Miracle-dz/UniFAR-FTUs huggingface dataset:
Cerebral blood flow during hypoxic hypoxia with plasma-based hemoglobin at reduced hematocrit.

We determined whether cerebral blood flow (CBF) remained related to arterial O2 content ([Formula: see text]) during hypoxic hypoxia when hematocrit and hemoglobin concentration were independently varied with cell-free, tetramerically stabilized hemoglobin transfusion. Three groups of pentobarbital sodium-anesthetized cats were studied with graded reductions in arterial O2saturation to 50%: 1) a control group with a hematocrit of 31 ± 1% (mean ± SE; n = 7); 2) an anemia group with a hematocrit of 21 ± 1% that underwent an isovolumic exchange transfusion with an albumin solution ( n = 8); and 3) a group transfused with an intramolecularly cross-linked hemoglobin solution to decrease hematocrit to 21 ± 1% ( n = 10). Total arterial hemoglobin concentration (g/dl) after hemoglobin transfusion (8.8 ± 0.2) was intermediate between that of the control (10.3 ± 0.3) and albumin (7.2 ± 0.4) groups. Forebrain CBF increased after albumin and hemoglobin transfusion at normoxic O2 tensions to levels attained at equivalent reductions in [Formula: see text] in the control group during graded hypoxia. Over a wide range of arterial O2 saturation and sagittal sinus[Formula: see text], CBF remained greater in the albumin group. When CBF was plotted against[Formula: see text] for all three groups, a single relationship was formed. Cerebral O2 transport, O2 consumption, and fractional O2 extraction were constant during hypoxia and equivalent among groups. We conclude that CBF remains related to [Formula: see text] during hypoxemia when hematocrit is reduced with and without proportional reductions in O2-carrying capacity. Thus O2 transport to the brain is well regulated at a constant level independently of alterations in hematocrit, hemoglobin concentration, and O2 saturation.
Podokinesis in endothelial cell migration: role of nitric oxide.

Previously, we demonstrated the role of nitric oxide (NO) in transforming epithelial cells from a stationary to locomoting phenotype [E. Noiri, T. Peresleni, N. Srivastava, P. Weber, W. F. Bahou, N. Peunova, and M. S. Goligorsky. Am. J. Physiol. 270 ( Cell Physiol. 39): C794-C802, 1996] and its permissive function in endothelin-1-stimulated endothelial cell migration (E. Noiri, Y. Hu, W. F. Bahou, C. Keese, I. Giaever, and M. S. Goligorsky. J. Biol. Chem. 272: 1747-1753, 1997). In the present study, the role of functional NO synthase in executing the vascular endothelial growth factor (VEGF)-guided program of endothelial cell migration and angiogenesis was studied in two independent experimental settings. First, VEGF, shown to stimulate NO release from simian virus 40-immortalized microvascular endothelial cells, induced endothelial cell transwell migration, whereas N G-nitro-l-arginine methyl ester (l-NAME) or antisense oligonucleotides to endothelial NO synthase suppressed this effect of VEGF. Second, in a series of experiments on endothelial cell wound healing, the rate of VEGF-stimulated cell migration was significantly blunted by the inhibition of NO synthesis. To gain insight into the possible mode of NO action, we next addressed the possibility that NO modulates cell matrix adhesion by performing impedance analysis of endothelial cell monolayers subjected to NO. The data showed the presence of spontaneous fluctuations of the resistance in ostensibly stationary endothelial cells. Spontaneous oscillations were induced by NO, which also inhibited cell matrix adhesion. This process we propose to term "podokinesis" to emphasize a scalar form of micromotion that, in the presence of guidance cues, e.g., VEGF, is transformed to a vectorial movement. In conclusion, execution of the program for directional endothelial cell migration requires two coexisting messages: NO-induced podokinesis (scalar motion) and guidance cues, e.g., VEGF, which imparts a vectorial component to the movement. Such a requirement for the dual signaling may explain a mismatch in the demand and supply with newly formed vessels in different pathological states accompanied by the inhibition of NO synthase.
The Distribution of Activation Markers and Selectins on Peripheral T Lymphocytes in Preeclampsia

Introduction Impaired maternal immune tolerance resulting in systemic inflammation plays a pivotal role in the pathogenesis of preeclampsia. Phenotypical changes of monocytes and neutrophil granulocytes have already been studied in preeclampsia, and some studies also included T lymphocyte activation markers; however, the results are controversial and a comprehensive analysis of activation markers is lacking. The characteristics of cellular adhesion molecules in preeclampsia are yet to be described. Material and Methods Peripheral blood samples of 18 preeclamptic patients and 20 healthy pregnant women in the third trimester were evaluated using flow cytometry to characterize the cell surface expression of T lymphocyte activation markers and selectins. Results We found an elevated ratio of HLA-DR and CD122-, CD62E-, and CD62L-expressing cells among the CD4+ T lymphocytes in PE in comparison to healthy pregnancy. No alterations were found in the prevalence of CD69-, CD25-, and CD62P-expressing lymphocytes and CD11c-expressing monocytes. Conclusions Our findings support the role of activated T lymphocytes and specific cell adhesion molecules in the pathogenesis of preeclampsia.
Collagen Solubility and Calcium Concentration and Their Effects on Tenderness in the M. longissimus lumborum

Collagen Solubility and Calcium Concentration and Their Effects on Tenderness in the M. longissimus lumborum. (December 2009) Daniel Phillip Genho, B.S., Utah State University Chair of Advisory Committee: Dr. Jeffrey W. Savell Strip steaks from the McGregor genome project were used to evaluate the effects of sarcomere length, myofibrillar fragmentation index, 3 h postmortem pH, 24 h postmortem pH, marbling, electrical stimulation (ES), sarcoplasmic free calcium concentration, and collagen characteristics on tenderness as measured by WarnerBratzler shear force (WBS). The WBS values were measured prior to this project so the animals were able to be separated into “tender” and “tough” groups using a WBS value of 30 N as the separating point, steaks with a WBS value less than 30 N being “tender” and the others being “tough”. It was found that ES sides had lower WBS values, however, “tough” steaks showed a greater response to ES than “tender” steaks. ES sides also had higher sarcoplasmic free calcium concentration and lower 3 h postmortem pH. Tenderness is best predicted by treatment (ES versus NON-ES), however, there is some efficacy in using total collagen and collagen solubility in conjunction with treatment.
Two Rab5 Homologs Are Essential for the Development and Pathogenicity of the Rice Blast Fungus Magnaporthe oryzae

The rice blast fungus, Magnaporthe oryzae, infects many economically important cereal crops, particularly rice. It has emerged as an important model organism for studying the growth, development, and pathogenesis of filamentous fungi. RabGTPases are important molecular switches in regulation of intracellular membrane trafficking in all eukaryotes. MoRab5A and MoRab5B are Rab5 homologs in M. oryzae, but their functions in the fungal development and pathogenicity are unknown. In this study, we have employed a genetic approach and demonstrated that both MoRab5A and MoRab5B are crucial for vegetative growth and development, conidiogenesis, melanin synthesis, vacuole fusion, endocytosis, sexual reproduction, and plant pathogenesis in M. oryzae. Moreover, both MoRab5A and MoRab5B show similar localization in hyphae and conidia. To further investigate possible functional redundancy between MoRab5A and MoRab5B, we overexpressed MoRAB5A and MoRAB5B, respectively, in MoRab5B:RNAi and MoRab5A:RNAi strains, but neither could rescue each other’s defects caused by the RNAi. Taken together, we conclude that both MoRab5A and MoRab5B are necessary for the development and pathogenesis of the rice blast fungus, while they may function independently.
Toxicity of TiO2 nanoparticles on soil nitrification at environmentally relevant concentrations: Lack of classical dose–response relationships

Abstract Titanium-dioxide nanoparticles (TiO2-NPs) are increasingly released in agricultural soils through, e.g. biosolids, irrigation or nanoagrochemicals. Soils are submitted to a wide range of concentrations of TiO2-NPs depending on the type of exposure. However, most studies have assessed the effects of unrealistically high concentrations, and the dose–response relationships are not well characterized for soil microbial communities. Here, using soil microcosms, we assessed the impact of TiO2-NPs at concentrations ranging from 0.05 to 500 mg kg−1 dry-soil, on the activity and abundance of ammonia-oxidizing archaea (AOA) and bacteria (AOB), and nitrite-oxidizing bacteria (Nitrobacter and Nitrospira). In addition, aggregation and oxidative potential of TiO2-NPs were measured in the spiking suspensions, as they can be important drivers of TiO2-NPs toxicity. After 90 days of exposure, non-classical dose–response relationships were observed for nitrifier abundance or activity, making threshold concentrations impossible to compute. Indeed, AOA abundance was reduced by 40% by TiO2-NPs whatever the concentration, while Nitrospira was never affected. Moreover, AOB and Nitrobacter abundances were decreased mainly at intermediate concentrations nitrification was reduced by 25% at the lowest (0.05 mg kg−1) and the highest (100 and 500 mg kg−1) TiO2-NPs concentrations. Path analyses indicated that TiO2-NPs affected nitrification through an effect on the specific activity of nitrifiers, in addition to indirect effects on nitrifier abundances. Altogether these results point out the need to include very low concentrations of NPs in soil toxicological studies, and the lack of relevance of classical dose–response tests and ecotoxicological dose metrics (EC50, IC50…) for TiO2-NPs impact on soil microorganisms.
Evidence that Calu-3 human airway cells secrete bicarbonate.

The Calu-3 cell line is being investigated as a model for human submucosal gland serous cells. In a previous investigation of basal short-circuit current ( I sc) in Calu-3 cells, high levels of bumetanide-insensitive basal I sc (∼60 μA/cm2) were measured in cells grown at an air interface. Basal I sc was reduced only 7% by bumetanide, and the largest component of basal I sc required both Cl- and[Formula: see text] in the bathing solutions. Because I sc could be partially inhibited by basolateral 4,4'-dinitrostilbene-2,2'-disulfonic acid and because the only known apical exit pathway for anions is the cystic fibrosis transmembrane conductance regulator, which has a relatively poor conductance for [Formula: see text], it was concluded that most basal I sc is[Formula: see text]-dependent Cl- secretion [M. Singh, M. Krouse, S. Moon, and J. J. Wine. Am. J. Physiol. 272 ( Lung Cell. Mol. Physiol. 16): L690-L698, 1997]. We have now measured isotopic fluxes of36Cl-and22Na+across short-circuited Calu-3 cells and found that virtually none of the basal I sc is Cl- secretion or Na+ absorption. Thus, in contrast to the earlier report, we conclude that the major component of basal I sc is[Formula: see text] secretion. Stimulation recruits primarily Cl- secretion, as previously proposed.
The 24h whole body leucine and urea kinetics at normal and high protein intakes with exercise in healthy adults

Forslund, Anders H. , Leif Hambraeus, Roger M. Olsson, Antoine E. El-Khoury, Yong-Ming Yu, and Vernon R. Young. The 24-h whole body leucine and urea kinetics at normal and high protein intakes with exercise in healthy adults. Am. J. Physiol. 275 (Endocrinol. Metab. 38): E310– E320, 1998. —In healthy adult men adapted to a diet/exercise regimen for 6 days, the effects of small, frequent meals supplying daily protein intakes of 1 (n 5 8) or 2.5 g·kg21 ·day21 (n 5 6) on leucine oxidation, urea production, and whole body protein synthesis (PS) and degradation (PD) have been compared with the use of a 24-h continuous intravenous [13C]leucine and [15N,15N]urea infusion protocol. Two 90-min periods of exercise (,50% maximal O2 consumption) were included during the fasting and the fed periods of the 24-h day. Subjects were determined to be at approximate energy, nitrogen, and leucine balances on both diets. Increased protein intake raised the urea production rate; the absolute rate of urea hydrolysis was the same on both diets. When the first-pass splanchnic uptake of leucine was taken to be 25% of intake, PS was stimulated by feeding (after an overnight fast) at both protein intake levels (P , 0.05 and P , 0.01), whereas PD declined significantly (P , 0.01) at both protein levels. Protein gain at a high protein intake appears to be the result of both a stimulation of PS and a marked decline in PD, whereas at a less generous intake, the gain appears to be a result of a fall in PD with a less evident change in PS. Exercise moderately decreased PS during and/or immediately after exercise at each protein level, and there was a postexercise-induced increase (P , 0.01) in PD, which was more dramatic when feeding was at the higher protein intake level.
Psychogenic non‐epileptic seizures among patients with functional neurological disorder: A case series from a Tanzanian referral hospital and literature review

Functional neurological disorders (FNDs) and psychogenic nonepileptic seizures (PNES) are likely as common in Sub‐Saharan Africa (SSA) as in the rest of the world, but there is a dearth of literature on the epidemiology and clinical presentation of these disorders in Africa. The purpose of this paper is to describe a case series of FNDs presenting to a referral hospital in SSA. In addition, we review the existing literature on FNDs in Africa.
Taurine prevents high-glucose-induced human vascular endothelial cell apoptosis.

Elevated blood glucose in uncontrolled diabetes is causally correlated with diabetic microangiopathy. Hyperglycemia-triggered accelerated endothelial cell apoptosis is a critical event in the process of diabetes-associated microvascular disease. The conditionally semiessential amino acid taurine has been previously shown to protect against human endothelial cell apoptosis. Therefore, this study was designed to investigate the role of taurine in the prevention of high-glucose-mediated cell apoptosis in human umbilical vein endothelial cells (HUVEC) and the mechanisms involved. Exposure of HUVEC to 30 mM glucose for 48 h (short-term) and 14 days (long-term) resulted in a significant increase in apoptosis, compared with normal glucose (5.5 mM; P < 0.05). High-glucose-induced DNA fragmentation preferentially occurred in the S phase cells. Mannitol (as osmotic control) at 30 mM failed to induce HUVEC apoptosis. Taurine prevented high-glucose-induced HUVEC apoptosis, which correlates with taurine attenuation of high-glucose-mediated increased intracellular reactive oxygen species (ROS) formation and elevated intracellular Ca2+ concentration ([Ca2+]i) level. Antioxidants, DMSO, N-acetyl cysteine, and glutathione, only partly attenuated high-glucose-induced HUVEC apoptosis. Glucose at 30 mM did not cause HUVEC necrosis. However, both glucose and mannitol at 60 mM caused HUVEC necrosis as represented by increased lactate dehydrogenase release and cell lysis. Taurine failed to prevent hyperosmolarity-induced cell necrosis. These results demonstrate that taurine attenuates hyperglycemia-induced HUVEC apoptosis through ROS inhibition and [Ca2+]istabilization and suggest that taurine may exert a beneficial effect in preventing diabetes-associated microangiopathy.
Pregnancy at Advanced Maternal Age Affects Behavior and Hippocampal Gene Expression in Mouse Offspring

Abstract There is growing evidence that advanced maternal age is a risk factor for neurological and neuropsychiatric disorders in offspring. However, it remains unclear whether the altered brain programming induced by advanced maternal age is mediated by pre- or postnatal factors. Here, a mouse model was used to investigate whether pregnancy at advanced age may provoke behavioral and brain gene expression changes in offspring. Swiss Albino mice conceived by 3-month-old males and either 15–18-month-old (n = 11) or 3-month-old control females (n = 5), were delivered by cesarean section, fostered after birth by 3-month-old dams and subjected to a battery of behavioral tests. Furthermore, genome-wide mRNA expression was analyzed in the hippocampi of 4-month-old males offspring using microarrays. Offspring conceived by old mothers exhibited increased ultrasound vocalization activity during separation from the foster mother, increased anxiety-like behaviors in adult life, and altered patterns of hippocampal gene expression, compared to controls. These effects were not reversed by the postnatal maternal care provided by the young foster mothers, suggesting that the altered brain programming is already established at birth, consistent with prenatal effects related to maternal aging.
Effectiveness of the I2AO2 interdisciplinary programme led by nurses on metabolic syndrome and cardiovascular risk: a randomized, controlled trial

Objective To evaluate the effectiveness of an interdisciplinary programme led by nurses in relation to metabolic syndrome (MS) and cardiovascular risk (CVR). Methods This randomized, controlled, clinical trial included 74 patients diagnosed with MS (experimental group [EG], n = 37; control group [CG], n = 37). The intervention consisted of a 12-month interdisciplinary programme (pre-test, 6 months of intervention, 12 months of intervention, and 1-year follow-up post-intervention) coordinated by nursing. Results We found a progressive and significant reduction for all clinical, biochemical, and anthropometric parameters analysed at different time points. In the EG, remission of MS by 48.1% in the short term was observed (83.8% in the medium term) and maintained at 1 year post-intervention. In the CG, the prevalence of MS increased by 2.7% from the initial evaluation to study completion. A similar trend was observed for CVR. In the EG, 100% of subjects had a moderate-low risk of CVR at 1 year post-intervention, whereas the CG had CVR in all categories. Conclusion An interdisciplinary, nurse-led programme improves participants’ metabolic and cardiovascular health, while maintaining long-term effects. Our findings suggest an important role of the professional nurse as a nexus between the patient, different professionals, and the community.
Exercise habituation is effective for improvement of periodontal disease status: a prospective intervention study

Background and purpose Periodontal disease is closely related to lifestyle-related diseases and obesity. It is widely known that moderate exercise habits lead to improvement in lifestyle-related diseases and obesity. However, little research has been undertaken into how exercise habits affect periodontal disease. The purpose of this study was to examine the effect of exercise habits on periodontal diseases and metabolic pathology. Methods We conducted a prospective intervention research for 12 weeks. The subjects were 71 obese men who participated in an exercise and/or dietary intervention program. Fifty subjects were assigned to exercise interventions (exercise intervention group) and 21 subjects were assigned to dietary interventions (dietary intervention group). This research was conducted before and after each intervention program. Results In the exercise intervention group, the number of teeth with a probing pocket depth (PPD) ≥4 mm significantly decreased from 14.4% to 5.6% (P<0.001), and the number of teeth with bleeding on probing (BOP) significantly decreased from 39.8% to 14.4% (P<0.001). The copy counts of Tannerella forsythia and Treponema denticola decreased significantly (P=0.001). A positive correlation was found between the change in the copy count of T. denticola and the number of teeth with PPD ≥4 mm (P=0.003) and the number of teeth with BOP (P=0.010). A positive correlation was also found between the change in the copy count of T. denticola and body weight (P=0.008), low-density lipoprotein cholesterol (P=0.049), and fasting insulin (P=0.041). However, in the dietary intervention group the copy count of T. denticola decreased significantly (P=0.007) and there was no correlation between the number of periodontal disease-causing bacteria and PPD and BOP. Conclusion Our results are the first to show that exercise might contribute to improvements in periodontal disease.
Function of Tumor Suppressors in Resistance to Antiandrogen Therapy and Luminal Epithelial Plasticity of Aggressive Variant Neuroendocrine Prostate Cancers

Combined loss of tumor suppressors (TSPs), PTEN, TP53, and RB1, is highly associated with small cell carcinoma of prostate phenotype. Recent genomic studies of human tumors as well as analyses in mouse genetic models have revealed a unique role for these TSPs in dictating epithelial lineage plasticity—a phenomenon that plays a critical role in the development of aggressive variant prostate cancer (PCa) and associated androgen therapy resistance. Here, we summarize recently published key observations on this topic and hypothesize a possible mechanism by which concurrent loss of TSPs could potentially regulate the PCa disease phenotype.
Combined single-cell quantitation of host and SIV genes and proteins ex vivo reveals host-pathogen interactions in individual cells

CD4 T cells harboring HIV-1/SIV represent a formidable hurdle to eradicating infection, and yet their detailed phenotype remains unknown. Here we integrate two single-cell technologies, flow cytometry and highly multiplexed quantitative RT-PCR, to characterize SIV-infected CD4 T cells directly ex vivo. Within individual cells, we correlate the cellular phenotype, in terms of host protein and RNA expression, with stages of the viral life cycle defined by combinatorial expression of viral RNAs. Spliced RNA+ infected cells display multiple memory and activation phenotypes, indicating virus production by diverse CD4 T cell subsets. In most (but not all) cells, progressive infection accompanies post-transcriptional downregulation of CD4 protein, while surface MHC class I is largely retained. Interferon-stimulated genes were also commonly upregulated. Thus, we demonstrate that combined quantitation of transcriptional and post-transcriptional regulation at the single-cell level informs in vivo mechanisms of viral replication and immune evasion.
Reduction in CD16/CD56 and CD16/CD3/CD56 Natural Killer Cells in Coronary Artery Disease

ABSTRACT Background: Natural killer (NK) cells are the potential modulators of inflammatory reactions that exert several unique biological effects and could lead to future adverse events of coronary artery disease (CAD). Hypothesis: The purpose of this study was to find out the possible association of modulation in NK cell, TNK cells, T cells, B cells, and tumor necrosis factor alpha (TNF-α) in CAD patients and various forms of myocardial infarction. Methods: The present study included total 190 subjects (98 confirmed CAD patients both men and women and 92 healthy control individuals). Serum concentration of TNF-α was measured by ELISA method. For the measurement of various immune cells, viz., NK cell, TNK cells, T cells, and B cells, flow-cytometric analysis was performed. Results: A significant reduction by 15% (P < 0.001) in CD16/CD56 NK cells was observed in CAD patients. Moreover, non-ST segment elevation myocardial infarction (NSTEMI), ST segment elevation myocardial infarction (STEMI), unstable angina (UA), and combined UA + NSTEMI group also showed a significant decline in NK cells compared with control individuals. CD16/CD56/CD3 TNK cells showed a significant reduction in CAD, NSTEMI, STEMI, and UA categories. However, UA + NSTEMI group did not show any significant change in TNK cells. On the other hand, the level of TNF-α was found to be significantly elevated in CAD, STEMI, and UA groups. NSTEMI and combined UA + NSTEMI group did not show any significant change in TNF-α level. Conclusion: Current study provides an insight toward the association of immune cells and inflammation with CAD.