Presentation is loading. Please wait.

Presentation is loading. Please wait.

Optimized STZ treatment leads to specific cytotoxicity of insulin-producing cells. Optimized STZ treatment leads to specific cytotoxicity of insulin-producing.

Published byBennett Riley Modified over 5 years ago

Similar presentations

Presentation on theme: "Optimized STZ treatment leads to specific cytotoxicity of insulin-producing cells. Optimized STZ treatment leads to specific cytotoxicity of insulin-producing."— Presentation transcript:

1 Optimized STZ treatment leads to specific cytotoxicity of insulin-producing cells.
Optimized STZ treatment leads to specific cytotoxicity of insulin-producing cells. Images are representative of guinea pigs developing hyperglycemia after treatment with an optimized SC dose of anomer-equilibrated STZ at 200 mg/kg administered after an intramuscular injection of yohimbine. (A) Pancreatic islets from a nondiabetic, normal-diet control guinea pig (arrow) demonstrating histological morphology in the absence of diabetogenic treatment. (B) Morphological changes 48 h after STZ treatment in pancreas of a guinea pig with confirmed hyperglycemia that was fed a normal diet. Cell death has occurred in the majority of islet cells (arrowheads), while a minority of the cells remain viable. (C) Immunofluorescent detection of pro-insulin (green) in pancreatic islets in a normal-diet control guinea pig indicates that the majority of islet cells are insulin-producing β cells (blue, Hoechst nuclear counterstain). (D,E) Immunofluorescent detection of pro-insulin in a guinea pig 48 h after receiving an optimized dose of STZ. Disruption of cellular and nuclear morphology is uniform across all islets and is specific to insulin-expressing β cells (arrows and inset). Scale bar: 100 µm. Brendan K. Podell et al. Dis. Model. Mech. 2017;10: © Published by The Company of Biologists Ltd

Download ppt "Optimized STZ treatment leads to specific cytotoxicity of insulin-producing cells. Optimized STZ treatment leads to specific cytotoxicity of insulin-producing."

Similar presentations

Mitochondria localize to both the front and the rear of neutrophils.

Mitochondria localize to both the front and the rear of neutrophils.
TMZ and Ara-C treatment of slice co-cultures.

TMZ and Ara-C treatment of slice co-cultures.
The gene encoding TP53INP1 is expressed in pancreatic endocrine cells A, B(A, B) Immunocytofluorescent staining of TP53INP1 (red) and insulin (green) in.

The gene encoding TP53INP1 is expressed in pancreatic endocrine cells A, B(A, B) Immunocytofluorescent staining of TP53INP1 (red) and insulin (green) in.
Morphological alterations in pancreatic islets demonstrate a compensatory response to HFHC diet and STZ-induced β-cell loss. Morphological alterations.

Morphological alterations in pancreatic islets demonstrate a compensatory response to HFHC diet and STZ-induced β-cell loss. Morphological alterations.
Visualisation of metabolic tissues in zebrafish.

Visualisation of metabolic tissues in zebrafish.
Development of stable STZ-induced diabetes requires coexisting diet-induced impaired glucose tolerance. Development of stable STZ-induced diabetes requires.

Development of stable STZ-induced diabetes requires coexisting diet-induced impaired glucose tolerance. Development of stable STZ-induced diabetes requires.
Percentage fractions of (β-Gal+) PCs in 32-week-old heterozygous females differ between cerebellar lobules affected and spared from degeneration of Purkinje.

Percentage fractions of (β-Gal+) PCs in 32-week-old heterozygous females differ between cerebellar lobules affected and spared from degeneration of Purkinje.
Effect of cxcr3.2 mutation on dissemination of local mycobacterial infection within 24 hpi. Effect of cxcr3.2 mutation on dissemination of local mycobacterial.

Effect of cxcr3.2 mutation on dissemination of local mycobacterial infection within 24 hpi. Effect of cxcr3.2 mutation on dissemination of local mycobacterial.
Fig. 8. In vitro effect of CMPs on adult DSS-treated stomach explants.

Fig. 8. In vitro effect of CMPs on adult DSS-treated stomach explants.
The human homolog of clu, CLUH, can rescue Drosophila clu mutant phenotypes. The human homolog of clu, CLUH, can rescue Drosophila clu mutant phenotypes.

The human homolog of clu, CLUH, can rescue Drosophila clu mutant phenotypes. The human homolog of clu, CLUH, can rescue Drosophila clu mutant phenotypes.
Fig. 8. CCA and ChQ treatment induce accumulation of F-actin rings.

Fig. 8. CCA and ChQ treatment induce accumulation of F-actin rings.
Fig. 2. Morphological changes of cultured adherent fibroblastic cells after OA treatment related to actin microfilament reorganization.(A) Cells observed.

Fig. 2. Morphological changes of cultured adherent fibroblastic cells after OA treatment related to actin microfilament reorganization.(A) Cells observed.
Nephrogenesis in vitro can be rescued in 3D co-cultures by siRNA treatment of Renca cells. Nephrogenesis in vitro can be rescued in 3D co-cultures by siRNA.

Nephrogenesis in vitro can be rescued in 3D co-cultures by siRNA treatment of Renca cells. Nephrogenesis in vitro can be rescued in 3D co-cultures by siRNA.
Representative histological images of aorta from WT, ApoEm/m and ApoE−/− pigs. Representative histological images of aorta from WT, ApoEm/m and ApoE−/−

Representative histological images of aorta from WT, ApoEm/m and ApoE−/− pigs. Representative histological images of aorta from WT, ApoEm/m and ApoE−/−
OA is found in the central and peripheral nervous systems.

OA is found in the central and peripheral nervous systems.
Tbx1 regulates the Mef2c AHF enhancer in vivo.

Tbx1 regulates the Mef2c AHF enhancer in vivo.
X-ray radiographic images showing structural alterations of the joints that are most commonly affected by OA. (A) Normal and (A′) severely affected joint.

X-ray radiographic images showing structural alterations of the joints that are most commonly affected by OA. (A) Normal and (A′) severely affected joint.
Embryonic corneal defects in E18.5 AP-2β NCC KO mutant embryos.

Embryonic corneal defects in E18.5 AP-2β NCC KO mutant embryos.
Inflammation is associated with increased basal-cell plasticity in the Nkx3.1 mutant prostate. Inflammation is associated with increased basal-cell plasticity.

Inflammation is associated with increased basal-cell plasticity in the Nkx3.1 mutant prostate. Inflammation is associated with increased basal-cell plasticity.
Expression of tomoregulin-1 in wild-type and cardiac hypertrophy mouse myocardium. Expression of tomoregulin-1 in wild-type and cardiac hypertrophy mouse.

Expression of tomoregulin-1 in wild-type and cardiac hypertrophy mouse myocardium. Expression of tomoregulin-1 in wild-type and cardiac hypertrophy mouse.

Similar presentations

Ads by Google