Publications on dementia in Medline 1974-2009: a quantitative bibliometric study.

Object: The aim is to describe the development of the scientific literature on dementia.

Methods: We present a quantitative, bibliometric study of the literature on dementia, based on Medline, covering 36 years (1974-2009). Two samples of references to dementia papers were retrieved: The main sample based on the MeSH term Dementia holds more than 88,500 references.

A 4-h hyperglycaemic excursion induces rapid and slow changes in major electrolytes in blood in healthy human subjects.

Hyperglycaemia is well known to cause reductions in plasma Na(+) levels or even hyponatraemia due to an osmotically induced dilution of the interstitium and blood. It is, however, unclear whether this dilution is significantly counteracted by ion regulatory homeostatic mechanism(s) or not. Furthermore, the effects of moderate hyperglycaemia on other major ions are less well known.

Schizophrenia in Medline 1950-2006: a bibliometric investigation.

The aim was to perform a bibliometric study, and compare the quantity of publications on schizophrenia with the total medical literature in Medline during 57 years, 1950-2006. The annual additions of literature to Medline are continually increasing and form the Medline growth curve. Comparisons of the number of publications on schizophrenia, or any other disease, to this curve, may be used to estimate the research activity.

Synaptotagmin VII splice variants alpha, beta, and delta are expressed in pancreatic beta-cells and regulate insulin exocytosis.

Synaptotagmins (SYT) are calcium-binding proteins that participate in regulated exocytosis. Although SYTI to IX isoforms are expressed in insulin-producing cell lines, hitherto only SYTIX has been associated with native beta-cell insulin granules and implicated in exocytosis. SYTVII was also proposed to regulate insulin exocytosis, but its subcellular location and number of alternative splice variants produced remain controversial.

The use of PubMed/Medline in psychiatry. 3: Searching PubMed.

This paper is the third in a series of three, intended as a tutorial in the use of PubMed/Medline for an inexperienced user. The papers have the following contents: I--a description of NLM, Medline, PubMed and the system of Medical Subject Headings (MeSH), which form the basis for the indexing of scientific articles, books and other items at NLM. II--A description and a tutorial of the PubMed search window.

The use of PubMed/Medline in psychiatry. 2: The PubMed search window: a description and a tutorial.

A previous paper, in a series of three, presented the National Library of Medicine, Medline, PubMed and the MeSH system. Connection to PubMed via the Internet opens the PubMed search window that is the tool for retrieving references to scientific medical literature. This paper is intended as a tutorial for an inexperienced visitor to PubMed, and describes the search window in some detail.

The use of PubMed/Medline in psychiatry. 1: Presentation of NLM and PubMed.

A comprehensive view of the available literature on a psychiatric problem can be found in the large electronic databases. Medline at the National Library of Medicine (NLM) in USA is the largest medical database. PubMed is the searchable database at the NLM, having Medline as its major content.

SV2A and SV2C are not vesicular Ca2+ transporters but control glucose-evoked granule recruitment.

Synaptic vesicle protein 2 (SV2) is expressed in neuroendocrine cells as three homologous isoforms, SV2A, SV2B and SV2C. Ca2+-dependent function in exocytosis has been attributed to SV2A and SV2B, without elucidation of the mechanism. The role of SV2C has not yet been addressed.

Glucose stimulates glucagon release in single rat alpha-cells by mechanisms that mirror the stimulus-secretion coupling in beta-cells.

In isolated rat pancreatic alpha-cells, glucose, arginine, and the sulfonylurea tolbutamide stimulated glucagon release. The effect of glucose was abolished by the KATP-channel opener diazoxide as well as by mannoheptulose and azide, inhibitors of glycolysis and mitochondrial metabolism. Glucose inhibited KATP-channel activity by 30% (P<0.

Beta-cell secretory products activate alpha-cell ATP-dependent potassium channels to inhibit glucagon release.

Glucagon, secreted from islet alpha-cells, mobilizes liver glucose. During hyperglycemia, glucagon secretion is inhibited by paracrine factors from other islet cells, but in type 1 and type 2 diabetic patients, this suppression is lost. We investigated the effects of beta-cell secretory products zinc and insulin on isolated rat alpha-cells, intact islets, and perfused pancreata.

Glucose sensitivity and metabolism-secretion coupling studied during two-year continuous culture in INS-1E insulinoma cells.

Rat insulinoma-derived INS-1 cells constitute a widely used beta-cell surrogate. However, due to their nonclonal nature, INS-1 cells are heterogeneous and are not stable over extended culture periods. We have isolated clonal INS-1E cells from parental INS-1 based on both their insulin content and their secretory responses to glucose.

Granule-specific ATP requirements for Ca2+-induced exocytosis in human neutrophils. Evidence for substantial ATP-independent release.

Ca2+-induced exocytosis in neuronal and neuroendocrine cells involves ATP-dependent steps believed to 'prime' vesicles for exocytosis. Primed, docked vesicles are released in response to Ca2+ influx through voltage-gated Ca2+ channels. Neutrophils, however, do not possess voltage-gated Ca2+ channels and appear to have no docked vesicles.