Miracle-dz/UniFAR-FTUs huggingface dataset:
Addressing Those Two That Go Together: The Angiotensin II Receptors and their Role in Blood-flow Regulation

In hypertension research and treatment, there is a milestone approximately every 50 years. The  rst theory of a connection between the kidney and high blood pressure (BP) was put forward in 1836 [1]. Tigerstedt in 1898 showed the existence of a renally produced substance mediating hypertension [2] and Goldblatt demonstrated the connection between blood  ow and vasopressor release in 1936 [3], about the same time as the  rst crude treatments for hypertension were being tested. Probably the most important antihypertensive drugs of the last decade, the angiotensin-converting enzyme (ACE) inhibitors, were introduced in 1982. This cycle of half centuries is set to be broken by the explosion in biomedical research in recent years. ACE inhibitors may still be the treatment of choice with demonstrated effects on mortality in congestive heart failure (CHF) [4, 5], but their “heir apparent” may already be on the market: the angiotensin II (Ang II)-receptor blockers (ARBs). Both ACE inhibitors and ARBs act on the renin– angiotensin system (RAS) to inhibit effects of Ang II, but in contrast to ACE inhibitors, ARBs block speci c actions of Ang II rather than its synthesis. Ang II has many different actions and it can function both as a circulating and as a locally produced hormone. As a circulating hormone Ang II is produced by the ACE, but locally acting Ang II can be synthesized both by ACE and through alternative pathways, e.g. by chymase [6]. These alternative enzymes are not sensitive to ACE inhibitors, which has been suggested to be a reason for the still high mortality in CHF, where residual levels of Ang II remain, despite treatments with ACE inhibitors [7, 8]. By using highly selective ARBs such as valsartan, local deleterious actions of Ang II can be effectively inhibited [9–11]. ARBs act on the Ang II AT1 receptor, which is responsible for most of the deleterious effects of Ang II. Its counterpart, the AT2 receptor, was long considered to be of importance during foetal development and upon tissue damage, as it was only detected in small amounts in normal tissues. This situation has changed in recent years and the AT2 receptor is now recognized to play a central role in the physiology of a range of organs, perhaps most importantly the endothelium, where AT2 stimulation is involved in, e.g., NO and bradykinin release, and opposes several AT1-mediated effects. This fact indicates that ARBs may have bene cial effects on blood  ow beyond those achieved by AT1 blockade.
Why Sex Matters

This inspiring book becomes one that is very booming. After published, this book can steal the market and book lovers to always run out of this book. And now, we will not let you run out any more to get this book. Why should be why sex matters? As a book lover, you must know that enjoying the book to read should be relevant to how you exactly need now. If they are not too much relevance, you can take the way of the inspirations to create for new inspirations.
K-to-W-band phased array antenna technology

A new phased array antenna (PAA) has been designed with frequency coverage from K- to W-band. This approach takes advantage of new 3D lithographic manufacturing techniques and Harris' Current Sheet Antenna (CSA) to cover 16-110 GHz from a single aperture. In this paper, analysis results will be presented, providing greater than 50% radiation efficiency over the entire instantaneous bandwidth and good scan performance to 60 degrees. To the author's knowledge, this is the first PAA capable of continuous operation from 16-110 GHz. This exciting new technology will be applicable to future avionics systems with direct integration to transmit and receive RF photonic back-ends.
Training of rowers before world championships.

In rowing, static and dynamic work of approximately 70% of the body's muscle mass is involved for 5.5 to 8 min at an average power of 450 to 550 W. In high load training phases before World Championships, training volume reaches 190 min.d-1, of which between 55 and 65% is performed as rowing, and the rest is nonspecific training like gymnastics and stretching and semispecific training like power training. Rowing training is mainly performed as endurance training, rowing 120 to 150 km or 12 h.wk-1. Rowing at higher intensities is performed between 4 and 10% of the total rowed time. The increase in training volume during the last years of about 20% was mainly reached by increasing nonspecific and semispecific training. The critical borderline to long-term overtraining in adapted athletes seems to be 2 to 3 wk of intensified prolonged training of about 3 h.d-1. Sufficient regeneration is required to avoid overtraining syndrome. The training principles of cross training, alternating hard and easy training days, and rest days reduce the risk of an overtraining syndrome in rowers.
Effect of human immunodeficiency virus on intensive care unit outcome of patients with Guillain-Barré syndrome.

OBJECTIVES The primary objective of this study was to investigate the effect of human immunodeficiency virus (HIV) infection on the outcome of patients admitted to the intensive care unit (ICU) with severe Guillain-Barré syndrome (GBS) requiring mechanical ventilation. A secondary objective was to compare the clinical and laboratory features of HIV-seronegative and HIV-seropositive patients admitted to the ICU with severe GBS. DESIGN Retrospective chart review. SETTING Two tertiary, academic hospitals in Johannesburg, South Africa. MATERIALS AND METHODS The case records of all patients admitted to the ICU with GBS between January 1995 and June 2002 were reviewed. Patients were included if their HIV status was known and if they had clinical features, electrophysiologic studies, and cerebrospinal fluid analyses consistent with GBS. Demographic data, days in ICU, days ventilated, CD4 T-lymphocyte counts (in the HIV group), cerebrospinal studies, infection rate, and mortality data were analyzed. RESULTS A total of 13 patients met the inclusion criteria: seven were HIV seronegative and six were HIV seropositive. The median age in the HIV group was 34.5 yrs, compared with 47 yrs in the non-HIV group. There was no significant difference between the two groups in days spent in the ICU or days ventilated. There were no significant differences in cerebrospinal studies, electrophysiologic studies, and blood culture-positive infections between the two groups. All patients received intravenous immunoglobulin (0.4 g/kg/day for 5 days). There was one death in the HIV-seropositive group and no deaths in the HIV-seronegative group. The median CD4 T-lymphocyte count in the HIV group was 322.5 x 106 cells/L. CONCLUSION HIV is commonly associated with GBS in South Africa. The ICU outcome in patients with HIV-associated GBS is similar to HIV-seronegative patients, particularly if the CD4 T-lymphocyte count is greater than 200 x 106 cells/L at admission.
Race and Mental Health Diagnosis Are Risk Factors for Highly Active Antiretroviral Therapy Failure in a Military Cohort Despite Equal Access to Care

Background:Data suggest that African Americans have lower rates of virologic suppression using highly active antiretroviral therapy (HAART), possibly because of socioeconomic status and access to care. In a US Military clinic, where beneficiaries have ready access to no-cost health care, the impact of several variables (including race) on HIV virologic suppression were examined. Methods:Retrospective analysis of antiretroviral-naive patients who began HAART between 1997 and 2003. Demographics, viral loads, CD4 cell counts, and mental health diagnoses were analyzed. Results:The charts of 129 individuals who initiated their first antiretroviral regimen during the period of observation were evaluated. The overall efficacy of reaching viral suppression was 71% at 12 months and 56% at 24 months. HIV suppression was achieved at 12 months by 63% of African Americans and 92% of whites (P = 0.001). Mental health diagnosis was associated with failure at 24 months (38 vs. 61%; P = 0.034). Being white (odds ratio = 3.5, 95% confidence interval [CI]: 1.2 to 10.3; P = 0.022) and lacking a mental health diagnosis (odds ratio = 8.7, 95% CI: 2.4 to 32.1; P = 0.001) were both associated with increased efficacy at 24 months by multivariate analysis. Conclusions:African-American race and the presence of a mental health diagnoses were independently associated with antiretroviral failure. Equal access to care yields high efficacy rates with HAART but does not fully equilibrate racial differences in virologic failure.
Early postoperative indicators of late outcome in acromegalic patients

objective According to current criteria, normalised serum IGF‐1 and glucose‐suppressed GH < 1 ng/ml are indicators of biochemical cure in acromegalic patients. We performed a retrospective study to assess whether the attainment of these values in the early postoperative period was predictive of future IGF‐1 normalisation and disease inactivity.
Differential expression of heat shock proteins in normal and failing human hearts.

BACKGROUND Heat shock proteins (hsp) constitute an endogenous stress response that protects cells from injury. Most work on these important proteins has focused on the immediate response to acute stress in cell culture systems and mammalian models of heart disease. Little is known about the expression of the hsps in human hearts. We were interested in whether there was increased expression of the hsps in heart failure, a setting of chronic, sustained stress. Five different hsps were examined: hsp27, hsp60, hsp72, hsc70 and hsp90. METHODS AND RESULTS Three groups of explanted hearts were studied: dilated cardiomyopathy (DCM), ischemic cardiomyopathy (IHD), and normal controls. Western-blotting with a standard curve of purified protein on each blot was used to quantify the expression of the hsps. Hsp27 was increased almost two-fold in DCM compared to normal hearts, and was significantly greater than in IHD hearts. Levels of hsp60 were doubled in both DCM and IHD hearts (P < 0.05). Hsp72, hsc70 and hsp90 were not significantly changed. CONCLUSIONS This study shows for the first time that differential changes in hsp levels occur in end-stage heart failure. Since hsps can render cells resistant to apoptosis, and are associated with the mitochondria and the cytoskeleton, which are known to be abnormal in heart failure, these studies may lead to new insights into the pathogenesis of cardiac decompensation.
Proline-rich synapse-associated proteins ProSAP1 and ProSAP2 interact with synaptic proteins of the SAPAP/GKAP family.

We have recently isolated a novel proline-rich synapse-associated protein-1 (ProSAP1) that is highly enriched in postsynaptic density (PSD). A closely related multidomain protein, ProSAP2, shares a highly conserved PDZ (PSD-95/discs-large/ZO-1) domain (80% identity), a ppI domain that mediates the interaction with cortactin, and a C-terminal SAM (sterile alpha-motif) domain. In addition, ProSAP2 codes for five ankyrin repeats and a SH3 (Src homology 3) domain. Transcripts for both proteins are coexpressed in many regions of rat brain, but show a distinct expression pattern in the cerebellum. Using the PDZ domains of ProSAP1 and 2 as bait in the yeast two-hybrid system, we isolated several clones of the SAPAP/GKAP (SAP90/PSD-95-associated protein/guanylate kinase-associated protein) family. The association of the proteins was verified by coimmunoprecipitation and cotransfection in HEK cells. Therefore, proteins of the ProSAP family represent a novel link between SAP90/PSD-95 bound membrane receptors and the cytoskeleton at glutamatergic synapses of the central nervous system.
Cholesterol 7α‐hydroxylase activities from human and rat liver are modulated in vitro posttranslationally by phosphorylation/dephosphorylation

Purified cholesterol 7α‐hydroxylases (C7αH) from human and rat liver microsomes, and from transformed Escherichia coli expression systems, were incubated with 0.3 mmol/L [gamma‐32P] adenosine triphosphate (ATP) in the presence and absence of bacterial alkaline phosphatase (AP) or rabbit muscle adenosine 3′,5′‐cyclic monophosphate (cAMP)‐dependent protein kinase. The amounts of 32P incorporation after separation of human and rat C7αH proteins by sodium dodecyl sulfate‐polyacrylamide gel electrophoresis (SDS‐PAGE) were related to C7αH catalytic activities (determined by a radioisotope incorporation method) and enzyme protein mass (determined by Western blotting and laser densitometry). Both human and rat C7αH activities significantly decreased after dephosphorylation by AP (‐57% ‐ ‐72%) and increased up to twofold with phosphorylation by rabbit muscle cAMP‐dependent protein kinase. The increases in C7αH activities were proportional to the amounts of cAMP‐dependent protein kinase used, and were coupled to 32P incorporation into the purified enzymes. Both the activation of C7αH and the amounts of 32P incorporation were time‐dependent and reached a maximum after 1 hour of incubation with 5 U of cAMP‐dependent protein kinase. In a second set of experiments, purified human and rat liver C7αH were dephosphorylated by 30‐minute incubation with AP, followed by inactivation of the phosphatase by the inhibitor NaF, and rephosphorylation of C7αH by 30‐minute incubation with rabbit muscle cAMP‐dependent protein kinase or bovine heart cAMP‐independent protein kinase. Rephosphorylation of the dephosphorylated C7αH proteins by cAMP‐dependent protein kinase increased C7αH catalytic activities up to fourfold, and the stimulation in catalytic activities paralleled the increases in 32P incorporation into the purified enzymes. Bovine heart protein kinase was as potent as rabbit muscle cAMP‐dependent protein kinase in stimulating catalytic activity and 32P incorporation into the human C7αH protein. Because the protein mass of these purified enzymes did not change, the short‐term regulation or catalytic efficiency of C7αH (activity per protein mass unit) is modulated, in vitro, posttranslationally by a phosphorylation/dephosphorylation mechanism in both the human and the rat enzymes.
Promoting medical student involvement in primary care research.

BACKGROUND AND OBJECTIVES As the growth of primary care continues, the need for strengthening the scientific foundations of practice becomes more pressing. Although there is general agreement on the importance of promoting primary care research by medical students, little has been reported on how this can be accomplished. The goal of the program described is to involve medical students in primary care research. METHODS Over the last 7 years, the Department of Family Medicine at the University of Colorado has promoted the involvement of medical students in primary care research through a program consisting of five elements: 1) a student development program (the Family Medicine Scholars Program), 2) financial support for student research, 3) a core of faculty mentors, 4) a strong coordinating effort by the predoctoral education office, and 5) research agendas geared to student schedules. RESULTS The number of students involved in primary care research, presentations, and publication of papers by students has increased since we initiated our medical student research program 7 years ago. CONCLUSIONS The elements discussed have proven successful at increasing student participation in primary care research.
Micro‐ and macrogeographical genetic structure of colonies of naked mole‐rats Heterocephalus glaber

Patterns of genetic structure in eusocial naked mole‐rat populations were quantified within and among geographically distant populations using multilocus DNA fingerprinting and mitochondrial DNA (mtDNA) sequence analysis. Individuals within colonies were genetically almost monomorphic, sharing the same mtDNA control region haplotype and having coefficients of band sharing estimated from DNA fingerprints ranging from 0.93 to 0.99. Family analysis of a hybrid captive colony of naked mole‐rats with increased levels of genetic variability using multilocus DNA fingerprinting gave results consistent with Mendelian inheritance, and has revealed for the first time that multiple paternity can occur. In a survey of wild colonies from Ethiopia, Somalia and locations in northern and southern Kenya, we have examined mtDNA control region sequence variation in 42 individuals from 15 colonies, and together with multilocus DNA fingerprinting and mtDNA cytochrome‐b sequence analysis in selected individuals have shown that these populations show considerable genetic divergence. Most of the variance in sequence divergence was found to be between geographical locations (Φct= 0.68) and there was a significant correlation between sequence divergence and geographical separation of haplotypes. Six colonies from Mtito Andei in southern Kenya shared the same control region haplotype, suggesting a recent common maternal ancestor. In contrast, out of four colonies at Lerata in north Kenya, three haplotypes were identified, and phylogenetic analysis suggests that this area may be a zone where two distinct lineages are in close proximity. Genetic distances were maximal between Ethiopian and southern Kenyan populations at 5.8% for cytochrome‐b, and are approaching interspecific values seen between other Bathyergids.
Nutritional Value of the Chilean Seaweeds Cryptonemia Obovata and Rhodymenia Corallina

Some nutritional components of the edible seaweeds Cryptonemia obovata and Rhodymenia corallina were determined. The amino acid content ranged from 1.0 ± 0.3 to 4174.2 ± 14.2 mg 100g−1 dry wt in C. obovata and between 0.9 ± 0.3 and 2657.0 ± 13.5 mg 100g−1 dry wt in R. corallina. The most abundant fatty acid in C. obovata was palmitic acid, reaching a value of 36.5 ± 0.2%, while in Rhodymenia corallina the main fatty acid was oleic acid, reaching a value of 24.7 ± 0.07%. Both seaweeds showed an important content of EPA (C20:5ω3). In C. obovata,α-tocopherol was the principal tocol (138.5 ± 4.9 mg kg−1 lipid), while in R. corallina, it was γ-tocotrienol (850.3 ± 9.4 mg kg−1 lipid). Furthermore, β-carotene was the main carotenoid pigment found in C. obovata.
Simultaneous measurement of free thyroxine and free 3,5,3'-triiodothyronine in undiluted serum by direct equilibrium dialysis/radioimmunoassay: evidence that free triiodothyronine and free thyroxine are normal in many patients with the low triiodothyronine syndrome.

UNLABELLED We have devised a practical, sensitive and specific method for simultaneous measurement of free thyroxine (FT4) and free triiodothyronine (FT3) in undiluted serum by direct equilibrium dialysis radioimmunoassay (RIA). Two hundred microliters serum sample was dialyzed against buffer (pH 7.4) for 20 hours at 37 degrees C and approximately 800 microL of the dialysate was used for measuring FT4 and FT3 simultaneously. The assay was set up in polystyrene tubes coated with anti-T4 antibody and available commercially for FT4 measurement (Quest-Nichols Institute, San Juan Capistrano, CA). The mean +/- SE (range) FT4 concentration (ng/dL) was 1.2 +/- 0.04 (0.7.0 to 2.30) in 54 normal subjects. It was significantly increased (3.6 +/- 0.4 [1.8 to 9.6], n = 20) in hyperthyroidism and clearly decreased (0.40 +/- 0.04 [1.10 to 0.70], n = 26] in hypothyroidism. All nonthyroid illness (NTI) patients had normal FT4 except 3, 2 of whom were on amiodarone and 1 had received heparin. Serum FT4 concentration was minimally elevated in 18 newborn cord blood serum (1.40 +/- 0.08 [0.90 to 2.2], cf. normal p < .05). The mean serum FT3 concentration (pg/dL) was 285 +/- 10 (134 to 454) in 54 normal sera. It was clearly increased in hyperthyroidism (1033 +/- 98 [593 to 2134], n = 20, p < .001). However, serum FT3 varied widely in hypothyroidism (27 to 597, mean 235 +/- 24, NS) as did serum total T3 (19 to 175). Interestingly, however, the mean serum FT3 concentration was normal (273 +/- 28 [62 to 575, NS]) in 25 NTI patients. All of these patients had low serum total T3 (46 +/- 5.0 [10 to 84], ng/dL; normal 84 to 160, p < 0.001), while FT3 was clearly normal in 21 of 25 patients and low in the remaining 4 patients. Similarly, among 18 newborn cord blood sera serum FT3 concentration was normal in 15 and subnormal only in the remaining 3 while all had clearly subnormal total T3 (28 to 74 ng/dL). CONCLUSIONS (1) A practical, sensitive, and specific assay for simultaneous measurement of FT4 and FT3 is described; (2) FT3 is consistently elevated in hyperthyroidism while FT4 is elevated in most (approximately 85%) cases; (3) FT4 is consistently decreased in hypothyroidism but FT3 varies widely; (4). Serum FT3 concentration is normal in approximately 83% of patients with the low T3 syndrome in NTI and newborn cord blood serum. These data suggest that normal FT3 may explain clinical euthyroidism in many patients with the low T3 syndrome.
A probable case of Muckle–Wells syndrome

Muckle–Wells syndrome is a rare autosomally dominant disorder belonging to the group of periodic fever syndromes. Three main features of the disease are: (i) urticarial eruptions; (ii) progressive perceptive deafness; and (iii) amyloid nephropathy. A 26‐year‐old Japanese woman had suffered at birth from an urticarial rash and episodic fever. The fever was frequently associated with chills and ill‐defined malaise. There was no familial history of urticarial rash or fever. Although she did not recognize hearing loss, audiometry revealed perceptive deafness. She also had hepatosplenomegaly and hyperimmunoglobulinemia, but did not have persistent arthritis, or any neurological or gastrointestinal disorder. No growth retardation was observed. Skin biopsy specimens from her buttock showed a sparse perivascular and interstitial infiltrate of neutrophils in the papillary dermis. Periodic fever syndrome was diagnosed. Muckle–Wells syndrome was most likely, although no amyloid nephropathy was observed and no gene mutations of CIAS1 (T785C, C778T, G907A, G1315A, G1075C) were detected. We treated her with prednisolone, which had a partial effect. Previous treatment with colchicines, antihistamines, dapsone, clarithromycin, minocycline hydrochloride and loxoprofen sodium had been unsuccessful. Muckle–Wells syndrome may go undiagnosed for many years or be misdiagnosed as refractory urticaria. Therefore, we should consider the possibility of periodic fever syndrome when we see patients with refractory urticaria and episodic fever.
Increased Infection-Related Mortality in KIR-Ligand–Mismatched Unrelated Allogeneic Hematopoietic Stem-Cell Transplantation

Recently, attention has been focused on the role of killer cell immunoglobulin-like receptor (KIR)-ligand incompatibility between donor and recipient in allogeneic hematopoietic stem-cell transplantation (ASCT). Although KIR-ligand mismatch is clearly associated with improved survival in haploidentical ASCT for acute myeloid leukemia, its role in unrelated human leukocyte antigen-mismatched ASCT is more controversial. Here we present a retrospective analysis of KIR-ligand–matched (n=167) and mismatched (n=23) unrelated ASCTs for hematologic malignancies performed at a single center. We observed that KIR-ligand mismatch was associated with increased transplantation-related mortality (P=0.02), leading to decreased overall survival (P=0.01). The increased transplantation-related mortality was a consequence of a higher rate of infections (P=0.01), whereas incidence of graft-versus-host disease and leukemic relapse did not differ significantly between the two groups. These results suggest that the presence of donor-derived, alloreactive natural killer cells may interfere with immunity to infection in the early posttransplantation period.
Differential Binding Profiles of StpA in Wild-Type and hns Mutant Cells: a Comparative Analysis of Cooperative Partners by Chromatin Immunoprecipitation-Microarray Analysis

ABSTRACT We performed chromatin immunoprecipitation-microarray analysis to investigate differences in function between StpA and H-NS in Escherichia coli cells. StpA binding regions essentially overlap those of H-NS in wild-type cells, while they are reduced to one-third in the hns mutant. The H-NS binding profile was unaffected by stpA inactivation.