Miracle-dz/UniFAR-FTUs huggingface dataset:
Streptozotocin treatment at birth induces a parallel depletion of thyrotropin-releasing hormone and insulin in the rat pancreas during development.

Elevated concentrations of TRH have been detected in the rat pancreas during the early days of life. The purpose of this study was to investigate further the cellular location of this peptide in the pancreas using streptozotocin (STZ) injected at birth. Pancreatic TRH and insulin contents were measured at different ages from birth until 35 days in rats injected with STZ and results compared with controls injected with the vehicle. A transitory hyperglycemic state was observed from day 1 to day 5 (maximum value 2.9 +/- 0.31 g/liter). After this period, although slightly hyperglycemic, STZ rats were not glucosuric . TRH and insulin contents followed two distinct patterns from days 1 to 5 and days 5 to 35. During the first period, an acute depletion of both substances was observed, the lower value observed reaching 2.7% and 9% of control values, respectively, for TRH and insulin. The TRH surge at day 2 was blunted. During the second period, insulin content increased to reach 42% of controls. On the contrary, recovery of TRH was not observed; TRH content was 9% of control at day 35. These results indicate that TRH is located in STZ-sensitive cells, in agreement with recent immunohistochemical data. The impaired capacity for TRH recovery remained unexplained and seems to indicate a difference in the biogenesis of insulin and TRH.
Donor leukocyte infusion as therapy of life-threatening adenoviral infections after T-cell-depleted bone marrow transplantation.

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All-female travel: what do women really want?

This paper examines the importance of the all-female element to women travellers and the possible benefits that can be gained from this type of travel. A self-administered mail survey questionnaire was completed by past clients (n=60) of an Australian all-female travel company, to measure their satisfaction with previous travel and to find out perceived benefits of all-female travel, personal plans for future travel and demographic information. Both quantitative and qualitative information was collected. The participants in the study were women over the age of 40 years, predominantly in the 50-69 age group. They were experienced travellers as 89% had travelled previously and 64% had travelled four or more times. The information collected allowed a comparison of the importance of certain criteria pre and post the tour. Confidence in tour leader, destination and its culture and not being a 'mass tourist' were seen as important both before and after the tour. Travelling with 'all female company', 'being cared for and pampered', and the 'sharing accommodation' increased in importance after the tour. There were a number of benefits identified in all-female travel. These included a more relaxed, congenial and intimate atmosphere in the group, sharing similar interests and absence of competition and tensions.
Aspergillus nidulans: association of certain alkaline phosphatase mutations with decreased virulence for mice.

are listed in table 1. All of these mutants carry, in addition to the mutation affecting the activity of phosphatase, an auxotrophic mutation (Ml) that determines a specific nutritional requirement for biotin. The strains Ml; palAl, Ml; palFIS, and Ml; pacAl were obtained from the Fungal Genetics Stock Center, Department of Biological Sciences, Dartmouth College, Hanover, New Hampshire. All other strains were supplied by Dr. Gordon L. Dorn of Dallas, Texas. Determination of virulence. The virulence of these mutants was assayed in male DBA/2J mice (24-26 g) by intravenous inoculation of saline suspensions of conidia obtained from cultures of these mutants grown at 37 C on a complete agar medium similar to that used by Barratt et al. [3].
Increased production of vascular endothelial growth factor by intestinal mucosa of patients with inflammatory bowel disease.

BACKGROUND/AIMS Vascular endothelial growth factor (VEGF) is a heparin-binding glycoprotein with potent angiogenic, mitogenic and vascular permeability-enhancing activities specific for endothelial cells. Recent studies have shown significantly increased VEGF serum levels in patients with active Crohn's disease and ulcerative colitis. The origin of the circulating VEGF is not yet completely described. The present investigation examines the VEGF production of colonic mucosa in consideration of mucosal disease activity in patients with inflammatory bowel disease. METHODOLOGY Fifteen patients with inflammatory bowel disease were studied, 9 patients with Crohn's disease and 6 patients with ulcerative colitis. Biopsies were taken from endoscopically inflamed and non-inflamed colonic mucosa. Therefore, an analysis of the spontaneous VEGF production of cultured biopsies without stimulus and of the histological grade of inflammation scored on a scale of 0-3 (normal mucosa--severe chronic colitis) were performed. Eight patients with irritable bowel syndrome served as controls. VEGF levels in the supernatant of cultured mucosal biopsies were measured using an enzyme linked immunosorbent assay. RESULTS VEGF production is expressed as pg/mg wet weight of the biopsies. Inflamed mucosa of patients with active ulcerative colitis (16.27 +/- 10.39, p = 0.003, n = 6) and active Crohn's disease (9.88 +/- 5.98, p < 0.012, n = 9) showed a significantly higher spontaneous production of VEGF by colonic mucosa than normal mucosa of controls (3.16 +/- 1.63, n = 8). In addition, there was an increased unstimulated VEGF production by cultured inflamed mucosa of patients with Crohn's disease compared with non-inflamed mucosa (3.88 +/- 3.66, p < 0.015, n = 9). In both Crohn's disease and ulcerative colitis, there was no significant difference between VEGF production by non-inflamed mucosa and normal mucosa of controls. CONCLUSIONS The present study identifies the intestinal mucosa as one of the origins of the elevated VEGF serum levels in patients with active inflammatory bowel disease and verifies the findings of recent studies about the importance of VEGF in Crohn's disease and ulcerative colitis.
Contrast enhanced subharmonic breast imaging: work in progress

Contrast enhanced subharmonic imaging (SHI) may enable combined imaging and estimation of quantifiable flow parameters such as perfusion. A modified Logiq 9 scanner (GE Healthcare, Milwaukee, WI) operating in grayscale SHI mode was used to measure in vivo SHI time intensity curves in 4 dogs. Renal SHI was performed following IV injections of the contrast agent Optison (GE Healthcare, Princeton, NJ). Following 3 contrast injections a neutron activation assay technique (BioPhysics Assay Laboratory Inc, Worcester, MA) was employed to quantify the degree of perfusion in 8 sections of each kidney. Digital clips were transferred to a PC and SHI time intensity curves acquired in each section. SHI fractional blood volumes (FBVs) were calculated and the perfusion estimated from the initial slope of the FBV uptake. SHI perfusion data was compared to the gold standard using linear regression analysis. As part of an ongoing study, women with breast lesions participated in a study of contrast enhanced breast SHI. Following baseline scans of grayscale ultrasound and power Doppler, Optison was administrated for power Doppler and grayscale SHI (0.5 and 4.0 ml dosages, respectively). Digital clips were acquired of each injection and SHI time intensity curves were determined within each lesion. In the dogs 270 SHI time intensity curves were acquired. SHI perfusion estimates correlated significantly with microsphere results (r = 0.57; p < 0.0001). To date six patients with seven benign breast masses have been studied. The internal morphology of the vascularity associated with the breast masses was visualized better with SHI than with power Doppler. SHI perfusion estimates of the breast lesions ranged from 1.67 to 2.46 ml/min/g. In conclusion, a new contrast specific imaging techniques, SHI, has been investigated for in vivo breast imaging and perfusion estimation, but further studies are required to substantiate these preliminary results.
Trp 1 , a Candidate Protein for the Store-operated Ca 2 1 Influx Mechanism in Salivary Gland Cells

The trp gene family has been proposed to encode the store-operated Ca influx (SOC) channel(s). This study examines the role of Trp1 in the SOC mechanism of salivary gland cells. htrp1, htrp3, and Trp1 were detected in the human submandibular gland cell line (HSG). HSG cells stably transfected with htrp1a cDNA displayed (i) a higher level of Trp1, (ii) a 3–5-fold increase in SOC (thapsigargin-stimulated Ca influx), determined by [Ca]i and Ca -activated K channel current measurements, and (iii) similar basal Ca permeability, and inhibition of SOC by Gd but not by Zn, as compared with control cells. Importantly, (i) transfection of HSG cells with antisense trp1a cDNA decreased endogenous Trp1 level and significantly attenuated SOC, and (ii) transfection of HSG cells with htrp3 cDNA did not increase SOC. These data demonstrate an association between Trp1 and SOC and strongly suggest that Trp1 is involved in this mechanism in HSG cells. Consistent with this suggestion, Trp1 was detected in the plasma membrane region, the proposed site of SOC, of acinar and ductal cells in intact rat submandibular glands. Based on these aggregate data, we propose Trp1 as a candidate protein for the SOC mechanism in salivary gland cells.
Use of Autologous Cultured Limbal and Conjunctival Epithelium in a Patient with Severe Bilateral Ocular Surface Disease Induced by Acid Injury: A Case Report of Unique Application

Purpose. Reconstruction of the ocular surface in a case of severe bilateral partial limbal stem cell deficiency (LSCD) with extensive symblephara using autologous cultured conjunctival and limbal epithelium. Case report. A 31-year-old woman presented with severe bilateral ocular surface disease with partial limbal stem cell deficiency, symblephara, lid and facial scarring, with a vision of 20/400 and counting fingers at 1 m in both eyes. Limbal and conjunctival tissue was harvested from the healthy-appearing left eye and used to generate two sheets of composite epithelium consisting of central limbal and peripheral conjunctival cells. The limbal tissues were explanted in the central region while the conjunctival tissues were explanted on the periphery of the deepithelialized human amniotic membrane (HAM) and nurtured using human corneal epithelial cell medium. After successful generation of a monolayer from both tissues had been confirmed, the composite of cultivated limbal and conjunctival epithelium with HAM was transplanted in each eye after excision of fibrous tissue and release of symblephara. One year postoperatively, the patient had a best spectacle-corrected visual acuity of 20/40 in the right eye (preoperative acuity 20/400) and counting fingers at 1 m in the left eye (same as preoperative) with a stable ocular surface. Conclusions. Autologous cultured epithelial transplantation is as an excellent option in selected patients with bilateral partial LSCD with small area(s) of healthy limbus in either eye and avoids the attendant risk of rejection and cost and potential toxicity of immunosuppression in allogeneic tissue transplantation. This case also highlights the feasibility of generating a composite culture of limbal and conjunctival epithelium using a single amniotic membrane.
ATP-binding cassette transporter A1 is significantly involved in the intestinal absorption of alpha- and gamma-tocopherol but not in that of retinyl palmitate in mice.

BACKGROUND It has long been assumed that newly absorbed vitamin A and E enter the body only via enterocyte-produced chylomicrons. However, recent results in cell cultures have shown that a fraction of alpha-tocopherol is secreted with intestinal HDL. OBJECTIVES The aims of this study were to identify this transporter and to assess whether it is significantly implicated in the in vivo intestinal absorption of the 2 main dietary forms of vitamin E (ie, alpha- and gamma-tocopherol) and in that of retinyl palmitate (vitamin A). DESIGN Having performed preliminary experiments in the Caco-2 cell model, we compared fasting and postprandial plasma concentrations of vitamins A and E in mice deficient in ATP-binding cassette A1 (ABCA1) transporter and in wild-type mice. RESULTS A substantial efflux of alpha- and gamma-tocopherol, but not of retinyl esters, was induced by the presence of apolipoprotein A-I at the basolateral side of Caco-2 monolayers. The efflux of alpha- and gamma-tocopherol was also impaired by glyburide and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. The postprandial response of plasma gamma-tocopherol was 4-fold lower in ABCA1(-/-) mice (P = 0.025) than in wild-type mice, whereas no significant difference was observed for retinyl esters. Fasting plasma alpha-tocopherol, but not vitamin A, concentrations were lower in mice bearing the genetic deletion. CONCLUSIONS ABCA1 is the transporter responsible for the in vivo secretion of alpha- and gamma-tocopherol with intestinal HDL, and this pathway is significantly implicated in the intestinal absorption and plasma status of vitamin E but not of vitamin A.
Efficient 2-D Convolution Algorithm with the Single-Data Multiple Kernel Approach

Abstract A fast implementation of convolution operation is described. The implementation takes advantage of various properties of commonly used kernels. First, the kernel elements are analyzed and rearranged, grouping the kernel elements of the same absolute value together and arranging trivial multiplication cases separately. Then the sequence of computing convolution sums is modified so that all the kernel elements could be multiplied by the same data element at each step. This new algorithm significantly reduces the number of multiplication operations for most widely used kernels. Our experiment shows that the performance improvement of two to seven over the direct implementation is achievable for most kernels. The required overhead (extra memory and preprocessing) is proportional to the kernel size and is negligible.
Further genetic analyses of skin tumor promoter susceptibility using inbred and recombinant inbred mice.

To explore further the genetics of susceptibility to skin tumor promotion in inbred mice, several aspects of responsiveness to 12-O-tetradecanoylphorbol-13-acetate (TPA) were examined in C3H/He mice and segregating crosses between this mouse strain and C57BL/6 mice as well as BXD and BXH recombinant inbred (RI) strains. Dose-response relationships were established for skin tumor promotion by TPA following initiation with 7,12-dimethylbenz[a]anthracene in C3H/He and B6C3F1, as well as several other mouse stocks and strains included for comparison. The relative responsiveness to TPA skin tumor promotion was: SENCAR much greater than DBA/2 greater than C3H/He approximately B6D2F1 greater than B6C3F1 much greater than C57BL/6. Analyses of the susceptibility of B6C3F2 and B6C3F1 x C57BL/6 backcross mice suggested that a minimum of two dominant genetic loci control responsiveness to phorbol ester promotion in these mice. Further analysis of BXH and BXD RI strains suggested the presence of four distinct promotion-responsive phenotypes controlled by a minimum of two genetic loci. The existence of a 'hyper-responsive' phenotype in the sets of RI strains, however, suggests that a third, recessive locus also may play a role in controlling responsiveness to TPA promotion. At 48 h after the last of four applications of TPA, marked hyperplasia and an increase in dark basal keratinocytes were observed in C3H/He mice, whereas in B6C3F1 mice the response in these parameters was intermediate between C3H/He and C57BL/6 mice. A marked dermal inflammation, as determined by infiltration of polymorphonuclear cells, was observed in C3H/He and B6C3F1 mice, whereas little was noted in C57BL/6 mice. Furthermore, histological evaluations of selected BXD RI strains revealed a significant correlation between the magnitude of the hyperplasia response and the percentage of mice bearing tumors. The present data, in conjunction with our previous studies, confirm that the major gene(s) controlling susceptibility to tumor promoter induced by TPA in two sensitive strains (i.e. DBA/2 C3H/He) are similar or closely linked to those for induction of sustained hyperplasia. In addition, the present data provide new evidence for a model where allelic differences at a minimum of three loci contribute to gene differences in susceptibility to phorbol ester promotion DBA/2 and C3H/He versus C57BL/6 mice.
Short Article: Effect of Click Trains on Duration Estimates by People with Parkinson's Disease

Patients with a diagnosis of Parkinson's disease and age- and IQ-matched controls estimated the duration of short 500-Hz tones (325–1,225 ms), on trials where the tone was either preceded by 3 s of 5-Hz clicks, or presented without clicks. The click manipulation had been shown in earlier studies with student participants to make verbal estimates longer. Patients were tested both on and off their dopaminergic medication, and controls were also tested in two sessions. Verbal estimates were markedly and significantly longer on trials with clicks than on those without clicks for both the patients and the controls, but there were no significant performance differences between patients or controls, nor between the on and off medication sessions in the patients. The study shows that a manipulation of subjective time, which has had small but consistent effects in student participants, also affects timing in patients and adds to a growing body of evidence that timing in patients with Parkinson's disease may in many cases have the same characteristics as those of neurologically intact control groups.
A New Gene Involved in the Transport-dependent Metabolism of Phosphatidylserine, PSTB2/PDR17, Shares Sequence Similarity with the Gene Encoding the Phosphatidylinositol/Phosphatidylcholine Transfer Protein,SEC14 *

A new yeast strain, designated pstB2, that is defective in the conversion of nascent phosphatidylserine (PtdSer) to phosphatidylethanolamine (PtdEtn) by PtdSer decarboxylase 2, has been isolated. The pstB2 strain requires ethanolamine for growth. Incubation of cells with [3H]serine followed by analysis of the aminoglycerophospholipids demonstrates a 50% increase in the labeling of PtdSer and a 72% decrease in PtdEtn formation in the mutant relative to the parental strain. The PSTB2 gene was isolated by complementation, and it restores ethanolamine prototrophy and corrects the defective lipid metabolism of the pstB2strain. The PSTB2 gene is allelic to the pleiotropic drug resistance gene, PDR17, and is homologous toSEC14, which encodes a phosphatidylinositol/phosphatidylcholine transfer protein. The protein, PstB2p, displays phosphatidylinositol but not PtdSer transfer activity, and its overexpression causes suppression of sec14mutants. However, overexpression of the SEC14 gene fails to suppress the conditional lethality of pstB2strains. The transport-dependent metabolism of PtdSer to PtdEtn occurs in permeabilized wild type yeast but is dramatically reduced in permeabilized pstB2 strains. Fractionation of permeabilized cells demonstrates that the pstB2 strain accumulates nascent PtdSer in the Golgi apparatus and a novel light membrane fraction, consistent with a defect in lipid transport processes that control substrate access to PtdSer decarboxylase 2.
ATRX tolerates activity-dependent histone H3 methyl/phos switching to maintain repetitive element silencing in neurons

ATRX (the alpha thalassemia/mental retardation syndrome X-linked protein) is a member of the switch2/sucrose nonfermentable2 (SWI2/SNF2) family of chromatin-remodeling proteins and primarily functions at heterochromatic loci via its recognition of “repressive” histone modifications [e.g., histone H3 lysine 9 tri-methylation (H3K9me3)]. Despite significant roles for ATRX during normal neural development, as well as its relationship to human disease, ATRX function in the central nervous system is not well understood. Here, we describe ATRX’s ability to recognize an activity-dependent combinatorial histone modification, histone H3 lysine 9 tri-methylation/serine 10 phosphorylation (H3K9me3S10ph), in postmitotic neurons. In neurons, this “methyl/phos” switch occurs exclusively after periods of stimulation and is highly enriched at heterochromatic repeats associated with centromeres. Using a multifaceted approach, we reveal that H3K9me3S10ph-bound Atrx represses noncoding transcription of centromeric minor satellite sequences during instances of heightened activity. Our results indicate an essential interaction between ATRX and a previously uncharacterized histone modification in the central nervous system and suggest a potential role for abnormal repetitive element transcription in pathological states manifested by ATRX dysfunction.
Two new glycosides from Leonurus japonicus

Two new glycosides, 1,6-di-O-syringoyl-β-d-glucopyranose (1) and quercetin 3-O-[(3-O-syringoyl-α-l-rhamnopyranosyl)-(1 → 6)-β-d-glucopyranoside] (2), along with seven known compounds were isolated from the MeOH extract of Leonurus japonicus. The structures of these compounds were elucidated by spectral analysis.
Standard guide for EDI (HL7) communication security.

This Standard Guide gives the framework for secure end-to-end communication of EDI messages focusing on HL7. It is based on the common security model that distinguishes the concepts of communication security as rather globally controlled and application security as rather locally controlled. The concepts of quality and safety are not considered. Each of these concepts defines a set of security services, which are provided by sets of security mechanisms based on security algorithms applied to data. The different levels of granularity allow views of different groups of users including medical users, system administrators, and implementers within the same specification framework. Additionally, for implementation, the protocol-services-mechanisms relationships with respect to standards and products also have to be considered.
GABAergic neocortical neurons are resistant to NMDA receptor‐mediated injury

N-methyl-D-aspartate (NMDA) receptors are thought to mediate much of the central neuronal loss produced by certain neurologic insults, including hypoxia-ischemia, hypoglycemia, and trauma. Therefore, the specific vulnerability of GABAergic inhibitory neurons to NMDA receptor-mediated toxicity might be an important determinant of the potential for epileptogenesis following these insults. We have examined the fate of GABAergic cortical neurons in mouse cell cultures exposed to toxic levels of NMDA. GABAergic cells (about 10% of the cultured neuronal population) were identified either by immunoreactivity with antisera to GABA or by autoradiography following high-affinity uptake of 3H-GABA. Cultures exposed for 5 min to 20 to 750 μM NMDA showed NMDA concentration-dependent, widespread neuronal loss. However, GABAergic neurons were relatively spared, and thus represented an enhanced fraction of neuronal survivors. These observations suggest that GABAergic cortical neurons may possess some intrinsic resistance to NMDA receptor-mediated neurotoxicity, a property which might convey an anticonvulsant “inhibitory safety factor” to neocortex against certain forms of injury.