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  • 92
    Gilead Sciences liposomal amphotericin b
    (A) Survival following 3 days of monotherapy or concomitant therapy with <t>liposomal</t> <t>amphotericin</t> B (“A”) and/or micafungin (“M”) in cyclophosphamide-immunosuppressed Swiss Webster mice infected i.v. with 5.2 × 10 4 A. fumigatus conidia/mouse. Beginning day 1 or day 4 postchallenge, the mice ( n = 7/group) were treated i.v. with D5W on days 1 to 6, 5 mg/kg micafungin on days 1 to 3, 5 mg/kg micafungin on days 4 to 6, 10 mg/kg liposomal amphotericin B on days 1 to 3, 10 mg/kg liposomal amphotericin B on days 4 to 6, 15 mg/kg liposomal amphotericin B on days 1 to 3, 15 mg/kg liposomal amphotericin B days 4 to 6, 5 mg/kg micafungin plus 10 mg/kg liposomal amphotericin B on days 1 to 3, or 5 mg/kg micafungin plus 15 mg/kg liposomal amphotericin B on days 1 to 3. All 3-day treatments initiated on day 1 versus D5W, P ≤ 0.005 for all comparisons. (B) Survival following 6 days of monotherapy or concomitant therapy with liposomal amphotericin B and/or micafungin. Beginning 24 h postchallenge, mice ( n = 7/group) were treated i.v. with D5W on days 1 to 6, 5 mg/kg micafungin on days 1 to 6, 10 mg/kg liposomal amphotericin B on days 1 to 6, 15 mg/kg liposomal amphotericin B on days 1 to 6, 5 mg/kg micafungin plus 10 mg/kg liposomal amphotericin B on days 1 to 6, or 5 mg/kg micafungin plus 15 mg/kg liposomal amphotericin B on days 1 to 6. All treatment groups versus D5W, P ≤ 0.003 for all comparisons. (C and D) Scatterplots of fungal burden (log 10 CFU per g) in the kidneys (C) and spleens (D) taken 24 h after the final dose in mice treated as described for panel A or B ( n = 7/group). Initiation of therapy on day 4 with 15 mg/kg liposomal amphotericin B versus D5W, P = 0.018 for kidney fungal burden; initiation of therapy on day 1, except for 5 mg/kg micafungin, versus D5W, P
    Liposomal Amphotericin B, supplied by Gilead Sciences, used in various techniques. Bioz Stars score: 92/100, based on 363 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Gilead Sciences bms
    (A) Survival following 3 days of monotherapy or concomitant therapy with <t>liposomal</t> <t>amphotericin</t> B (“A”) and/or micafungin (“M”) in cyclophosphamide-immunosuppressed Swiss Webster mice infected i.v. with 5.2 × 10 4 A. fumigatus conidia/mouse. Beginning day 1 or day 4 postchallenge, the mice ( n = 7/group) were treated i.v. with D5W on days 1 to 6, 5 mg/kg micafungin on days 1 to 3, 5 mg/kg micafungin on days 4 to 6, 10 mg/kg liposomal amphotericin B on days 1 to 3, 10 mg/kg liposomal amphotericin B on days 4 to 6, 15 mg/kg liposomal amphotericin B on days 1 to 3, 15 mg/kg liposomal amphotericin B days 4 to 6, 5 mg/kg micafungin plus 10 mg/kg liposomal amphotericin B on days 1 to 3, or 5 mg/kg micafungin plus 15 mg/kg liposomal amphotericin B on days 1 to 3. All 3-day treatments initiated on day 1 versus D5W, P ≤ 0.005 for all comparisons. (B) Survival following 6 days of monotherapy or concomitant therapy with liposomal amphotericin B and/or micafungin. Beginning 24 h postchallenge, mice ( n = 7/group) were treated i.v. with D5W on days 1 to 6, 5 mg/kg micafungin on days 1 to 6, 10 mg/kg liposomal amphotericin B on days 1 to 6, 15 mg/kg liposomal amphotericin B on days 1 to 6, 5 mg/kg micafungin plus 10 mg/kg liposomal amphotericin B on days 1 to 6, or 5 mg/kg micafungin plus 15 mg/kg liposomal amphotericin B on days 1 to 6. All treatment groups versus D5W, P ≤ 0.003 for all comparisons. (C and D) Scatterplots of fungal burden (log 10 CFU per g) in the kidneys (C) and spleens (D) taken 24 h after the final dose in mice treated as described for panel A or B ( n = 7/group). Initiation of therapy on day 4 with 15 mg/kg liposomal amphotericin B versus D5W, P = 0.018 for kidney fungal burden; initiation of therapy on day 1, except for 5 mg/kg micafungin, versus D5W, P
    Bms, supplied by Gilead Sciences, used in various techniques. Bioz Stars score: 92/100, based on 436 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Gilead Sciences msd
    (A) Survival following 3 days of monotherapy or concomitant therapy with <t>liposomal</t> <t>amphotericin</t> B (“A”) and/or micafungin (“M”) in cyclophosphamide-immunosuppressed Swiss Webster mice infected i.v. with 5.2 × 10 4 A. fumigatus conidia/mouse. Beginning day 1 or day 4 postchallenge, the mice ( n = 7/group) were treated i.v. with D5W on days 1 to 6, 5 mg/kg micafungin on days 1 to 3, 5 mg/kg micafungin on days 4 to 6, 10 mg/kg liposomal amphotericin B on days 1 to 3, 10 mg/kg liposomal amphotericin B on days 4 to 6, 15 mg/kg liposomal amphotericin B on days 1 to 3, 15 mg/kg liposomal amphotericin B days 4 to 6, 5 mg/kg micafungin plus 10 mg/kg liposomal amphotericin B on days 1 to 3, or 5 mg/kg micafungin plus 15 mg/kg liposomal amphotericin B on days 1 to 3. All 3-day treatments initiated on day 1 versus D5W, P ≤ 0.005 for all comparisons. (B) Survival following 6 days of monotherapy or concomitant therapy with liposomal amphotericin B and/or micafungin. Beginning 24 h postchallenge, mice ( n = 7/group) were treated i.v. with D5W on days 1 to 6, 5 mg/kg micafungin on days 1 to 6, 10 mg/kg liposomal amphotericin B on days 1 to 6, 15 mg/kg liposomal amphotericin B on days 1 to 6, 5 mg/kg micafungin plus 10 mg/kg liposomal amphotericin B on days 1 to 6, or 5 mg/kg micafungin plus 15 mg/kg liposomal amphotericin B on days 1 to 6. All treatment groups versus D5W, P ≤ 0.003 for all comparisons. (C and D) Scatterplots of fungal burden (log 10 CFU per g) in the kidneys (C) and spleens (D) taken 24 h after the final dose in mice treated as described for panel A or B ( n = 7/group). Initiation of therapy on day 4 with 15 mg/kg liposomal amphotericin B versus D5W, P = 0.018 for kidney fungal burden; initiation of therapy on day 1, except for 5 mg/kg micafungin, versus D5W, P
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    Gilead Sciences tenofovir
    Proposed model of <t>tenofovir's</t> effects on virus replication. (A) Without drug treatment, virulent virus can replicate to high titers because of high infection rates of CD4 + -T-helper cells and antigen-presenting cells and insufficient CD8 + -cell-mediated immune responses. (B) Tenofovir acts (i) as an inhibitor of RT, reducing the number of CD4 + -T-helper cells and antigen-presenting cells that become newly infected and (ii) possibly also as an immunomodulator. Potent CD8 + -cell-mediated immune responses help to reduce the half-life ( T 1/2 ) and thus the burst of viral progeny for those cells that became infected. Both tenofovir and antiviral CD8 + cells are required to induce and maintain low viremia. The role of the CD8 + cells becomes even more pronounced after the emergence of drug-resistant K65R viral mutants. (C) During artificial CD8 + -cell depletion, productively infected cells survive longer and produce more progeny virus, resulting in an increase in viremia.
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    Gilead Sciences ledipasvir sofosbuvir
    Lichen planus. Photographs taken 6 months before initiation of therapy ( left ) and 1 month after initiation of <t>ledipasvir-sofosbuvir</t> ( right ) show marked visible improvement of cutaneous lesions.
    Ledipasvir Sofosbuvir, supplied by Gilead Sciences, used in various techniques. Bioz Stars score: 91/100, based on 122 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Gilead Sciences sofosbuvir
    HCV genotype 1-specific virologic response of <t>sofosbuvir</t>
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    Gilead Sciences covid 19
    SARS-COV-2 virus binding ACE2 and the renin-angiotensin system axis. Top left shows the virus structure identifying protruding surface spike proteins (enlarged to show S1 and S2 segments with the Receptor Binding Domain (RBD)), the most abundant Membrane protein, the Envelope protein that forms a simple multimeric ion channel, and the Nucleocapsid protein with the bound positive sense single strand (ss) RNA. Below: Furin pre-cleaves spike proteins at the S1/S2 site and promotes subsequent TMPRSS2-dependent entry into host cells. The RBD in the S1 segment binds with high affinity the protease domain (PD) in ACE2. Subsequent conformational changes in S2 facilitate fusion between the viral envelope and the host cell membrane, and internalization by endocytosis with ACE2. Ang II-AT-1 receptor activation of ADAM17 cleaves/sheds cell surface ACE2 which can no longer cleave Ang II or Ang I to protective peptides (Ang (1-9) and Ang (1-7)), resulting in myocardial dysfunction. This action is blocked by AT-1 receptor blockers upregulating ACE2 levels. The AT-1 receptor-mediated effects are opposite to that of Mas and MrgD (not shown) receptors. The catalytic subunit of ACE2 is independent of PD and may operate as long as ACE2 is not internalized. The protective axis comprising of recombinant ACE2, Ang (1–7), Mas receptor agonists, and RAS inhibitors enhance ACE2 action and serve as potential therapies in <t>Covid-19.</t> In addition, ACE inhibitors prevent the metabolism of Ang (1-7) by ACE to the inactive metabolite Ang (1-5) (see Table 1 ).
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    Gilead Sciences sof ldv
    Longitudinal changes in serum total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglyceride during and after the treatment in <t>SOF</t> + <t>LDV-SVR</t> group. Mean value of serum TC, LDL-C, HDL-C, TG at baseline (0W), 4 wk (4W), 8 wk (8W), 12 wk (12W) of SOF + LDV treatment and 4 wk (P4W), and 12 wk (12W) after the end of SOF + LDV treatment was plotted. Vertical line expressed the range of mean ± SD. Statistical significance from baseline was indicated at upper part of each graph. Statistical significance at P4W and P12W compared to the end of therapy was indicated at the lower part of each graph ( b P
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    Gilead Sciences echosens
    Longitudinal changes in serum total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglyceride during and after the treatment in <t>SOF</t> + <t>LDV-SVR</t> group. Mean value of serum TC, LDL-C, HDL-C, TG at baseline (0W), 4 wk (4W), 8 wk (8W), 12 wk (12W) of SOF + LDV treatment and 4 wk (P4W), and 12 wk (12W) after the end of SOF + LDV treatment was plotted. Vertical line expressed the range of mean ± SD. Statistical significance from baseline was indicated at upper part of each graph. Statistical significance at P4W and P12W compared to the end of therapy was indicated at the lower part of each graph ( b P
    Echosens, supplied by Gilead Sciences, used in various techniques. Bioz Stars score: 90/100, based on 25 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Gilead Sciences remdesivir
    The structures of sofosbuvir ( 1 ) and <t>remdesivir</t> ( 2 ).
    Remdesivir, supplied by Gilead Sciences, used in various techniques. Bioz Stars score: 93/100, based on 44 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Gilead Sciences emtricitabine
    Univariate linear regression analyses are shown for the dependent variable Ln (cerebrospinal fluid [CSF] <t>emtricitabine</t> [FTC] concentration) and significant predictor variables a ) Ln (Plasma FTC concentration) was a significant predictor of Ln (CSF FTC concentration), R 2 = 0.7, p
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    Gilead Sciences research grants
    Univariate linear regression analyses are shown for the dependent variable Ln (cerebrospinal fluid [CSF] <t>emtricitabine</t> [FTC] concentration) and significant predictor variables a ) Ln (Plasma FTC concentration) was a significant predictor of Ln (CSF FTC concentration), R 2 = 0.7, p
    Research Grants, supplied by Gilead Sciences, used in various techniques. Bioz Stars score: 92/100, based on 54 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Gilead Sciences cidofovir
    Representative chromatogram of cyclic <t>cidofovir</t> prodrugs (a) B-C2-cCDF, (b) B-C6–cCDF, (c) B-C12–cCDF, (d) C6-cCDF, and (e) C12-cCDF.
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    Gilead Sciences tenofovir alafenamide
    Median (IQR) <t>tenofovir</t> and tenofovir-dp in blood plasma and PBMCs following a single dose of tenofovir <t>alafenamide.</t> Tenofovir over 14 days in plasma (a) and tenofovir-dp in PBMCs (b). Plot inserts depict concentrations over 24 h for each matrix. Concentration values BLQ were imputed at half the LLOQ for graphing purposes. Broken horizontal lines represent the LLOQ. At least 32% of plasma samples had unquantifiable tenofovir and at least 8% of PBMC samples had unquantifiable tenofovir-dp. Percentage of samples that were BLQ at each sampling time is tabulated below each graph. TAF, tenofovir alafenamide.
    Tenofovir Alafenamide, supplied by Gilead Sciences, used in various techniques. Bioz Stars score: 90/100, based on 56 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Gilead Sciences sofosbuvir velpatasvir
    Median (IQR) <t>tenofovir</t> and tenofovir-dp in blood plasma and PBMCs following a single dose of tenofovir <t>alafenamide.</t> Tenofovir over 14 days in plasma (a) and tenofovir-dp in PBMCs (b). Plot inserts depict concentrations over 24 h for each matrix. Concentration values BLQ were imputed at half the LLOQ for graphing purposes. Broken horizontal lines represent the LLOQ. At least 32% of plasma samples had unquantifiable tenofovir and at least 8% of PBMC samples had unquantifiable tenofovir-dp. Percentage of samples that were BLQ at each sampling time is tabulated below each graph. TAF, tenofovir alafenamide.
    Sofosbuvir Velpatasvir, supplied by Gilead Sciences, used in various techniques. Bioz Stars score: 91/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Gilead Sciences stock shareholder
    Median (IQR) <t>tenofovir</t> and tenofovir-dp in blood plasma and PBMCs following a single dose of tenofovir <t>alafenamide.</t> Tenofovir over 14 days in plasma (a) and tenofovir-dp in PBMCs (b). Plot inserts depict concentrations over 24 h for each matrix. Concentration values BLQ were imputed at half the LLOQ for graphing purposes. Broken horizontal lines represent the LLOQ. At least 32% of plasma samples had unquantifiable tenofovir and at least 8% of PBMC samples had unquantifiable tenofovir-dp. Percentage of samples that were BLQ at each sampling time is tabulated below each graph. TAF, tenofovir alafenamide.
    Stock Shareholder, supplied by Gilead Sciences, used in various techniques. Bioz Stars score: 95/100, based on 81 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Gilead Sciences nih
    Median (IQR) <t>tenofovir</t> and tenofovir-dp in blood plasma and PBMCs following a single dose of tenofovir <t>alafenamide.</t> Tenofovir over 14 days in plasma (a) and tenofovir-dp in PBMCs (b). Plot inserts depict concentrations over 24 h for each matrix. Concentration values BLQ were imputed at half the LLOQ for graphing purposes. Broken horizontal lines represent the LLOQ. At least 32% of plasma samples had unquantifiable tenofovir and at least 8% of PBMC samples had unquantifiable tenofovir-dp. Percentage of samples that were BLQ at each sampling time is tabulated below each graph. TAF, tenofovir alafenamide.
    Nih, supplied by Gilead Sciences, used in various techniques. Bioz Stars score: 92/100, based on 50 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Gilead Sciences tibotec
    Median (IQR) <t>tenofovir</t> and tenofovir-dp in blood plasma and PBMCs following a single dose of tenofovir <t>alafenamide.</t> Tenofovir over 14 days in plasma (a) and tenofovir-dp in PBMCs (b). Plot inserts depict concentrations over 24 h for each matrix. Concentration values BLQ were imputed at half the LLOQ for graphing purposes. Broken horizontal lines represent the LLOQ. At least 32% of plasma samples had unquantifiable tenofovir and at least 8% of PBMC samples had unquantifiable tenofovir-dp. Percentage of samples that were BLQ at each sampling time is tabulated below each graph. TAF, tenofovir alafenamide.
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    Gilead Sciences tdf ftc
    Mean plasma concentration vs . time on day 14 for (A) tenofovir disoproxil fumarate <t>(TDF)</t> and (B) emtricitabine <t>(FTC)</t> each alone and with GSK2248761. (A) TDF ( ); TDF + GSK2248761 ( ). (B) FTC ( ); FTC + GSK2248761 ( )
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    Gilead Sciences truvada
    Mean plasma concentration vs . time on day 14 for (A) tenofovir disoproxil fumarate <t>(TDF)</t> and (B) emtricitabine <t>(FTC)</t> each alone and with GSK2248761. (A) TDF ( ); TDF + GSK2248761 ( ). (B) FTC ( ); FTC + GSK2248761 ( )
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    Gilead Sciences ask1
    Western blots and densitometric analysis of p-JNK translocation to the mitochondria at 6 h. Mice were treated with 30 mg/kg <t>ASK1</t> inhibitor GS-459679 or the vehicle (55% PEG in water) 30 min before 300 mg/kg APAP injection. Western blotting was performed
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    Gilead Sciences adefovir dipivoxil
    Analysis of Th1/Th2 cytokine producing CD3+CD4+ cells at <t>adefovir</t> <t>dipivoxil</t> treatment week (TW) between mutation and no mutation.
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    Gilead Sciences tenofovir gel
    Longitudinal analyses of NK cell activated ADCC (antibody-specific- %CD107a + cells [Log10]) in the plasma and GT (CVL) of women at 3 months, 6 months and 12 months, for the <t>tenofovir</t> and placebo arms for gp41. Analyses for cytotoxic activities (gp41-specific %CD107a + cells [Log10]) in the plasma on the left (A) for gp41 and the genital tract on the right to (B) for gp41. Solid lines indicate the minimum and maximum values of box and whisker plots, with black solid lines across the dots indicate the median at each time point for each study arm. Wilcoxon signed-rank tests were done to determine statistical differences between NK cell activated ADCC activities within each arm of the study, for each protein. Statistically significant values were defined as p
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    Gilead Sciences research funding
    Longitudinal analyses of NK cell activated ADCC (antibody-specific- %CD107a + cells [Log10]) in the plasma and GT (CVL) of women at 3 months, 6 months and 12 months, for the <t>tenofovir</t> and placebo arms for gp41. Analyses for cytotoxic activities (gp41-specific %CD107a + cells [Log10]) in the plasma on the left (A) for gp41 and the genital tract on the right to (B) for gp41. Solid lines indicate the minimum and maximum values of box and whisker plots, with black solid lines across the dots indicate the median at each time point for each study arm. Wilcoxon signed-rank tests were done to determine statistical differences between NK cell activated ADCC activities within each arm of the study, for each protein. Statistically significant values were defined as p
    Research Funding, supplied by Gilead Sciences, used in various techniques. Bioz Stars score: 93/100, based on 50 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Gilead Sciences ic87114
    Attenuation of cockroach antigen (CRA)-induced airway inflammation in a mouse model by inhibiting PI3K p110δ activity. A : recruitment of total inflammatory cells to the airways determined by microscopic evaluation of Hema 3-stained cytocentrifuged slides of bronchoalveolar lavage fluid (BALF) in control and CRA-exposed mice treated with <t>IC87114</t> (50 mg/kg) or vehicle alone (PEG-400). B and C : cellular infiltration of lung tissue after hematoxylin and eosin staining of paraformaldehyde-fixed lung sections (representative images are shown at magnification ×200) and scoring of peribronchial inflammation. Combined data from 2 experiments are shown in C . n = 7–9 mice/group. D : differential cell counts in BALF of control and CRA-exposed mice treated with IC87114 or vehicle alone. Eos, eosinophils; Monos, monocytes and macrophages; Neu, neutrophils; Lymphs, lymphocytes. Combined data from experiments repeated at least 3 times are shown in A and D . n = 6 mice for control group and 13–17 mice for CRA-exposed groups. E and F : infiltration of lung tissue by eosinophils after staining with rat mAb against murine major basic protein (MBP). Representative images are shown in E . Magnification ×200. MBP-positive cells in 5–6 randomly selected nonoverlapping microscopic fields were counted at magnification of ×400. Combined data from 2 experiments are shown in F . n = 4 mice for control group and 7 for CRA-exposed groups. G : airway hyperresponsiveness (AHR) assessed by whole body plethysmography in control and CRA-exposed mice treated with IC87114 or vehicle alone. The enhanced pause (PenH) in breathing when exposed to increasing amounts of nebulized methacholine (MCh) after initial exposure to saline was monitored. Combined data from 2 experiments are shown. n = 5 mice for control group and 6–10 mice for CRA-exposed groups. Data represent means ± SE in A , C , D , F , and G . * P
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    (A) Survival following 3 days of monotherapy or concomitant therapy with liposomal amphotericin B (“A”) and/or micafungin (“M”) in cyclophosphamide-immunosuppressed Swiss Webster mice infected i.v. with 5.2 × 10 4 A. fumigatus conidia/mouse. Beginning day 1 or day 4 postchallenge, the mice ( n = 7/group) were treated i.v. with D5W on days 1 to 6, 5 mg/kg micafungin on days 1 to 3, 5 mg/kg micafungin on days 4 to 6, 10 mg/kg liposomal amphotericin B on days 1 to 3, 10 mg/kg liposomal amphotericin B on days 4 to 6, 15 mg/kg liposomal amphotericin B on days 1 to 3, 15 mg/kg liposomal amphotericin B days 4 to 6, 5 mg/kg micafungin plus 10 mg/kg liposomal amphotericin B on days 1 to 3, or 5 mg/kg micafungin plus 15 mg/kg liposomal amphotericin B on days 1 to 3. All 3-day treatments initiated on day 1 versus D5W, P ≤ 0.005 for all comparisons. (B) Survival following 6 days of monotherapy or concomitant therapy with liposomal amphotericin B and/or micafungin. Beginning 24 h postchallenge, mice ( n = 7/group) were treated i.v. with D5W on days 1 to 6, 5 mg/kg micafungin on days 1 to 6, 10 mg/kg liposomal amphotericin B on days 1 to 6, 15 mg/kg liposomal amphotericin B on days 1 to 6, 5 mg/kg micafungin plus 10 mg/kg liposomal amphotericin B on days 1 to 6, or 5 mg/kg micafungin plus 15 mg/kg liposomal amphotericin B on days 1 to 6. All treatment groups versus D5W, P ≤ 0.003 for all comparisons. (C and D) Scatterplots of fungal burden (log 10 CFU per g) in the kidneys (C) and spleens (D) taken 24 h after the final dose in mice treated as described for panel A or B ( n = 7/group). Initiation of therapy on day 4 with 15 mg/kg liposomal amphotericin B versus D5W, P = 0.018 for kidney fungal burden; initiation of therapy on day 1, except for 5 mg/kg micafungin, versus D5W, P

    Journal: Antimicrobial Agents and Chemotherapy

    Article Title: Liposomal Amphotericin B and Echinocandins as Monotherapy or Sequential or Concomitant Therapy in Murine Disseminated and Pulmonary Aspergillus fumigatus Infections ▿

    doi: 10.1128/AAC.01554-09

    Figure Lengend Snippet: (A) Survival following 3 days of monotherapy or concomitant therapy with liposomal amphotericin B (“A”) and/or micafungin (“M”) in cyclophosphamide-immunosuppressed Swiss Webster mice infected i.v. with 5.2 × 10 4 A. fumigatus conidia/mouse. Beginning day 1 or day 4 postchallenge, the mice ( n = 7/group) were treated i.v. with D5W on days 1 to 6, 5 mg/kg micafungin on days 1 to 3, 5 mg/kg micafungin on days 4 to 6, 10 mg/kg liposomal amphotericin B on days 1 to 3, 10 mg/kg liposomal amphotericin B on days 4 to 6, 15 mg/kg liposomal amphotericin B on days 1 to 3, 15 mg/kg liposomal amphotericin B days 4 to 6, 5 mg/kg micafungin plus 10 mg/kg liposomal amphotericin B on days 1 to 3, or 5 mg/kg micafungin plus 15 mg/kg liposomal amphotericin B on days 1 to 3. All 3-day treatments initiated on day 1 versus D5W, P ≤ 0.005 for all comparisons. (B) Survival following 6 days of monotherapy or concomitant therapy with liposomal amphotericin B and/or micafungin. Beginning 24 h postchallenge, mice ( n = 7/group) were treated i.v. with D5W on days 1 to 6, 5 mg/kg micafungin on days 1 to 6, 10 mg/kg liposomal amphotericin B on days 1 to 6, 15 mg/kg liposomal amphotericin B on days 1 to 6, 5 mg/kg micafungin plus 10 mg/kg liposomal amphotericin B on days 1 to 6, or 5 mg/kg micafungin plus 15 mg/kg liposomal amphotericin B on days 1 to 6. All treatment groups versus D5W, P ≤ 0.003 for all comparisons. (C and D) Scatterplots of fungal burden (log 10 CFU per g) in the kidneys (C) and spleens (D) taken 24 h after the final dose in mice treated as described for panel A or B ( n = 7/group). Initiation of therapy on day 4 with 15 mg/kg liposomal amphotericin B versus D5W, P = 0.018 for kidney fungal burden; initiation of therapy on day 1, except for 5 mg/kg micafungin, versus D5W, P

    Article Snippet: Twenty-four hours later, intravenous drug therapy with one of the following agents was initiated ( n = 12/group) and continued for 3 or 6 days: liposomal amphotericin B (5, 10, or 15 mg/kg), micafungin (5, 10, or 15 mg/kg), caspofungin (5 mg/kg), or 5% dextrose (D5W; controls).

    Techniques: Mouse Assay, Infection

    (A) Survival following 6 days of monotherapy or concomitant therapy with liposomal amphotericin B (“A”) and/or caspofungin (“C”) in cyclophosphamide-immunosuppressed Swiss Webster mice infected i.v. with 5.3 × 10 4 A. fumigatus conidia/mouse. Beginning 24 h postchallenge, the mice ( n = 7/group) were treated i.v. with D5W on days 1 to 6, 10 mg/kg liposomal amphotericin B on days 1 to 6, 15 mg/kg liposomal amphotericin B on days 1 to 6, 5 mg/kg caspofungin on days 1 to 6, 5 mg/kg caspofungin plus 10 mg/kg liposomal amphotericin B on days 1 to 6, or 5 mg/kg caspofungin plus 15 mg/kg liposomal amphotericin B on days 1 to 6. All treatment groups versus D5W, P ≤ 0.001. (B and C) Scatterplots of fungal burden (log 10 CFU per g) in the kidneys (B) or spleens (C) taken 24 h after the final dose in mice treated as described for panel A ( n = 7/group). Five or 10 mg/kg liposomal amphotericin B versus caspofungin or D5W, P = 0.002 and P

    Journal: Antimicrobial Agents and Chemotherapy

    Article Title: Liposomal Amphotericin B and Echinocandins as Monotherapy or Sequential or Concomitant Therapy in Murine Disseminated and Pulmonary Aspergillus fumigatus Infections ▿

    doi: 10.1128/AAC.01554-09

    Figure Lengend Snippet: (A) Survival following 6 days of monotherapy or concomitant therapy with liposomal amphotericin B (“A”) and/or caspofungin (“C”) in cyclophosphamide-immunosuppressed Swiss Webster mice infected i.v. with 5.3 × 10 4 A. fumigatus conidia/mouse. Beginning 24 h postchallenge, the mice ( n = 7/group) were treated i.v. with D5W on days 1 to 6, 10 mg/kg liposomal amphotericin B on days 1 to 6, 15 mg/kg liposomal amphotericin B on days 1 to 6, 5 mg/kg caspofungin on days 1 to 6, 5 mg/kg caspofungin plus 10 mg/kg liposomal amphotericin B on days 1 to 6, or 5 mg/kg caspofungin plus 15 mg/kg liposomal amphotericin B on days 1 to 6. All treatment groups versus D5W, P ≤ 0.001. (B and C) Scatterplots of fungal burden (log 10 CFU per g) in the kidneys (B) or spleens (C) taken 24 h after the final dose in mice treated as described for panel A ( n = 7/group). Five or 10 mg/kg liposomal amphotericin B versus caspofungin or D5W, P = 0.002 and P

    Article Snippet: Twenty-four hours later, intravenous drug therapy with one of the following agents was initiated ( n = 12/group) and continued for 3 or 6 days: liposomal amphotericin B (5, 10, or 15 mg/kg), micafungin (5, 10, or 15 mg/kg), caspofungin (5 mg/kg), or 5% dextrose (D5W; controls).

    Techniques: Mouse Assay, Infection

    Survival following 3 or 6 days of monotherapy (A) or 6 days of sequential therapy (B) with liposomal amphotericin B (“A”) and/or caspofungin (“C”) in cyclophosphamide-immunosuppressed Swiss Webster mice infected i.v. with 5.3 × 10 4 A. fumigatus conidia/mouse. Beginning 24 h postchallenge, the mice ( n = 7/group) were treated i.v. as follows. (A) Monotherapy with D5W on days 1 to 6, 5 mg/kg caspofungin on days 1 to 3, 5 mg/kg caspofungin on days 1 to 6, 10 mg/kg liposomal amphotericin B on days 1 to 3, 10 mg/kg liposomal amphotericin B on days 1 to 6, 15 mg/kg liposomal amphotericin B on days 1 to 3, or 15 mg/kg liposomal amphotericin B on days 1 to 6. Ten or 15 mg/kg liposomal amphotericin B or 5 mg/kg caspofungin on days 1 to 3 versus D5W, P ≤ 0.002; 10 or 15 mg/kg liposomal amphotericin B versus 5 mg/kg caspofungin on days 1 to 6, P = 0.02. (B) Sequential therapy with 5 mg/kg caspofungin on days 1 to 3, and 10 mg/kg liposomal amphotericin B on days 4 to 6; 5 mg/kg caspofungin on days 1 to 3 and 15 mg/kg liposomal amphotericin B on days 4 to 6; 10 mg/kg liposomal amphotericin B on days 1 to 3 and 5 mg/kg caspofungin on days 4 to 6; or 15 mg/kg liposomal amphotericin B on days 1 to 3 and 5 mg/kg caspofungin on days 4 to 6. Combinations versus D5W, P ≤ 0.001; 10 or 15 mg/kg liposomal amphotericin B followed by 5 mg/kg caspofungin versus 5 mg/kg caspofungin on days 1 to 6, P = 0.02. (C and E) Scatterplots of fungal burden (log 10 CFU per g) in kidneys (C) and spleen (E) taken 24 h after the final dose in mice ( n = 7/group) treated as described for panels A and B. (C) For kidney fungal burden, liposomal amphotericin B monotherapies, sequential therapies beginning with liposomal amphotericin B, or 5 mg/kg caspofungin followed by 15 mg/kg liposomal amphotericin B versus D5W, P

    Journal: Antimicrobial Agents and Chemotherapy

    Article Title: Liposomal Amphotericin B and Echinocandins as Monotherapy or Sequential or Concomitant Therapy in Murine Disseminated and Pulmonary Aspergillus fumigatus Infections ▿

    doi: 10.1128/AAC.01554-09

    Figure Lengend Snippet: Survival following 3 or 6 days of monotherapy (A) or 6 days of sequential therapy (B) with liposomal amphotericin B (“A”) and/or caspofungin (“C”) in cyclophosphamide-immunosuppressed Swiss Webster mice infected i.v. with 5.3 × 10 4 A. fumigatus conidia/mouse. Beginning 24 h postchallenge, the mice ( n = 7/group) were treated i.v. as follows. (A) Monotherapy with D5W on days 1 to 6, 5 mg/kg caspofungin on days 1 to 3, 5 mg/kg caspofungin on days 1 to 6, 10 mg/kg liposomal amphotericin B on days 1 to 3, 10 mg/kg liposomal amphotericin B on days 1 to 6, 15 mg/kg liposomal amphotericin B on days 1 to 3, or 15 mg/kg liposomal amphotericin B on days 1 to 6. Ten or 15 mg/kg liposomal amphotericin B or 5 mg/kg caspofungin on days 1 to 3 versus D5W, P ≤ 0.002; 10 or 15 mg/kg liposomal amphotericin B versus 5 mg/kg caspofungin on days 1 to 6, P = 0.02. (B) Sequential therapy with 5 mg/kg caspofungin on days 1 to 3, and 10 mg/kg liposomal amphotericin B on days 4 to 6; 5 mg/kg caspofungin on days 1 to 3 and 15 mg/kg liposomal amphotericin B on days 4 to 6; 10 mg/kg liposomal amphotericin B on days 1 to 3 and 5 mg/kg caspofungin on days 4 to 6; or 15 mg/kg liposomal amphotericin B on days 1 to 3 and 5 mg/kg caspofungin on days 4 to 6. Combinations versus D5W, P ≤ 0.001; 10 or 15 mg/kg liposomal amphotericin B followed by 5 mg/kg caspofungin versus 5 mg/kg caspofungin on days 1 to 6, P = 0.02. (C and E) Scatterplots of fungal burden (log 10 CFU per g) in kidneys (C) and spleen (E) taken 24 h after the final dose in mice ( n = 7/group) treated as described for panels A and B. (C) For kidney fungal burden, liposomal amphotericin B monotherapies, sequential therapies beginning with liposomal amphotericin B, or 5 mg/kg caspofungin followed by 15 mg/kg liposomal amphotericin B versus D5W, P

    Article Snippet: Twenty-four hours later, intravenous drug therapy with one of the following agents was initiated ( n = 12/group) and continued for 3 or 6 days: liposomal amphotericin B (5, 10, or 15 mg/kg), micafungin (5, 10, or 15 mg/kg), caspofungin (5 mg/kg), or 5% dextrose (D5W; controls).

    Techniques: Mouse Assay, Infection

    Proposed model of tenofovir's effects on virus replication. (A) Without drug treatment, virulent virus can replicate to high titers because of high infection rates of CD4 + -T-helper cells and antigen-presenting cells and insufficient CD8 + -cell-mediated immune responses. (B) Tenofovir acts (i) as an inhibitor of RT, reducing the number of CD4 + -T-helper cells and antigen-presenting cells that become newly infected and (ii) possibly also as an immunomodulator. Potent CD8 + -cell-mediated immune responses help to reduce the half-life ( T 1/2 ) and thus the burst of viral progeny for those cells that became infected. Both tenofovir and antiviral CD8 + cells are required to induce and maintain low viremia. The role of the CD8 + cells becomes even more pronounced after the emergence of drug-resistant K65R viral mutants. (C) During artificial CD8 + -cell depletion, productively infected cells survive longer and produce more progeny virus, resulting in an increase in viremia.

    Journal: Journal of Virology

    Article Title: CD8+-Cell-Mediated Suppression of Virulent Simian Immunodeficiency Virus during Tenofovir Treatment

    doi: 10.1128/JVI.78.10.5324-5337.2004

    Figure Lengend Snippet: Proposed model of tenofovir's effects on virus replication. (A) Without drug treatment, virulent virus can replicate to high titers because of high infection rates of CD4 + -T-helper cells and antigen-presenting cells and insufficient CD8 + -cell-mediated immune responses. (B) Tenofovir acts (i) as an inhibitor of RT, reducing the number of CD4 + -T-helper cells and antigen-presenting cells that become newly infected and (ii) possibly also as an immunomodulator. Potent CD8 + -cell-mediated immune responses help to reduce the half-life ( T 1/2 ) and thus the burst of viral progeny for those cells that became infected. Both tenofovir and antiviral CD8 + cells are required to induce and maintain low viremia. The role of the CD8 + cells becomes even more pronounced after the emergence of drug-resistant K65R viral mutants. (C) During artificial CD8 + -cell depletion, productively infected cells survive longer and produce more progeny virus, resulting in an increase in viremia.

    Article Snippet: Tenofovir (Gilead Sciences) was suspended in distilled water, dissolved by the addition of NaOH to a final pH of 7.0 at 60 mg/ml, filter sterilized (0.2-μm pore size; Nalgene), and stored at 4°C.

    Techniques: Infection

    Lichen planus. Photographs taken 6 months before initiation of therapy ( left ) and 1 month after initiation of ledipasvir-sofosbuvir ( right ) show marked visible improvement of cutaneous lesions.

    Journal: JAAD Case Reports

    Article Title: Treatment with ledipasvir-sofosbuvir for hepatitis C resulting in improvement of lichen planus

    doi: 10.1016/j.jdcr.2016.12.005

    Figure Lengend Snippet: Lichen planus. Photographs taken 6 months before initiation of therapy ( left ) and 1 month after initiation of ledipasvir-sofosbuvir ( right ) show marked visible improvement of cutaneous lesions.

    Article Snippet: Albeit temporary, to our knowledge, this is the first reported case of LP improving after the use of ledipasvir-sofosbuvir and may pave the way for potential future therapies for the cutaneous manifestation.

    Techniques:

    HCV genotype 1-specific virologic response of sofosbuvir

    Journal: World Journal of Hepatology

    Article Title: Sofosbuvir treatment and hepatitis C virus infection

    doi: 10.4254/wjh.v8.i3.183

    Figure Lengend Snippet: HCV genotype 1-specific virologic response of sofosbuvir

    Article Snippet: Sofosbuvir (formerly known as GS-7977; Gilead Sciences, Foster City, CA, United States) is a nucleotide NS5B inhibitor[ ].

    Techniques:

    HCV genotype 3-specific virologic response of sofosbuvir

    Journal: World Journal of Hepatology

    Article Title: Sofosbuvir treatment and hepatitis C virus infection

    doi: 10.4254/wjh.v8.i3.183

    Figure Lengend Snippet: HCV genotype 3-specific virologic response of sofosbuvir

    Article Snippet: Sofosbuvir (formerly known as GS-7977; Gilead Sciences, Foster City, CA, United States) is a nucleotide NS5B inhibitor[ ].

    Techniques:

    HCV genotype 2-specific virologic response of sofosbuvir

    Journal: World Journal of Hepatology

    Article Title: Sofosbuvir treatment and hepatitis C virus infection

    doi: 10.4254/wjh.v8.i3.183

    Figure Lengend Snippet: HCV genotype 2-specific virologic response of sofosbuvir

    Article Snippet: Sofosbuvir (formerly known as GS-7977; Gilead Sciences, Foster City, CA, United States) is a nucleotide NS5B inhibitor[ ].

    Techniques:

    SARS-COV-2 virus binding ACE2 and the renin-angiotensin system axis. Top left shows the virus structure identifying protruding surface spike proteins (enlarged to show S1 and S2 segments with the Receptor Binding Domain (RBD)), the most abundant Membrane protein, the Envelope protein that forms a simple multimeric ion channel, and the Nucleocapsid protein with the bound positive sense single strand (ss) RNA. Below: Furin pre-cleaves spike proteins at the S1/S2 site and promotes subsequent TMPRSS2-dependent entry into host cells. The RBD in the S1 segment binds with high affinity the protease domain (PD) in ACE2. Subsequent conformational changes in S2 facilitate fusion between the viral envelope and the host cell membrane, and internalization by endocytosis with ACE2. Ang II-AT-1 receptor activation of ADAM17 cleaves/sheds cell surface ACE2 which can no longer cleave Ang II or Ang I to protective peptides (Ang (1-9) and Ang (1-7)), resulting in myocardial dysfunction. This action is blocked by AT-1 receptor blockers upregulating ACE2 levels. The AT-1 receptor-mediated effects are opposite to that of Mas and MrgD (not shown) receptors. The catalytic subunit of ACE2 is independent of PD and may operate as long as ACE2 is not internalized. The protective axis comprising of recombinant ACE2, Ang (1–7), Mas receptor agonists, and RAS inhibitors enhance ACE2 action and serve as potential therapies in Covid-19. In addition, ACE inhibitors prevent the metabolism of Ang (1-7) by ACE to the inactive metabolite Ang (1-5) (see Table 1 ).

    Journal: Cellular Signalling

    Article Title: Drugs targeting various stages of the SARS-CoV-2 life cycle: Exploring promising drugs for the treatment of Covid-19

    doi: 10.1016/j.cellsig.2020.109721

    Figure Lengend Snippet: SARS-COV-2 virus binding ACE2 and the renin-angiotensin system axis. Top left shows the virus structure identifying protruding surface spike proteins (enlarged to show S1 and S2 segments with the Receptor Binding Domain (RBD)), the most abundant Membrane protein, the Envelope protein that forms a simple multimeric ion channel, and the Nucleocapsid protein with the bound positive sense single strand (ss) RNA. Below: Furin pre-cleaves spike proteins at the S1/S2 site and promotes subsequent TMPRSS2-dependent entry into host cells. The RBD in the S1 segment binds with high affinity the protease domain (PD) in ACE2. Subsequent conformational changes in S2 facilitate fusion between the viral envelope and the host cell membrane, and internalization by endocytosis with ACE2. Ang II-AT-1 receptor activation of ADAM17 cleaves/sheds cell surface ACE2 which can no longer cleave Ang II or Ang I to protective peptides (Ang (1-9) and Ang (1-7)), resulting in myocardial dysfunction. This action is blocked by AT-1 receptor blockers upregulating ACE2 levels. The AT-1 receptor-mediated effects are opposite to that of Mas and MrgD (not shown) receptors. The catalytic subunit of ACE2 is independent of PD and may operate as long as ACE2 is not internalized. The protective axis comprising of recombinant ACE2, Ang (1–7), Mas receptor agonists, and RAS inhibitors enhance ACE2 action and serve as potential therapies in Covid-19. In addition, ACE inhibitors prevent the metabolism of Ang (1-7) by ACE to the inactive metabolite Ang (1-5) (see Table 1 ).

    Article Snippet: At present, worldwide, more than 15 clinical trials in several phases are investigating the efficacy and safety of intravenous remdesivir for Covid-19.

    Techniques: Binding Assay, Activation Assay, Recombinant

    Longitudinal changes in serum total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglyceride during and after the treatment in SOF + LDV-SVR group. Mean value of serum TC, LDL-C, HDL-C, TG at baseline (0W), 4 wk (4W), 8 wk (8W), 12 wk (12W) of SOF + LDV treatment and 4 wk (P4W), and 12 wk (12W) after the end of SOF + LDV treatment was plotted. Vertical line expressed the range of mean ± SD. Statistical significance from baseline was indicated at upper part of each graph. Statistical significance at P4W and P12W compared to the end of therapy was indicated at the lower part of each graph ( b P

    Journal: World Journal of Gastroenterology

    Article Title: Impact of interferon-free antivirus therapy on lipid profiles in patients with chronic hepatitis C genotype 1b

    doi: 10.3748/wjg.v23.i13.2355

    Figure Lengend Snippet: Longitudinal changes in serum total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglyceride during and after the treatment in SOF + LDV-SVR group. Mean value of serum TC, LDL-C, HDL-C, TG at baseline (0W), 4 wk (4W), 8 wk (8W), 12 wk (12W) of SOF + LDV treatment and 4 wk (P4W), and 12 wk (12W) after the end of SOF + LDV treatment was plotted. Vertical line expressed the range of mean ± SD. Statistical significance from baseline was indicated at upper part of each graph. Statistical significance at P4W and P12W compared to the end of therapy was indicated at the lower part of each graph ( b P

    Article Snippet: That of SOF + LDV was oral administration of one tablet of combination drug (Harvoni® , Gilead sciences, California, United States) containing 400 mg of SOF and 90 mg of LDV once a day for 12 wk.

    Techniques:

    Differences in the ΔTC (A), ΔLDL-C (B) between DCV + ASV-SVR and SOF + LDV-SVR group. The mean value of the difference from the baseline value in TC and LDL-C was plotted. Vertical line expressed the range of mean ± SD. The difference of ΔTC and ΔLDL-C between DCV + ASV-SVR and SOF + LDV-SVR group at 4 wk (4W), 8 wk (8W), and 12 wk (12W) of treatment and 4 wk (P4W) and 12 wk (12W) after the end of treatment. Statistical significance of differences between DCV + ASV-SVR and SOF + LDV-SVR group at 4W, 8W, 12W, P4W, and P12W was expressed at the upper part of each graph ( e P

    Journal: World Journal of Gastroenterology

    Article Title: Impact of interferon-free antivirus therapy on lipid profiles in patients with chronic hepatitis C genotype 1b

    doi: 10.3748/wjg.v23.i13.2355

    Figure Lengend Snippet: Differences in the ΔTC (A), ΔLDL-C (B) between DCV + ASV-SVR and SOF + LDV-SVR group. The mean value of the difference from the baseline value in TC and LDL-C was plotted. Vertical line expressed the range of mean ± SD. The difference of ΔTC and ΔLDL-C between DCV + ASV-SVR and SOF + LDV-SVR group at 4 wk (4W), 8 wk (8W), and 12 wk (12W) of treatment and 4 wk (P4W) and 12 wk (12W) after the end of treatment. Statistical significance of differences between DCV + ASV-SVR and SOF + LDV-SVR group at 4W, 8W, 12W, P4W, and P12W was expressed at the upper part of each graph ( e P

    Article Snippet: That of SOF + LDV was oral administration of one tablet of combination drug (Harvoni® , Gilead sciences, California, United States) containing 400 mg of SOF and 90 mg of LDV once a day for 12 wk.

    Techniques:

    The structures of sofosbuvir ( 1 ) and remdesivir ( 2 ).

    Journal: Angewandte Chemie (International Ed. in English)

    Article Title: Thoughts on What Chemists Can Contribute to Fighting SARS‐CoV‐2 – A Short Note on Hand Sanitizers, Drug Candidates and Outreach

    doi: 10.1002/anie.202004721

    Figure Lengend Snippet: The structures of sofosbuvir ( 1 ) and remdesivir ( 2 ).

    Article Snippet: Remdesivir was developed by Gilead Sciences to combat Ebola and related filoviruses, but did not have sufficient activity against these targets.

    Techniques:

    Univariate linear regression analyses are shown for the dependent variable Ln (cerebrospinal fluid [CSF] emtricitabine [FTC] concentration) and significant predictor variables a ) Ln (Plasma FTC concentration) was a significant predictor of Ln (CSF FTC concentration), R 2 = 0.7, p

    Journal: Journal of clinical pharmacology

    Article Title: Cerebrospinal Fluid Concentrations of Tenofovir and Emtricitabine in the Setting of HIV-1 Protease Inhibitor-Based Regimens

    doi: 10.1002/jcph.612

    Figure Lengend Snippet: Univariate linear regression analyses are shown for the dependent variable Ln (cerebrospinal fluid [CSF] emtricitabine [FTC] concentration) and significant predictor variables a ) Ln (Plasma FTC concentration) was a significant predictor of Ln (CSF FTC concentration), R 2 = 0.7, p

    Article Snippet: Emtricitabine [package insert] Foster City, CA: Gilead Sciences, Inc; 2012.

    Techniques: Concentration Assay

    Representative chromatogram of cyclic cidofovir prodrugs (a) B-C2-cCDF, (b) B-C6–cCDF, (c) B-C12–cCDF, (d) C6-cCDF, and (e) C12-cCDF.

    Journal: Journal of pharmaceutical sciences

    Article Title: Transporter-Targeted Lipid Prodrugs of Cyclic Cidofovir: A Potential Approach for the Treatment of Cytomegalovirus Retinitis

    doi: 10.1002/jps.23140

    Figure Lengend Snippet: Representative chromatogram of cyclic cidofovir prodrugs (a) B-C2-cCDF, (b) B-C6–cCDF, (c) B-C12–cCDF, (d) C6-cCDF, and (e) C12-cCDF.

    Article Snippet: Cidofovir was a generous gift from the Gilead Science (Foster city, California) for this project.

    Techniques:

    Schematic representation of the synthesis of lipid prodrugs of cyclic cidofovir.

    Journal: Journal of pharmaceutical sciences

    Article Title: Transporter-Targeted Lipid Prodrugs of Cyclic Cidofovir: A Potential Approach for the Treatment of Cytomegalovirus Retinitis

    doi: 10.1002/jps.23140

    Figure Lengend Snippet: Schematic representation of the synthesis of lipid prodrugs of cyclic cidofovir.

    Article Snippet: Cidofovir was a generous gift from the Gilead Science (Foster city, California) for this project.

    Techniques:

    Schematic representation of the synthesis of biotin-conjugated lipid prodrugs of cyclic cidofovir.

    Journal: Journal of pharmaceutical sciences

    Article Title: Transporter-Targeted Lipid Prodrugs of Cyclic Cidofovir: A Potential Approach for the Treatment of Cytomegalovirus Retinitis

    doi: 10.1002/jps.23140

    Figure Lengend Snippet: Schematic representation of the synthesis of biotin-conjugated lipid prodrugs of cyclic cidofovir.

    Article Snippet: Cidofovir was a generous gift from the Gilead Science (Foster city, California) for this project.

    Techniques:

    Median (IQR) tenofovir and tenofovir-dp in blood plasma and PBMCs following a single dose of tenofovir alafenamide. Tenofovir over 14 days in plasma (a) and tenofovir-dp in PBMCs (b). Plot inserts depict concentrations over 24 h for each matrix. Concentration values BLQ were imputed at half the LLOQ for graphing purposes. Broken horizontal lines represent the LLOQ. At least 32% of plasma samples had unquantifiable tenofovir and at least 8% of PBMC samples had unquantifiable tenofovir-dp. Percentage of samples that were BLQ at each sampling time is tabulated below each graph. TAF, tenofovir alafenamide.

    Journal: Journal of Antimicrobial Chemotherapy

    Article Title: Single-dose pharmacokinetics of tenofovir alafenamide and its active metabolite in the mucosal tissues

    doi: 10.1093/jac/dkx064

    Figure Lengend Snippet: Median (IQR) tenofovir and tenofovir-dp in blood plasma and PBMCs following a single dose of tenofovir alafenamide. Tenofovir over 14 days in plasma (a) and tenofovir-dp in PBMCs (b). Plot inserts depict concentrations over 24 h for each matrix. Concentration values BLQ were imputed at half the LLOQ for graphing purposes. Broken horizontal lines represent the LLOQ. At least 32% of plasma samples had unquantifiable tenofovir and at least 8% of PBMC samples had unquantifiable tenofovir-dp. Percentage of samples that were BLQ at each sampling time is tabulated below each graph. TAF, tenofovir alafenamide.

    Article Snippet: Cells were incubated with 0.5 and 10 μM tenofovir alafenamide (i.e. 238.2 and 4764 ng/mL, respectively) or tenofovir (i.e. 143.6 and 2872 ng/mL, respectively) for 3, 12, 24, 48 and 72 h. Differences in drug stock diluents were controlled by matching concentrations of DMSO and purified water for the tenofovir- and tenofovir alafenamide-treated media, respectively.

    Techniques: Concentration Assay, Sampling

    Median (IQR) tenofovir and tenofovir-dp in rectal tissues following a single dose of tenofovir alafenamide. Tenofovir (continuous lines) and tenofovir-dp (broken lines) over 14 days in rectal tissue. Concentration values BLQ were imputed at half the sample-specific LLOQ for graphing purposes. Representative LLOQs are depicted for tenofovir (continuous horizontal line) and tenofovir-dp (broken horizontal line). At least 25% and 69% of samples had unquantifiable tenofovir and tenofovir-dp, respectively. Percentage of samples that were BLQ at each sampling time is tabulated below the graph. TAF, tenofovir alafenamide; TFV, tenofovir; TFVdp, tenofovir-dp.

    Journal: Journal of Antimicrobial Chemotherapy

    Article Title: Single-dose pharmacokinetics of tenofovir alafenamide and its active metabolite in the mucosal tissues

    doi: 10.1093/jac/dkx064

    Figure Lengend Snippet: Median (IQR) tenofovir and tenofovir-dp in rectal tissues following a single dose of tenofovir alafenamide. Tenofovir (continuous lines) and tenofovir-dp (broken lines) over 14 days in rectal tissue. Concentration values BLQ were imputed at half the sample-specific LLOQ for graphing purposes. Representative LLOQs are depicted for tenofovir (continuous horizontal line) and tenofovir-dp (broken horizontal line). At least 25% and 69% of samples had unquantifiable tenofovir and tenofovir-dp, respectively. Percentage of samples that were BLQ at each sampling time is tabulated below the graph. TAF, tenofovir alafenamide; TFV, tenofovir; TFVdp, tenofovir-dp.

    Article Snippet: Cells were incubated with 0.5 and 10 μM tenofovir alafenamide (i.e. 238.2 and 4764 ng/mL, respectively) or tenofovir (i.e. 143.6 and 2872 ng/mL, respectively) for 3, 12, 24, 48 and 72 h. Differences in drug stock diluents were controlled by matching concentrations of DMSO and purified water for the tenofovir- and tenofovir alafenamide-treated media, respectively.

    Techniques: Concentration Assay, Sampling

    Median (IQR) tenofovir and tenofovir-dp in female genital tissues following a single dose of tenofovir alafenamide. Tenofovir (continuous lines) and tenofovir-dp (broken lines) over 14 days in FGT tissue. Concentration values BLQ were imputed at half the sample-specific LLOQ for graphing purposes. Representative LLOQs are depicted for tenofovir (continuous horizontal line) and tenofovir-dp (broken horizontal line). At least 31% and 87.5% of samples had unquantifiable tenofovir and tenofovir-dp, respectively. Percentage of samples that were BLQ at each sampling time is tabulated below the graph. TAF, tenofovir alafenamide; TFV, tenofovir; TFVdp, tenofovir-dp.

    Journal: Journal of Antimicrobial Chemotherapy

    Article Title: Single-dose pharmacokinetics of tenofovir alafenamide and its active metabolite in the mucosal tissues

    doi: 10.1093/jac/dkx064

    Figure Lengend Snippet: Median (IQR) tenofovir and tenofovir-dp in female genital tissues following a single dose of tenofovir alafenamide. Tenofovir (continuous lines) and tenofovir-dp (broken lines) over 14 days in FGT tissue. Concentration values BLQ were imputed at half the sample-specific LLOQ for graphing purposes. Representative LLOQs are depicted for tenofovir (continuous horizontal line) and tenofovir-dp (broken horizontal line). At least 31% and 87.5% of samples had unquantifiable tenofovir and tenofovir-dp, respectively. Percentage of samples that were BLQ at each sampling time is tabulated below the graph. TAF, tenofovir alafenamide; TFV, tenofovir; TFVdp, tenofovir-dp.

    Article Snippet: Cells were incubated with 0.5 and 10 μM tenofovir alafenamide (i.e. 238.2 and 4764 ng/mL, respectively) or tenofovir (i.e. 143.6 and 2872 ng/mL, respectively) for 3, 12, 24, 48 and 72 h. Differences in drug stock diluents were controlled by matching concentrations of DMSO and purified water for the tenofovir- and tenofovir alafenamide-treated media, respectively.

    Techniques: Concentration Assay, Sampling

    Mean plasma concentration vs . time on day 14 for (A) tenofovir disoproxil fumarate (TDF) and (B) emtricitabine (FTC) each alone and with GSK2248761. (A) TDF ( ); TDF + GSK2248761 ( ). (B) FTC ( ); FTC + GSK2248761 ( )

    Journal: British Journal of Clinical Pharmacology

    Article Title: Drug interaction profile for GSK2248761, a next generation non-nucleoside reverse transcriptase inhibitor

    doi: 10.1111/j.1365-2125.2012.04194.x

    Figure Lengend Snippet: Mean plasma concentration vs . time on day 14 for (A) tenofovir disoproxil fumarate (TDF) and (B) emtricitabine (FTC) each alone and with GSK2248761. (A) TDF ( ); TDF + GSK2248761 ( ). (B) FTC ( ); FTC + GSK2248761 ( )

    Article Snippet: In addition, all plasma TDF and FTC PK parameters were comparable after co-administration of TDF/FTC and GSK2248761 relative to administration of TDF/FTC alone.

    Techniques: Concentration Assay

    Western blots and densitometric analysis of p-JNK translocation to the mitochondria at 6 h. Mice were treated with 30 mg/kg ASK1 inhibitor GS-459679 or the vehicle (55% PEG in water) 30 min before 300 mg/kg APAP injection. Western blotting was performed

    Journal: Toxicology and applied pharmacology

    Article Title: Inhibitor of Apoptosis Signal-Regulating Kinase 1 Protects Against Acetaminophen-induced Liver Injury

    doi: 10.1016/j.taap.2015.03.019

    Figure Lengend Snippet: Western blots and densitometric analysis of p-JNK translocation to the mitochondria at 6 h. Mice were treated with 30 mg/kg ASK1 inhibitor GS-459679 or the vehicle (55% PEG in water) 30 min before 300 mg/kg APAP injection. Western blotting was performed

    Article Snippet: It has been demonstrated that mice deficient in ASK1 were significantly protected against APAP hepatotoxicity (Nakagawa et al., 1998).

    Techniques: Western Blot, Translocation Assay, Mouse Assay, Injection

    Effect of ASK1 inhibitor GS-459679 post-treatment on APAP-induced JNK activation. Western blots (A) and densitometry analysis of p-JNK in the cytosolic (B) and mitochondrial (C) fractions. Mice were treated with 500 mg/kg N -acetylcysteine (NAC) (A), 30

    Journal: Toxicology and applied pharmacology

    Article Title: Inhibitor of Apoptosis Signal-Regulating Kinase 1 Protects Against Acetaminophen-induced Liver Injury

    doi: 10.1016/j.taap.2015.03.019

    Figure Lengend Snippet: Effect of ASK1 inhibitor GS-459679 post-treatment on APAP-induced JNK activation. Western blots (A) and densitometry analysis of p-JNK in the cytosolic (B) and mitochondrial (C) fractions. Mice were treated with 500 mg/kg N -acetylcysteine (NAC) (A), 30

    Article Snippet: It has been demonstrated that mice deficient in ASK1 were significantly protected against APAP hepatotoxicity (Nakagawa et al., 1998).

    Techniques: Activation Assay, Western Blot, Mouse Assay

    Effect of the ASK1 inhibitor on the regeneration response after APAP-induced liver injury. Proliferating Cell Nuclear Antigen (PCNA) levels was determined by western blotting (A) and immunohistochemistry (C) 24 h after APAP in animals treated either with

    Journal: Toxicology and applied pharmacology

    Article Title: Inhibitor of Apoptosis Signal-Regulating Kinase 1 Protects Against Acetaminophen-induced Liver Injury

    doi: 10.1016/j.taap.2015.03.019

    Figure Lengend Snippet: Effect of the ASK1 inhibitor on the regeneration response after APAP-induced liver injury. Proliferating Cell Nuclear Antigen (PCNA) levels was determined by western blotting (A) and immunohistochemistry (C) 24 h after APAP in animals treated either with

    Article Snippet: It has been demonstrated that mice deficient in ASK1 were significantly protected against APAP hepatotoxicity (Nakagawa et al., 1998).

    Techniques: Western Blot, Immunohistochemistry

    Effect of ASK1 inhibitor GS-459679 on APAP-induced GSH depletion. Mice were treated with 30 mg/kg GS-459679 or equivalent amount of vehicle (55% PEG in water) 30 min before 300 mg/kg APAP administration. GSH levels (μmol/g liver) were measured

    Journal: Toxicology and applied pharmacology

    Article Title: Inhibitor of Apoptosis Signal-Regulating Kinase 1 Protects Against Acetaminophen-induced Liver Injury

    doi: 10.1016/j.taap.2015.03.019

    Figure Lengend Snippet: Effect of ASK1 inhibitor GS-459679 on APAP-induced GSH depletion. Mice were treated with 30 mg/kg GS-459679 or equivalent amount of vehicle (55% PEG in water) 30 min before 300 mg/kg APAP administration. GSH levels (μmol/g liver) were measured

    Article Snippet: It has been demonstrated that mice deficient in ASK1 were significantly protected against APAP hepatotoxicity (Nakagawa et al., 1998).

    Techniques: Mouse Assay

    Effect of the ASK1 inhibitor GS-459679 on hepatic GSH and GSSG levels after APAP treatment. Mice were treated with 30 mg/kg GS-459679 or equivalent amount of vehicle (55% PEG in water) 30 min before 300 mg/kg APAP administration. GSH levels were measured

    Journal: Toxicology and applied pharmacology

    Article Title: Inhibitor of Apoptosis Signal-Regulating Kinase 1 Protects Against Acetaminophen-induced Liver Injury

    doi: 10.1016/j.taap.2015.03.019

    Figure Lengend Snippet: Effect of the ASK1 inhibitor GS-459679 on hepatic GSH and GSSG levels after APAP treatment. Mice were treated with 30 mg/kg GS-459679 or equivalent amount of vehicle (55% PEG in water) 30 min before 300 mg/kg APAP administration. GSH levels were measured

    Article Snippet: It has been demonstrated that mice deficient in ASK1 were significantly protected against APAP hepatotoxicity (Nakagawa et al., 1998).

    Techniques: Mouse Assay

    Effect of the ASK1 inhibitor on JNK activation. Western blot analysis (A) of p-JNK and total JNK in the cytosolic fraction of livers from untreated mice (Ctrl), mice treated with 30 mg/kg ASK1 inhibitor or mice treated with the same volume of vehicle

    Journal: Toxicology and applied pharmacology

    Article Title: Inhibitor of Apoptosis Signal-Regulating Kinase 1 Protects Against Acetaminophen-induced Liver Injury

    doi: 10.1016/j.taap.2015.03.019

    Figure Lengend Snippet: Effect of the ASK1 inhibitor on JNK activation. Western blot analysis (A) of p-JNK and total JNK in the cytosolic fraction of livers from untreated mice (Ctrl), mice treated with 30 mg/kg ASK1 inhibitor or mice treated with the same volume of vehicle

    Article Snippet: It has been demonstrated that mice deficient in ASK1 were significantly protected against APAP hepatotoxicity (Nakagawa et al., 1998).

    Techniques: Activation Assay, Western Blot, Mouse Assay

    Effect of ASK1 inhibitor GS-459679 post-treatment against APAP hepatotoxicity at 24 h. Mice were treated with 500 mg/kg N -acetylcysteine (NAC) (A), 30 mg/kg ASK1i (B) and the combination of both (C) either 1.5 or 3 h after 300 mg/kg of APAP administration.

    Journal: Toxicology and applied pharmacology

    Article Title: Inhibitor of Apoptosis Signal-Regulating Kinase 1 Protects Against Acetaminophen-induced Liver Injury

    doi: 10.1016/j.taap.2015.03.019

    Figure Lengend Snippet: Effect of ASK1 inhibitor GS-459679 post-treatment against APAP hepatotoxicity at 24 h. Mice were treated with 500 mg/kg N -acetylcysteine (NAC) (A), 30 mg/kg ASK1i (B) and the combination of both (C) either 1.5 or 3 h after 300 mg/kg of APAP administration.

    Article Snippet: It has been demonstrated that mice deficient in ASK1 were significantly protected against APAP hepatotoxicity (Nakagawa et al., 1998).

    Techniques: Mouse Assay

    Protective effect of the ASK1 inhibitor GS-459679 against APAP -induced liver injury. C57BL/6 mice were pretreated with either 10 or 30 mg/kg GS-459679 or an equivalent dose of the vehicle (55% PEG in water) 30 min before 300 mg/kg APAP administration.

    Journal: Toxicology and applied pharmacology

    Article Title: Inhibitor of Apoptosis Signal-Regulating Kinase 1 Protects Against Acetaminophen-induced Liver Injury

    doi: 10.1016/j.taap.2015.03.019

    Figure Lengend Snippet: Protective effect of the ASK1 inhibitor GS-459679 against APAP -induced liver injury. C57BL/6 mice were pretreated with either 10 or 30 mg/kg GS-459679 or an equivalent dose of the vehicle (55% PEG in water) 30 min before 300 mg/kg APAP administration.

    Article Snippet: It has been demonstrated that mice deficient in ASK1 were significantly protected against APAP hepatotoxicity (Nakagawa et al., 1998).

    Techniques: Mouse Assay

    Analysis of Th1/Th2 cytokine producing CD3+CD4+ cells at adefovir dipivoxil treatment week (TW) between mutation and no mutation.

    Journal: Mediators of Inflammation

    Article Title: Th1 and Th2 Immune Response in Chronic Hepatitis B Patients during a Long-Term Treatment with Adefovir Dipivoxil

    doi: 10.1155/2010/143026

    Figure Lengend Snippet: Analysis of Th1/Th2 cytokine producing CD3+CD4+ cells at adefovir dipivoxil treatment week (TW) between mutation and no mutation.

    Article Snippet: Large clinical trials of adefovir dipivoxil, in HBeAg-positive chronic HBV patients in China have proven that adefovir dipivoxil can significantly improve HBV serology and liver biochemistry after 48 and 52 weeks of treatment [ , ].

    Techniques: Mutagenesis

    Biochemical and virological responses after adefovir dipivoxil treatment. ALT (a), AST (b), HBV-DNA loading (c), and HBsAg levels (d) were examined in the serum samples from chronic HBV patients at adefovir dipivoxil treatment week of 0 (baseline), 12, 24, 36, 52, 65, 78, 92, and 104 ( P value for all treatment were statistically different from baseline

    Journal: Mediators of Inflammation

    Article Title: Th1 and Th2 Immune Response in Chronic Hepatitis B Patients during a Long-Term Treatment with Adefovir Dipivoxil

    doi: 10.1155/2010/143026

    Figure Lengend Snippet: Biochemical and virological responses after adefovir dipivoxil treatment. ALT (a), AST (b), HBV-DNA loading (c), and HBsAg levels (d) were examined in the serum samples from chronic HBV patients at adefovir dipivoxil treatment week of 0 (baseline), 12, 24, 36, 52, 65, 78, 92, and 104 ( P value for all treatment were statistically different from baseline

    Article Snippet: Large clinical trials of adefovir dipivoxil, in HBeAg-positive chronic HBV patients in China have proven that adefovir dipivoxil can significantly improve HBV serology and liver biochemistry after 48 and 52 weeks of treatment [ , ].

    Techniques: AST Assay

    Longitudinal analyses of NK cell activated ADCC (antibody-specific- %CD107a + cells [Log10]) in the plasma and GT (CVL) of women at 3 months, 6 months and 12 months, for the tenofovir and placebo arms for gp41. Analyses for cytotoxic activities (gp41-specific %CD107a + cells [Log10]) in the plasma on the left (A) for gp41 and the genital tract on the right to (B) for gp41. Solid lines indicate the minimum and maximum values of box and whisker plots, with black solid lines across the dots indicate the median at each time point for each study arm. Wilcoxon signed-rank tests were done to determine statistical differences between NK cell activated ADCC activities within each arm of the study, for each protein. Statistically significant values were defined as p

    Journal: Frontiers in Immunology

    Article Title: Topical Tenofovir Pre-exposure Prophylaxis and Mucosal HIV-Specific Fc-Mediated Antibody Activities in Women

    doi: 10.3389/fimmu.2020.01274

    Figure Lengend Snippet: Longitudinal analyses of NK cell activated ADCC (antibody-specific- %CD107a + cells [Log10]) in the plasma and GT (CVL) of women at 3 months, 6 months and 12 months, for the tenofovir and placebo arms for gp41. Analyses for cytotoxic activities (gp41-specific %CD107a + cells [Log10]) in the plasma on the left (A) for gp41 and the genital tract on the right to (B) for gp41. Solid lines indicate the minimum and maximum values of box and whisker plots, with black solid lines across the dots indicate the median at each time point for each study arm. Wilcoxon signed-rank tests were done to determine statistical differences between NK cell activated ADCC activities within each arm of the study, for each protein. Statistically significant values were defined as p

    Article Snippet: Gilead Sciences supplied the tenofovir gel that was manufactured by CONRAD for the CAPRISA 004 trial.

    Techniques: Whisker Assay

    Correlations between CD4 + T cell counts and ADNP (Log 10 Phagoscores) and NK cell activated ADCC in the plasma for the tenofovir arm at 6 months. (A) V1V2-gp70-specific phagoscores (Log10) correlation with CD4 + T cell counts and (B) p24-specific- %CD107a + cells (Log10]) correlation with CD4 + T cell counts. Significant values were identified as p

    Journal: Frontiers in Immunology

    Article Title: Topical Tenofovir Pre-exposure Prophylaxis and Mucosal HIV-Specific Fc-Mediated Antibody Activities in Women

    doi: 10.3389/fimmu.2020.01274

    Figure Lengend Snippet: Correlations between CD4 + T cell counts and ADNP (Log 10 Phagoscores) and NK cell activated ADCC in the plasma for the tenofovir arm at 6 months. (A) V1V2-gp70-specific phagoscores (Log10) correlation with CD4 + T cell counts and (B) p24-specific- %CD107a + cells (Log10]) correlation with CD4 + T cell counts. Significant values were identified as p

    Article Snippet: Gilead Sciences supplied the tenofovir gel that was manufactured by CONRAD for the CAPRISA 004 trial.

    Techniques:

    HIV-specific ADNP [phagoscores (Log10)] in the genital tract (CVL) in women from the tenofovir and placebo arms. Cross-sectional analyses between the tenofovir and placebo arms to HIV proteins (A) gp41 and (B) p24 and longitudinal analyses for tenofovir and placebo (C) p66. Solid lines indicate the minimum and maximum values of box and whisker plots, with black solid lines across the dots indicate the median at each time point for each study arm. Wilcoxon signed-rank test was used to analyse ADNP activity over time and Wilcoxon-Mann-Whitney test was used for cross sectional analysis. Statistically significant values were defined as p

    Journal: Frontiers in Immunology

    Article Title: Topical Tenofovir Pre-exposure Prophylaxis and Mucosal HIV-Specific Fc-Mediated Antibody Activities in Women

    doi: 10.3389/fimmu.2020.01274

    Figure Lengend Snippet: HIV-specific ADNP [phagoscores (Log10)] in the genital tract (CVL) in women from the tenofovir and placebo arms. Cross-sectional analyses between the tenofovir and placebo arms to HIV proteins (A) gp41 and (B) p24 and longitudinal analyses for tenofovir and placebo (C) p66. Solid lines indicate the minimum and maximum values of box and whisker plots, with black solid lines across the dots indicate the median at each time point for each study arm. Wilcoxon signed-rank test was used to analyse ADNP activity over time and Wilcoxon-Mann-Whitney test was used for cross sectional analysis. Statistically significant values were defined as p

    Article Snippet: Gilead Sciences supplied the tenofovir gel that was manufactured by CONRAD for the CAPRISA 004 trial.

    Techniques: Whisker Assay, Activity Assay, MANN-WHITNEY

    Longitudinal analyses of plasma HIV-specific ADNP [phagoscores (Log10)] in both the tenofovir and the placebo arms. Phagocytic activities [phagoscores (Log10)] to HIV proteins (A) gp120, (B) gp41, (C) p66, and (D) p24. Solid lines indicate the minimum and maximum values of box and whisker plots, with black solid lines across the dots indicate the median at each time point for each study arm. Statistical differences were defined as p

    Journal: Frontiers in Immunology

    Article Title: Topical Tenofovir Pre-exposure Prophylaxis and Mucosal HIV-Specific Fc-Mediated Antibody Activities in Women

    doi: 10.3389/fimmu.2020.01274

    Figure Lengend Snippet: Longitudinal analyses of plasma HIV-specific ADNP [phagoscores (Log10)] in both the tenofovir and the placebo arms. Phagocytic activities [phagoscores (Log10)] to HIV proteins (A) gp120, (B) gp41, (C) p66, and (D) p24. Solid lines indicate the minimum and maximum values of box and whisker plots, with black solid lines across the dots indicate the median at each time point for each study arm. Statistical differences were defined as p

    Article Snippet: Gilead Sciences supplied the tenofovir gel that was manufactured by CONRAD for the CAPRISA 004 trial.

    Techniques: Whisker Assay

    Correlations between ADNP (Log 10 Phagoscores) and NK cell activated ADCC (antibody-specific- %CD107a + cells [Log10]) activities in the plasma of women in the tenofovir arm. (A) gp41-specific- phagoscores (Log10) at 3 months in the tenofovir arm, (B) p66-specific- %CD107a + cells (Log10) at 12 months. Spearman R correlation analyses were performed. Significant values were identified as p

    Journal: Frontiers in Immunology

    Article Title: Topical Tenofovir Pre-exposure Prophylaxis and Mucosal HIV-Specific Fc-Mediated Antibody Activities in Women

    doi: 10.3389/fimmu.2020.01274

    Figure Lengend Snippet: Correlations between ADNP (Log 10 Phagoscores) and NK cell activated ADCC (antibody-specific- %CD107a + cells [Log10]) activities in the plasma of women in the tenofovir arm. (A) gp41-specific- phagoscores (Log10) at 3 months in the tenofovir arm, (B) p66-specific- %CD107a + cells (Log10) at 12 months. Spearman R correlation analyses were performed. Significant values were identified as p

    Article Snippet: Gilead Sciences supplied the tenofovir gel that was manufactured by CONRAD for the CAPRISA 004 trial.

    Techniques:

    Attenuation of cockroach antigen (CRA)-induced airway inflammation in a mouse model by inhibiting PI3K p110δ activity. A : recruitment of total inflammatory cells to the airways determined by microscopic evaluation of Hema 3-stained cytocentrifuged slides of bronchoalveolar lavage fluid (BALF) in control and CRA-exposed mice treated with IC87114 (50 mg/kg) or vehicle alone (PEG-400). B and C : cellular infiltration of lung tissue after hematoxylin and eosin staining of paraformaldehyde-fixed lung sections (representative images are shown at magnification ×200) and scoring of peribronchial inflammation. Combined data from 2 experiments are shown in C . n = 7–9 mice/group. D : differential cell counts in BALF of control and CRA-exposed mice treated with IC87114 or vehicle alone. Eos, eosinophils; Monos, monocytes and macrophages; Neu, neutrophils; Lymphs, lymphocytes. Combined data from experiments repeated at least 3 times are shown in A and D . n = 6 mice for control group and 13–17 mice for CRA-exposed groups. E and F : infiltration of lung tissue by eosinophils after staining with rat mAb against murine major basic protein (MBP). Representative images are shown in E . Magnification ×200. MBP-positive cells in 5–6 randomly selected nonoverlapping microscopic fields were counted at magnification of ×400. Combined data from 2 experiments are shown in F . n = 4 mice for control group and 7 for CRA-exposed groups. G : airway hyperresponsiveness (AHR) assessed by whole body plethysmography in control and CRA-exposed mice treated with IC87114 or vehicle alone. The enhanced pause (PenH) in breathing when exposed to increasing amounts of nebulized methacholine (MCh) after initial exposure to saline was monitored. Combined data from 2 experiments are shown. n = 5 mice for control group and 6–10 mice for CRA-exposed groups. Data represent means ± SE in A , C , D , F , and G . * P

    Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

    Article Title: The p110? subunit of PI3K regulates bone marrow-derived eosinophil trafficking and airway eosinophilia in allergen-challenged mice

    doi: 10.1152/ajplung.00005.2012

    Figure Lengend Snippet: Attenuation of cockroach antigen (CRA)-induced airway inflammation in a mouse model by inhibiting PI3K p110δ activity. A : recruitment of total inflammatory cells to the airways determined by microscopic evaluation of Hema 3-stained cytocentrifuged slides of bronchoalveolar lavage fluid (BALF) in control and CRA-exposed mice treated with IC87114 (50 mg/kg) or vehicle alone (PEG-400). B and C : cellular infiltration of lung tissue after hematoxylin and eosin staining of paraformaldehyde-fixed lung sections (representative images are shown at magnification ×200) and scoring of peribronchial inflammation. Combined data from 2 experiments are shown in C . n = 7–9 mice/group. D : differential cell counts in BALF of control and CRA-exposed mice treated with IC87114 or vehicle alone. Eos, eosinophils; Monos, monocytes and macrophages; Neu, neutrophils; Lymphs, lymphocytes. Combined data from experiments repeated at least 3 times are shown in A and D . n = 6 mice for control group and 13–17 mice for CRA-exposed groups. E and F : infiltration of lung tissue by eosinophils after staining with rat mAb against murine major basic protein (MBP). Representative images are shown in E . Magnification ×200. MBP-positive cells in 5–6 randomly selected nonoverlapping microscopic fields were counted at magnification of ×400. Combined data from 2 experiments are shown in F . n = 4 mice for control group and 7 for CRA-exposed groups. G : airway hyperresponsiveness (AHR) assessed by whole body plethysmography in control and CRA-exposed mice treated with IC87114 or vehicle alone. The enhanced pause (PenH) in breathing when exposed to increasing amounts of nebulized methacholine (MCh) after initial exposure to saline was monitored. Combined data from 2 experiments are shown. n = 5 mice for control group and 6–10 mice for CRA-exposed groups. Data represent means ± SE in A , C , D , F , and G . * P

    Article Snippet: However, leukotriene B4-induced neutrophil emigration was inhibited by IC87114 ( , ).

    Techniques: Activity Assay, Staining, Mouse Assay

    Effect of PI3K p110δ inhibition on eosinophil trafficking in vivo. A : rolling of infused murine eosinophils in inflamed cremaster muscle microvessels of mice treated with IC87114 [100 μl of 7.5 mg/ml (30 mg/kg)] or vehicle, polyethylene glycol (PEG-400), evaluated by intravital microscopy (IVM). The number of rolling cells is expressed as rolling fraction, which is a percentage of the total number of cells passing through the same reference point. B : rolling velocity of interacting eosinophils determined by offline analysis of recorded video images by choosing 4–6 rolling eosinophils per venule and measuring the time taken for the cells to travel between 2 reference points (50–200 μm). Results represent mean rolling velocity of 144 cells in the control group and 54 cells in the IC87114-treated group. C : adhesion of infused eosinophils in cremaster muscle microvessels of mice treated with IC87114 or vehicle. D : representative photomicrographs showing examples of rolling and adherent eosinophils in cremaster muscle microvessels of vehicle- and IC87114-treated mice (magnification ×100). White arrows indicate rolling and/or adherent cells. V; veins. Combined data from 4 mice for the control group and 5 mice for IC87114-treated group are shown in A–C . Rolling and adhesion were evaluated in 4–12 vessels/mouse for the control group and 4–8 vessels/mouse for IC87114-treated group. Data represent means ± SE for A–C . * P

    Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

    Article Title: The p110? subunit of PI3K regulates bone marrow-derived eosinophil trafficking and airway eosinophilia in allergen-challenged mice

    doi: 10.1152/ajplung.00005.2012

    Figure Lengend Snippet: Effect of PI3K p110δ inhibition on eosinophil trafficking in vivo. A : rolling of infused murine eosinophils in inflamed cremaster muscle microvessels of mice treated with IC87114 [100 μl of 7.5 mg/ml (30 mg/kg)] or vehicle, polyethylene glycol (PEG-400), evaluated by intravital microscopy (IVM). The number of rolling cells is expressed as rolling fraction, which is a percentage of the total number of cells passing through the same reference point. B : rolling velocity of interacting eosinophils determined by offline analysis of recorded video images by choosing 4–6 rolling eosinophils per venule and measuring the time taken for the cells to travel between 2 reference points (50–200 μm). Results represent mean rolling velocity of 144 cells in the control group and 54 cells in the IC87114-treated group. C : adhesion of infused eosinophils in cremaster muscle microvessels of mice treated with IC87114 or vehicle. D : representative photomicrographs showing examples of rolling and adherent eosinophils in cremaster muscle microvessels of vehicle- and IC87114-treated mice (magnification ×100). White arrows indicate rolling and/or adherent cells. V; veins. Combined data from 4 mice for the control group and 5 mice for IC87114-treated group are shown in A–C . Rolling and adhesion were evaluated in 4–12 vessels/mouse for the control group and 4–8 vessels/mouse for IC87114-treated group. Data represent means ± SE for A–C . * P

    Article Snippet: However, leukotriene B4-induced neutrophil emigration was inhibited by IC87114 ( , ).

    Techniques: Inhibition, In Vivo, Mouse Assay, Intravital Microscopy

    Phosphatidylinositol 3-kinase (PI3K) p110δ promotes eosinophil adhesion and changes in cell morphology. A : expression of PI3K p110α, p110β, p110γ, and p110δ in bone marrow-derived eosinophil (BM-Eos) by RT-PCR with isoform-specific primers. Expression of β-actin served as the internal control. Representative image is shown. Combined data from 3 experiments with BM-Eos from 3 different mice are shown for densitometry. B : adhesion of fluorescently labeled BM-Eos treated with IC87114 or vehicle to immobilized recombinant murine (rm) vascular cell adhesion molecule (VCAM)-1 or rm intercellular adhesion molecule (ICAM)-1 in 96-well plates under static conditions. The number of cells adhered was quantitated against a standard curve generated with fluorescently labeled eosinophils using a microplate reader. Combined data from 3 experiments in triplicate are shown. C : confocal microscopy of FITC-phalloidin-stained BM-Eos adhering to VCAM-1 or ICAM-1 on coverslips in the presence of vehicle or 10 μM IC87114 for 20 min. Magnification ×600. D : quantitation of adherent BM-Eos exhibiting changes in morphology after IC87114 treatment. Cells in 5 different fields of each coverslip exhibiting cell spreading with leading edges, lamellipodia, or filopodia after treatment with vehicle or IC87114 were counted and expressed as a percentage of the total number of cells in the field. Combined data of 3 experiments for adhesion to VCAM-1 and 2 experiments for adhesion to ICAM-1 are shown. Data represent means ± SE in A , B , and D . * P

    Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

    Article Title: The p110? subunit of PI3K regulates bone marrow-derived eosinophil trafficking and airway eosinophilia in allergen-challenged mice

    doi: 10.1152/ajplung.00005.2012

    Figure Lengend Snippet: Phosphatidylinositol 3-kinase (PI3K) p110δ promotes eosinophil adhesion and changes in cell morphology. A : expression of PI3K p110α, p110β, p110γ, and p110δ in bone marrow-derived eosinophil (BM-Eos) by RT-PCR with isoform-specific primers. Expression of β-actin served as the internal control. Representative image is shown. Combined data from 3 experiments with BM-Eos from 3 different mice are shown for densitometry. B : adhesion of fluorescently labeled BM-Eos treated with IC87114 or vehicle to immobilized recombinant murine (rm) vascular cell adhesion molecule (VCAM)-1 or rm intercellular adhesion molecule (ICAM)-1 in 96-well plates under static conditions. The number of cells adhered was quantitated against a standard curve generated with fluorescently labeled eosinophils using a microplate reader. Combined data from 3 experiments in triplicate are shown. C : confocal microscopy of FITC-phalloidin-stained BM-Eos adhering to VCAM-1 or ICAM-1 on coverslips in the presence of vehicle or 10 μM IC87114 for 20 min. Magnification ×600. D : quantitation of adherent BM-Eos exhibiting changes in morphology after IC87114 treatment. Cells in 5 different fields of each coverslip exhibiting cell spreading with leading edges, lamellipodia, or filopodia after treatment with vehicle or IC87114 were counted and expressed as a percentage of the total number of cells in the field. Combined data of 3 experiments for adhesion to VCAM-1 and 2 experiments for adhesion to ICAM-1 are shown. Data represent means ± SE in A , B , and D . * P

    Article Snippet: However, leukotriene B4-induced neutrophil emigration was inhibited by IC87114 ( , ).

    Techniques: Expressing, Derivative Assay, Reverse Transcription Polymerase Chain Reaction, Mouse Assay, Labeling, Recombinant, Generated, Confocal Microscopy, Staining, Quantitation Assay

    CRA-induced mucus secretion and expression of proinflammatory molecules found in inflammatory zone 1 (FIZZ1) and intelectin-1 are reduced by inhibition of PI3K p110δ activity. Lung sections from control and CRA-exposed mice treated with IC87114 or vehicle alone were evaluated for mucus secretion based on periodic acid-Schiff's (PAS) staining as well as expression of FIZZ1 and intelectin-1 by immunohistology. Representative microscopic images ( left , magnification ×200) and combined quantitative data ( right ) of 3–6 airways from control group ( n = 5) and 8–13 airways from CRA-exposed groups ( n = 6–7) are shown. Data represent means ± SE. * P

    Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

    Article Title: The p110? subunit of PI3K regulates bone marrow-derived eosinophil trafficking and airway eosinophilia in allergen-challenged mice

    doi: 10.1152/ajplung.00005.2012

    Figure Lengend Snippet: CRA-induced mucus secretion and expression of proinflammatory molecules found in inflammatory zone 1 (FIZZ1) and intelectin-1 are reduced by inhibition of PI3K p110δ activity. Lung sections from control and CRA-exposed mice treated with IC87114 or vehicle alone were evaluated for mucus secretion based on periodic acid-Schiff's (PAS) staining as well as expression of FIZZ1 and intelectin-1 by immunohistology. Representative microscopic images ( left , magnification ×200) and combined quantitative data ( right ) of 3–6 airways from control group ( n = 5) and 8–13 airways from CRA-exposed groups ( n = 6–7) are shown. Data represent means ± SE. * P

    Article Snippet: However, leukotriene B4-induced neutrophil emigration was inhibited by IC87114 ( , ).

    Techniques: Expressing, Inhibition, Activity Assay, Mouse Assay, Staining

    Inactivation of PI3K p110δ with IC87114 inhibits eosinophil migration and prevents eotaxin-1-induced changes in cell morphology. A : migration of fluorescently labeled BM-Eos treated with IC87114 or vehicle toward 100 nM murine eotaxin-1 in Transwell plates after 2 h at 37°C. Combined data from 5 independent experiments in duplicate are shown. B : expression of CCR3, the receptor for eotaxin-1, by vehicle- and IC87114-treated eosinophils by flow cytometry using FITC-conjugated anti-mouse CCR3 (5 μg/ml). Rat IgG2a was used as the isotype control. Histogram shown is representative of 3 experiments with eosinophils from 3 different mice. C : confocal microscopy of FITC-phalloidin-stained BM-Eos adhering to VCAM-1 or ICAM-1 in the presence of vehicle or 10 μM IC87114 for 20 min followed by eotaxin-1 (100 nM, 5 min). Magnification ×600. D : quantitation of adherent vehicle- and IC87114-treated BM-Eos exhibiting changes in morphology after eotaxin-1 treatment. Adhered cells in 5 different fields of each coverslip exhibiting cell spreading with distinct leading edges, lamellipodia, or filopodia after eotaxin-1 treatment were counted and expressed as a percentage of the total number of cells in the field. Combined data of 3 experiments for adhesion on VCAM-1 and 2 experiments for adhesion on ICAM-1 are shown. Data represent means ± SE in A and D . * P

    Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

    Article Title: The p110? subunit of PI3K regulates bone marrow-derived eosinophil trafficking and airway eosinophilia in allergen-challenged mice

    doi: 10.1152/ajplung.00005.2012

    Figure Lengend Snippet: Inactivation of PI3K p110δ with IC87114 inhibits eosinophil migration and prevents eotaxin-1-induced changes in cell morphology. A : migration of fluorescently labeled BM-Eos treated with IC87114 or vehicle toward 100 nM murine eotaxin-1 in Transwell plates after 2 h at 37°C. Combined data from 5 independent experiments in duplicate are shown. B : expression of CCR3, the receptor for eotaxin-1, by vehicle- and IC87114-treated eosinophils by flow cytometry using FITC-conjugated anti-mouse CCR3 (5 μg/ml). Rat IgG2a was used as the isotype control. Histogram shown is representative of 3 experiments with eosinophils from 3 different mice. C : confocal microscopy of FITC-phalloidin-stained BM-Eos adhering to VCAM-1 or ICAM-1 in the presence of vehicle or 10 μM IC87114 for 20 min followed by eotaxin-1 (100 nM, 5 min). Magnification ×600. D : quantitation of adherent vehicle- and IC87114-treated BM-Eos exhibiting changes in morphology after eotaxin-1 treatment. Adhered cells in 5 different fields of each coverslip exhibiting cell spreading with distinct leading edges, lamellipodia, or filopodia after eotaxin-1 treatment were counted and expressed as a percentage of the total number of cells in the field. Combined data of 3 experiments for adhesion on VCAM-1 and 2 experiments for adhesion on ICAM-1 are shown. Data represent means ± SE in A and D . * P

    Article Snippet: However, leukotriene B4-induced neutrophil emigration was inhibited by IC87114 ( , ).

    Techniques: Migration, Labeling, Expressing, Flow Cytometry, Cytometry, Mouse Assay, Confocal Microscopy, Staining, Quantitation Assay

    Treatment with PI3K p110δ inhibitor alters adhesion molecule expression and distribution by eosinophils. A : expression of adhesion molecules by vehicle- and IC87114-treated BM-Eos by flow cytometry using rat monoclonal antibodies (mAbs) against α4 (CD49), lymphocyte function associated antigen (LFA)-1 (CD11a), Mac-1 (CD11b), and CD62L. Depending on the mAb, rat IgG2a or 2b was used as the isotype-matched control. All antibodies were used at a final concentration of 5 μg/ml. B : immunofluorescence staining to evaluate distribution of Mac-1 and α4 on the cell surface of vehicle- or IC87114-treated eosinophils adhered to ICAM-1 and VCAM-1, respectively. Adhered cells were stained with goat anti-mouse α4 (5 μg/ml) or rat anti-mouse Mac-1 (10 μg/ml) followed by rhodamine-conjugated secondary antibodies. Goat IgG (for anti-α4) or rat IgG2b (for anti-Mac-1) was used as the isotype control. Magnification ×600. Data shown in A and B are representative of 3 independent experiments with eosinophils from 3 different mice.

    Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

    Article Title: The p110? subunit of PI3K regulates bone marrow-derived eosinophil trafficking and airway eosinophilia in allergen-challenged mice

    doi: 10.1152/ajplung.00005.2012

    Figure Lengend Snippet: Treatment with PI3K p110δ inhibitor alters adhesion molecule expression and distribution by eosinophils. A : expression of adhesion molecules by vehicle- and IC87114-treated BM-Eos by flow cytometry using rat monoclonal antibodies (mAbs) against α4 (CD49), lymphocyte function associated antigen (LFA)-1 (CD11a), Mac-1 (CD11b), and CD62L. Depending on the mAb, rat IgG2a or 2b was used as the isotype-matched control. All antibodies were used at a final concentration of 5 μg/ml. B : immunofluorescence staining to evaluate distribution of Mac-1 and α4 on the cell surface of vehicle- or IC87114-treated eosinophils adhered to ICAM-1 and VCAM-1, respectively. Adhered cells were stained with goat anti-mouse α4 (5 μg/ml) or rat anti-mouse Mac-1 (10 μg/ml) followed by rhodamine-conjugated secondary antibodies. Goat IgG (for anti-α4) or rat IgG2b (for anti-Mac-1) was used as the isotype control. Magnification ×600. Data shown in A and B are representative of 3 independent experiments with eosinophils from 3 different mice.

    Article Snippet: However, leukotriene B4-induced neutrophil emigration was inhibited by IC87114 ( , ).

    Techniques: Expressing, Flow Cytometry, Cytometry, Concentration Assay, Immunofluorescence, Staining, Mouse Assay