A focus on Gozo

A slim manuscript volume containing sixty-four pages and three pages of a rudimentary index throws considerable light on life in Gozo in the mid-1800s. The volume written in Italian and measuring 22 cm by 16 cm has a very modest and unobtrusive title page. In block letters we find the word 'GOZO' to which the words 'memorie sul' were subsequently added, thus resulting in the title of 'Memorie sul Gozo'. The origin and authorship of the volume is unknown. It was found among the papers of my late father and there are no indications at all of how, why and when it came to be written. It is penned in a very clear hand and by a very organised and observant person who, it seems, was determined to record certain events, incidents and personalities. He was also remarkably interested in the topography of Gozo, very carefully listing places and minutely describing locations. It appears to have been written over a span of time, maybe years. There are indications that he added on to what he had written earlier and in very few cases are there traces of 'pentimento'.peer-reviewe

A role for autophagy in β-cell life and death.

Autophagy is a vacuolar, self-digesting mechanism responsible for the removal of organelles and defined regions of the cytoplams. This process has, in general, a beneficial role for the cell, since it regulates the turnover of aged proteins and eliminates damaged structures. However, cells that undergo altered autophagy may be triggered to die in a non-apoptotic manner. As a matter of fact, in recent years it has become clear that dysregulated autophagy may be implicated in several disorders, such as cancer, neurodegenerative diseases and hepatic encephalopathy. We have recently shown that β-cells of type 2 diabetic subjects show signs of autophagy associated death, which may contribute to the overall loss of β-cell mass in type 2 diabetes. In addition, studies with cell lines and rodent models have demonstrated the importance of autophagy in β-cell function and survival. Altogether, the available evidence supports the view that autophagy is implicated in β-cell pathophysiology, and suggests that addressing the molecular mechanisms involved in autophagic regulation might provide clues for preventing or treating β-cell damage in diabetes

Hepatitis C Virus Infection and Human Pancreatic β-Cell Dysfunction

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3D multiphysics transient modeling of vertical Ge-on-Si pin waveguide photodetectors

We report transient simulations of Ge-on-Si vertical pin waveguide photodetectors (WPDs), where the optical generation term used by the time-domain model is the FDTD solution of the electromagnetic problem treated as a spatially-distributed pulsed signal. This approach, validated against experimental measurements of the frequency response, paves the way to future studies of the dynamic response of WPDs, enabling the description of complex modulation schemes including saturation effects and current tails due to slow carriers

Type D personality in never depressed patients at their first acute coronary syndrome

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Histopathology and ex vivo insulin secretion of pancreatic islets in gestational diabetes: A case report

Gestational diabetes (GD) results from insufficient endogenous insulin supply. No information is available on features of islet cells in human GD. Herein, we describe several properties of islets from a woman with GD. Immunohistochemical stainings and EM analyses were performed on pancreatic samples. Islet isolation was achieved by enzymatic dissociation and density gradient centrifugation. Ex vivo insulin secretion was studied in response to fuel secretagogues. Control islets were obtained from matched non-pregnant, non-diabetic women. Total insulin positive area was lower in GD, mainly due to the presence of smaller islets. β-cell apoptosis and the presence of Ki67 positive islet cells were similar in GD and controls, whereas the amount of insulin positive cells in or close to the ducts was decreased in GD. Ex vivo insulin secretion did not differ between GD and non-pregnant, non-diabetic islets. These findings suggest that in this case of human GD there might mainly be a defect of β-cell amount, not due to increased apoptosis, but possibly to insufficient regeneration

Co-localization of acinar markers and insulin in pancreatic cells of subjects with type 2 diabetes

To search for clues suggesting that beta cells may generate by transdifferentiation in humans, we assessed the presence of cells double positive for exocrine (amylase, carboxypeptidase A) and endocrine (insulin) markers in the pancreas of non-diabetic individuals (ND) and patients with type 2 diabetes (T2D). Samples from twelve ND and twelve matched T2D multiorgan donors were studied by electron microscopy, including amylase and insulin immunogold labeling; carboxypeptidase A immunofluorescence light microscopy assessment was also performed. In the pancreas from four T2D donors, cells containing both zymogen-like and insulin-like granules were observed, scattered in the exocrine compartment. Nature of granules was confirmed by immunogold labeling for amylase and insulin. Double positive cells ranged from 0.82 to 1.74 per mm2, corresponding to 0.26±0.045% of the counted exocrine cells. Intriguingly, cells of the innate immune systems (mast cells and/or macrophages) were adjacent to 33.3±13.6% of these hybrid cells. No cells showing co-localization of amylase and insulin were found in ND samples by electron microscopy. Similarly, cells containing both carboxypeptidase A and insulin were more frequently observed in the diabetic pancreata. These results demonstrate more abundant presence of cells containing both acinar markers and insulin in the pancreas of T2D subjects, which suggests possible conversion from one cellular type to the other and specific association with the diseased condition