Miracle-dz/UniFAR-FTUs huggingface dataset:
Chronic central infusion of ANG II potentiates cardiac sympathetic afferent reflex in dogs.

The aims of this study were to determine whether ANG II is involved in the central integration of the cardiac sympathetic afferent reflex (CSAR), and if this central effect of ANG II is mediated by the AT1 receptor. Experiments were undertaken in dogs that were anesthetized with α-chloralose, sinoaortic denervated, and vagotomized. The renal sympathetic nerve activity (RSNA) responses to varying frequency and voltage stimulation of cardiac sympathetic afferent nerves were used to evaluate the central sensitivity of the CSAR. In two groups of dogs, two doses (50 and 100 ng/min icv) of ANG II were acutely infused. In a third group of dogs, ANG II was chronically infused for 3 days (100 ng/min, 1 μl/h icv). We found that acute infusion into the cerebroventricle of two doses of ANG II did not affect the central sensitivity of the CSAR or the baseline hemodynamics, but the baseline RSNA increased significantly during the infusion of the higher dose of ANG II. However, chronic intracerebroventricular infusion of ANG II enhanced the central sensitivity of the CSAR significantly. In addition, chronic intracerebrovetricular infusion of ANG II elicited a significant increase in water intake and in arterial pressure from the first and second day of infusion, respectively. In the group that received chronic intracerebroventricular infusion of ANG II, the administration of an AT1-receptor antagonist losartan (0.125 mg/kg icv) abolished ANG II-induced augmentation of the CSAR. These results suggest that chronic elevation of central ANG II can sensitize the CSAR via central AT1 receptors.
CK inhibition accelerates transcytosolic energy signaling during rapid workload steps in isolated rabbit hearts.

The effect of graded creatine kinase (CK) inhibition on the response time of mitochondrial O2 consumption to dynamic workload jumps ( t mito) was studied in isolated rabbit hearts. Tyrode-perfused hearts ( n = 7/group) were exposed to 15 min of 0, 0.1, 0.2, or 0.4 mM iodoacetamide (IA) (CK activity = 100, 14, 6, and 3%, respectively). Pretreatment t mito was similar across groups at 6.5 ± 0.5 s (mean ± SE). The increase observed over time in control hearts (33 ± 8%) was progressively reversed to 16 ± 6, -20 ± 6 ( P< 0.01 vs. control), and -46 ± 6 ( P < 0.01 vs. control) % in the 0.1, 0.2 and 0.4 mM IA groups, respectively. The faster response times occurred without reductions in mitochondrial oxidative capacity (assessed in vitro) or myocardial O2 consumption of the whole heart during workload steps. Isovolumic contractile function assessed as rate-pressure product (RPP) and contractile reserve (increase in RPP during heart rate steps) were significantly reduced by IA. We conclude that CK in the myofibrils and/or cytosol does not speed up transfer of the energy-related signal to the mitochondria but rather acts as an energetic buffer, effectively slowing the stimulus between myofibrils/ion pumps and oxidative phosphorylation. This argues against the existence of an obligatory creatine phosphate energy shuttle, because CK is effectively bypassed.
Arterial O2 content and tension in regulation of cardiac output and leg blood flow during exercise in humans.

A universal O2 sensor presumes that compensation for impaired O2delivery is triggered by low O2tension, but in humans, comparisons of compensatory responses to altered arterial O2 content ([Formula: see text]) or tension ([Formula: see text]) have not been reported. To directly compare cardiac output (Q˙TOT) and leg blood flow (LBF) responses to a range of[Formula: see text] and[Formula: see text], seven healthy young men were studied during two-legged knee extension exercise with control hemoglobin concentration ([Hb] = 144.4 ± 4 g/l) and at least 1 wk later after isovolemic hemodilution ([Hb] = 115 ± 2 g/l). On each study day, subjects exercised twice at 30 W and on to voluntary exhaustion with an[Formula: see text] of 0.21 or 0.11. The interventions resulted in two conditions with matched[Formula: see text] but markedly different [Formula: see text] (hypoxia and anemia) and two conditions with matched[Formula: see text] and different[Formula: see text] (hypoxia and anemia + hypoxia). [Formula: see text] varied from 46 ± 3 Torr in hypoxia to 95 ± 3 Torr (range 37 to >100) in anemia ( P < 0.001), yet LBF at exercise was nearly identical. However, as[Formula: see text] dropped from 190 ± 5 ml/l in control to 132 ± 2 ml/l in anemia + hypoxia ( P < 0.001),Q˙TOT and LBF at 30 W rose to 12.8 ± 0.8 and 7.2 ± 0.3 l/min, respectively, values 23 and 47% above control ( P< 0.01). Thus regulation ofQ˙TOT, LBF, and arterial O2 delivery to contracting intact human skeletal muscle is dependent for signaling primarily on[Formula: see text], not[Formula: see text]. This finding suggests that factors related to [Formula: see text]or [Hb] may play an important role in the regulation of blood flow during exercise in humans.
Endothelial cell nitric oxide production in acute chest syndrome.

Acute chest syndrome (ACS) is the most common form of acute pulmonary disease associated with sickle cell disease. To investigate the possibility that alterations in endothelial cell (EC) production and metabolism of nitric oxide (NO) products might be contributory, we measured NO products from cultured pulmonary EC exposed to red blood cells and/or plasma from sickle cell patients during crisis. Exposure to plasma from patients with ACS caused a 5- to 10-fold increase in S-nitrosothiol (RSNO) and a 7- to 14-fold increase in total nitrogen oxide (NOx) production by both pulmonary arterial and microvascular EC. Increases occurred within 2 h of exposure to plasma in a concentration-dependent manner and were associated with increases in endothelial nitric oxide synthase (eNOS) protein and eNOS enzymatic activity, but not with changes in nitric oxide synthase (NOS) III or NOS II transcripts, inducible NOS (iNOS) protein nor iNOS enzymatic activity. RSNO and NOx increased whether plasma was obtained from patients with ACS or other forms of vasoocclusive crisis. Furthermore, an oxidative state occurred and oxidative metabolites of NO, particularly peroxynitrite, were produced. These findings suggest that altered NO production and metabolism to damaging oxidative molecules contribute to the pathogenesis of ACS.
Diet, nutrition, and cancer.

As the second leading cause of death in the United States, cancer is a major public health problem today. Cancer incidence varies worldwide and tends to change with migration. These epidemiological observations have led to the concept that environmental factors may be important in carcinogenesis. Diet and nutrition are receiving increased attention and the National Cancer Institute, as mandated by the Nation Cancer Act Amendments of 1974, is playing a major leadership role in expanding research efforts in the areas of environmental carcinogenesis, and nutrition in relation to cancer. The subject of diet, nutrition, and cancer is complex. Different types of cancer are not necessarily affected by dietary components in the same manner. Although the development of certain neoplasms may be repressed by specific dietary deficiencies, other types, particularly those of the liver and upper gastrointestinal tract, are actually augmented or potentiated by such deficienceis. In extrapolating results from animal experiments to humans, caution must be exercised because of possible differences in species response to the same dietary stimulus and because spontaneous tumors may react differently from experimentally-induced tumors. Diet and nutrition are viewed more appropriately as modifiers, rather than initiators, of tumorigenesis. Caloric intake, type and amount of fat, protein, amino acids, vitamins, minerals, fiber, and other dietary constituents have been studied in regard to their influence on the development of neoplasms. Dietary components may have opposing effects on tumorigenesis, i.e., protective and predisposing, and the consequence to the host will depend on the balance between these opposing forces. Studies conducted to date indicate that the modifying effect of diet and nutrition may be exerted through specific effects on 1) intestinal bacteria and substrates for bacterial metabolism, 2) microsomal mixed-function oxidase system, 3) endocrine system, 4) immunological system, 5) availability of metabolites for cell proliferations, and 6) rate of carcinogen transfer and duration of exposure to the carcinogen. More research is needed to elucidate the interaction between diet and each of these factors and to test the validity of the mechanisms proposed to explain such interactions. These studies will lead not only to a better understanding of carcinogenesis itself but also to a new understanding of the influence of diet on human physiology and metabolism.
Integrating and Accessing Heterogeneous Information Sources in TSIMMIS

A common problem facing many organizations today is that of multiple, disparate information sources and repositories, including databases, object stores, knowledge file systems, digital libraries, information retrieval systems, and electronic mail systems. Decision makers often need information from multiple sources, but are unable to get and fuse the required information in a timely fashion due to the diffculties of accessing the different systems, and due to the fact that the information obtained can be inconsistent and contradictory. The goal of the TSIMMIS 1 project is to provide tools for accessing, in an integrated fashion, multiple information sources. Numerous other recent projects have similar goals and are discussed briefly at the end of this abstract. For the following description of the TSIMMIS architecture refer to Figure 1. 1.1 T ranslators and Common Model Figure 1 shows a collection of (disk-shaped) heterogeneous information sources. Above each source is a translator (or wrapper ) that logically converts the underlying data objects to a common information model. To do this logical translation, the translator converts This work was supported by ARPA Contract F33615-93-1-1339, by the Anderson Faculty Scholar Fund, by the Center for Integrated Systems at Stanford University, and by equipment grants from Digital Equipment Corporation and IBM Corporation. The US Government is authorized to reproduce and distribute reprints for Government purposes notwithstanding any copyright notation thereon. The views and conclusions contained in this document are those of the authors and should not be interpreted as necessarily representing the offcial policies or endorsements, either express or implied, of the US Government.
Visual Memories Bypass Normalization

How distinct are visual memory representations from visual perception? Although evidence suggests that briefly remembered stimuli are represented within early visual cortices, the degree to which these memory traces resemble true visual representations remains something of a mystery. Here, we tested whether both visual memory and perception succumb to a seemingly ubiquitous neural computation: normalization. Observers were asked to remember the contrast of visual stimuli, which were pitted against each other to promote normalization either in perception or in visual memory. Our results revealed robust normalization between visual representations in perception, yet no signature of normalization occurring between working memory stores—neither between representations in memory nor between memory representations and visual inputs. These results provide unique insight into the nature of visual memory representations, illustrating that visual memory representations follow a different set of computational rules, bypassing normalization, a canonical visual computation.
The relationship between alliance and outcome: Analysis of a two-person perspective on alliance and session outcome.

OBJECTIVE Better alliance is known to predict better psychotherapy outcomes, but the interdependent and interactive effects of both therapist- and patient-reported alliance levels have yet to be systematically investigated. METHOD Using actor-partner interdependence model analysis the authors estimated actor, partner, and 2 types of interactive effects of alliance on session outcome in a sample of 241 patient-therapist dyads across 30 sessions of cognitive-behavioral and alliance-focused therapy. RESULTS Findings suggest that the most robust predictors of session outcome are within-treatment changes in patient reports of the alliance, which predict both patient and therapist report on outcome. Within-treatment changes in therapist reports of the alliance, as well as differences between patients and between therapists in their average ratings of alliance levels across treatment, predict outcome as reported by the specific individual. Although alliance was found to be a significant predictor of outcome in both treatments, for therapist-reported alliance and outcome it had a stronger effect in alliance-focused therapy than in cognitive-behavioral therapy. Additionally, dyads with the highest pooled level of alliance from both partners fared best on session outcome. CONCLUSIONS The results are consistent with a 2-person perspective on psychotherapy, demonstrating the importance of considering the interdependent and interactive nature of both patient and therapist alliance levels on session outcome. (PsycINFO Database Record
Regulation of mesangial cell hexokinase activity by PKC and the classic MAPK pathway.

Phorbol esters increase glucose (Glc) uptake and utilization in a variety of cell types, and, in some cells, these changes have been attributed to increased Glc phosphorylation and better functional coupling of hexokinases (HKs) to facilitative Glc transporters. Phorbol esters are potent mesangial cell mitogens, but their effects on HK-catalyzed Glc phosphorylation and metabolism are unknown. When examined in murine mesangial cells, active, but not inactive, phorbol esters increased HK activity in a time- and dose-dependent manner. Maximal induction of HK activity at 12-24 h was accompanied by parallel increases in both Glc utilization and lactate production and was blocked by the specific MEK1/2 inhibitor PD-98059 (IC50∼3 μM). This effect involved early activation of protein kinase C (PKC), MEK1/2, and ERK1/2, and the prolonged time course of subsequent HK induction was attributable, in part, to requirements for ongoing gene transcription and de novo protein synthesis. Mesangial cell HK activity thus exhibits novel regulatory behavior involving both PKC and classic MAPK pathway activation, suggesting specific mechanisms whereby PKC activation may influence Glc metabolism.
Thermal sensitivity of carbon nanotube and graphene oxide containing responsive hydrogels

Comparative investigations are reported on poly(N-isopropylacrylamide) (PNIPA) gels of various carbon nanotube (CNT) and graphene oxide (GO) contents synthesized under identical conditions. The kind and concentration of the incor- porated carbon nanoparticles (CNPs) influence the swelling and stress-strain behaviour of the composites. Practically inde- pendently of the filler content, incorporation of CNPs appreciably improves the fracture stress properties of the gels. The time constant and the swelling ratio of the shrinkage following an abrupt increase in temperature of the swelling medium from 20 to 50 °C can be adjusted by selecting both the type and the amount of nanoparticle loading. This offers a means of accurately controlling the deswelling kinetics of drug release with PNIPA systems, and could be employed in sensor appli- cations where fast and excessive shrinkage are a significant drawback. Both CNTs and GO enhance the infrared sensitivity of the PNIPA gel, thus opening a route for the design of novel drug transport and actuator systems. It is proposed that the in- fluence of the CNPs depends more on their surface reactivity during the gel synthesis rather than on their morphology. One of the important findings of this study is the existence of a thermally conducting network in the GO filled gels.
Endogenous ATP release regulates Cl- secretion in cultured human and rat biliary epithelial cells.

P2Y receptor stimulation increases membrane Cl- permeability in biliary epithelial cells, but the source of extracellular nucleotides and physiological relevance of purinergic signaling to biliary secretion are unknown. Our objectives were to determine whether biliary cells release ATP under physiological conditions and whether extracellular ATP contributes to cell volume regulation and transepithelial secretion. With the use of a sensitive bioluminescence assay, constitutive ATP release was detected from human Mz-ChA-1 cholangiocarcinoma cells and polarized normal rat cholangiocyte monolayers. ATP release increased rapidly during cell swelling induced by hypotonic exposure. In Mz-ChA-1 cells, removal of extracellular ATP (apyrase) and P2 receptor blockade (suramin) reversibly inhibited whole cell Cl- current activation and prevented cell volume recovery during hypotonic stress. Moreover, exposure to apyrase induced cell swelling under isotonic conditions. In intact normal rat cholangiocyte monolayers, hypotonic perfusion activated apical Cl-currents, which were inhibited by addition of apyrase and suramin to bathing media. These findings indicate that modulation of ATP release by the cellular hydration state represents a potential signal coordinating cell volume with membrane Cl- permeability and transepithelial Cl-secretion.
Clinical Features, Risk Factors and Outcomes of Bacteremia due to Enterococci with High-Level Gentamicin Resistance: Comparison with Bacteremia due to Enterococci without High-Level Gentamicin Resistance

High-level gentamicin resistance (HLGR) in enterococci has increased since the 1980s, but the clinical significance of the resistance and its impact on outcome have not been established. One hundred and thirty-six patients with bacteremia caused by enterococci with HLGR (HLGR group) were compared with 79 patients with bacteremia caused by enterococci without HLGR (non-HLGR group). Hematologic malignancy, neutropenia, Enterococcus faecium infection, nosocomial infection and monomicrobial bacteremia were more common in the HLGR group than the non-HLGR group, and APACHE II scores were also higher (P<0.05, in each case). Neutropenia, monomicrobial infection, stay in intensive care at culture, and use of 3rd generation cephalosporin, were independent risk factors for acquisition of HLGR enterococcal bacteremia. Fourteen-day and 30-day mortalities were higher in the HLGR group than the non-HLGR group in univariate analysis (37% vs. 15%, P=0.001; 50% vs. 22%, P<0.001). However, HLGR was not an independent risk factor for mortality due to enterococcal bacteremia in multivariate analysis. Therefore, HLGR enterococcal bacteremia is associated with more severe comorbid conditions and higher mortality than non-HLGR enterococcal bacteremia but the HLGR itself does not contribute significantly to mortality.
Caffeine Improves Basketball Performance in Experienced Basketball Players

The aim of this study was to determine the effect of caffeine intake on overall basketball performance in experienced players. A double-blind, placebo-controlled, randomized experimental design was used for this investigation. In two different sessions separated by one week, 20 experienced basketball players ingested 3 mg of caffeine/kg of body mass or a placebo. After 60 min, participants performed 10 repetitions of the following sequence: Abalakov jump, Change-of-Direction and Acceleration Test (CODAT) and two free throws. Later, heart rate, body impacts and game statistics were recorded during a 20-min simulated basketball game. In comparison to the placebo, the ingestion of caffeine increased mean jump height (37.3 ± 6.8 vs. 38.2 ± 7.4 cm; p = 0.012), but did not change mean time in the CODAT test or accuracy in free throws. During the simulated game, caffeine increased the number of body impacts (396 ± 43 vs. 410 ± 41 impacts/min; p < 0.001) without modifying mean or peak heart rate. Caffeine also increased the performance index rating (7.2 ± 8.6 vs. 10.6 ± 7.1; p = 0.037) during the game. Nevertheless, players showed a higher prevalence of insomnia (19.0 vs. 54.4%; p = 0.041) after the game. Three mg of caffeine per kg of body mass could be an effective ergogenic substance to increase physical performance and overall success in experienced basketball players.
Prevalence and Associated Factors of Low Back Pain among Clinicians of A Major Referral Hospital.

OBJECTIVES Low back pain (LBP) is one of the most common health problems faced by health care professionals due to their occupational lifestyle. This study aimed to quantify the prevalence of LBP among clinicians, and to identify its associated factors. METHODS A cross sectional study was carried out in King Khalid University Hospital (KKUH) among 460 clinicians from different specialties. A validated questionnaire of 21 items was used to collect data. Chi-square test and odds ratios were used to observe and measure the association between categorical variables. Binary logistic regression by Wald method was used to identify independent factors associated with LBP (yes/no). RESULTS The prevalence of LBP was found to be 59.4% (244) with 38% of them reported as severe. The distribution of prevalence among consultants, registrars and residents was 110 (45.1%), 91 (37.3%) and 43 (17.6%) respectively. Out of 114 (46.7%) surgeons who suffer from LBP we found, orthopaedic surgeons had 10.2% prevalence of LBP. Male clinician (odds ratio: 1.7; 95% Confidence Interval (CI): 1.1- 2.8), consultant (4.1; 95% CI: 2.1-8.3), registrar (2.2; 95% CI: 1.2-4.2), more than 10 hours/week near bedside (1.8; 95% CI: 1.1-3.0), bending backwards at work (8.3; 95% CI: 5.1-13.4) and pulling objects during work (3.1; 95% CI: 1.7-5.6) were found to be independent statistically significant associated factors of LBP. CONCLUSION The high prevalence of LBP among clinicians and its associated factors indicates that clinicians should maintain good posture and avoid sudden movements during working hours in hospital to reduce this occupational health problem.
Ksp-cadherin gene promoter. II. Kidney-specific activity in transgenic mice.

Kidney-specific cadherin (Ksp-cadherin, cadherin 16) is a tissue-specific member of the cadherin superfamily that is expressed exclusively in the basolateral membrane of tubular epithelial cells in the kidney. To determine the basis for tissue-specific expression of Ksp-cadherin in vivo, we evaluated the activity of the promoter in transgenic mice. Transgenic mice containing 3.3 kb of the mouse Ksp-cadherin promoter and an Escherichia coli lacZ reporter gene were generated by pronuclear microinjection. Assays of β-galactosidase enzyme activity showed that the transgene was expressed exclusively in the kidney in both adult and developing mice. Within the kidney, the transgene was expressed in a subset of renal tubular epithelial cells that endogenously expressed Ksp-cadherin and that were identified as collecting ducts by colabeling with Dolichos biflorus agglutinin. In the developing metanephros, expression of the transgene in the branching ureteric bud correlated with the developmental expression of Ksp-cadherin. Identical patterns of expression were observed in multiple founder mice, indicating that kidney specificity was independent of transgene integration site. However, heterocellular expression was observed consistent with repeat-induced gene silencing. We conclude that the Ksp-cadherin gene promoter directs kidney-specific expression in vivo. Regulatory elements that are sufficient to recapitulate the tissue- and differentiation-specific expression of Ksp-cadherin in the renal collecting duct are located within 3.3 kb upstream to the transcriptional start site.