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New Developments in Oral Insulin Delivery
Published in Emmanuel Opara, Controlled Drug Delivery Systems, 2020
Alec Jost, Mmesoma Anike, Emmanuel Opara
Prior to 1920, and beginning with the seminal work of Mering and Minkowski in 1889 showing that total pancreatectomy induces severe diabetes, a hypothesis had been established that an internal secretion of the pancreas controlled glucose disposal. Subsequently, while doing routine autopsies, the American pathologist Moses Barron had observed in a rare case of the formation of a pancreatic stone (pancreatic lithiasis) that the stone had completely occluded the main pancreatic duct causing all the acinar cells to disappear through atrophy while most of the islet cells survived (Barron 1920). These findings were consistent with other observations made when pancreatic ducts were blocked by ligation, and all together laid the foundation for Frederick Banting’s quest for the pancreatic internal secretion later named as “insulin.” Also, it is known that, at the first meeting of Banting with J.J.R Macleod, the professor of physiology, in whose lab Banting and Best worked at the University of Toronto, part of their discussion was that many others had tried to prepare an extract of the pancreas which contained the internal secretion and failed. Both agreed that the problem with previous extracts was that they also contained potent digestive components of the external secretion, now known as enzymes, which may have destroyed the internal secretion (Bliss 1982).
Trout and Salmon (Salmonidae)
Published in John A Plumb, Health Maintenance Of Cultured Fishes, 1994
Pathological changes resulting from IPNV are typical of a viremia.57 The most profound histopathological change is the obliteration of most of the acinar tissue of the pancreas, and its replacement by necrotic detritus containing fragmented acinar cells, pyknotic nuclei, and zymogen granules. In advanced cases, monocytes, and polymorphonuclear lymphocytes increase indicating the presence of some inflammation. Initially, foci of necrosis are scattered throughout the acinar tissue, and necrosis rapidly spreads to surrounding tissue. At the periphery of the necrotic areas, many acinar cells will contain intracytoplasmic inclusions. Fatty tissues surrounding the pancreatic tissue often become necrotic, and necrosis frequently occurs in the islet of Langerhans.
Tissue Engineering in Reconstruction and Regeneration of Visceral Organs
Published in Rajesh K. Kesharwani, Raj K. Keservani, Anil K. Sharma, Tissue Engineering, 2022
Soma Mondal Ghorai, Sudhanshu Mishra
Pancreas lies in the upper abdomen and is a part of gastrointestinal system and acts both as an exocrine and an endocrine organ. It secretes digestive juices into the intestine as well as hormones into the blood for metabolism and storage. Basically, it is made up of clusters of cells known as the pancreatic acini that produce digestive enzymes and some other structures called pancreatic islets or the islets of Langerhans are involved in endocrine function (Figure 7.6). The exocrine part of the pancreas is a complex tubular network of acini and the cells are situated along with a small ductile at the intersection of acinar tubule or acinus. The complex duct system is a key to prevent the entry of exocrine enzymes into the interstitial space, which, if disrupted, may cause tissue damage that manifest as pancreatitis. The central and interlobular ducts have thick compact collagenous walls. The connective tissue becomes narrow and progressively becomes thin as the ducts branch out, arising incidence of leakage of the duct system. To prevent this, intercellular tight junctions (zonula occludens) are found between duct cells, the acinar cells, and the centroacinar cells (Longnecker, 2014). The endocrine part of the pancreas constitutes islets of Langerhans that substantially differ in size. In humans, the average size ranges between 100 and 150 m wherein about 70% are in the size range of 50–250 m in diameter (Hellman, 1959 a). Most islets are spherical or ellipsoid, wherein the smaller islets are dispersed throughout the acinar lobules and larger islets underline the main and interlobular ducts of the pancreas. Glucagon secreted from α-cells, insulin secreted from ß-cells, and somatostatin secreted from δ-cells are the main pancreatic islet cell types that produce the peptide hormones. Also, cells secreting pancreatic polypeptide are regarded as the fourth most predominant endocrine cell type in the islets (Hellman, 1959 b). Thus, designing a tissue-engineered pancreatic substitute (TEPS), which consists of insulin-producing cells appropriately encapsulated to support cellular function, poses major challenge.
Tear osmolarity is sensitive to exercise-induced fluid loss but is not associated with common hydration measures in a field setting
Published in Journal of Sports Sciences, 2018
Justin J. Holland, Michelle Ray, Christopher Irwin, Tina L. Skinner, Michael Leveritt, Ben Desbrow
To assess whether spot Tosm collections would be sensitive to total body fluid shifts within an ecologically valid temperature range we had participants complete a 10 km run in the field. We found that the osmolarity of tear fluid increased from 294 ± 8 pre-exercise to 302 ± 13 mOsm.L−1 post-exercise. Under states of fluid restriction at 1% and 2% BML it has been reported that Tosm will rise to 299 ± 9 and 301 ± 9 mOsm.L−1 respectfully (Ungaro et al., 2015), which is not dissimilar to what was observed in the present study. The acinar cells of the lacrimal gland secrete fluid that is isotonic and reflective filtrate of plasma (Mircheff, 1989; Sollanek et al., 2012). Thus, given the similar and expected changes in Posm under fluid loss it may in part explain the reason for increase in Tosm. This is consistent with animal models where reductions in lacrimal gland flow rate subsequently increase lacrimal gland fluid osmolality (Dartt, Moller, & Poulsen, 1981; Fortes et al., 2011; Gilbard & Dartt, 1982). The exact reason for changes in tear fluid under field conditions requires further research, particularly where environmental factors (dust, wind and sunlight) may interact with the tear film.