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Fluka Chemical mucicarmine
Mucicarmine, supplied by Fluka Chemical, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mucicarmine/mucicarmine/10__1134_slash_s1062359023090194-27-4-5
Average 90 stars, based on 1 article reviews
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Article Title: Helminth Fauna of Black-Legged Kittiwakes (Rissa tridactyla, Laridae, Charadriiformes) in the Northern Part of the Kara Sea
Article Snippet: The results of original studies on the helminth fauna of the black-legged kittiwake (Rissa tridactyla L.) (ten ad. and ten juv.) in the northern part of the Kara Sea (Severnaya Zemlya Archipelago and Wiese Island) carried out in the years 2019–2020 are presented.. Eight species of helminths (one trematode, four cestodes, and three nematodes) have been registered.. For the first time in seabirds in the high latitudes of the Arctic, the trematode Diplostomum sp. and the nematode Paracuaria adunca have been recorded.



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Ferroptosis-related genes play a role in DSS-induced colitis and MSCs reverse the process of ferroptosis. ( A ) The qPCR detection <t>of</t> <t>MUC-1</t> gene in colitis tissues. ( B ) The immunohistochemistry images of NC, DSS+PBS, and DSS+MSC groups in colon tissues (scale bar: 100µm). ( C ) The CCK-8 analysis of IEC-6 cell viability. The different concentration (10, 5, and 2.5µM) of GO-203 (MUC-1 inhibitor) was used to measure the cell viability at 48 h, GO-203 10, 5, and 2.5µM vs control. ( D ) The proliferation level of IEC-6 cells in the presence of GO-203 (5µM) at 24 h and 48 h measured by CCK-8 assay. ( E ) The cell viability of IEC-6 cells in the presence of GO-203 and co-culture with MSCs. ( F ) The Western blot analysis of MUC-1 expression after transfected with overexpressing MUC-1 lentivirus in IEC-6 cells. ( G ) The proliferation level of IEC-6 cells transfected with overexpressing MUC-1 lentivirus in 24 h, 48 h, and 72 h. ( H ) The IEC-6 cell viability after treated with erastin and RSL3 with the comparison of control and overexpressed MUC-1 group. ( I ) qRT-PCR analysis of MUC-1, SLC7A11 , and GPX4 after treated with GO-203 (5µM) for 48 h in IEC-6 cells. ( J ) qRT-PCR analysis of SLC7A11 and GPX4 after overexpressed MUC-1 in IEC-6 cells. ( K ) qRT-PCR analysis of SLC7A11 and GPX4 in the presence of erastin in the control and overexpressed MUC-1 group. ( L ) qRT-PCR analysis of SLC7A11, GPX4 , and ACSL4 in the presence of RSL3 in the control and overexpressed MUC-1 group. Data are presented as mean ± SD. ***P < 0.001, **P < 0.01, *P < 0.05.
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Ferroptosis-related genes play a role in DSS-induced colitis and MSCs reverse the process of ferroptosis. ( A ) The qPCR detection <t>of</t> <t>MUC-1</t> gene in colitis tissues. ( B ) The immunohistochemistry images of NC, DSS+PBS, and DSS+MSC groups in colon tissues (scale bar: 100µm). ( C ) The CCK-8 analysis of IEC-6 cell viability. The different concentration (10, 5, and 2.5µM) of GO-203 (MUC-1 inhibitor) was used to measure the cell viability at 48 h, GO-203 10, 5, and 2.5µM vs control. ( D ) The proliferation level of IEC-6 cells in the presence of GO-203 (5µM) at 24 h and 48 h measured by CCK-8 assay. ( E ) The cell viability of IEC-6 cells in the presence of GO-203 and co-culture with MSCs. ( F ) The Western blot analysis of MUC-1 expression after transfected with overexpressing MUC-1 lentivirus in IEC-6 cells. ( G ) The proliferation level of IEC-6 cells transfected with overexpressing MUC-1 lentivirus in 24 h, 48 h, and 72 h. ( H ) The IEC-6 cell viability after treated with erastin and RSL3 with the comparison of control and overexpressed MUC-1 group. ( I ) qRT-PCR analysis of MUC-1, SLC7A11 , and GPX4 after treated with GO-203 (5µM) for 48 h in IEC-6 cells. ( J ) qRT-PCR analysis of SLC7A11 and GPX4 after overexpressed MUC-1 in IEC-6 cells. ( K ) qRT-PCR analysis of SLC7A11 and GPX4 in the presence of erastin in the control and overexpressed MUC-1 group. ( L ) qRT-PCR analysis of SLC7A11, GPX4 , and ACSL4 in the presence of RSL3 in the control and overexpressed MUC-1 group. Data are presented as mean ± SD. ***P < 0.001, **P < 0.01, *P < 0.05.
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Ferroptosis-related genes play a role in DSS-induced colitis and MSCs reverse the process of ferroptosis. ( A ) The qPCR detection <t>of</t> <t>MUC-1</t> gene in colitis tissues. ( B ) The immunohistochemistry images of NC, DSS+PBS, and DSS+MSC groups in colon tissues (scale bar: 100µm). ( C ) The CCK-8 analysis of IEC-6 cell viability. The different concentration (10, 5, and 2.5µM) of GO-203 (MUC-1 inhibitor) was used to measure the cell viability at 48 h, GO-203 10, 5, and 2.5µM vs control. ( D ) The proliferation level of IEC-6 cells in the presence of GO-203 (5µM) at 24 h and 48 h measured by CCK-8 assay. ( E ) The cell viability of IEC-6 cells in the presence of GO-203 and co-culture with MSCs. ( F ) The Western blot analysis of MUC-1 expression after transfected with overexpressing MUC-1 lentivirus in IEC-6 cells. ( G ) The proliferation level of IEC-6 cells transfected with overexpressing MUC-1 lentivirus in 24 h, 48 h, and 72 h. ( H ) The IEC-6 cell viability after treated with erastin and RSL3 with the comparison of control and overexpressed MUC-1 group. ( I ) qRT-PCR analysis of MUC-1, SLC7A11 , and GPX4 after treated with GO-203 (5µM) for 48 h in IEC-6 cells. ( J ) qRT-PCR analysis of SLC7A11 and GPX4 after overexpressed MUC-1 in IEC-6 cells. ( K ) qRT-PCR analysis of SLC7A11 and GPX4 in the presence of erastin in the control and overexpressed MUC-1 group. ( L ) qRT-PCR analysis of SLC7A11, GPX4 , and ACSL4 in the presence of RSL3 in the control and overexpressed MUC-1 group. Data are presented as mean ± SD. ***P < 0.001, **P < 0.01, *P < 0.05.
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Ferroptosis-related genes play a role in DSS-induced colitis and MSCs reverse the process of ferroptosis. ( A ) The qPCR detection <t>of</t> <t>MUC-1</t> gene in colitis tissues. ( B ) The immunohistochemistry images of NC, DSS+PBS, and DSS+MSC groups in colon tissues (scale bar: 100µm). ( C ) The CCK-8 analysis of IEC-6 cell viability. The different concentration (10, 5, and 2.5µM) of GO-203 (MUC-1 inhibitor) was used to measure the cell viability at 48 h, GO-203 10, 5, and 2.5µM vs control. ( D ) The proliferation level of IEC-6 cells in the presence of GO-203 (5µM) at 24 h and 48 h measured by CCK-8 assay. ( E ) The cell viability of IEC-6 cells in the presence of GO-203 and co-culture with MSCs. ( F ) The Western blot analysis of MUC-1 expression after transfected with overexpressing MUC-1 lentivirus in IEC-6 cells. ( G ) The proliferation level of IEC-6 cells transfected with overexpressing MUC-1 lentivirus in 24 h, 48 h, and 72 h. ( H ) The IEC-6 cell viability after treated with erastin and RSL3 with the comparison of control and overexpressed MUC-1 group. ( I ) qRT-PCR analysis of MUC-1, SLC7A11 , and GPX4 after treated with GO-203 (5µM) for 48 h in IEC-6 cells. ( J ) qRT-PCR analysis of SLC7A11 and GPX4 after overexpressed MUC-1 in IEC-6 cells. ( K ) qRT-PCR analysis of SLC7A11 and GPX4 in the presence of erastin in the control and overexpressed MUC-1 group. ( L ) qRT-PCR analysis of SLC7A11, GPX4 , and ACSL4 in the presence of RSL3 in the control and overexpressed MUC-1 group. Data are presented as mean ± SD. ***P < 0.001, **P < 0.01, *P < 0.05.
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Ferroptosis-related genes play a role in DSS-induced colitis and MSCs reverse the process of ferroptosis. ( A ) The qPCR detection <t>of</t> <t>MUC-1</t> gene in colitis tissues. ( B ) The immunohistochemistry images of NC, DSS+PBS, and DSS+MSC groups in colon tissues (scale bar: 100µm). ( C ) The CCK-8 analysis of IEC-6 cell viability. The different concentration (10, 5, and 2.5µM) of GO-203 (MUC-1 inhibitor) was used to measure the cell viability at 48 h, GO-203 10, 5, and 2.5µM vs control. ( D ) The proliferation level of IEC-6 cells in the presence of GO-203 (5µM) at 24 h and 48 h measured by CCK-8 assay. ( E ) The cell viability of IEC-6 cells in the presence of GO-203 and co-culture with MSCs. ( F ) The Western blot analysis of MUC-1 expression after transfected with overexpressing MUC-1 lentivirus in IEC-6 cells. ( G ) The proliferation level of IEC-6 cells transfected with overexpressing MUC-1 lentivirus in 24 h, 48 h, and 72 h. ( H ) The IEC-6 cell viability after treated with erastin and RSL3 with the comparison of control and overexpressed MUC-1 group. ( I ) qRT-PCR analysis of MUC-1, SLC7A11 , and GPX4 after treated with GO-203 (5µM) for 48 h in IEC-6 cells. ( J ) qRT-PCR analysis of SLC7A11 and GPX4 after overexpressed MUC-1 in IEC-6 cells. ( K ) qRT-PCR analysis of SLC7A11 and GPX4 in the presence of erastin in the control and overexpressed MUC-1 group. ( L ) qRT-PCR analysis of SLC7A11, GPX4 , and ACSL4 in the presence of RSL3 in the control and overexpressed MUC-1 group. Data are presented as mean ± SD. ***P < 0.001, **P < 0.01, *P < 0.05.
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(a) Nest of mucin-secreting tumor cells, lined by squamoid tumor cells (H&E, 20x). (b) Diffuse CK7 positivity (CK7 stain, 20x). (c) Tumor cells immunoreactive for MUC1 (MUC1 stain, 20x). (d) Glandular luminal mucin-secreting tumor cells focally stained for CK20 (CK20 stain, 20x). (e) MUC4 positivity in the apical aspect of luminal mucin-secreting tumor cells (MUC4 stain, 20x). (f) CEA positivity in glandular luminal tumor cells (CEA stain, 20x). (g) MUC5 staining in the luminal tumor cells (MUC5 stain, 20x). (h) <t>Mucicarmine</t> stain highlighting the intracytoplasmic mucin in the tumor cells (mucicarmine stain, 20x). (i) Outer squamoid tumor cells showed diffuse p63 staining (p63 stain, 20x). (j) Outer squamoid tumor cells showed diffuse CK5/6 staining (CK5/6 stain, 20x).
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(a) Organ load determination: BALB/c mice (6–8 weeks) were infected intra-nasally with 10 5 yeast cells of the WT, can2, or can2+CAN2 strain (3 mice/strain). After 14 days, mice were sacrificed, and their lungs were removed aseptically, weighed, homogenized, and diluted in PBS, and cultured on YPD agar in high CO 2 for CFU enumeration. Results were expressed as CFU per gram of tissue. No significant difference in organ load of WT or can2 mutant was observed (p>0.05). (b) In vivo capsule production: WT, can2, and can2+CAN2 strains recovered from mice lungs were visualized with India ink (magnification, × 100). (c) Histopathological examination of lungs: Left lung lobes from mice infected with the WT, the can2 mutant, or the can2+CAN2 reconstituted strain for 14-days were fixed, sectioned, and stained with Mayer’s <t>mucicarmine.</t> Alveoli (single arrow) and airways (double arrow) showed the presence of numerous organisms for each of the infecting strain and similar tissue response was noted for WT, can2 and can2 + CAN2 .
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(a) Organ load determination: BALB/c mice (6–8 weeks) were infected intra-nasally with 10 5 yeast cells of the WT, can2, or can2+CAN2 strain (3 mice/strain). After 14 days, mice were sacrificed, and their lungs were removed aseptically, weighed, homogenized, and diluted in PBS, and cultured on YPD agar in high CO 2 for CFU enumeration. Results were expressed as CFU per gram of tissue. No significant difference in organ load of WT or can2 mutant was observed (p>0.05). (b) In vivo capsule production: WT, can2, and can2+CAN2 strains recovered from mice lungs were visualized with India ink (magnification, × 100). (c) Histopathological examination of lungs: Left lung lobes from mice infected with the WT, the can2 mutant, or the can2+CAN2 reconstituted strain for 14-days were fixed, sectioned, and stained with Mayer’s <t>mucicarmine.</t> Alveoli (single arrow) and airways (double arrow) showed the presence of numerous organisms for each of the infecting strain and similar tissue response was noted for WT, can2 and can2 + CAN2 .
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Ferroptosis-related genes play a role in DSS-induced colitis and MSCs reverse the process of ferroptosis. ( A ) The qPCR detection of MUC-1 gene in colitis tissues. ( B ) The immunohistochemistry images of NC, DSS+PBS, and DSS+MSC groups in colon tissues (scale bar: 100µm). ( C ) The CCK-8 analysis of IEC-6 cell viability. The different concentration (10, 5, and 2.5µM) of GO-203 (MUC-1 inhibitor) was used to measure the cell viability at 48 h, GO-203 10, 5, and 2.5µM vs control. ( D ) The proliferation level of IEC-6 cells in the presence of GO-203 (5µM) at 24 h and 48 h measured by CCK-8 assay. ( E ) The cell viability of IEC-6 cells in the presence of GO-203 and co-culture with MSCs. ( F ) The Western blot analysis of MUC-1 expression after transfected with overexpressing MUC-1 lentivirus in IEC-6 cells. ( G ) The proliferation level of IEC-6 cells transfected with overexpressing MUC-1 lentivirus in 24 h, 48 h, and 72 h. ( H ) The IEC-6 cell viability after treated with erastin and RSL3 with the comparison of control and overexpressed MUC-1 group. ( I ) qRT-PCR analysis of MUC-1, SLC7A11 , and GPX4 after treated with GO-203 (5µM) for 48 h in IEC-6 cells. ( J ) qRT-PCR analysis of SLC7A11 and GPX4 after overexpressed MUC-1 in IEC-6 cells. ( K ) qRT-PCR analysis of SLC7A11 and GPX4 in the presence of erastin in the control and overexpressed MUC-1 group. ( L ) qRT-PCR analysis of SLC7A11, GPX4 , and ACSL4 in the presence of RSL3 in the control and overexpressed MUC-1 group. Data are presented as mean ± SD. ***P < 0.001, **P < 0.01, *P < 0.05.

Journal: Journal of Inflammation Research

Article Title: Mesenchymal Stem Cells Ameliorate DSS-Induced Experimental Colitis by Modulating the Gut Microbiota and MUC-1 Pathway

doi: 10.2147/JIR.S402592

Figure Lengend Snippet: Ferroptosis-related genes play a role in DSS-induced colitis and MSCs reverse the process of ferroptosis. ( A ) The qPCR detection of MUC-1 gene in colitis tissues. ( B ) The immunohistochemistry images of NC, DSS+PBS, and DSS+MSC groups in colon tissues (scale bar: 100µm). ( C ) The CCK-8 analysis of IEC-6 cell viability. The different concentration (10, 5, and 2.5µM) of GO-203 (MUC-1 inhibitor) was used to measure the cell viability at 48 h, GO-203 10, 5, and 2.5µM vs control. ( D ) The proliferation level of IEC-6 cells in the presence of GO-203 (5µM) at 24 h and 48 h measured by CCK-8 assay. ( E ) The cell viability of IEC-6 cells in the presence of GO-203 and co-culture with MSCs. ( F ) The Western blot analysis of MUC-1 expression after transfected with overexpressing MUC-1 lentivirus in IEC-6 cells. ( G ) The proliferation level of IEC-6 cells transfected with overexpressing MUC-1 lentivirus in 24 h, 48 h, and 72 h. ( H ) The IEC-6 cell viability after treated with erastin and RSL3 with the comparison of control and overexpressed MUC-1 group. ( I ) qRT-PCR analysis of MUC-1, SLC7A11 , and GPX4 after treated with GO-203 (5µM) for 48 h in IEC-6 cells. ( J ) qRT-PCR analysis of SLC7A11 and GPX4 after overexpressed MUC-1 in IEC-6 cells. ( K ) qRT-PCR analysis of SLC7A11 and GPX4 in the presence of erastin in the control and overexpressed MUC-1 group. ( L ) qRT-PCR analysis of SLC7A11, GPX4 , and ACSL4 in the presence of RSL3 in the control and overexpressed MUC-1 group. Data are presented as mean ± SD. ***P < 0.001, **P < 0.01, *P < 0.05.

Article Snippet: The MUC-1 gene inhibitor GO-203 (MCE) was added to IEC-6 cells with different concentrations (10, 5, and 2.5μM).

Techniques: Immunohistochemistry, CCK-8 Assay, Concentration Assay, Control, Co-Culture Assay, Western Blot, Expressing, Transfection, Comparison, Quantitative RT-PCR

(a) Nest of mucin-secreting tumor cells, lined by squamoid tumor cells (H&E, 20x). (b) Diffuse CK7 positivity (CK7 stain, 20x). (c) Tumor cells immunoreactive for MUC1 (MUC1 stain, 20x). (d) Glandular luminal mucin-secreting tumor cells focally stained for CK20 (CK20 stain, 20x). (e) MUC4 positivity in the apical aspect of luminal mucin-secreting tumor cells (MUC4 stain, 20x). (f) CEA positivity in glandular luminal tumor cells (CEA stain, 20x). (g) MUC5 staining in the luminal tumor cells (MUC5 stain, 20x). (h) Mucicarmine stain highlighting the intracytoplasmic mucin in the tumor cells (mucicarmine stain, 20x). (i) Outer squamoid tumor cells showed diffuse p63 staining (p63 stain, 20x). (j) Outer squamoid tumor cells showed diffuse CK5/6 staining (CK5/6 stain, 20x).

Journal: Case Reports in Pathology

Article Title: Mucoepidermoid Carcinoma of the Intrapancreatic Common Bile Duct: Immunohistochemical Profile, Prognosis, and Review of the Literature

doi: 10.1155/2013/192458

Figure Lengend Snippet: (a) Nest of mucin-secreting tumor cells, lined by squamoid tumor cells (H&E, 20x). (b) Diffuse CK7 positivity (CK7 stain, 20x). (c) Tumor cells immunoreactive for MUC1 (MUC1 stain, 20x). (d) Glandular luminal mucin-secreting tumor cells focally stained for CK20 (CK20 stain, 20x). (e) MUC4 positivity in the apical aspect of luminal mucin-secreting tumor cells (MUC4 stain, 20x). (f) CEA positivity in glandular luminal tumor cells (CEA stain, 20x). (g) MUC5 staining in the luminal tumor cells (MUC5 stain, 20x). (h) Mucicarmine stain highlighting the intracytoplasmic mucin in the tumor cells (mucicarmine stain, 20x). (i) Outer squamoid tumor cells showed diffuse p63 staining (p63 stain, 20x). (j) Outer squamoid tumor cells showed diffuse CK5/6 staining (CK5/6 stain, 20x).

Article Snippet: Tumor sections were stained with mucicarmine stain (Dako) and immunohistochemistry using the Dako EnVision system with the following antibodies: CK7 (Dako, mouse monoclonal, RTU), CK20 (Dako, mouse monoclonal, RTU), carcinoembryonic antigen (CEA, Dako, mouse monoclonal, RTU), p63 (BioCARE, mouse monoclonal, 1 : 20), CK5/6 (Dako, mouse monoclonal, RTU), MUC1 (BioCARE, mouse monoclonal, 1 : 100), MUC2 (Dako, mouse monoclonal, RTU), MUC4 (Invitrogen, mouse monoclonal, 1 : 400), MUC5 (Leica, mouse monoclonal, 1 : 50), and HER2-neu (c-erbB2, Dako, rabbit polyclonal, 1 : 3000).

Techniques: Staining

(a) Organ load determination: BALB/c mice (6–8 weeks) were infected intra-nasally with 10 5 yeast cells of the WT, can2, or can2+CAN2 strain (3 mice/strain). After 14 days, mice were sacrificed, and their lungs were removed aseptically, weighed, homogenized, and diluted in PBS, and cultured on YPD agar in high CO 2 for CFU enumeration. Results were expressed as CFU per gram of tissue. No significant difference in organ load of WT or can2 mutant was observed (p>0.05). (b) In vivo capsule production: WT, can2, and can2+CAN2 strains recovered from mice lungs were visualized with India ink (magnification, × 100). (c) Histopathological examination of lungs: Left lung lobes from mice infected with the WT, the can2 mutant, or the can2+CAN2 reconstituted strain for 14-days were fixed, sectioned, and stained with Mayer’s mucicarmine. Alveoli (single arrow) and airways (double arrow) showed the presence of numerous organisms for each of the infecting strain and similar tissue response was noted for WT, can2 and can2 + CAN2 .

Journal: PLoS ONE

Article Title: Carbon Dioxide is a Powerful Inducer of Monokaryotic Hyphae and Spore Development in Cryptococcus gattii and Carbonic Anhydrase Activity is Dispensable in This Dimorphic Transition

doi: 10.1371/journal.pone.0113147

Figure Lengend Snippet: (a) Organ load determination: BALB/c mice (6–8 weeks) were infected intra-nasally with 10 5 yeast cells of the WT, can2, or can2+CAN2 strain (3 mice/strain). After 14 days, mice were sacrificed, and their lungs were removed aseptically, weighed, homogenized, and diluted in PBS, and cultured on YPD agar in high CO 2 for CFU enumeration. Results were expressed as CFU per gram of tissue. No significant difference in organ load of WT or can2 mutant was observed (p>0.05). (b) In vivo capsule production: WT, can2, and can2+CAN2 strains recovered from mice lungs were visualized with India ink (magnification, × 100). (c) Histopathological examination of lungs: Left lung lobes from mice infected with the WT, the can2 mutant, or the can2+CAN2 reconstituted strain for 14-days were fixed, sectioned, and stained with Mayer’s mucicarmine. Alveoli (single arrow) and airways (double arrow) showed the presence of numerous organisms for each of the infecting strain and similar tissue response was noted for WT, can2 and can2 + CAN2 .

Article Snippet: For histopathology, the left lung lobe was dissected and immersion-fixed in formalin; it was embedded and processed into paraffin blocks, sectioned at 4µm and stained with mucicarmine (Richard-Allan Scientific, Kalamazoo, MI).

Techniques: Infection, Cell Culture, Mutagenesis, In Vivo, Staining