scholarly journals Collection, Packaging and Cold Shipping of Fresh Non-Islet Pancreatic (Acinar) Tissue v1 (protocols.io.bimpkc5n)

protocols.io ◽  
2020 ◽  
Author(s):  
Integrated Islet
Keyword(s):  
1960 ◽  
Vol 20 (1) ◽  
pp. 69-77 ◽  
Author(s):  
R. E. COUPLAND

SUMMARY Pieces of foetal rat pancreas obtained from specimens of 18–40 mm c.r. length were implanted into the anterior chamber of the mother's eye. The subsequent changes were followed using histological methods. Acinar tissue degenerates and completely disappears during the first 2 weeks after implantation. Duct epithelium proliferates and large numbers of islets of Langerhans are produced which contain both α and β cells. In grafts of 1 year's duration islets form the main bulk of the graft. Methods of staining the islet tissue of the rat are discussed.


2020 ◽  
Vol 117 (20) ◽  
pp. 10876-10887 ◽  
Author(s):  
Mirza Muhammad Fahd Qadir ◽  
Silvia Álvarez-Cubela ◽  
Dagmar Klein ◽  
Jasmijn van Dijk ◽  
Rocío Muñiz-Anquela ◽  
...  

We have described multipotent progenitor-like cells within the major pancreatic ducts (MPDs) of the human pancreas. They express PDX1, its surrogate surface marker P2RY1, and the bone morphogenetic protein (BMP) receptor 1A (BMPR1A)/activin-like kinase 3 (ALK3), but not carbonic anhydrase II (CAII). Here we report the single-cell RNA sequencing (scRNA-seq) of ALK3bright+-sorted ductal cells, a fraction that harbors BMP-responsive progenitor-like cells. Our analysis unveiled the existence of multiple subpopulations along two major axes, one that encompasses a gradient of ductal cell differentiation stages, and another featuring cells with transitional phenotypes toward acinar tissue. A third potential ducto-endocrine axis is revealed upon integration of the ALK3bright+ dataset with a single-cell whole-pancreas transcriptome. When transplanted into immunodeficient mice, P2RY1+/ALK3bright+ populations (enriched in PDX1+/ALK3+/CAII− cells) differentiate into all pancreatic lineages, including functional β-cells. This process is accelerated when hosts are treated systemically with an ALK3 agonist. We found PDX1+/ALK3+/CAII− progenitor-like cells in the MPDs of types 1 and 2 diabetes donors, regardless of the duration of the disease. Our findings open the door to the pharmacological activation of progenitor cells in situ.


1978 ◽  
Vol 26 (3) ◽  
pp. 487
Author(s):  
AW White ◽  
CJF Harrop

The development of the endocrine pancreas in kangaroos was examined histologically with tissue from three kangaroo species, the red kangaroo Megaleia rufa, the euro Macropus robustus erubescens, and the grey kangaroo Macropus giganteus. The relative size of the pancreas of the pouch young was found not to differ significantly from that of adults. Stages of pancreatic development were described from the frequency of the occurrence of the pancreatic epithelial ducts and the B or insulin-secreting cells, while the development and distribution of the A2 or glucagon-producing cells was also observed. In pouch young of less than 22 days of age the pancreas is dominated by ductular epithelial and undifferentiated pancreatic cells. From days 42 to 97 of pouch life B endocrine cells tend to be concentrated together and ductular tissue encroaches into areas previously dominated by connective tissue. After 120-135 days the first A2 cells are apparent and are usually located at the periphery of the islets, which now take on a distinctive appearance as the acinar tissue expands and separates them. After 135 days of pouch life A2 cells outnumber B cells; the endocrine tissue assumes an adult appearance after 150-160 days. The major difference between the development of pancreatic tissue in foetal sheep and pouch-young kangaroo is the prolonged dominance of connective tissue and the slow development of endocrine tissue in the former.


1997 ◽  
Vol 6 (1) ◽  
pp. 39-45 ◽  
Author(s):  
Josá F. Mendola ◽  
Helena Corominola ◽  
Enric Esmatjes ◽  
Alex Saenz ◽  
Laureano Fernandez-Cruz ◽  
...  

We examined in fully mismatched rats, the survival of pancreatic islet allografts in recipients treated with either fusidic acid (FA), an antistaphyllococcal antibiotic that has been shown to possess an immunosuppressive effect in vitro and in vivo, or cyclosporin-A (CsA). Islets were isolated by collagenase digestion, separated from acinar tissue by handpicking under a dissecting microscope and transplanted into the liver by portal vein injection of streptozotocin(STZ)-induced diabetic rats. The results indicated that while a temporary immunosuppression with CsA achieved an indefinite islet allograft survival, FA administered to recipients daily was not able to prevent islet allograft rejection across a major histocompatibility barrier. We conclude that despite the fact that fusidic acid has been claimed to act as an immunosuppressant drug in vitro with effects similar to those of CsA, unlike CsA, FA given either orally or by s.c. injection was not effective to prolong islet allograft survival in vivo. Copyright © 1997 Elsevier Science Inc.


1964 ◽  
Vol 207 (2) ◽  
pp. 423-430 ◽  
Author(s):  
S. J. Cooperstein ◽  
Arnold Lazarow

These studies on the mechanism by which alloxan selectively destroys the ß cells in the islets of Langerhans have been carried out in the toadfish because the islet tissue in this species is segregated into a discrete mass, separated from the acinar tissue. We have measured the C14 content of several tissues at various times after intravenous injection of tracer doses of alloxan-2-C14. The islet C14 content never exceeded 50% of that of blood and was no greater than that found in many other tissues. Thus the selectivity of alloxan is not due to selective concentration by islet tissue. The distribution of alloxan-2-C14 was compared with that of d-mannitol-1-H3. A mixture of both isotopic substances was injected and the C14 and H3 in each tissue determined. The distribution of alloxan-2-C14 was very similar to that of d-mannitol-1-H3. This suggests that tracer doses of injected alloxan do not enter islet cells but remain in the extracellular compartment, and that the ß-cell membrane may be a primary site of alloxan action.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Luke Ternes ◽  
Ge Huang ◽  
Christian Lanciault ◽  
Guillaume Thibault ◽  
Rachelle Riggers ◽  
...  

AbstractMechanistic disease progression studies using animal models require objective and quantifiable assessment of tissue pathology. Currently quantification relies heavily on staining methods which can be expensive, labor/time-intensive, inconsistent across laboratories and batch, and produce uneven staining that is prone to misinterpretation and investigator bias. We developed an automated semantic segmentation tool utilizing deep learning for rapid and objective quantification of histologic features relying solely on hematoxylin and eosin stained pancreatic tissue sections. The tool segments normal acinar structures, the ductal phenotype of acinar-to-ductal metaplasia (ADM), and dysplasia with Dice coefficients of 0.79, 0.70, and 0.79, respectively. To deal with inaccurate pixelwise manual annotations, prediction accuracy was also evaluated against biological truth using immunostaining mean structural similarity indexes (SSIM) of 0.925 and 0.920 for amylase and pan-keratin respectively. Our tool’s disease area quantifications were correlated to the quantifications of immunostaining markers (DAPI, amylase, and cytokeratins; Spearman correlation score = 0.86, 0.97, and 0.92) in unseen dataset (n = 25). Moreover, our tool distinguishes ADM from dysplasia, which are not reliably distinguished with immunostaining, and demonstrates generalizability across murine cohorts with pancreatic disease. We quantified the changes in histologic feature abundance for murine cohorts with oncogenic Kras-driven disease, and the predictions fit biological expectations, showing stromal expansion, a reduction of normal acinar tissue, and an increase in both ADM and dysplasia as disease progresses. Our tool promises to accelerate and improve the quantification of pancreatic disease in animal studies and become a unifying quantification tool across laboratories.


1997 ◽  
Vol 63 (10) ◽  
pp. 1537-1540 ◽  
Author(s):  
Laurence Kessler ◽  
Cathy Jesser ◽  
Alain Belcourt ◽  
Michel Pinget

2002 ◽  
Vol 50 (12) ◽  
pp. 1625-1632 ◽  
Author(s):  
Fang-Xu Jiang ◽  
Gaetano Naselli ◽  
Leonard C. Harrison

Tissue function is regulated by the extracellular microenvironment including cell basement membranes, in which laminins are a major component. Previously, we found that laminin-1 promotes differentiation and survival of pancreatic islet cells. Here we characterize the expression pattern of laminins and their integrin receptors in adult pancreas. Although they are expressed in the basement membrane of acinar cells and duct epithelium, no laminin chains examined were detected extracellularly in the pancreatic islets. In contrast to laminin β1- and γ1-chains, the α1-chain, unique to laminin-1, was not detected. Laminin-10 (α5β1γ1) was expressed in acinar tissue, whereas laminins-2 (α2β1γ1) and -10 were expressed in the blood vessels. The laminin connector molecule, nidogen-1, had a distribution similar to that of laminin β1 and γ1, whereas fibulin-1 and -2, which compete with nidogen-1, were mostly confined to blood vessels. Integrin subunits α6 and α3 were detected in acinar cells and duct epithelial cells, but α6 was absent in islet cells. Integrin α6β4 was detected only in duct cells, α6β1 in both acinar and ductal cells, and α3β1 in acinar, duct, and islet cells. These findings are a basis for further investigation of the role of extracellular matrix molecules and their receptors in pancreas function.


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