tnf α concentrations Search Results


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GeneTex rabbit anti-tnf- α gtx26671
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LINCO tnf-α concentrations
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Genzyme tnf-α concentrations
P. carinii detection by histology and PCR. P. carinii organisms were undetectable by silver methenamine staining of lung sections from parasite-exposed healthy mutants (A, represented by IFN-γ-R−/−), in contrast to morbid mutant mice (B, represented by TCRβ−/−). Magnification of the diseased lung section is shown to distinguish stained sporangia (C). Whole lung digests were used for detection of P. carinii by PCR, products of which were blotted on nitrocellulose and hybridized with a P. carinii-specific gene fragment (D). Parasitized lung tissues of TCRβ−/−, Aβ−/−, and RAG-1−/− mutant mice gave positive signals, whereas tissues from P. carinii-exposed heterozygous control mice (+/−) and from exposed IFN-γ-R−/− or <t>TNF-α-RI−/−</t> mutants did not reveal a detectable PCR signal. Bars, 50 μm.
Tnf α Concentrations, supplied by Genzyme, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Nanjing Jiancheng Bioengineering Research Institute Co Ltd cytokine concentrations of tnf-α
P. carinii detection by histology and PCR. P. carinii organisms were undetectable by silver methenamine staining of lung sections from parasite-exposed healthy mutants (A, represented by IFN-γ-R−/−), in contrast to morbid mutant mice (B, represented by TCRβ−/−). Magnification of the diseased lung section is shown to distinguish stained sporangia (C). Whole lung digests were used for detection of P. carinii by PCR, products of which were blotted on nitrocellulose and hybridized with a P. carinii-specific gene fragment (D). Parasitized lung tissues of TCRβ−/−, Aβ−/−, and RAG-1−/− mutant mice gave positive signals, whereas tissues from P. carinii-exposed heterozygous control mice (+/−) and from exposed IFN-γ-R−/− or <t>TNF-α-RI−/−</t> mutants did not reveal a detectable PCR signal. Bars, 50 μm.
Cytokine Concentrations Of Tnf α, supplied by Nanjing Jiancheng Bioengineering Research Institute Co Ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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PeproTech cytokine concentrations of tnf-α
P. carinii detection by histology and PCR. P. carinii organisms were undetectable by silver methenamine staining of lung sections from parasite-exposed healthy mutants (A, represented by IFN-γ-R−/−), in contrast to morbid mutant mice (B, represented by TCRβ−/−). Magnification of the diseased lung section is shown to distinguish stained sporangia (C). Whole lung digests were used for detection of P. carinii by PCR, products of which were blotted on nitrocellulose and hybridized with a P. carinii-specific gene fragment (D). Parasitized lung tissues of TCRβ−/−, Aβ−/−, and RAG-1−/− mutant mice gave positive signals, whereas tissues from P. carinii-exposed heterozygous control mice (+/−) and from exposed IFN-γ-R−/− or <t>TNF-α-RI−/−</t> mutants did not reveal a detectable PCR signal. Bars, 50 μm.
Cytokine Concentrations Of Tnf α, supplied by PeproTech, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Medience Co Ltd serum cytokine concentrations of tnf-α and il-6
P. carinii detection by histology and PCR. P. carinii organisms were undetectable by silver methenamine staining of lung sections from parasite-exposed healthy mutants (A, represented by IFN-γ-R−/−), in contrast to morbid mutant mice (B, represented by TCRβ−/−). Magnification of the diseased lung section is shown to distinguish stained sporangia (C). Whole lung digests were used for detection of P. carinii by PCR, products of which were blotted on nitrocellulose and hybridized with a P. carinii-specific gene fragment (D). Parasitized lung tissues of TCRβ−/−, Aβ−/−, and RAG-1−/− mutant mice gave positive signals, whereas tissues from P. carinii-exposed heterozygous control mice (+/−) and from exposed IFN-γ-R−/− or <t>TNF-α-RI−/−</t> mutants did not reveal a detectable PCR signal. Bars, 50 μm.
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Huangshi Feiyun Pharmaceutical Co Ltd serum concentrations tnf-α
Pathological images of the ileum and serum inflammatory factors in each group. ( A ) H & E staining (n=4). Serum LPS ( B ) <t>and</t> <t>TNF-α</t> ( C ) levels were detected with ELISA kits. Data are shown as the mean ± SEM. **p < 0.01 (n = 8).
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Loss of insertion and probe depth.
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Dakewe Biotech Co tnf-α and il-6 concentrations via elisa analysis
Aloin inhibits the LPS-induced expression of IL-6 <t>and</t> <t>TNF-α</t> RAW 264.7 cells were pre-treated with aloin for 2 h prior to LPS (100 ng/mL) stimulation. Cell-free supernatants were collected to detect ( A ) Interleukin 6 (IL-6) and ( B ) Tumor necrosis factor <t>alpha</t> <t>(TNF-α)</t> concentrations via ELISA after LPS treatment for 9 h and 24 h, respectively. The mRNA expression levels of ( C ) IL-6 and ( D ) TNF-α were determined by qPCR in RAW264.7 cells pre-treated with aloin (400 μM) followed by LPS (100 ng/mL) stimulation for 6 h. The data shown are the means ± SD of three experiments. ### p < 0.001 is significantly different from the control. * p < 0.05, ** p < 0.01, and *** p < 0.001 are different from the LPS alone.
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GeneticLab Co Ltd plasma concentrations of leptin and tnf-α
Aloin inhibits the LPS-induced expression of IL-6 <t>and</t> <t>TNF-α</t> RAW 264.7 cells were pre-treated with aloin for 2 h prior to LPS (100 ng/mL) stimulation. Cell-free supernatants were collected to detect ( A ) Interleukin 6 (IL-6) and ( B ) Tumor necrosis factor <t>alpha</t> <t>(TNF-α)</t> concentrations via ELISA after LPS treatment for 9 h and 24 h, respectively. The mRNA expression levels of ( C ) IL-6 and ( D ) TNF-α were determined by qPCR in RAW264.7 cells pre-treated with aloin (400 μM) followed by LPS (100 ng/mL) stimulation for 6 h. The data shown are the means ± SD of three experiments. ### p < 0.001 is significantly different from the control. * p < 0.05, ** p < 0.01, and *** p < 0.001 are different from the LPS alone.
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Elabscience Biotechnology elisa kits for determination of concentrations of il-6 and tnf-α
Aloin inhibits the LPS-induced expression of IL-6 <t>and</t> <t>TNF-α</t> RAW 264.7 cells were pre-treated with aloin for 2 h prior to LPS (100 ng/mL) stimulation. Cell-free supernatants were collected to detect ( A ) Interleukin 6 (IL-6) and ( B ) Tumor necrosis factor <t>alpha</t> <t>(TNF-α)</t> concentrations via ELISA after LPS treatment for 9 h and 24 h, respectively. The mRNA expression levels of ( C ) IL-6 and ( D ) TNF-α were determined by qPCR in RAW264.7 cells pre-treated with aloin (400 μM) followed by LPS (100 ng/mL) stimulation for 6 h. The data shown are the means ± SD of three experiments. ### p < 0.001 is significantly different from the control. * p < 0.05, ** p < 0.01, and *** p < 0.001 are different from the LPS alone.
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Purdue University Cytometry serum concentrations of il-1β, tnf-α and vegf
Aloin inhibits the LPS-induced expression of IL-6 <t>and</t> <t>TNF-α</t> RAW 264.7 cells were pre-treated with aloin for 2 h prior to LPS (100 ng/mL) stimulation. Cell-free supernatants were collected to detect ( A ) Interleukin 6 (IL-6) and ( B ) Tumor necrosis factor <t>alpha</t> <t>(TNF-α)</t> concentrations via ELISA after LPS treatment for 9 h and 24 h, respectively. The mRNA expression levels of ( C ) IL-6 and ( D ) TNF-α were determined by qPCR in RAW264.7 cells pre-treated with aloin (400 μM) followed by LPS (100 ng/mL) stimulation for 6 h. The data shown are the means ± SD of three experiments. ### p < 0.001 is significantly different from the control. * p < 0.05, ** p < 0.01, and *** p < 0.001 are different from the LPS alone.
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Image Search Results


P. carinii detection by histology and PCR. P. carinii organisms were undetectable by silver methenamine staining of lung sections from parasite-exposed healthy mutants (A, represented by IFN-γ-R−/−), in contrast to morbid mutant mice (B, represented by TCRβ−/−). Magnification of the diseased lung section is shown to distinguish stained sporangia (C). Whole lung digests were used for detection of P. carinii by PCR, products of which were blotted on nitrocellulose and hybridized with a P. carinii-specific gene fragment (D). Parasitized lung tissues of TCRβ−/−, Aβ−/−, and RAG-1−/− mutant mice gave positive signals, whereas tissues from P. carinii-exposed heterozygous control mice (+/−) and from exposed IFN-γ-R−/− or TNF-α-RI−/− mutants did not reveal a detectable PCR signal. Bars, 50 μm.

Journal:

Article Title: Activated Pulmonary Macrophages Are Insufficient for Resistance against Pneumocystis carinii

doi:

Figure Lengend Snippet: P. carinii detection by histology and PCR. P. carinii organisms were undetectable by silver methenamine staining of lung sections from parasite-exposed healthy mutants (A, represented by IFN-γ-R−/−), in contrast to morbid mutant mice (B, represented by TCRβ−/−). Magnification of the diseased lung section is shown to distinguish stained sporangia (C). Whole lung digests were used for detection of P. carinii by PCR, products of which were blotted on nitrocellulose and hybridized with a P. carinii-specific gene fragment (D). Parasitized lung tissues of TCRβ−/−, Aβ−/−, and RAG-1−/− mutant mice gave positive signals, whereas tissues from P. carinii-exposed heterozygous control mice (+/−) and from exposed IFN-γ-R−/− or TNF-α-RI−/− mutants did not reveal a detectable PCR signal. Bars, 50 μm.

Article Snippet: Standard TNF-α concentrations (Genzyme Corporation, Cambridge, Mass.) or experimental supernatants (50 μl) were added and incubated at 37°C for a further 24 h. To control for TNF-β secretion, selected samples were additionally preincubated with an excess of anti-TNF-α polyclonal Ab (Genzyme).

Techniques: Staining, Mutagenesis

Detection of iNOS expression in lung sections and cytospins of BAL cells by immunohistology. Lung sections of diseased TCRβ−/−, Aβ−/−, and RAG-1−/− mutant mice consistently stained positively with a polyclonal Ab against iNOS (A, represented by Aβ−/−). Lung sections from P. carinii-exposed IFN-γ-R−/− (B) and TNF-α-RI−/− (C) mutant mice were iNOS negative. Staining of cytospin preparations of BAL cells derived from parasitized mutant mice revealed that iNOS expression was restricted to alveolar macrophages (D, represented by Aβ−/−). Arrow, multinucleated giant cell. (A to C) AP-conjugated anti-iNOS polyclonal Ab developed with NBT-BCIP and counterstained with nuclear fast red; (D) AP-conjugated anti-iNOS Ab developed with NBT-BCIP-INT and counterstained with hematoxylin. Bars, 50 μm.

Journal:

Article Title: Activated Pulmonary Macrophages Are Insufficient for Resistance against Pneumocystis carinii

doi:

Figure Lengend Snippet: Detection of iNOS expression in lung sections and cytospins of BAL cells by immunohistology. Lung sections of diseased TCRβ−/−, Aβ−/−, and RAG-1−/− mutant mice consistently stained positively with a polyclonal Ab against iNOS (A, represented by Aβ−/−). Lung sections from P. carinii-exposed IFN-γ-R−/− (B) and TNF-α-RI−/− (C) mutant mice were iNOS negative. Staining of cytospin preparations of BAL cells derived from parasitized mutant mice revealed that iNOS expression was restricted to alveolar macrophages (D, represented by Aβ−/−). Arrow, multinucleated giant cell. (A to C) AP-conjugated anti-iNOS polyclonal Ab developed with NBT-BCIP and counterstained with nuclear fast red; (D) AP-conjugated anti-iNOS Ab developed with NBT-BCIP-INT and counterstained with hematoxylin. Bars, 50 μm.

Article Snippet: Standard TNF-α concentrations (Genzyme Corporation, Cambridge, Mass.) or experimental supernatants (50 μl) were added and incubated at 37°C for a further 24 h. To control for TNF-β secretion, selected samples were additionally preincubated with an excess of anti-TNF-α polyclonal Ab (Genzyme).

Techniques: Expressing, Mutagenesis, Staining, Negative Staining, Derivative Assay

Constitutive IFN-γ (A), TNF-α (B), and IL-12 (C) production by 105 BAL cells from healthy and diseased mouse mutants with indicated deficiencies. Each data point corresponds to one mouse, for which at least two replicates were performed. Average values are indicated by horizontal bars. Asterisks indicate significant differences (Student t test, P < 0.05) between cytokine levels attained by healthy and diseased mice of each mutant strain. Statistics are not applicable in panel A, since healthy animals do not produce any IFN-γ. h, healthy; d, diseased.

Journal:

Article Title: Activated Pulmonary Macrophages Are Insufficient for Resistance against Pneumocystis carinii

doi:

Figure Lengend Snippet: Constitutive IFN-γ (A), TNF-α (B), and IL-12 (C) production by 105 BAL cells from healthy and diseased mouse mutants with indicated deficiencies. Each data point corresponds to one mouse, for which at least two replicates were performed. Average values are indicated by horizontal bars. Asterisks indicate significant differences (Student t test, P < 0.05) between cytokine levels attained by healthy and diseased mice of each mutant strain. Statistics are not applicable in panel A, since healthy animals do not produce any IFN-γ. h, healthy; d, diseased.

Article Snippet: Standard TNF-α concentrations (Genzyme Corporation, Cambridge, Mass.) or experimental supernatants (50 μl) were added and incubated at 37°C for a further 24 h. To control for TNF-β secretion, selected samples were additionally preincubated with an excess of anti-TNF-α polyclonal Ab (Genzyme).

Techniques: Mutagenesis

Cytokine production by alveolar macrophages from healthy and diseased mice after stimulation

Journal:

Article Title: Activated Pulmonary Macrophages Are Insufficient for Resistance against Pneumocystis carinii

doi:

Figure Lengend Snippet: Cytokine production by alveolar macrophages from healthy and diseased mice after stimulation

Article Snippet: Standard TNF-α concentrations (Genzyme Corporation, Cambridge, Mass.) or experimental supernatants (50 μl) were added and incubated at 37°C for a further 24 h. To control for TNF-β secretion, selected samples were additionally preincubated with an excess of anti-TNF-α polyclonal Ab (Genzyme).

Techniques:

Pathological images of the ileum and serum inflammatory factors in each group. ( A ) H & E staining (n=4). Serum LPS ( B ) and TNF-α ( C ) levels were detected with ELISA kits. Data are shown as the mean ± SEM. **p < 0.01 (n = 8).

Journal: Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy

Article Title: Electroacupuncture at Lower He-Sea and Front-Mu Acupoints Ameliorates Insulin Resistance in Type 2 Diabetes Mellitus by Regulating the Intestinal Flora and Gut Barrier

doi: 10.2147/DMSO.S374843

Figure Lengend Snippet: Pathological images of the ileum and serum inflammatory factors in each group. ( A ) H & E staining (n=4). Serum LPS ( B ) and TNF-α ( C ) levels were detected with ELISA kits. Data are shown as the mean ± SEM. **p < 0.01 (n = 8).

Article Snippet: A mouse TNF-α ELISA Kit (Beyotime) was used to determine the serum concentrations of TNF-α (Huangshi Yanke Biotechnology Co., Ltd., Product number: CK-E20852) and LPS (Huangshi Yanke Biotechnology Co., Ltd., Product number: CK-E31044).

Techniques: Staining, Enzyme-linked Immunosorbent Assay

Loss of insertion and probe depth.

Journal: BioMed Research International

Article Title: Quantification of TNF- α in Patients with Periodontitis and Type 2 Diabetes

doi: 10.1155/2019/7984891

Figure Lengend Snippet: Loss of insertion and probe depth.

Article Snippet: Interstudy variation in TNF- α concentrations may be due to several factors including periodontal disease severity, subject age, sample type, population type, and technique details such as storage temperature and pretest storage time [ ].

Techniques: Control

Aloin inhibits the LPS-induced expression of IL-6 and TNF-α RAW 264.7 cells were pre-treated with aloin for 2 h prior to LPS (100 ng/mL) stimulation. Cell-free supernatants were collected to detect ( A ) Interleukin 6 (IL-6) and ( B ) Tumor necrosis factor alpha (TNF-α) concentrations via ELISA after LPS treatment for 9 h and 24 h, respectively. The mRNA expression levels of ( C ) IL-6 and ( D ) TNF-α were determined by qPCR in RAW264.7 cells pre-treated with aloin (400 μM) followed by LPS (100 ng/mL) stimulation for 6 h. The data shown are the means ± SD of three experiments. ### p < 0.001 is significantly different from the control. * p < 0.05, ** p < 0.01, and *** p < 0.001 are different from the LPS alone.

Journal: Molecules : A Journal of Synthetic Chemistry and Natural Product Chemistry

Article Title: Aloin Suppresses Lipopolysaccharide-Induced Inflammatory Response and Apoptosis by Inhibiting the Activation of NF-κB

doi: 10.3390/molecules23030517

Figure Lengend Snippet: Aloin inhibits the LPS-induced expression of IL-6 and TNF-α RAW 264.7 cells were pre-treated with aloin for 2 h prior to LPS (100 ng/mL) stimulation. Cell-free supernatants were collected to detect ( A ) Interleukin 6 (IL-6) and ( B ) Tumor necrosis factor alpha (TNF-α) concentrations via ELISA after LPS treatment for 9 h and 24 h, respectively. The mRNA expression levels of ( C ) IL-6 and ( D ) TNF-α were determined by qPCR in RAW264.7 cells pre-treated with aloin (400 μM) followed by LPS (100 ng/mL) stimulation for 6 h. The data shown are the means ± SD of three experiments. ### p < 0.001 is significantly different from the control. * p < 0.05, ** p < 0.01, and *** p < 0.001 are different from the LPS alone.

Article Snippet: Cell-free supernatants were collected for the determination of TNF-α and IL-6 concentrations via ELISA analysis (Dakewe), according the manufacturer’s protocols.

Techniques: Expressing, Enzyme-linked Immunosorbent Assay