Miracle-dz/UniFAR-FTUs huggingface dataset:
Influence of a high-intensity interval training session on peripheral and central blood pressure at rest and during stress testing in healthy individuals.

BACKGROUND Regular physical activity is known to reduce arterial pressure (BP). In a previous investigation, we could prove that even a single bout of moderate-intensity continuous exercise (MICE) causes a prolonged reduction in BP. Whether high-intensity interval training (HIIT) has a favourable influence on BP, and therefore may be followed subjects and methods by a prolonged BP reduction, should be examined on the basis of blood pressure response after exercise and during a subsequent stress test. PATIENTS AND METHODS In 39 healthy men (aged 34 ± 8 years, BMI 24 ± 2), peripheral and central BP were measured noninvasively at rest and at the end of a 2-min cold pressor test (CPT) using a Mobil-O-Graph (24 PWA monitor, IEM). Following HIIT (6 x 1 min at 98% of the previously determined maximum wattage, 4-min rest between intervals) BP was measured again throughout 60 min of rest and thereafter during a CPT. The results were compared with those obtained before HIIT. RESULTS Similar to MICE, peripheral and central BPs were significantly (p < 0.05) lower 45 min after HIIT. When analysing peripheral BP during a CPT before and after exercise, significantly lower systolic (p < 0.001) and diastolic (p = 0.008) pressures were established after HIIT. This was true for systolic (p = 0.002) and diastolic (p = 0.006) central BP as well. Although there were no more significant differences between pressures at rest before and 60 min after exercise, the increase in peripheral systolic pressure due to CPT was significantly slower after HIIT (p = 0.019) when compared with BP during CPT before exercise. This was true for central systolic BP as well (p = 0.017). CONCLUSION HIIT leads to a BP reduction, which can still be detected up to 45 min after completion of the training. Even 60 min after exercise, pressures during a CPT showed a reduced augmentation, indicating an attenuated hemodynamic response to stress testing after HIIT.
New insights into the cellular makeup and progenitor potential of palatal connective tissues

The present study investigated the regenerative potential of connective tissues harvested from two palatal areas widely used as donor sites for muco‐gingival surgical approaches. Connective tissue grafts (CTGs) were obtained by de‐epithelialisation of a free gingival graft (deCTG) and by a split flap approach from a previous donor site (reCTG). Two types of mesenchymal stem cell (MSCs) were isolated and were named de‐epithelialised MSCs (deMSCs) and re‐entry MSCs (reMSCs). The cells were characterised and cellular functionality was investigated. CTGs were evaluated using immunohistochemical and ultrastructural approaches. No significant differences were observed regarding the frequency of colony‐forming unit‐ fibroblasts, migration potential, and population doubling time between the two cell lines (p > 0.05). Both cell lines showed positivity for CD105, CD73, CD90, and CD44 and negative expression for CD34/45, CD14, CD79a, and HLA‐DR. MSCs from both cell lines successfully differentiated into osteogenic, adipogenic, and chondrogenic lineages. Cells expressing antigens characteristic of CD34+ stromal cells (CD34+, αSMA−, CD31−) were traced in both CTGs. Ultrastructural analysis highlighted the presence of putative progenitors, namely fibroblasts,—in the pericapillary regions and in remote regions of the lamina propria‐ and pericytes—surrounding the capillaries. This study provides supplementary arguments for the use of CTG grafts in clinical practice due to the presence of putative progenitor cell. However, results were inconclusive regarding clinical decision‐making to determine optimal harvesting area. Prior harvesting in the donor area did not appear to alter the regenerative capabilities of the connective tissue.
Sometimes you simply have to wait: sympathetic activity in women with hypertensive pregnancies.

C ardiovascular organ damage takes many years or even decades to ensue. Large epidemiological studies, such as the Framingham Heart Study, have been indispensable in delineating hitherto unknown cardiovascular risk factors. Yet, the sheer size of these studies limits invasiveness and intensity of the physiological characterization. Much of the research applying more sophisticated methodologies in smaller samples has a rather limited time frame. In real life, the data have to be in within a few years to support the next manuscript, grant proposals, or academic promotions. Another approach is to carefully assess patients, to document the findings, and to keep the data in a safe place for the next generation of clinical scientists. Approximately 40 years ago, Swedish scientists laid the foundation for a manuscript published in the present issue of the Journal of Hypertension [1]. Collén et al. [1] tested the hypothesis that events earlier in life, in this case hypertensive pregnancies, are associated with long-term alterations in sympathetic nervous system activity. The target is well chosen given the pivotal role exerted by neuroadrenergic factors in cardiovascular regulation [2]. Indeed, rare patients at the extreme ends of sympathetic control illustrate the utmost importance of the sympathetic nervous system. Excessive sympathetic activity predisposes to arterial hypertension and cardiovascular organ damage [2]. In fact, an excessive cardiovascular sympathetic drive can acutely damage the heart in rare patients with Takotsubo cardiomyopathy [3,4]. The sympathetically damaged heart often recovers once sympathetic overactivity has resolved. However, sympathetic excitation is also involved, on a chronic basis, in more common organ manifestations of cardiovascular disease. This is the case, for example, in patients with hypertension, in which the sympathetic activation may favor on a chronic
Connexin 46 and Connexin 50 in Selenite Cataract

The purpose of this work was to determine if the lens gap junction proteins connexin 46 (Cx46) and connexin 50 (Cx50) were altered with the development of selenite-induced cataract. Cataracts were induced in young Sprague-Dawley rats with a single subcutaneous injection of sodium selenite; age-matched uninjected rats served as controls. Membrane fractions were isolated from homogenates of cortex and nucleus of normal and cataractous lenses by differential and discontinuous sucrose gradient centrifugation. Aliquots of urea-insoluble protein from membrane fractions were analyzed by quantitative densitometry of Western blots probed with antibodies to Cx46 and Cx50. A significant decrease in the more slowly migrating Cx46-reactive band, which represents phosphorylated Cx46, was found in the major membrane fraction of the cortex of cataractous lenses. There was no significant difference in the amounts of either Cx46 or Cx50 associated with selenite cataract in any of the membrane fractions examined. These results suggest that alteration of gap junction function (as evidenced by the change in phosphorylation of Cx46) may be associated with the development of the selenite cataract, but that neither Cx46 nor Cx50 is subject to the well-characterized proteolysis associated with the selenite cataract model.
MASSIVE ALVEOLAR THROMBIN ACTIVATION IN PSEUDOMONAS AERUGINOSA-INDUCED ACUTE LUNG INJURY

In acute lung injury (ALI), a coagulation/fibrinolysis imbalance leads to fibrin deposition, persistence of which contributes to fibrotic evolution. Our study evaluated the effects of early inhibition of coagulation in Pseudomonas aeruginosa (Pa)-induced ALI through the use of recombinant human antithrombin (rhAT). The study was conducted in vivo on a murine model of Pa-induced ALI. Intravenous rhAT was administered simultaneously with intratracheal Pa. Four experimental groups were compared: CTR, intratracheal saline (0.5 mL/kg)/intravenous saline (1 mL); PNP, intratracheal Pa (0.5 mL/kg of 2 × 109 cfu)/intravenous saline; AT, intratracheal saline/intravenous rhAT (500 IU/kg); ATPNP, intratracheal Pa/intravenous rhAT. Epithelial and endothelial permeabilities were evaluated with radiolabeled albumin flux across the alveolar barrier (125I- and 131I-labeled albumin). Thrombin-antithrombin (TAT) complexes levels were used as markers of coagulation activation in blood samples and in BAL fluid. Epithelial and endothelial protein permeability were increased in Pa-induced ALI versus control. Intravenous rhAT administration led to further permeability disorders. Administration of rhAT in Pa ALI led to a rise in TAT complexes in ATPNP blood serum and BAL fluids compared with the other groups. In Pa-induced ALI the administration intravenous rhAT leads to major histologic damage, alveolar capillary barrier injury, and permeability increase. Such effects of the inhibition of thrombin activation by rhAT lead to the hypothesis of a probable beneficial role of early coagulation activation in ALI as a factor limiting both the extent of injury and permeability disorders. Our study suggests that inhibition of this initial procoagulative imbalance is potentially dangerous.
Impact of Climate Change on Twenty-First Century Crop Yields in the U.S.

Crop yields are strongly dependent on the average climate, extreme temperatures, and carbon dioxide concentrations, all of which are projected to increase in the coming century. In this study, a statistical model was created to predict US yields to 2100 for three crops using low and high-emissions future scenarios (RCP 4.5 and 8.5). The model is based on linear regressions between historical crop yields and daily weather observations since 1970 for every county in the US. Yields were found to be most strongly dependent on heat waves, summer average temperatures, and killing degree days; these relationships were hence used to predict future yields. The model shows that warming temperatures will significantly decrease corn and soybean yields, but will not have as strong of an influence on rice. Before accounting for CO2 fertilization, crops in the high-emissions scenario are predicted to produce 77%, 85%, and 96% of their expected yield without climate change for corn, soybeans, and rice, respectively. When a simple CO2 fertilization factor is included, corn, a C4 plant, increases slightly, while the yields of the C3 plants (soybeans and rice) are actually predicted to increase compared to today’s yields. This study exhibits the wide range of possible impacts of climate change on crop yields in the coming century, and emphasizes the need for field research on the combined effects of CO2 fertilization and heat extremes.
Differential Regulation of Glucose Transport and Transporters by Glucose in Vascular Endothelial and Smooth Muscle Cells

Hyperglycemia has been implicated in the pathogenesis of both micro- and macrovascular complications in diabetes. Little is known, however, about glucose transporters and their regulation in thevascular system. In this study, the regulation of glucose transporters by glucose was examined in cultured BAECs and BSMCs, and in human arterial smooth muscle cells. Both BAECs and BSMCs transported glucose via the facilitated diffusion transport system. Glucose-transport activity in vascular smooth muscle cells was inversely and reversibly regulated by glucose. Exposure of BSMCs and HSMCs to high glucose decreased Vmax for 2DG and 3-O-MG uptake, whereas Km remained unchanged. The hexose-transport system of BAECs exhibited lower 2DG and 3-O-MG uptake compared with BSMCs and showed little or no adaptation to changes in ambient glucose. Northern blot analysis. GLUT1 protein, quantified by Western blot analysis, was more abundant in BSMCs than in BAECs and was decreased by ∼50% when medium glucose was elevated from 1.2 to 22 mM for 24 h. The alterations in the level of GLUT1 protein correlated with the changes observed in transport activity. These observations suggest differential regulation of glucose transporter in response to glucose between smooth muscle and endothelial cells. The sites of autoregulation may involve translational control and/or the stability of the protein in the smooth muscle cells. The ability of vascular smooth muscle cells to down-regulate glucose transport in response to chronic hyperglycemia may serve as a protective mechanism against possible adverse effects of increased intracellular glucose.
Kinetic and dynamic components of increased benzodiazepine sensitivity in aging animals.

Male CD-1 mice (age 6 weeks, 6 months, 1 and 2 years) received single 2-mg/kg i.p. doses of clonazepam. Plasma and cortex clonazepam concentrations, rotarod ataxia and in vivo benzodiazepine receptor occupancy were measured at multiple times up to 14 hr after dosage. Elimination of clonazepam from plasma and cortex became slower with age, but cortex concentrations always exceeded those in plasma. The mean ratio was 1.82, and was not influenced by age. Rotarod ataxia was quantitatively greater and of longer duration in aging animals. This was not explained entirely by kinetic changes, as ataxia at any given cortex clonazepam concentration or degree of receptor occupancy was greater in 1-year-old animals than in those age 6 weeks or 6 months. In a second study, 6-week and 1-year-old animals were tested at a fixed time (1 hr) after variable doses of clonazepam (0.01-2.0 mg/kg); findings were consistent with results from the fixed-dose study. In vitro studies evaluated benzodiazepine receptor binding, chloride channel binding and muscimol-stimulated chloride uptake in cortical membrane preparations from animals of the four age groups. Binding affinity and number of binding sites were not influenced by age, or was gamma-aminobutyric acid-dependent muscimol-stimulated chloride uptake (either with or without addition of lorazepam) significantly related to age. Thus, increased overall sensitivity of aging animals to the central depressant effects of clonazepam is evident in the described model. (ABSTRACT TRUNCATED AT 250 WORDS)
Does Governmental Assistance Affect Private Decisions to Insure? An Empirical Analysis of Flood Insurance Purchases

In this paper, we empirically examine whether the Federal Emergency Management Agency’s Public Assistance (PA) program, which targets postdisaster cleanup and infrastructure rehabilitation, affects household purchases of flood insurance. Using the fixed-effects model with instrumental variables to address the endogeneity of disaster aid, we find that increased PA grants reduce a county’s flood insurance take-up rates, thereby driving down its total insurance coverage and premiums paid. Our findings provide empirical evidence on the crowding-out effect of public disaster programs, and shed light on their implicit social costs and increased federal financial exposure to natural disasters and climate change. (JEL Q54, Q58)
Mal de debarquement syndrome: new insights

Mal de Debarquement Syndrome (MdDS) is an enigmatic neurotological disorder with high morbidity, psychosocial burden, and few treatment options. Fortunately, there has been recent growth in scientific interest in understanding the biological basis of and in treating MdDS. Recent studies using functional neuroimaging have shown increased glucose metabolism in the left entorhinal cortex (EC) and amygdala in the setting of decreased prefrontal and temporal cortex metabolism in subjects with persistent MdDS. The EC is a key player in processing and gating spatial information to be stored in the hippocampus and is a major driver of brain oscillations. A limbic focus may also be key to spontaneous MdDS‐like symptoms occurring in individuals with a history of anxiety or chronic stress. Treatment with repetitive transcranial magnetic stimulation over the dorsolateral prefrontal cortex can decrease the rocking dizziness of MdDS, with successful responses associated with decreases in the coherence between brain networks with nodes in the parietal and occipital lobes. A new theory of MdDS is proposed as pathology secondary to entrainment of intrinsic brain networks driven by oscillatory motion exposure coupled with an inability to subsequently desynchronize the activity of these nodes. Future treatment strategies may be directed toward unyoking these networks.
Genetic Features of Chinese Patients with Gitelman Syndrome: Sixteen Novel SLC12A3 Mutations Identified in a New Cohort

Background: Gitelman syndrome (GS) is an autosomal recessive renal tubulopathy caused by inactivating mutations in the SLC12A3 gene. Although hundreds of different mutations across the SLC12A3 gene have been reported worldwide, data from mainland China are limited. We investigated the clinical manifestations and genetic features of Chinese patients with GS. Methods: Fifty-four unrelated Chinese patients with clinically diagnosed GS were included. Clinical manifestations and biochemical parameters were collected and analyzed. All exons and flanking regions of the SLC12A3 and CLCNKB genes were screened by direct sequencing. Results: Weakness was the most commonly reported symptom in this cohort of patients with GS. In gender-based analyses, higher systolic blood pressure and urine protein excretion were observed in male patients. For genetic screening, 2 pathogenic SLC12A3 mutations were identified in 38 patients (70.4%), 1 mutation in 11 patients (20.4%) and no mutation in 5 patients (9.3%). In total, 42 distinct pathogenic mutations throughout SLC12A3 were identified; 16 were novel, including 9 missense, 1 deletion, 1 insertion, 3 splice site and 2 nonsense mutations. Eleven mutations were recurrently found in different patients. Among them, T60M and D486N were identified in 11 individuals. No CLCNKB mutations were found. Conclusion: Sixteen novel SLC12A3 pathogenic mutations were identified in a cohort of Chinese patients with GS. T60M and D486N were most frequent and appear to be important candidate alleles in Chinese patients with GS.
Compliance with neuromuscular training and anterior cruciate ligament injury risk reduction in female athletes: a meta-analysis.

CONTEXT No consensus exists about the influence of compliance with neuromuscular training programs on reduction of the risk of anterior cruciate ligament (ACL) injury. OBJECTIVE To systematically review and synthesize the published literature to determine if compliance with neuromuscular training is associated with reduced incidence of ACL injury in young female athletes. DATA SOURCES We searched PubMed, SPORTDiscus, CINAHL, and MEDLINE for articles published from 1995 to 2010 using the key words anterior cruciate ligament prevention, ACL prevention, knee prevention, prospective knee prevention, neuromuscular training, and neuromuscular intervention. STUDY SELECTION Criteria for inclusion required that (1) the number of ACL injuries was reported, (2) a neuromuscular training program was used, (3) females were included as participants, (4) the study design was prospective and controlled, and (5) compliance data for the neuromuscular training program were provided. DATA EXTRACTION Extracted data included the number of ACL injuries, total number of participants per group, observation time period, number of participants who completed each session, number of sessions completed by an entire team, and number of total sessions. Attendance was calculated as the number of participants who completed each session converted into a percentage of the total number of participants. Intervention completion was calculated as the number of sessions completed by an entire team converted into a percentage of the total number of training sessions. These data were used to calculate an overall rate of compliance. DATA SYNTHESIS Six of 205 identified studies were included. Incidence rates of ACL injury were lower in studies with high rates of compliance with neuromuscular training than in studies with low compliance rates (incidence rate ratio = 0.27 [95% confidence interval = 0.07, 0.80]). Tertile analysis indicated rates of ACL injury incidence were lower in studies with high compliance rates than in studies with moderate and low compliance rates (incidence rate ratio = 0.18 [95% confidence interval = 0.02, 0.77]). CONCLUSIONS A potential inverse dose-response relationship exists between compliance with neuromuscular training and incidence of ACL injury. Attending and completing recommended neuromuscular sessions appears to be an important factor for preventing ACL injuries.
T-cell activation by recombinant receptors: CD28 costimulation is required for interleukin 2 secretion and receptor-mediated T-cell proliferation but does not affect receptor-mediated target cell lysis.

Recombinant T-cell receptors with antibody-like specificity are successfully used to direct CTLs toward a MHC-independent immune response against target cells. Here we monitored the specific activation of receptor grafted CTLs in the context of CD28 costimulation. Peripheral blood T cells were retrovirally engrafted with recombinant anti-CD30 and anti-carcinoembryonic antigen receptors, respectively, that harbor either the Fc epsilonRI-gamma or the CD3-zeta intracellular signaling domain. Cross-linking of recombinant receptors by solid-phase bound ligand, i.e., CD30 and a carcinoembryonic antigen receptor-specific anti-idiotypic antibody, respectively, induces IFN-gamma secretion that is further enhanced by CD28 costimulation of grafted T cells. Induction of interleukin (IL)-2 secretion, in contrast, requires CD28 costimulation in addition to receptor cross-linking, irrespective of T-cell preactivation by anti-CD3 monoclonal antibody plus IL-2 or by anti-CD3 monoclonal antibody plus anti-CD28 monoclonal antibody. Accordingly, induction of IL-2 secretion upon receptor cross-linking by membrane-bound antigen requires CD28/B7 costimulation whereas IFN-gamma secretion and cell proliferation does not. The efficiency of cytolysis by receptor-grafted CTLs does not depend on and is not affected by CD28 costimulation. The data demonstrate that CTL proliferation, cytokine secretion, and cytolysis upon receptor cross-linking are differentially modulated by CD28 costimulation and that cytolysis does not require B7 expression on target cells.
Nod Factor and Elicitors Activate Different Phospholipid Signaling Pathways in Suspension-Cultured Alfalfa Cells1

Lipo-chitooligosaccharides (Nod factors) are produced by symbiotic Rhizobium sp. bacteria to elicit Nod responses on their legume hosts. One of the earliest responses is the formation of phosphatidic acid (PA), a novel second messenger in plant cells. Remarkably, pathogens have also been reported to trigger the formation of PA in nonlegume plants. To investigate how host plants can distinguish between symbionts and pathogens, the effects of Nod factor and elicitors (chitotetraose and xylanase) on the formation of PA were investigated in suspension-cultured alfalfa (Medicago sativa) cells. Theoretically, PA can be synthesized via two signaling pathways, i.e. via phospholipase D (PLD) and via phospholipase C in combination with diacylglycerol (DAG) kinase. Therefore, a strategy involving differential radiolabeling with [32P]orthophosphate was used to determine the contribution of each pathway to PA formation. In support, PLD activity was specifically measured by using the ability of the enzyme to transfer the phosphatidyl group of its substrate to a primary alcohol. In practice, Nod factor, chitotetraose, and xylanase induced the formation of PA and its phosphorylated product DAG pyrophosphate within 2 min of treatment. However, whereas phospholipase C and DAG kinase were activated during treatment with all three different compounds, PLD was only activated by Nod factor. No evidence was obtained for the activation of phospholipase A2.