Miracle-dz/UniFAR-FTUs huggingface dataset:
Age‐ and sex‐based patterns of positional behavior and substrate utilization in the golden snub‐nosed monkey (Rhinopithecus roxellana)

Body mass plays an important role in primate positional behavior and in sexually dimorphic arboreal primate species may influence how immature and adult individuals travel through the forest canopy and access food resources. In this study, we examined age‐ and sex‐based patterns of positional behavior and substrate utilization in wild golden snub‐nosed monkeys (Rhinopithecus roxellana), an endangered species of Asian colobine. Our results indicated that among all age and sex classes, sitting was the most common feeding and resting posture and during travel, quadrupedal walking was the dominant locomotor behavior. Despite the fact that adult male R. roxellana are reported to exhibit a body mass nearly two times that of adult females, we found no significant sex differences in the positional repertoire during feeding and traveling. In addition, we found that while infants and juveniles used similar postural and locomotor behaviors as their adult counterparts, younger golden snub‐nosed monkeys more frequently engaged in risky or escape‐oriented behaviors such as climbing, running, leaping, and forelimb suspension. With increasing age, the use of quadrupedal walking and dropping (downward in‐air displacement of body mass that does not require hindlimb propulsion) increased and the use of leaping, suspensory postures, and bridging decreased. Finally, given differences in the positional repertoire of adult and immature golden snub‐nosed monkeys, we argue that studies of ontogenetic patterns of positional behavior should emphasize what it takes to survive at each life stage rather than what it takes to match an adult repertoire. Am. J. Primatol. 77:98–108, 2015. © 2014 Wiley Periodicals, Inc.
Is Congenital Amusia a Disconnection Syndrome? A Study Combining Tract- and Network-Based Analysis

Previous studies on congenital amusia mainly focused on the impaired fronto-temporal pathway. It is possible that neural pathways of amusia patients on a larger scale are affected. In this study, we investigated changes in structural connections by applying both tract-based and network-based analysis to DTI data of 12 subjects with congenital amusia and 20 demographic-matched normal controls. TBSS (tract-based spatial statistics) was used to detect microstructural changes. The results showed that amusics had higher diffusivity indices in the corpus callosum, the right inferior/superior longitudinal fasciculus, and the right inferior frontal-occipital fasciculus (IFOF). The axial diffusivity values of the right IFOF were negatively correlated with musical scores in the amusia group. Network-based analysis showed that the efficiency of the brain network was reduced in amusics. The impairments of WM tracts were also found to be correlated with reduced network efficiency in amusics. This suggests that impaired WM tracts may lead to the reduced network efficiency seen in amusics. Our findings suggest that congenital amusia is a disconnection syndrome.
A Vision for the Systematic Monitoring and Improvement of the Quality of Electronic Health Data

In parallel with the implementation of information and communications systems, health care organizations are beginning to amass large-scale repositories of clinical and administrative data. Many nations seek to leverage so-called Big Data repositories to support improvements in health outcomes, drug safety, health surveillance, and care delivery processes. An unsupported assumption is that electronic health care data are of sufficient quality to enable the varied use cases envisioned by health ministries. The reality is that many electronic health data sources are of suboptimal quality and unfit for particular uses. To more systematically define, characterize and improve electronic health data quality, we propose a novel framework for health data stewardship. The framework is adapted from prior data quality research outside of health, but it has been reshaped to apply a systems approach to data quality with an emphasis on health outcomes. The proposed framework is a beginning, not an end. We invite the biomedical informatics community to use and adapt the framework to improve health data quality and outcomes for populations in nations around the world.
Viral infection of the myocardium in endocardial fibroelastosis. Molecular evidence for the role of mumps virus as an etiologic agent.

BACKGROUND Endocardial fibroelastosis, previously a common disease of children, often resulted in congestive heart failure and death. Virus-induced myocarditis was the suspected first step in the pathogenesis of the disease, with enteroviruses and mumps virus considered potential causes. Direct evidence for their involvement was limited, however, and during the past two decades, a significant decline in the incidence of endocardial fibroelastosis occurred. Recently, we demonstrated polymerase chain reaction to be a rapid and sensitive method for identification of the viral genome in the myocardium of patients with myocarditis and dilated cardiomyopathy. The purpose of this study was to analyze myocardial samples of patients with endocardial fibroelastosis for the viral genome. METHODS AND RESULTS Myocardial samples from 29 patients with autopsy-proven endocardial fibroelastosis were analyzed for viral genome (enterovirus, adenovirus, mumps, cytomegalovirus, parvovirus, influenza, herpes simplex virus) by use of polymerase chain reaction or reverse transcriptase-polymerase chain reaction. In 90% of samples, the viral genome was amplified; > 70% of the samples were positive for mumps viral RNA, while 28% amplified adenovirus. In contrast, only 1 of 65 control samples amplified a virus (enterovirus). Two regions of mumps virus were amplified: the nucleocapsid gene and the polymerase-associated protein gene. Interestingly, only 3 of the 21 samples that were positive for mumps RNA were positive with both sets of primers, indicating that the persistence of mumps virus in the myocardium may be related to the selection of defective virus mutants. CONCLUSIONS These data suggest an etiologic role for viral infection in endocardial fibroelastosis, supporting the hypothesis that endocardial fibroelastosis is a sequela of a viral myocarditis, in particular of that due to mumps virus.
The effect of tamoxifen and hormone replacement therapy on serum cholesterol, bone mineral density and coagulation factors in healthy postmenopausal women participating in a randomised, controlled tamoxifen prevention study.

BACKGROUND The role of hormone replacement therapy (HRT) in women who have been treated for breast cancer remains controversial. The addition of tamoxifen may protect these women from any proliferative effect of exogenous oestrogen on the breast. The aim of this analysis was to determine if tamoxifen and HRT may be safely administered together. METHODS We studied the interaction between HRT and tamoxifen on serum cholesterol, fibrinogen, antithrombin III (AT III) and bone mineral density (BMD) in postmenopausal healthy women enrolled in a randomised tamoxifen chemoprevention trial. RESULTS Tamoxifen decreased serum cholesterol by a mean of 13% from pretreatment values (n = 153). The addition of HRT to tamoxifen did not result in further reduction in serum cholesterol (n = 20). HRT alone led to a reduction of serum cholesterol by a mean of 5% in 14 women on placebo. The addition of tamoxifen to HRT resulted in further reduction in serum cholesterol by a mean of 7% (n = 44). Significant reductions of plasma fibrinogen by 14% and AT III by 8% were seen in women who received tamoxifen. There were no further significant changes in these coagulation factors in women on tamoxifen/HRT combinations. Tamoxifen resulted in an annual increase in BMD of the femur and spine by 2% and 1.5%, respectively, when compared to placebo (n = 38). The addition of HRT to tamoxifen resulted in further 2% annual increase in BMD of the femur. CONCLUSIONS We conclude that there were no significant adverse intereactions with tamoxifen and HRT in this small series of patients. The combination results in a reduction of serum cholesterol, increase in BMD especially in the femur and appears not to have any adverse effect on coagulation factors. Multicentre studies should be conducted to evaluate the effect of this combination on relieving menopausal symptoms, disease relapse and overall survival in women who have received treatment for breast cancer.
Lack of evidence that obesity is a cause of pilonidal sinus disease.

OBJECTIVE To find out whether pilonidal sinus is more common among obese people. DESIGN Retrospective study from hospital records. SETTING Two university hospitals, Turkey. SUBJECTS 419 patients who were operated on for pilonidal sinus disease; and 213 age and sex matched patients with benign diseases other than pilonidal sinus disease and who were not morbidly obese acted as controls. MAIN OUTCOME MEASURES Comparison of body mass index (BMI) in the two groups. RESULTS Patients with BMI of 25-30 were classified as overweight (61/419, 15% compared with 28/213, 13%), and those with BMI of 30 or more as obese (7/419 compared with 4/213, 2% in each group). Mean (SD) BMI of patients with pilonidal sinus disease was 26.0 (3.9) compared with 25.6 (3.9) in the control group (p = 0.4). CONCLUSION Obesity alone is not an important factor in the aetiology of pilonidal sinus disease.
Feasibility of Shortening 14‐day Hybrid Therapy While Maintaining an Excellent Helicobacter pylori Eradication Rate

The need for new effective Helicobacter pylori eradication therapy has focused efforts on the development and optimization of regimens with excellent eradication rates such as 14‐day hybrid therapy. This study evaluated whether the duration of hybrid therapy could be reduced while maintaining a high eradication rate and to examine the effect of antibiotic resistance on outcome.
Inter-firm alliances networks in nanotechnology: The roles of network position and technological uncertainty

The emerging nanotechnology has attracted much attention with respect to its potential economic growth. Interdisciplinary collaboration is a key mechanism for accessing different domains technology and knowledge for developing nanotechnology commercialization opportunities. The need for effective inter-firm collaboration is of particular importance in emerging nanotechnology domains. Thus, the present study explores interfirm alliance networking behavior in nanotechnology firms to determine fully what types of factors drive interfirm nanotechnology alliance activities. In this study we proposed theoretical frameworks attempt to fill the gap in knowledge regarding emerging nanotechnology alliance behavior and to explore the alliance decisions driving inter-firm alliances that are grounded in deeper nanotechnology of interfirm alliances. The primary focus of nanotechnology alliance for nanotechnology-based firms confirms that interfirm alliances in nanotechnology are influenced directly by inter-firm R&D ties and by joint interactions among inter-firm R&D ties, network positions, and technological uncertainty. Specifically, we propose that a nanotechnology-based firm is highly likely to engage in alliances regarding decision-making activity. Using an original dataset of nanotechnology-based firms in the emerging nanotechnology alliance activity, we found that the joint effect of a position of high network centrality and a high level of technological uncertainty weaken inter-firm nanotechnology alliances.
A case of the rare variant of Klinefelter syndrome 47,XY,i(X)(q10)

Klinefelter syndrome is the most common genetic form of male hypogonadism, but the phenotype becomes evident only after puberty. It is characterized by infertility, small testes, sparse body and facial hair, increased body weight, gynecomastia, increased LH and FSH, and a low level of testosterone. Early recognition and treatment of Klinefelter syndrome can significantly improve the patient's quality of life and prevent serious consequences. Here, we report an infertile man with a rare variant of Klinefelter syndrome with a 47, XY, i(X)(q10) karyotype.
Elimination and Biochemical Responses to Intravenous Alendronate in Postmenopausal Osteoporosis

Postmenopausal women with established vertebral osteoporosis were studied for 2 years to determine the terminal elimination half‐life and the duration of response to treatment with intravenous alendronate (30 mg) given over 4 days. The urinary excretion of alendronate followed a multiexponential decline. Approximately 50% of the total dose was excreted over the first 5 days, and a further 17% was excreted in the succeeding 6 months. Thereafter, there was a much slower elimination phase with an estimated mean terminal half‐life of greater than 10 years (n = 11). Urinary excretion of hydroxyproline and calcium decreased significantly from pretreatment values by day 3, reaching a nadir by 1 week (40% and 67% decrease, respectively). Thereafter, hydroxyproline remained suppressed for the following 2 years. In contrast, urinary calcium excretion returned gradually toward pretreatment values over the first year and during the second year was comparable to pretreatment values. Serum activity of alkaline phosphatase activity decreased over 3 months (23% reduction), increased gradually thereafter, and returned to pretreatment values at month 24. Bone mineral density measured at the spine increased by approximately 5% during the first year and remained significantly higher than pretreatment values at 2 years. We conclude that a short course of high doses of intravenous alendronate is associated with a prolonged skeletal retention of the agent. This open study also suggests that this regimen has a sustained effect on bone turnover persisting for at least 1 year.
Stocking activities for the Arctic charr in Lake Geneva: Genetic effects in space and time

Abstract Artificial stocking practices are widely used by resource managers worldwide, in order to sustain fish populations exploited by both recreational and commercial activities, but their benefits are controversial. Former practices involved exotic strains, although current programs rather consider artificial breeding of local fishes (supportive breeding). Understanding the complex genetic effects of these management strategies is an important challenge with economic and conservation implications, especially in the context of population declines. In this study, we focus on the declining Arctic charr (Salvelinus alpinus) population from Lake Geneva (Switzerland and France), which has initially been restocked with allochtonous fishes in the early eighties, followed by supportive breeding. In this context, we conducted a genetic survey to document the evolution of the genetic diversity and structure throughout the last 50 years, before and after the initiation of hatchery supplementation, using contemporary and historical samples. We show that the introduction of exotic fishes was associated with a genetic bottleneck in the 1980–1990s, a break of Hardy–Weinberg Equilibrium (HWE), a reduction in genetic diversity, an increase in genetic structure among spawning sites, and a change in their genetic composition. Together with better environmental conditions, three decades of subsequent supportive breeding using local fishes allowed to re‐establish HWE and the initial levels of genetic variation. However, current spawning sites have not fully recovered their original genetic composition and were extensively homogenized across the lake. Our study demonstrates the drastic genetic consequences of different restocking tactics in a comprehensive spatiotemporal framework and suggests that genetic alteration by nonlocal stocking may be partly reversible through supportive breeding. We recommend that conservation‐based programs consider local diversity and implement adequate protocols to limit the genetic homogenization of this Arctic charr population.
Indomethacin Attenuates Oxytocin and Hypothalamic‐Pituitary‐Adrenal Axis Responses to Systemic Interleukin‐1β

Systemic administration of the cytokine IL‐1β produces a significant release of ACTH into the plasma and activation of hypothalamic oxytocin (OT) and corticotropin releasing factor (CRF) cells. However, the mechanism(s) by which systemic IL‐1β induces these responses is not clear. In the present study, we have investigated the proposal that catecholamine cells of the ventrolateral medulla (VLM) and nucleus of the solitary tract (NTS) can relay circulating IL‐1 signals via a prostaglandin‐dependent mechanism to effect the HPA axis responses in the rat. Intra‐arterial administration of IL‐1β (1 pg/kg) to otherwise untreated animals produced a prominent release of ACTH into the plasma, substantial c‐fos expression in paraventricular medial parvocellular (mPVN) corticotropin releasing factor (CRF) cells, supraoptic (SON) and paraventricular nucleus (PVN) OT cells, area postrema cells, NTS and VLM catecholamine cells and cells of the central amygdala. Pretreatment with the prostaglandin synthesis inhibitor, indomethacin (10 mg/kg body weight ia) 15 min before IL‐1β administration (1 pg/kg ia) significantly reduced plasma ACTH release and c‐fos expression in PVN and SON OT cells and MPVN CRF cells. In addition, the area postrema, A1 and C1 catecholamine cell groups of the VLM and A2 and C2 catecholamine cell groups of the NTS, all exhibited concomitant reductions in c‐fos expression. Conversely indomethacin administration did not alter the IL1β‐induced expression of c‐fos in the central amygdala. These data suggest that central pathways involved in the IL‐1β‐induced activation of the HPA axis and OT cells are, at least in part, dependent upon prostaglandin synthesis. It is proposed that neurons in the area postrema, NTS and VLM might mediate this IL‐1β‐induced activation of hypothalamic CRF and OT cells and release of ACTH into the plasma.
Detection of Escherichia coli O157:H7 by multiplex PCR

In order to develop a PCR assay for Escherichia coli O157:H7, a portion of the 60-MDa plasmid harbored by enterohemorrhagic E. coli (EHEC) was sequenced and PCR primers were designed. A multiplex PCR method was then designed by employing primers specific for the EHEC eaeA gene, conserved sequences of Shiga-like toxins I (SLT-I) and II (SLT-II), and the 60-MDa plasmid. PCR products of 1,087 bp (eaeA), 227 and/or 224 bp (SLT-I and/or SLT-II), and 166 bp (plasmid) were successfully amplified simultaneously in a single reaction. The multiplex PCR method can be used to specifically identify EHEC of serogroup O157.
An Organoselenium Compound Inhibits Staphylococcus aureus Biofilms on Hemodialysis Catheters In Vivo

ABSTRACT Colonization of central venous catheters (CVCs) by pathogenic bacteria leads to catheter-related bloodstream infections (CRBSIs). These colonizing bacteria form highly antibiotic-resistant biofilms. Staphylococcus aureus is one of the most frequently isolated pathogens in CRBSIs. Impregnating CVC surfaces with antimicrobial agents has various degrees of effectiveness in reducing the incidence of CRBSIs. We recently showed that organoselenium covalently attached to disks as an antibiofilm agent inhibited the development of S. aureus biofilms. In this study, we investigated the ability of an organoselenium coating on hemodialysis catheters (HDCs) to inhibit S. aureus biofilms in vitro and in vivo. S. aureus failed to develop biofilms on HDCs coated with selenocyanatodiacetic acid (SCAA) in either static or flowthrough continuous-culture systems. The SCAA coating also inhibited the development of S. aureus biofilms on HDCs in vivo for 3 days. The SCAA coating was stable and nontoxic to cell culture or animals. This new method for coating the internal and external surfaces of HDCs with SCAA has the potential to prevent catheter-related infections due to S. aureus.
Lens epithelium-derived growth factor (LEDGF) delays photoreceptor degeneration in explants of rd/rd mouse retina

Lens epithelium derived growth factor (LEDGF) has been shown to rescue embryonic chick photoreceptor cells from serum starvation and heat stress, light damaged photoreceptor cells in Lewis rats, and photoreceptor cells in RCS rats. The aim of our study is to study the rescue effect of LEDGF on photoreceptor cells in the rd/rd mouse using our long-term serum free organ culture. At the end of this culture period of 21–26 days LEDGF treated rd mouse retina showed an increased photoreceptor survival compared to the untreated controls. LEDGF has no effect on expression and localization of opsin and arrestin in the rod photoreceptor cells when RPE is present. The protective potency of LEDGF on the retinal photoreceptor cells is similar to that of BDNF. LEDGF is known to activate heat shock proteins (Hsps) and the elevated Hsps are also reported to suppress apoptosis.
Proteomic analysis reveals novel binding partners of MIP‐T3 in human cells

MIP‐T3 (microtubule‐interacting protein associated with TRAF3) is a microtubule‐interacting protein that evolutionarily conserved from worms to humans, but whose cellular functions remains unknown. To get insight into the functions of MIP‐T3, we set out to identify MIP‐T3 interacting proteins by immunoprecipitation in human embryonic kidney 293 cells and MS analysis. As the results, a total of 34 proteins were identified and most of them were novel MIP‐T3 putative partners. The MIP‐T3‐associated proteins could be grouped into nine clusters based on their molecule functions, including cytoskeleton, chaperone, nucleic acid binding, kinase and so on. Three MIP‐T3‐interacted proteins – actin, HSPA8 and tubulin – were further confirmed by reciprocal coimmunoprecipitations and colocalization analysis. The interaction of MIP‐T3 with both actin filaments and microtubule suggested that MIP‐T3 may play an important role in regulation of cytoskeleton dynamics in cells. Our results therefore not only uncover a large number of MIP‐T3‐associated proteins that possess a variety of cellular functions, but also provide new research directions for the study of the functions of MIP‐T3.
Oxygen debt and metabolic acidemia as quantitative predictors of mortality and the severity of the ischemic insult in hemorrhagic shock

Background and MethodsAn experimental canine model of hemorrhagic, hypovolemic shock is described that uses oxygen debt and its metabolic consequences of lactic acidemia and metabolic base deficit as independent variables for the prediction of probability of death. ResultsLactic acidemia and metabolic base deficit are compared with the conventional hemodynamic variables of BP and cardiac output (&OV0422;t) as predictors of outcome and are shown to be superior using a modified Kaplan-Meier probability statistic. The LD50 for oxygen debt is shown to be 113.5 mL/kg, 12.9 mmol/L for lactate, and −18.8 mmol/L for base excess (BE). Comparison is made between the ability of &OV0422;t, BP, shed blood, BE, and lactate to predict oxygen debt. ConclusionsOf the single-variable predictors, BE shows the highest explained variability. However, a combined prediction from both lactate and BE appears superior to the use of either alone. Using this regression to compute the oxygen debt, it is possible to estimate accurately the actual level of oxygen debt from the BE and lactate values obtained during hemorrhagic hypovolemia. From serial determinations over time of the increase in these biochemical variables above the oxygen debt baseline, it is possible to estimate the rate of oxygen debt accumulation and the time remaining until the LD50 will be reached as indicators of the severity of the total body ischemia resulting from hemorrhagic shock. (Crit Care Med 1991; 19:231)