hank s balanced salt solution hbss  (Thermo Fisher)


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    Name:
    HBSS no calcium no magnesium
    Description:
    Hanks Balanced Salt Solution HBSS is used for a variety of cell culture applications such as washing cells before dissociation transporting cells or tissue diluting cells for counting and preparing reagents Formulations without calcium and magnesium are required for rinsing chelators from the culture before cell dissociation We offer a variety of Gibco HBSS formulations for a range of cell culture applications Find the right formulation using the media selector tool This HBSS is modified as follows WithWithout• Phenol Red• Calcium• Glucose• Magnesium• Sodium BicarbonateThe complete formulation is available Product Intended UseFor in vitro diagnostic use CAUTION Not for human or animal therapeutic use Uses other than the intended use may be a violation of local law cGMP Manufacturing and Quality SystemGibco HBSS is manufactured at a cGMP compliant facility located in Paisley Scotland UK The facility is registered with the FDA as a medical device manufacturer and is certified to the ISO 13485 standard For supply chain continuity we offer an identical Gibco HBSS product made in our Grand Island facility 14170 120 This facility is registered with the FDA as a medical device manufacturer and is certified to the ISO 13485 standards
    Catalog Number:
    14170070
    Price:
    None
    Applications:
    Cell Culture|Mammalian Cell Culture
    Category:
    Cell Culture Transfection Reagents
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    Structured Review

    Thermo Fisher hank s balanced salt solution hbss
    Effects of JH4 on ASC-stimulated blood perfusion and ischemic limb salvage. The ischemic limbs were injected with ASCs in the absence or presence of JH4. For negative control, <t>HBSS</t> was injected into ischemic limbs. (A) Representative images of the ischemia-induced mouse hind limb on day 28. (B) Quantitative analysis of blood flow measured by laser doppler perfusion imaging analysis. (C) Analysis of the necrosis score on day 28. (B, C) The data represent the mean ± standard error of the mean. HBSS, <t>Hank's</t> balanced salt solution; ASC, adipose tissue-derived mesenchymal stem cell; ANOVA, analysis of variance. * p
    Hanks Balanced Salt Solution HBSS is used for a variety of cell culture applications such as washing cells before dissociation transporting cells or tissue diluting cells for counting and preparing reagents Formulations without calcium and magnesium are required for rinsing chelators from the culture before cell dissociation We offer a variety of Gibco HBSS formulations for a range of cell culture applications Find the right formulation using the media selector tool This HBSS is modified as follows WithWithout• Phenol Red• Calcium• Glucose• Magnesium• Sodium BicarbonateThe complete formulation is available Product Intended UseFor in vitro diagnostic use CAUTION Not for human or animal therapeutic use Uses other than the intended use may be a violation of local law cGMP Manufacturing and Quality SystemGibco HBSS is manufactured at a cGMP compliant facility located in Paisley Scotland UK The facility is registered with the FDA as a medical device manufacturer and is certified to the ISO 13485 standard For supply chain continuity we offer an identical Gibco HBSS product made in our Grand Island facility 14170 120 This facility is registered with the FDA as a medical device manufacturer and is certified to the ISO 13485 standards
    https://www.bioz.com/result/hank s balanced salt solution hbss/product/Thermo Fisher
    Average 99 stars, based on 59 article reviews
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    hank s balanced salt solution hbss - by Bioz Stars, 2020-10
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    Images

    1) Product Images from "Mesenchymal Stem Cell-Mediated Therapy of Peripheral Artery Disease Is Stimulated by a Lamin A-Progerin Binding Inhibitor"

    Article Title: Mesenchymal Stem Cell-Mediated Therapy of Peripheral Artery Disease Is Stimulated by a Lamin A-Progerin Binding Inhibitor

    Journal: Journal of Lipid and Atherosclerosis

    doi: 10.12997/jla.2020.9.3.460

    Effects of JH4 on ASC-stimulated blood perfusion and ischemic limb salvage. The ischemic limbs were injected with ASCs in the absence or presence of JH4. For negative control, HBSS was injected into ischemic limbs. (A) Representative images of the ischemia-induced mouse hind limb on day 28. (B) Quantitative analysis of blood flow measured by laser doppler perfusion imaging analysis. (C) Analysis of the necrosis score on day 28. (B, C) The data represent the mean ± standard error of the mean. HBSS, Hank's balanced salt solution; ASC, adipose tissue-derived mesenchymal stem cell; ANOVA, analysis of variance. * p
    Figure Legend Snippet: Effects of JH4 on ASC-stimulated blood perfusion and ischemic limb salvage. The ischemic limbs were injected with ASCs in the absence or presence of JH4. For negative control, HBSS was injected into ischemic limbs. (A) Representative images of the ischemia-induced mouse hind limb on day 28. (B) Quantitative analysis of blood flow measured by laser doppler perfusion imaging analysis. (C) Analysis of the necrosis score on day 28. (B, C) The data represent the mean ± standard error of the mean. HBSS, Hank's balanced salt solution; ASC, adipose tissue-derived mesenchymal stem cell; ANOVA, analysis of variance. * p

    Techniques Used: Injection, Negative Control, Imaging, Derivative Assay

    Effects of JH4 treatment on ASC-stimulated neovascularization in ischemic muscle. Tissues from the ischemic limbs on day 28 were analyzed by immunostaining. (A) Effects of JH4 treatment on ASC-stimulated angiogenesis in vivo . Sections were stained with anti-CD31 antibodies (red) and nuclei were counterstained with DAPI (blue). (B) The number of CD31+ capillaries per HPF was counted. (C) Effects of JH4 treatment on ASC-stimulated arteriogenesis in vivo . Sections were stained with anti-α-SMA antibodies (green) and nuclei were counterstained with DAPI (blue). (D) The number of α-SMA-positive arteries/arterioles per HPF was counted. The data represent the mean ± standard error of the mean. Scale bar, 100 μm. HBSS, Hank's balanced salt solution; ASC, adipose tissue-derived mesenchymal stem cell; DAPI, 4′,6-diamidino-2-phenylindole; HPF, high power field; α-SMA, α-smooth muscle actin. * p
    Figure Legend Snippet: Effects of JH4 treatment on ASC-stimulated neovascularization in ischemic muscle. Tissues from the ischemic limbs on day 28 were analyzed by immunostaining. (A) Effects of JH4 treatment on ASC-stimulated angiogenesis in vivo . Sections were stained with anti-CD31 antibodies (red) and nuclei were counterstained with DAPI (blue). (B) The number of CD31+ capillaries per HPF was counted. (C) Effects of JH4 treatment on ASC-stimulated arteriogenesis in vivo . Sections were stained with anti-α-SMA antibodies (green) and nuclei were counterstained with DAPI (blue). (D) The number of α-SMA-positive arteries/arterioles per HPF was counted. The data represent the mean ± standard error of the mean. Scale bar, 100 μm. HBSS, Hank's balanced salt solution; ASC, adipose tissue-derived mesenchymal stem cell; DAPI, 4′,6-diamidino-2-phenylindole; HPF, high power field; α-SMA, α-smooth muscle actin. * p

    Techniques Used: Immunostaining, In Vivo, Staining, Derivative Assay

    2) Product Images from "Direct Effect of Carbon Monoxide on Relaxation Induced by Electrical Field Stimulation in Rat Corpus Cavernosum"

    Article Title: Direct Effect of Carbon Monoxide on Relaxation Induced by Electrical Field Stimulation in Rat Corpus Cavernosum

    Journal: Korean Journal of Urology

    doi: 10.4111/kju.2010.51.8.572

    Effect of different carbon monoxide (CO) concentrations (1%, 2%, and 5%) on relaxation in Phe-precontracted corpus cavernosum smooth muscle before exposure to electrical field stimulation. HBSS: Hank's balanced salt solution.
    Figure Legend Snippet: Effect of different carbon monoxide (CO) concentrations (1%, 2%, and 5%) on relaxation in Phe-precontracted corpus cavernosum smooth muscle before exposure to electrical field stimulation. HBSS: Hank's balanced salt solution.

    Techniques Used:

    Effect of carbon monoxide (5%) on corpus cavernosum smooth muscle (CCSM) relaxation induced by electrical field stimulation (EFS). Rat CCSM was phenylephrine-precontracted and responded to EFS (0.5 to 32 Hz, 0.2 ms duration). HBSS: Hank's balanced salt solution.
    Figure Legend Snippet: Effect of carbon monoxide (5%) on corpus cavernosum smooth muscle (CCSM) relaxation induced by electrical field stimulation (EFS). Rat CCSM was phenylephrine-precontracted and responded to EFS (0.5 to 32 Hz, 0.2 ms duration). HBSS: Hank's balanced salt solution.

    Techniques Used: Mass Spectrometry

    Effect of nitric oxide synthase inhibitor, N G -nitro-L-arginine, on rat corpus cavernosum smooth muscle relaxation induced by electrical field stimulation in the presence of carbon monoxide (5%). CO: carbon monoxide, HBSS: Hank's balanced salt solution, L-NOARG: N G -nitro-L-arginine, EFS: electrical field stimulation.
    Figure Legend Snippet: Effect of nitric oxide synthase inhibitor, N G -nitro-L-arginine, on rat corpus cavernosum smooth muscle relaxation induced by electrical field stimulation in the presence of carbon monoxide (5%). CO: carbon monoxide, HBSS: Hank's balanced salt solution, L-NOARG: N G -nitro-L-arginine, EFS: electrical field stimulation.

    Techniques Used:

    3) Product Images from "Oral Azathioprine Leads to Higher Incorporation of 6-Thioguanine in DNA of Skin than Liver: The Protective Role of the Keap1/Nrf2/ARE Pathway"

    Article Title: Oral Azathioprine Leads to Higher Incorporation of 6-Thioguanine in DNA of Skin than Liver: The Protective Role of the Keap1/Nrf2/ARE Pathway

    Journal: Cancer prevention research (Philadelphia, Pa.)

    doi: 10.1158/1940-6207.CAPR-11-0137

    Protection against UVA radiation-induced oxidative stress by sulforaphane in Hepa1c1c7 cells ( A ) Cells (3.5 ×10 5 per well) were plated on 6-well plates. After 24 h hours, they were treated with either vehicle (0.1% acetonitrile, white bars), 2 μM 6-thioguanine (6-TG, black bars), or co-treated with 2 μM 6-thioguanine and 5 μM sulforaphane (SF, grey bars) for further 24 h. Cells were then washed with Hank’s buffered saline solution (HBSS), and exposed to UVA (1, 2, or 3 J/cm 2 ) in 1.0 ml of HBSS. ROI generated by the UV radiation were quantified by the fluorescent probe 2′,7′- dichlorodihydrofluorescein and fluorescence intensity was measured 1 h post-irradiation. ( B ) Cells (1.75 × 10 5 per well in 6-well plates) were transiently transfected with a mixture of two siRNAs targeting Mrp4 , or with a non-targeting control oligo. The medium was changed 18 h after transfection with either medium containing 0.1% acetonitrile (black bars) or 5 μM SF (grey bars). Six hours later, the medium was changed, and the cells were treated with 6- thioguanine, in the presence of SF, for further 24 h. Cells were prepared and exposed to UVA (3 J/cm 2 ) as described under panel A . ( C ) Cells were seeded, treated, and exposed to UVA radiation as described under panel A . Reduced glutathione (GSH) was quantified using monochlorobimane and the fluorescence intensity of the GS-monochlorobimane adduct was determined 2 h post-irradiation. For all panels, means ± S.D. are shown (n = 3).
    Figure Legend Snippet: Protection against UVA radiation-induced oxidative stress by sulforaphane in Hepa1c1c7 cells ( A ) Cells (3.5 ×10 5 per well) were plated on 6-well plates. After 24 h hours, they were treated with either vehicle (0.1% acetonitrile, white bars), 2 μM 6-thioguanine (6-TG, black bars), or co-treated with 2 μM 6-thioguanine and 5 μM sulforaphane (SF, grey bars) for further 24 h. Cells were then washed with Hank’s buffered saline solution (HBSS), and exposed to UVA (1, 2, or 3 J/cm 2 ) in 1.0 ml of HBSS. ROI generated by the UV radiation were quantified by the fluorescent probe 2′,7′- dichlorodihydrofluorescein and fluorescence intensity was measured 1 h post-irradiation. ( B ) Cells (1.75 × 10 5 per well in 6-well plates) were transiently transfected with a mixture of two siRNAs targeting Mrp4 , or with a non-targeting control oligo. The medium was changed 18 h after transfection with either medium containing 0.1% acetonitrile (black bars) or 5 μM SF (grey bars). Six hours later, the medium was changed, and the cells were treated with 6- thioguanine, in the presence of SF, for further 24 h. Cells were prepared and exposed to UVA (3 J/cm 2 ) as described under panel A . ( C ) Cells were seeded, treated, and exposed to UVA radiation as described under panel A . Reduced glutathione (GSH) was quantified using monochlorobimane and the fluorescence intensity of the GS-monochlorobimane adduct was determined 2 h post-irradiation. For all panels, means ± S.D. are shown (n = 3).

    Techniques Used: Generated, Fluorescence, Irradiation, Transfection

    4) Product Images from "Activated Rac1 regulates the degradation of IκBα and the nuclear translocation of STAT3–NFκB complexes in starved cancer cells"

    Article Title: Activated Rac1 regulates the degradation of IκBα and the nuclear translocation of STAT3–NFκB complexes in starved cancer cells

    Journal: Experimental & Molecular Medicine

    doi: 10.1038/emm.2016.17

    Rac1 is activated and colocalized with STAT3 or p65 in starved cancer cells. ( a ) HeLa cells were incubated in HBSS for the indicated time periods, and total cell lysates were incubated with PAK PBD agarose beads. Bound Rac1 was detected with western blotting using a Rac1 Ab (upper panel). The amount of total Rac1 was also measured with western blotting (lower panel). PC, positive control (GTPγS), NC, negative control (GDP). ( b ) HeLa cells incubated in HBSS for 4 h were fluorescence-stained with anti-Rac1 Ab, anti-STAT3 Ab, anti-p65 Ab and DAPI. ( c ) HeLa cells expressing vector or Rac1 wild-type HA (Rac1WT-HA) and STAT3 wild-type V5 (ST3WT-V5) were western blotted with V5 Ab, HA Ab and tubulin Ab (left). HeLa cells expressing Rac1WT-HA and ST3WT-V5 were incubated with HBSS for 0 or 8 h. Nuclear and cytoplasmic fractions were prepared, immunoprecipitated with anti-STAT3 Ab and western blotted with anti-HA Ab and anti-V5 Ab (right). DAPI, 4′,6-diamidino-2-phenylindole; HBSS, Hank's balanced salt solution; STAT3, signal transducer and activator of transcription 3.
    Figure Legend Snippet: Rac1 is activated and colocalized with STAT3 or p65 in starved cancer cells. ( a ) HeLa cells were incubated in HBSS for the indicated time periods, and total cell lysates were incubated with PAK PBD agarose beads. Bound Rac1 was detected with western blotting using a Rac1 Ab (upper panel). The amount of total Rac1 was also measured with western blotting (lower panel). PC, positive control (GTPγS), NC, negative control (GDP). ( b ) HeLa cells incubated in HBSS for 4 h were fluorescence-stained with anti-Rac1 Ab, anti-STAT3 Ab, anti-p65 Ab and DAPI. ( c ) HeLa cells expressing vector or Rac1 wild-type HA (Rac1WT-HA) and STAT3 wild-type V5 (ST3WT-V5) were western blotted with V5 Ab, HA Ab and tubulin Ab (left). HeLa cells expressing Rac1WT-HA and ST3WT-V5 were incubated with HBSS for 0 or 8 h. Nuclear and cytoplasmic fractions were prepared, immunoprecipitated with anti-STAT3 Ab and western blotted with anti-HA Ab and anti-V5 Ab (right). DAPI, 4′,6-diamidino-2-phenylindole; HBSS, Hank's balanced salt solution; STAT3, signal transducer and activator of transcription 3.

    Techniques Used: Incubation, Western Blot, Positive Control, Negative Control, Fluorescence, Staining, Expressing, Plasmid Preparation, Immunoprecipitation

    Degradation of IκB kinase by Rac1 in starved cancer cells is independent of IκBα serine phosphorylation by IKK. ( a ) HeLa cells expressing NT shRNA or Rac1 shRNA were western blotted with Rac1 Ab and tubulin Ab (left). HeLa cells expressing NT shRNA or Rac1 shRNA were incubated in HBSS for the indicated time periods and western blotted with IκBα Ab and tubulin Ab (right). ( b ) HeLa cells expressing NT or Rac1 shRNA incubated in HBSS for the indicated time periods were fluorescence-stained with anti-Rac1 Ab, anti-IκBα and DAPI. Arrow indicate p105 (upper) and p50 (lower), respectively. ( c ) HeLa cells expressing control vector, Rac1WT-HA, Rac1Q61L-HA or Rac1N17-HA were western blotted with HA Ab and tubulin Ab (left). HeLa cells expressing control vector, Rac1WT-HA, Rac1Q61L-HA or Rac1N17-HA were incubated in HBSS for the indicated time periods and western blotted with IκBα Ab and tubulin Ab (right). ( d ) HeLa cells expressing NT shRNA, STAT3 shRNA or Rac1 shRNA were western blotted with STAT3 Ab, Rac1 Ab and tubulin Ab (left). HeLa cells expressing NT shRNA, STAT3 shRNA or Rac1 shRNA were incubated in HBSS for 6 h with and without MG132 (25 μ M ), and western blotted to detect phospho-serine IκBα, IκBα or tubulin (right). Ab, antibody; DAPI, 4′,6-diamidino-2-phenylindole; HBSS, Hank's balanced salt solution; NT, non-target; short hairpin RNA; STAT3, signal transducer and activator of transcription 3.
    Figure Legend Snippet: Degradation of IκB kinase by Rac1 in starved cancer cells is independent of IκBα serine phosphorylation by IKK. ( a ) HeLa cells expressing NT shRNA or Rac1 shRNA were western blotted with Rac1 Ab and tubulin Ab (left). HeLa cells expressing NT shRNA or Rac1 shRNA were incubated in HBSS for the indicated time periods and western blotted with IκBα Ab and tubulin Ab (right). ( b ) HeLa cells expressing NT or Rac1 shRNA incubated in HBSS for the indicated time periods were fluorescence-stained with anti-Rac1 Ab, anti-IκBα and DAPI. Arrow indicate p105 (upper) and p50 (lower), respectively. ( c ) HeLa cells expressing control vector, Rac1WT-HA, Rac1Q61L-HA or Rac1N17-HA were western blotted with HA Ab and tubulin Ab (left). HeLa cells expressing control vector, Rac1WT-HA, Rac1Q61L-HA or Rac1N17-HA were incubated in HBSS for the indicated time periods and western blotted with IκBα Ab and tubulin Ab (right). ( d ) HeLa cells expressing NT shRNA, STAT3 shRNA or Rac1 shRNA were western blotted with STAT3 Ab, Rac1 Ab and tubulin Ab (left). HeLa cells expressing NT shRNA, STAT3 shRNA or Rac1 shRNA were incubated in HBSS for 6 h with and without MG132 (25 μ M ), and western blotted to detect phospho-serine IκBα, IκBα or tubulin (right). Ab, antibody; DAPI, 4′,6-diamidino-2-phenylindole; HBSS, Hank's balanced salt solution; NT, non-target; short hairpin RNA; STAT3, signal transducer and activator of transcription 3.

    Techniques Used: Expressing, shRNA, Western Blot, Incubation, Fluorescence, Staining, Plasmid Preparation

    STAT3, p65 and IκBα relocated to the membrane ruffles in starved cancer cells. ( a , b ) HeLa cells were incubated in HBSS for the indicated time periods. Confocal microscopy analysis showing STAT3, p65 and IκBα ( a ), and a merged image of STAT3 and p65 ( b ). Arrows indicate membrane ruffles. DAPI, 4′,6-diamidino-2-phenylindole; HBSS, Hank's balanced salt solution; STAT3, signal transducer and activator of transcription 3.
    Figure Legend Snippet: STAT3, p65 and IκBα relocated to the membrane ruffles in starved cancer cells. ( a , b ) HeLa cells were incubated in HBSS for the indicated time periods. Confocal microscopy analysis showing STAT3, p65 and IκBα ( a ), and a merged image of STAT3 and p65 ( b ). Arrows indicate membrane ruffles. DAPI, 4′,6-diamidino-2-phenylindole; HBSS, Hank's balanced salt solution; STAT3, signal transducer and activator of transcription 3.

    Techniques Used: Incubation, Confocal Microscopy

    Rac1 is required for nuclear translocation of the STAT3–NFκB complex in starved cancer cells. ( a ) Parental HeLa cells and HeLa cells expressing STAT3WT-V5 and p65-HA, and STAT3WT-V5, p65-HA and Rac1 shRNA were western blotted with V5 Ab, HA Ab, Rac1 Ab and tubulin Ab. ( b ) HeLa cells expressing ST3WT-V5 and p65-HA, and ST3WT-V5, p65-HA and Rac1 shRNA were incubated in HBSS for 8 h and had their nuclear and cytoplasmic fraction extracted and immunoprecipitated with anti-p65 Ab, followed by western blotting with STAT3 Ab and p65 Ab. ( c ) HeLa cells expressing NT shRNA, STAT3 shRNA, p65 shRNA or Rac1 shRNA were incubated in HBSS for 16 h, and the amounts of IL6 mRNA were measured by real-time PCR. Data are presented as relative quantitation (RQ)±s.d. Ab, antibody; C.F., cytoplasmic fraction; HBSS, Hank's balanced salt solution; IP, immunoprecipitate; mRNA, messenger RNA; NT, non-target; N.F., nuclear fraction; NFκB, nuclear factor κB; shRNA, short hairpin RNA; STAT3, signal transducer and activator of transcription 3.
    Figure Legend Snippet: Rac1 is required for nuclear translocation of the STAT3–NFκB complex in starved cancer cells. ( a ) Parental HeLa cells and HeLa cells expressing STAT3WT-V5 and p65-HA, and STAT3WT-V5, p65-HA and Rac1 shRNA were western blotted with V5 Ab, HA Ab, Rac1 Ab and tubulin Ab. ( b ) HeLa cells expressing ST3WT-V5 and p65-HA, and ST3WT-V5, p65-HA and Rac1 shRNA were incubated in HBSS for 8 h and had their nuclear and cytoplasmic fraction extracted and immunoprecipitated with anti-p65 Ab, followed by western blotting with STAT3 Ab and p65 Ab. ( c ) HeLa cells expressing NT shRNA, STAT3 shRNA, p65 shRNA or Rac1 shRNA were incubated in HBSS for 16 h, and the amounts of IL6 mRNA were measured by real-time PCR. Data are presented as relative quantitation (RQ)±s.d. Ab, antibody; C.F., cytoplasmic fraction; HBSS, Hank's balanced salt solution; IP, immunoprecipitate; mRNA, messenger RNA; NT, non-target; N.F., nuclear fraction; NFκB, nuclear factor κB; shRNA, short hairpin RNA; STAT3, signal transducer and activator of transcription 3.

    Techniques Used: Translocation Assay, Expressing, shRNA, Western Blot, Incubation, Immunoprecipitation, Real-time Polymerase Chain Reaction, Quantitation Assay

    5) Product Images from "Trans-basement membrane migration of eosinophils induced by LPS-stimulated neutrophils from human peripheral blood in vitro"

    Article Title: Trans-basement membrane migration of eosinophils induced by LPS-stimulated neutrophils from human peripheral blood in vitro

    Journal: ERJ Open Research

    doi: 10.1183/23120541.00003-2015

    Effect of neutrophils or lipopolysaccharide (LPS)-stimulated neutrophils from severe asthmatics on eosinophil trans-basement membrane migration. Neutrophils and eosinophils were isolated from the peripheral blood of severe asthmatics. Eosinophils (1×10 5 cells) were added to the upper compartment of a chamber with a Matrigel-coated Transwell insert. Hank's balanced salt solution (HBSS)/bovine serum albumin (BSA) (Control), neutrophils (2×10 4 cells) in HBSS/BSA (+Neut), LPS (10 µg·mL −1 ) in HBSS/BSA (+LPS) or the combination of LPS and neutrophils (+LPS+Neut) were placed into the lower compartment. After 120 min of incubation, migrated eosinophils in the lower chamber were measured by eosinophil peroxidase assays (n=4). Data are presented as mean± sem . **: p
    Figure Legend Snippet: Effect of neutrophils or lipopolysaccharide (LPS)-stimulated neutrophils from severe asthmatics on eosinophil trans-basement membrane migration. Neutrophils and eosinophils were isolated from the peripheral blood of severe asthmatics. Eosinophils (1×10 5 cells) were added to the upper compartment of a chamber with a Matrigel-coated Transwell insert. Hank's balanced salt solution (HBSS)/bovine serum albumin (BSA) (Control), neutrophils (2×10 4 cells) in HBSS/BSA (+Neut), LPS (10 µg·mL −1 ) in HBSS/BSA (+LPS) or the combination of LPS and neutrophils (+LPS+Neut) were placed into the lower compartment. After 120 min of incubation, migrated eosinophils in the lower chamber were measured by eosinophil peroxidase assays (n=4). Data are presented as mean± sem . **: p

    Techniques Used: Migration, Isolation, Incubation

    Lipopolysaccharide (LPS)-stimulated neutrophils from healthy volunteers induce the trans-basement membrane migration of eosinophils. Neutrophils and eosinophils were isolated from peripheral blood of healthy volunteers. Eosinophils (1×10 5 cells) were added to the upper compartment of a chamber with a Matrigel-coated Transwell insert. Hank's balanced salt solution (HBSS)/bovine serum albumin (BSA) (Control), neutrophils (2×10 4 cells) in HBSS/BSA (+Neut), LPS (10 µg·mL −1 ) in HBSS/BSA (+LPS) or the combination of LPS and neutrophils (+LPS+Neut) were placed into the lower compartment. After 120 min of incubation, migrated eosinophils in the lower chamber were measured by eosinophil peroxidase assays (n=5). Data are presented as mean± sem . ***: p
    Figure Legend Snippet: Lipopolysaccharide (LPS)-stimulated neutrophils from healthy volunteers induce the trans-basement membrane migration of eosinophils. Neutrophils and eosinophils were isolated from peripheral blood of healthy volunteers. Eosinophils (1×10 5 cells) were added to the upper compartment of a chamber with a Matrigel-coated Transwell insert. Hank's balanced salt solution (HBSS)/bovine serum albumin (BSA) (Control), neutrophils (2×10 4 cells) in HBSS/BSA (+Neut), LPS (10 µg·mL −1 ) in HBSS/BSA (+LPS) or the combination of LPS and neutrophils (+LPS+Neut) were placed into the lower compartment. After 120 min of incubation, migrated eosinophils in the lower chamber were measured by eosinophil peroxidase assays (n=5). Data are presented as mean± sem . ***: p

    Techniques Used: Migration, Isolation, Incubation

    6) Product Images from "Misoprostol Inhibits Equine Neutrophil Adhesion, Migration, and Respiratory Burst in an In Vitro Model of Inflammation"

    Article Title: Misoprostol Inhibits Equine Neutrophil Adhesion, Migration, and Respiratory Burst in an In Vitro Model of Inflammation

    Journal: Frontiers in Veterinary Science

    doi: 10.3389/fvets.2017.00159

    Misoprostol pretreatment inhibits CXCL8-, LTB 4 -, and PAF-induced equine neutrophil chemotaxis. Calcein AM-labeled equine neutrophils were pretreated with multiple concentrations of misoprostol, dibutyryl cyclic-AMP (db-cAMP), or the vehicle control (VC) for each inhibitor [Hank’s balanced salt solution (HBSS)]. The phosphatidylinositol-3 kinase (PI3K)-inhibitor wortmannin was used as a positive control for inhibition. Neutrophils were stimulated for 1 h with the following chemoattractants or vehicles: (A) 100 ng/ml CXCL8 (or HBSS vehicle), (B) 10 nM LTB 4 (or EtOH vehicle), or (C) 10 nM PAF (or EtOH vehicle). Percent chemotaxis was calculated by dividing florescence in each bottom well by 100% migration control wells. Data are expressed as mean% chemotaxis ± SEM. ** p
    Figure Legend Snippet: Misoprostol pretreatment inhibits CXCL8-, LTB 4 -, and PAF-induced equine neutrophil chemotaxis. Calcein AM-labeled equine neutrophils were pretreated with multiple concentrations of misoprostol, dibutyryl cyclic-AMP (db-cAMP), or the vehicle control (VC) for each inhibitor [Hank’s balanced salt solution (HBSS)]. The phosphatidylinositol-3 kinase (PI3K)-inhibitor wortmannin was used as a positive control for inhibition. Neutrophils were stimulated for 1 h with the following chemoattractants or vehicles: (A) 100 ng/ml CXCL8 (or HBSS vehicle), (B) 10 nM LTB 4 (or EtOH vehicle), or (C) 10 nM PAF (or EtOH vehicle). Percent chemotaxis was calculated by dividing florescence in each bottom well by 100% migration control wells. Data are expressed as mean% chemotaxis ± SEM. ** p

    Techniques Used: Chemotaxis Assay, Labeling, Positive Control, Inhibition, Migration

    Related Articles

    Infection:

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    Article Snippet: .. Detection of Ca2+ Accumulation The culture medium of infected or control cells was changed to HBSS that contained 5 μM Fluo4-AM (Invitrogen, Carlsbad, CA, USA), an indicator of Ca2+ in the cytosol. .. After incubation at 37 °C for 30 min, cells were washed twice with HBSS.

    Mouse Assay:

    Article Title: KML001, a Telomere-Targeting Drug, Sensitizes Glioblastoma Cells to Temozolomide Chemotherapy and Radiotherapy through DNA Damage and Apoptosis
    Article Snippet: .. To establish the orthotopic xenograft models, U87MG cells (2 × 105 /5 μ L Hank's balanced salt solution (HBSS), Gibco) were stereotypically injected into the left striata of mice (coordinate; AP +0.5, ML +1.7, DV −3.2 mm from Bregma). .. Each group had eight mice, and mice were medicated by KML001 (5 mg/kg for every day via per oral) at 1 day after tumor cells injection.

    Concentration Assay:

    Article Title: Monitoring mRNA Translation in Neuronal Processes Using Fluorescent Non-Canonical Amino Acid Tagging
    Article Snippet: .. In brief, HPG was diluted in HBSS (Life Technologies) to a concentration of 2 mM. .. Before HPG application, the culture medium was replaced with HBSS to deplete methionine from the cells for 30 min. During this pre-incubation, the appropriate samples were also treated with 100 µM cycloheximide (Sigma-Aldrich) to inhibit protein synthesis.

    Incubation:

    Article Title: Lysosomal Interaction of Akt with Phafin2: A Critical Step in the Induction of Autophagy
    Article Snippet: .. 12 hours later, the cells were treated with 10 µM Rapamycin (Sigma) or washed with PBS three times and subsequently incubated in HBSS (GIBCO,14025). .. The cells were then imaged using an Olympus IX-71 microscope equipped with a CoolSNAP HQ cooled charge-coupled device (Photometrics, Tucson, AZ).

    Article Title: Role of Bone Marrow-Derived Monocytes/Macrophages in the Repair of Mucosal Damage Caused by Irradiation and/or Anticancer Drugs in Colitis Model
    Article Snippet: .. Preparation of Damaged Mucosa and Identification of Injected BMCs Dissected mucosa was incubated in calcium and magnesium-free HBSS (GIBCO) containing 2.5% heat-inactivated FBS and 1 mM DTT (Sigma-Aldrich) to remove mucus. .. The mucosa was then incubated in HBSS containing 1 mM EDTA (GIBCO) for 45 min at 37°C.

    Staining:

    Article Title: Novel method for rapid toxicity screening of magnetic nanoparticles
    Article Snippet: .. To detect ROS in cells after MNPs addition, unfixed cells were washed with HBSS supplemented with 2 mM L-glutamine and 10 mM HEPES (pH 7,4 adjusted with 1 N NaOH), and stained with 2 µM H2DCFDA solution (life technologies) for 30 min at 37 °C in darkness. ..

    Injection:

    Article Title: In vivo distribution of U87MG cells injected into the lateral ventricle of rats with spinal cord injury
    Article Snippet: .. Then 20 nM Cy5.5 fluorescent dye (Amersham CyDye™ mono-reactive NHS Ester, GE Healthcare, Piscataway, NJ, USA) or 5 × 106 U87MG cells in 50 μL HBSS (Gibco) was injected into the lateral ventricle (4 mm deep from the skull) using a syringe pump (LEGATO™ 111, KD scientific, Holliston, MA, USA) for 10 minutes. .. After injection, the injection needle was maintained for 5 minutes to prevent leakage.

    Article Title: KML001, a Telomere-Targeting Drug, Sensitizes Glioblastoma Cells to Temozolomide Chemotherapy and Radiotherapy through DNA Damage and Apoptosis
    Article Snippet: .. To establish the orthotopic xenograft models, U87MG cells (2 × 105 /5 μ L Hank's balanced salt solution (HBSS), Gibco) were stereotypically injected into the left striata of mice (coordinate; AP +0.5, ML +1.7, DV −3.2 mm from Bregma). .. Each group had eight mice, and mice were medicated by KML001 (5 mg/kg for every day via per oral) at 1 day after tumor cells injection.

    Article Title: Role of Bone Marrow-Derived Monocytes/Macrophages in the Repair of Mucosal Damage Caused by Irradiation and/or Anticancer Drugs in Colitis Model
    Article Snippet: .. Preparation of Damaged Mucosa and Identification of Injected BMCs Dissected mucosa was incubated in calcium and magnesium-free HBSS (GIBCO) containing 2.5% heat-inactivated FBS and 1 mM DTT (Sigma-Aldrich) to remove mucus. .. The mucosa was then incubated in HBSS containing 1 mM EDTA (GIBCO) for 45 min at 37°C.

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    Thermo Fisher hank s balanced salt solution hbss
    Misoprostol pretreatment inhibits CXCL8-, LTB 4 -, and PAF-induced equine neutrophil chemotaxis. Calcein AM-labeled equine neutrophils were pretreated with multiple concentrations of misoprostol, dibutyryl cyclic-AMP (db-cAMP), or the vehicle control (VC) for each inhibitor <t>[Hank’s</t> balanced salt solution <t>(HBSS)].</t> The phosphatidylinositol-3 kinase (PI3K)-inhibitor wortmannin was used as a positive control for inhibition. Neutrophils were stimulated for 1 h with the following chemoattractants or vehicles: (A) 100 ng/ml CXCL8 (or HBSS vehicle), (B) 10 nM LTB 4 (or EtOH vehicle), or (C) 10 nM PAF (or EtOH vehicle). Percent chemotaxis was calculated by dividing florescence in each bottom well by 100% migration control wells. Data are expressed as mean% chemotaxis ± SEM. ** p
    Hank S Balanced Salt Solution Hbss, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 59 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Misoprostol pretreatment inhibits CXCL8-, LTB 4 -, and PAF-induced equine neutrophil chemotaxis. Calcein AM-labeled equine neutrophils were pretreated with multiple concentrations of misoprostol, dibutyryl cyclic-AMP (db-cAMP), or the vehicle control (VC) for each inhibitor [Hank’s balanced salt solution (HBSS)]. The phosphatidylinositol-3 kinase (PI3K)-inhibitor wortmannin was used as a positive control for inhibition. Neutrophils were stimulated for 1 h with the following chemoattractants or vehicles: (A) 100 ng/ml CXCL8 (or HBSS vehicle), (B) 10 nM LTB 4 (or EtOH vehicle), or (C) 10 nM PAF (or EtOH vehicle). Percent chemotaxis was calculated by dividing florescence in each bottom well by 100% migration control wells. Data are expressed as mean% chemotaxis ± SEM. ** p

    Journal: Frontiers in Veterinary Science

    Article Title: Misoprostol Inhibits Equine Neutrophil Adhesion, Migration, and Respiratory Burst in an In Vitro Model of Inflammation

    doi: 10.3389/fvets.2017.00159

    Figure Lengend Snippet: Misoprostol pretreatment inhibits CXCL8-, LTB 4 -, and PAF-induced equine neutrophil chemotaxis. Calcein AM-labeled equine neutrophils were pretreated with multiple concentrations of misoprostol, dibutyryl cyclic-AMP (db-cAMP), or the vehicle control (VC) for each inhibitor [Hank’s balanced salt solution (HBSS)]. The phosphatidylinositol-3 kinase (PI3K)-inhibitor wortmannin was used as a positive control for inhibition. Neutrophils were stimulated for 1 h with the following chemoattractants or vehicles: (A) 100 ng/ml CXCL8 (or HBSS vehicle), (B) 10 nM LTB 4 (or EtOH vehicle), or (C) 10 nM PAF (or EtOH vehicle). Percent chemotaxis was calculated by dividing florescence in each bottom well by 100% migration control wells. Data are expressed as mean% chemotaxis ± SEM. ** p

    Article Snippet: Experimental Reagents Lipopolysaccharide (LPS) from E. coli 055:B5, phorbol 12-myristate 13-acetate (PMA), CXCL8, dibutyryl cyclic AMP (db-cAMP), wortmannin, staurosporine, bovine serum albumin (BSA), and anti-BSA antibody were from Sigma Aldrich (St. Louis, MO, USA); heat-inactivated fetal bovine serum (FBS) was from Gemini-Bioproducts (West Sacramento, CA, USA); misoprostol, LTB4 , and PAF were from Cayman Chemical (Ann Arbor, MI, USA); equine recombinant granulocyte-monocyte colony-stimulating factor (GM-CSF) was from Kingfisher Biotech (Saint Paul, MN, USA); and Hank’s balanced salt solution (HBSS) was from Thermo Fisher Scientific (Grand Island, NY, USA).

    Techniques: Chemotaxis Assay, Labeling, Positive Control, Inhibition, Migration