Miracle-dz/UniFAR-FTUs huggingface dataset:
Physiological Demands of Playing Field Hockey Game at Sub Elite Players

The purpose of this study was to identify the physiological demands and distance covered during national competitive 2016. Method used 9 female players including 2 backs, 3 halves, 4 forwards. Data was collected by measuring heart rate, blood lactate, distance covered and time spent walking/running. Data was analysed using mean, standard deviation, and range. Results found that the mean heart rate and blood lactate concentration during warm up were 96,4±12,7 bpm and 1,7±0,8 mmol•L-1; at the end of the first half of the match was 171,2±6,3 bpm and 5,2±3,1 mmol•L-1; prior to start at the second half was 130,8±3,8 bpm and 3,7±3,6 mmol•L-1; and the end of the second half was 157,4±12,7 bpm and 5,8±0,2 mmol•L-1. A mean of total distance covered during the complete field hockey game was 4372,5±263,9 m. Mean value of time spent walking and running were 41,42 minutes and 28,18 minutes, respectively. Conclusion of this study was female field hockey players have lower heart rate, blood lactate concentration, distance covered and time spent walking/running than other players in the literature reviews. Implication of this study can be used to evaluate the training program in order to improve performance enhancement of the players.
Does Bank Stakeholder Orientation Enhance Financial Stability?

Using the staggered enactment of constituency statutes across US states, we find that banks with directors whose legal duties are expanded to consider stakeholder and long-term interests significantly reduce risk-taking by increasing capital and shifting to safer borrowers. Additionally, we find that the effect of statute enactment on bank performance is insignificant on average but significantly positive for banks that take excessive risk. Furthermore, we find that banks that previously received a statute enactment fared significantly better during the crises. Our findings support the increasing calls for greater emphasis on stakeholder interests amidst the current bank regulatory and governance reforms.
Professional Pitchers With Glenohumeral Internal Rotation Deficit (GIRD) Display Greater Humeral Retrotorsion Than Pitchers Without GIRD

Background: Dominant shoulder glenohumeral internal rotation deficit (GIRD) has been associated with pitching arm injuries. The relationship of humeral torsion on development of GIRD is not clear. Hypothesis: Pitchers displaying GIRD will display greater humeral retrotorsion when compared with those without GIRD. Study Design: Cross-sectional study; Level of evidence, 3. Methods: Humeral torsion and shoulder range of motion (ROM) were measured in 222 professional pitchers before spring training from 2009 to 2012. Shoulder external rotation (ER) and internal rotation (IR) ROM were assessed in 90° of abduction with the scapula stabilized. Humeral torsion was measured via ultrasound using previously described and validated methods. Side-to-side differences in total arc of motion (ER + IR), ER, and IR ROM and humeral torsion were calculated as nondominant minus dominant arm measures for analysis. Pitchers were classified as having GIRD if their dominant arm displayed an IR deficit ≥15° concomitant with a total arc of motion deficit ≥10° compared with their nondominant arm. A mixed-model analysis of variance (side × GIRD) was used to compare dominant and nondominant humeral torsion between pitchers with GIRD (n = 60) and those without GIRD (n = 162). Independent t tests were used to compare the side-to-side difference in humeral torsion between pitchers with GIRD and those without GIRD (α = 0.05). Results: Pitchers with GIRD displayed significantly less humeral torsion (ie, greater retrotorsion) in their dominant arm as compared with those without GIRD (GIRD = 4.5° ± 11.8°, no GIRD = 10.4° ± 11.7°; P = .002). Pitchers with GIRD also displayed a greater side-to-side difference in humeral torsion (GIRD = 19.5° ± 11.9°, no GIRD = 12.3° ± 12.4°; P = .001). However, pitchers with GIRD did not display an increase in dominant ER ROM (dominant ER = 131.8° ± 14.3°, nondominant ER 126.6° ± 13.1°) when compared with those without GIRD (dominant ER = 132.0° ± 14.2°, nondominant ER 122.6° ± 13.1°; P = .03). Pitchers with GIRD displayed expected alterations in ROM (IR = 28.8° ± 9.6°, total arc = 160.6° ± 15.4°; P < .01 for both) when compared with those without GIRD (IR = 39.9° ± 9.9°, total arc = 171.2° ± 15.5°). Conclusion: Pitchers with GIRD displayed greater side-to-side differences and dominant humeral retrotorsion as compared with those without GIRD. The greater humeral retrotorsion may place greater stress on the posterior shoulder resulting in ROM deficits. Pitchers with greater humeral retrotorsion appear to be more susceptible to developing ROM deficits associated with injury and may need increased monitoring and customized treatment programs to mitigate their increased injury risk.
Effect of phorbol ester and pertussis toxin on the enhancement of noradrenaline release by angiotensin II in mouse atria

1 Mouse atria were incubated with [3H]‐noradrenaline, and the outflow of radioactivity due to electrical field stimulation (5 Hz, 60 s) was used as an index of noradrenaline release. Angiotensin II (0.01 and 0.1 μm) significantly enhanced the stimulation‐induced (S‐I) outflow of radioactivity. 2 Phorbol 12‐myristate 13‐acetate (0.001, 0.03, 0.1 and 1.0 μm), a protein kinase C activating phorbol ester, significantly enhanced the S‐I outflow of radioactivity. When angiotensin II (0.1 μm) was present with the concentration of phorbol 12‐myristate 13‐acetate that was maximally effective in increasing the S‐I outflow (0.1 μm), the enhancement of S‐I outflow produced by angiotensin II was maintained. 3 Polymyxin B (70 μm), an inhibitor of protein kinase C, significantly inhibited the S‐I outflow. Polymyxin B also inhibited the enhancement of the S‐I outflow produced by angiotensin II (0.1 μm). 4 In another series of experiments mice were injected with pertussis toxin (1.5 μg per mouse), 4 days before their atria were removed. The effectiveness of pertussis toxin pretreatment was determined indirectly using carbachol. Carbachol caused a concentration‐dependent fall in both the rate and force of beating of isolated spontaneously beating atria from mice pretreated with vehicle. This effect of carbachol was not seen with atria from mice pretreated with pertussis toxin. 5 Pertussis toxin pretreatment did not alter the enhancement of the S‐I outflow of radioactivity produced by angiotensin II (0.01 and 0.1 μm). 6 These results suggest that angiotensin II receptor modulation of noradrenaline release is not mediated through either a pertussis toxin sensitive guanine nucleotide‐binding protein or activation of protein kinase C.
Employer Resistance to Works Councils: Evidence from Surveys amongst Trade Unions

Employer resistance to works councils is not a phenomenon that has been closely associated with German labour relations. While classic studies characterise the ‘German model’ in terms of social partnership, more recent accounts seem to observe a ‘dualisation’ if not liberalisation of German labour relations. In somewhat of a contradiction to the ‘social partnership’ perspective, we find that incidents of employers’ hostility towards the establishment of works councils are widespread. Based on data provided by the WSI Survey of paid union representatives (2012, 2015), we find that employers disrupt every sixth attempt to establish a works council. Among the measures taken by employers, the most common strategy is to intimidate works council candidates. Furthermore, we show that employers’ hostility to works councils is evenly distributed between manufacturing (core) and private services (periphery), which suggests that the transformation of the ‘German model’ over the past decade follows a more nuanced path than suggested by accounts of dualisation. In contrast to the liberalisation hypothesis, our results also indicate that rather than affecting establishments across the board, attempts by employers to obstruct employees’ participation rights are focused on a certain type of establishment: medium-sized and owner-managed firms.
Glutamate regulation of non‐quantal release of acetylcholine in the rat neuromuscular junction

Glutamate, previously demonstrated to participate in regulation of the resting membrane potential in skeletal muscles, also regulates non‐quantal acetylcholine (ACh) secretion from rat motor nerve endings. Non‐quantal ACh secretion was estimated by the amplitude of endplate hyperpolarization (H‐effect) following blockade of skeletal muscle post‐synaptic nicotinic receptors by (+)‐tubocurarine and cholinesterase by armin (diethoxy‐p‐nitrophenyl phosphate). Glutamate was shown to inhibit non‐quantal release but not spontaneous and evoked quantal secretion of ACh. Glutamate‐induced decrease of the H‐effect was enhanced by glycine. Glycine alone also lowered the H‐effect, probably due to potentiation of the effect of endogenous glutamate present in the synaptic cleft. Inhibition of N‐methyl‐d‐aspartate (NMDA) receptors with (+)‐5‐methyl‐10,11‐dihydro‐5H‐dibenzocyclohepten‐5,10‐imine (MK801), dl‐2‐amino‐5‐phosphopentanoic acid (AP5) and 7‐chlorokynurenic acid or the elimination of Ca2+ from the bathing solution prevented the glutamate‐induced decrease of the H‐effect with or without glycine. Inhibition of muscle nitric oxide synthase by NG‐nitro‐l‐arginine methyl ester (l‐NAME), soluble guanylyl cyclase by 1H[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ) and binding and inactivation of extracellular nitric oxide (NO) by haemoglobin removed the action of glutamate and glycine on the H‐effect. The results suggest that glutamate, acting on post‐synaptic NMDA receptors to induce sarcoplasmic synthesis and release of NO, selectively inhibits non‐quantal secretion of ACh from motor nerve terminals. Non‐quantal ACh is known to modulate the resting membrane potential of muscle membrane via control of activity of chloride transport and a decrease in secretion of non‐quantal transmitter following muscle denervation triggers the early post‐denervation depolarization of muscle fibres.
Zoledronate can induce colorectal cancer microenvironment expressing BTN3A1 to stimulate effector γδ T cells with antitumor activity

ABSTRACT Amino-bis-phosphonates (N-BPs) such as zoledronate (Zol) have been used in anticancer clinical trials due to their ability to upregulate pyrophosphate accumulation promoting antitumor Vγ9Vδ2 T cells. The butyrophilin 3A (BTN3A, CD277) family, mainly the BTN3A1 isoform, has emerged as an important structure contributing to Vγ9Vδ2 T cells stimulation. It has been demonstrated that the B30.2 domain of BTN3A1 can bind phosphoantigens (PAg) and drive the activation of Vγ9Vδ2 T cells through conformational changes of the extracellular domains. Moreover, BTN3A1 binding to the cytoskeleton, and its consequent membrane stabilization, is crucial to stimulate the PAg-induced tumor cell reactivity by human Vγ9Vδ2 T cells. Aim of this study was to investigate the relevance of BTN3A1 in N-BPs-induced antitumor response in colorectal cancer (CRC) and the cell types involved in the tumor microenvironment. In this paper, we show that (i) CRC, exposed to Zol, stimulates the expansion of Vδ2 T lymphocytes with effector memory phenotype and antitumor cytotoxic activity, besides sensitizing cancer cells to γδ T cell-mediated cytotoxicity; (ii) this effect is partially related to BTN3A1 expression and in particular with its cellular re-distribution in the membrane and cytoskeleton-associated fraction; (iii) BTN3A1 is detected in CRC at the tumor site, both on epithelial cells and on tumor-associated fibroblasts (TAF), close to areas infiltrated by Vδ2 T lymphocytes; (iv) Zol is effective in stimulating antitumor effector Vδ2 T cells from ex-vivo CRC cell suspensions; and (v) both CRC cells and TAF can be primed by Zol to trigger Vδ2 T cells.
Research Note: Trade Name Franchise Membership as a Human Resource Management Strategy: Does Buying Group Training Deliver ‘True Value’ for Small Retailers?

Human resource management (HRM) is an important source of competitive advantage. However, recent reports document that HRM, and in particular employee training, is less likely to occur in small firms. One possible remedy of special interest to small retailers is trade name franchise membership. Trade name franchises, or buying groups, claim to offer small firms advantages not otherwise realizable, including bulk buying discounts, brand name recognition and workforce training. We report results from our study of over 300 small and medium-sized hardware stores, which tested the effects of employee training and trade name franchise membership, on small firm performance. Trade name franchisees achieve higher mean performance; however, the contribution to performance made by franchisees’ training does not appear to be significantly better than that of independent stores.
Separation and modulation of calcium currents in bullfrog sympathetic neurons.

The calcium current of frog sympathetic neurons has relatively rapid activation kinetics (tau < 3 ms) in response to changes in voltage. Pharmacologically, the current is blocked approximately 90% of omega-conotoxin, but < 10% by dihydropyridine antagonists. This suggests that nearly all of the current is N type. However, inactivation is slow and incomplete even for depolarizations lasting > 1 s, consistent with recent evidence that N-type channels do not always inactivate rapidly. The calcium current is partially inhibited via receptors for acetylcholine, luteinizing hormone releasing hormone, substance P, ATP, and norepinephrine. These effects are mimicked by internal dialysis with GTP-gamma-S, suggesting involvement of a G protein. The transmitters affect the activation kinetics of the calcium current in a voltage-dependent manner, which can be modeled as a reversible shift of some channels to "reluctant" states in which strong depolarization is needed to produce channel opening. The effects of transmitters develop and recover with t1/2 approximately 1-2 s, so if a second messenger is involved in receptor-calcium channel coupling, it must act rapidly.
Mortality Associated with Benzodiazepines and Benzodiazepine-Related Drugs among Community-Dwelling Older People in Finland: A Population-Based Retrospective Cohort Study

Objective: To investigate the association between the use of benzodiazepines (BDZs) and BDZ-related drugs and mortality among community-dwelling people aged 65 years and older in Finland. Method: This was a population-based retrospective cohort study. Records of all reimbursed drugs purchased by all 2224 residents of Leppävirta, Finland, aged 65 years and older in 2000 were extracted from the Finnish National Prescription Register. Diagnostic data were extracted from the Special Reimbursement Register. All-cause mortality was assessed after 9 years using national registers. Cox proportional hazards models were used to compute unadjusted and adjusted hazard ratios (HRs) and 95% confidence intervals for mortality among prevalent users of BDZs and BDZ-related drugs in 2000 (n = 325), compared with nonusers of BDZs and BDZ-related drugs between 2000 and 2008 (n = 1520). Results: BDZs and BDZ-related drugs were used by 325 out of the 2224 residents (14.6%) in 2000. The 9-year mortality was 50.2% among BDZ and BDZ-related drug users in 2000 and 36.3% among BDZ and BDZ-related drug nonusers between 2000 and 2008 (HR 1.53; 95% CI 1.28 to 1.82). After adjusting for baseline age, sex, antipsychotic drug use, and diagnostic confounders, the HR was 1.01 (95% CI 0.84 to 1.21). Conclusions: Use of BDZs and BDZ-related drugs was associated with an increased mortality hazard in unadjusted analyses. However, after adjusting for age, sex, antipsychotic drug use, and diagnostic confounders, the use of BDZs and BDZ-related drugs was not associated with excess mortality.
MIF rediscovered: cytokine, pituitary hormone, and glucocorticoid‐induced regulator of the immune response

The protein that has been historically called macrophage migration inhibitory factor (MIF) was one of the first cytokine activities to be discovered and was originally described to be a T lymphocyte product that inhibited the random migration of macrophages. Over the years, additional molecules with MIF “activity” have been described and the precise role of the original MIF “protein” remained enigmatic. Recent studies have led to the discovery of a pituitary mediator that appears to act as the counter‐ regulatory hormone for glucocorticoid action within the immune system. Isolated as a product of murine anterior pituitary cells, this peptide was sequenced and found to be the mouse homolog of MIF. MIF has the unique property of being released from macrophages and T cells in response to physiological con‐centrations of glucocorticoids. The secretion of MIF is tightly regulated and decreases at high, anti‐inflam‐ matory steroid concentrations. Once released, MIF “overrides” or counterregulates the immunosuppressive effects of steroids on immune cell activation and cytokine production. These observations suggest that MIF fills an important gap in our understanding of how the host initiates and controls immunity. Because glucocorticoids are an integral part of the host's global response to infection or tissue invasion, the physiological role of MIF is to act at an inflammatory site or lymph node to counterbalance the profound inhibitory effects of steroids on the immune response. — Bucala, R. MIF rediscovered: cytokine, pituitary hormone, and glucocorticoid‐induced regulator of the immune response. FASEBJ. 10, 1607‐1613 (1996)
The idiopathic intracranial hypertension treatment trial: clinical profile at baseline.

IMPORTANCE To our knowledge, there are no large prospective cohorts of untreated patients with idiopathic intracranial hypertension (IIH) to characterize the disease. OBJECTIVE To report the baseline clinical and laboratory features of patients enrolled in the Idiopathic Intracranial Hypertension Treatment Trial. DESIGN, SETTING, AND PARTICIPANTS We collected data at baseline from questionnaires, examinations, automated perimetry, and fundus photography grading. Patients (n = 165) were enrolled from March 17, 2010, to November 27, 2012, at 38 academic and private practice sites in North America. All participants met the modified Dandy criteria for IIH and had a perimetric mean deviation between -2 dB and -7 dB. All but 4 participants were women. MAIN OUTCOMES AND MEASURES Baseline and laboratory characteristics. RESULTS The mean (SD) age of our patients was 29.0 (7.4) years and 4 (2.4%) were men. The average (SD) body mass index (calculated as weight in kilograms divided by height in meters squared) was 39.9 (8.3). Headache was the most common symptom (84%). Transient visual obscurations occurred in 68% of patients, back pain in 53%, and pulse synchronous tinnitus in 52%. Only 32% reported visual loss. The average (SD) perimetric mean deviation in the worst eye was -3.5 (1.1) dB, (range, -2.0 to -6.4 dB) and in the best eye was -2.3 (1.1) dB (range, -5.2 to 0.8 dB). A partial arcuate visual field defect with an enlarged blind spot was the most common perimetric finding. Visual acuity was 85 letters or better (20/20) in 71% of the worst eyes and 77% of the best eyes. Quality of life measures, including the National Eye Institute Visual Function Questionnaire-25 and the Short Form-36 physical and mental health summary scales, were lower compared with population norms. CONCLUSIONS AND RELEVANCE The Idiopathic Intracranial Hypertension Treatment Trial represents the largest prospectively analyzed cohort of untreated patients with IIH. Our data show that IIH is almost exclusively a disease of obese young women. Patients with IIH with mild visual loss have typical symptoms, may have mild acuity loss, and have visual field defects, with predominantly arcuate loss and enlarged blind spots that require formal perimetry for detection. TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT01003639.
Survival and complications of stereotactic radiosurgery

Background: Utilization of stereotactic radiosurgery (SRS) for treatment of high-grade gliomas (HGGs) has been slowly increasing with variable reported success rates. Objective: Systematic review of the available data to evaluate the efficacy of SRS as a treatment for HGG with regards to median overall survival (OS) and progression-free survival (PFS), in addition to ascertaining the rate of radiation necrosis and other SRS-related major neurological complications. Methods: Literature searches were performed for publications from 1992 to 2016. The pooled estimates of median PFS and median OS were calculated as a weighted estimate of population medians. Meta-analyses of published rates of radiation necrosis and other major neurological complications were also performed. Results: Twenty-nine studies reported the use of SRS for recurrent HGG, and 16 studies reported the use of SRS for newly diagnosed HGG. For recurrent HGG, the pooled estimates of median PFS and median OS were 5.42 months (3–16 months) and 20.19 months (9–65 months), respectively; the pooled radiation necrosis rate was 5.9% (0–44%); and the pooled estimates of major neurological complications rate was 3.3% (0–23%). For newly diagnosed HGG, the pooled estimates of median PFS and median OS were 7.89 months (5.5–11 months) and 16.87 months (9.5–33 months) respectively; the pooled radiation necrosis rate was 6.5% (0–33%); and the pooled estimates of other major neurological complications rate was 1.5% (0–25%). Conclusion: Our results suggest that SRS holds promise as a relatively safe treatment option for HGG. In terms of efficacy at this time, there are inadequate data to support routine utilization of SRS as the standard of care for newly diagnosed or recurrent HGG. Further studies should be pursued to define more clearly the therapeutic role of SRS.
Detection of monocyte/macrophage cell populations in effusions: A comparative study using flow cytometric immunophenotyping and immunocytochemistry

The objective of the present study was to compare the efficiency of immunophenotyping using flow cytometry (FCM) and immunocytochemistry (ICC) in the detection of macrophages in serous effusions. Cytoblock sections from 90 effusions were stained for the monocyte/macrophage marker CD14, using ICC. Fresh‐frozen samples of all cases were analyzed for CD14 expression, using FCM. Epithelial, lymphoid, and mesothelial cell populations were identified using antibodies against Ber‐EP4, CD45, and N‐cadherin, respectively. Results were compared with clinical parameters and morphological diagnosis. Thirty‐nine specimens were cytologically diagnosed as malignant, containing tumor cells of nonhematologic origin, whereas 46 were interpreted as benign. Two additional specimens were diagnosed as indeterminate or suspicious for malignancy, and 3 specimens contained lymphoma cells. CD14‐positive cells were detected in 85/90 (94%) of effusions using FCM, and in all 90 specimens using ICC. The percentage of CD14‐positive cells was highly variable, but in some specimens was as high as 76% using FCM and 85% using ICC. A good association was observed between the two methods in the detection of CD14‐positive cells (P < 0.001). The presence of macrophages in effusions showed an association with female gender, using both FCM (P = 0.002) and ICC (P = 0.011), but none with effusion site, patient age, clinical and cytological diagnosis, or presence of Ber‐EP4‐positive cells (P > 0.05). The presence of Ber‐EP4‐positive cells showed a strong association with the cytological diagnosis of malignancy (P < 0.001). In conclusion, macrophages are a significant cell population in effusions, of both benign and malignant etiology, due to both their size and their possible confusion with cancer cells. Both FCM and ICC aid in the recognition of these cells, and thus provide an effective tool for the identification of different cell populations in effusions. Diagn. Cytopathol. 25:214–219, 2001. © 2001 Wiley‐Liss, Inc.