Miracle-dz/UniFAR-FTUs huggingface dataset:
A PSYCHO-PHYSIOLOGICAL COMPARISON OF POST-TRAUMATIC AND PROLONGED DURESS STRESS DISORDERS

It has been proposed that post-traumatic stress disorder (PTSD) and so-called “prolonged duress stress disorder” (PDSD) have similar symptom profiles and differ only with regard to the presence or absence of a “traumatic event”. This single case experiment investigated whether PTSD can be distinguished from PDSD at the level of patho-physiology. The results indicate that both PTSD and PDSD imagery elicit physiological responses, but these are more readily and more strongly evoked by the former than the latter. These findings suggest that physiological response differences between PTSD and PDSD may be only a matter of degree. Implications are drawn for the psycho-physiological assessment of PDSD and recommendations for further research are made.
A Gravity Dual of Localized Tachyon Condensation in Intersecting Branes

The method of probe brane is the powerful one to obtain the effective action living on the probe brane from supergravity. We apply this method to the unstable brane systems, and understand the tachyon condensation in the context of the open/closed duality. First, we probe the parallel coincident branes by the anti-brane. In this case, the mass squared of the stretched string becomes negative infinite in the decoupling limit. So that the dual open string field theory is difficult to understand. Next, we probe parallel coincident branes by a brane intersecting with an angle. In this case, the stretched strings have the tachyonic modes localized near the intersecting point, and by taking the appropriate limit for the intersection angle, we can leave mass squared of this modes negative finite in the decoupling limit. Then we can obtain the information about the localized tachyon condensation from the probe brane action obtained using supergravity.
Saints, and the Rest of Us: Broadening the Perspective on Moral Identity Development

In the field of psychology, the construct of moral identity emerged as one response to the perceived gaps between moral judgment and action [Blasi, 1983, 1984]. As such, moral identity was conceptualized as the extent to which being a moral person is important to people’s sense of who they are and who they want to be, and posited to act as an intervening psychological structure between moral thinking and conduct. In other words, it was thought that, for people for whom morality is central to and integrated within their identity, the desire to live in a manner consistent with their sense of self would serve as a key moral motivation [Aquino & Reed, 2002; Colby & Damon, 1992; Hardy & Carlo, 2005; Matsuba & Walker, 2005]. In the target article, Krettenauer and Hertz [this issue] place the construct of moral identity in its right intellectual context and briefly summarize the main findings of three decades of research: Measures of moral identity, framed largely in terms of the self-reported centrality a person places on possessing and enacting moral values, have repeatedly yielded findings of individual differences that, while theoretically consistent (inasmuch as moral identity centrality has been shown to be associated with readiness to engage in prosocial action and to abstain from antisocial behavior), have also been relatively small and not unique. Krettenauer and Hertz, however, are not much concerned in this article with the staying power of the moral identity construct as a means for predicting individual differences in moral behavior. Their main concern, one that has also been articulated by other researchers in the field [e.g., Hardy & Carlo, 2011; Lapsley & Stey, 2014], relates to the paucity of findings regarding age differences in moral identity. Indeed, Krettenauer and Hertz are faced with a quandary. The most broadly used measures of moral identity have consistently and reliably yielded findings of no age differences.
Bacterial Vaginosis, Race, and Sexually Transmitted Infections: Does Race Modify the Association?

Background: There are significant racial disparities in the prevalence of sexually transmitted infections (STIs) in the United States. The purpose of this study was to evaluate whether the association of bacterial vaginosis and incident STI is modified by race even after adjustment for sexual practices and other potential confounding variables. Methods: We evaluated the association of bacterial vaginosis (BV) and STI acquisition in a group of 523 women at high risk for unplanned pregnancies and STI. BV was diagnosed by both Gram stain and Amsel criteria. STIs included Chlamydia trachomatis, Neisseria gonorrhoeae, pelvic inflammatory disease, trichomoniasis, syphilis, and HIV. Cox regression estimated the associations and the synergy index assessed whether race modified the association of BV and incident STI. Results: Sixteen percent of participants developed an STI during the 2-year follow-up. Compared with white women without BV at baseline, the adjusted hazard ratios were as follows: white women with BV = 0.59; African American women without BV = 1.96; and African American women with BV = 2.86. The synergy index of 3.38 implies a combined association of BV and African American race with STI in excess of each factor individually. Conclusions: African American race modifies the association of BV and incident STI. Future research should strive to determine the relative contributions of other factors, such as biologic variation, social network or the consequences of socioeconomic position, in this disparity.
In Vitro Simulation of Corneal Epithelium Microenvironment Induces a Corneal Epithelial-like Cell Phenotype from Human Adipose Tissue Mesenchymal Stem Cells

Abstract Purpose: Transplantation of autologous corneal stem cells in not possible in cases of bilateral limbal stem cell deficiency (LSCD). To restore the ocular surface in these patients, an autologous extraocular source of stem cells is desirable to avoid dependence on deceased donor tissue and host immunosuppression of allogenic transplants. While bone marrow-derived mesenchymal stem cells (MSCs) can acquire certain characteristics of corneal epithelial cells, subcutaneous adipose tissue (AT) is more readily available and accessible. The aim of this study was to determine if extraocular human AT-derived MSCs (hAT-MSCs) can acquire in vitro some features of corneal epithelial-like cells. Methods: hAT-MSCs were isolated from human lipoaspirates and expanded up to 3–4 passages. We studied the immunophenotype of MSCs and demonstrated its multipotent capacity to differentiate toward osteoblasts, adipocytes and chondrocytes. To test the capacity of differentiation of hAT-MSCs toward corneal epithelial-like cells, hAT-MSCs were cultured on substrata of plastic or collagen IV. We used basal culture medium (BM), BM conditioned with human corneal epithelial cells (HCEcBM) and BM conditioned with limbal fibroblasts (LFcBM). Results: The hAT-MSCs incubated for 15 days with HCEcBM acquired more polygonal and complex morphology as evaluated by phase-contrast microscopy and flow cytometry. Additionally, the expression of transforming growth factor-β receptor CD105 and corneal epithelial marker CK12 got increased as evaluated by flow cytometry, real-time reverse-transcription polymerase chain reaction, western blot and immunostaining. These changes were absent in hAT-MSCs incubated with unconditioned BM or with LFcBM. Conclusions: Corneal epithelial-like cells can be induced from extraocular hAT-MSCs by subjecting them to an in vitro microenvironment containing conditioning signals derived from differentiated human corneal epithelial cells. Our results suggest that hAT-MSCs could provide a novel source of stem cells that hold the potential to restore sight lost in patients suffering from bilateral ocular surface failure due to LSCD.
Immediate extubation versus standard postoperative ventilation: Our experience in on pump open heart surgery

Elective postoperative ventilation in patients undergoing “on pump” open heart surgery has been a standard practice. Ultra fast-track extubation in the operating room is now an accepted technique for “off pump” coronary artery bypass grafting. We tried to incorporate these experiences in on pump open heart surgery and compare the haemodynamic and respiratory parameters in the immediate postoperative period, in patients on standard postoperative ventilation for 8-12 hours. After ethical committee’s approval and informed consent were obtained, 72 patients, between 28 and 45 years of age, undergoing on pump open heart surgery, were selected for our study. We followed same standard anaesthetic, cardiopulmonary bypass (CPB) and cardioplegic protocol. Thirty-six patients (Group E) were randomly allocated for immediate extubation following operation, after fulfillment of standard extubation criteria. Those who failed to meet these criteria were not extubated and were excluded from the study. The remaining 36 patients (Group V) were electively ventilated and extubated after 8-12 hours. Standard monitoring for on pump open heart surgery, including bispectral index was done. The demographic data, surgical procedures, preoperative parameters, aortic cross clamp and cardiopulmonary bypass times were comparable in both the groups. Extubation was possible in more than 88% of cases (n=32 out of 36 cases) in Group E and none required reintubation for respiratory insufficiency. Respiratory, haemodynamic parameters and postoperative complications were comparable in both the groups in the postoperative period. Therefore, we can safely conclude that immediate extubation in the operating room after on pump open heart surgery is an alternative acceptable method to avoid postoperative ventilation and its related complications in selected patients.
The School Transitions Project: A Comprehensive Preventive Intervention

Some children who transfer into new schools are at risk for later school and life difficulties. Such children often enter the new schools with several life stressors and academic lags, and they are often members of lower socioeconomic status groups. Described are a series of preventive interventions for high-risk elementary school transfer children. All transfers initially received an orientation program. Some children received no further interventions, others were provided tutoring in the school, and others were provided school tutoring plus parent tutoring. The findings from several cohorts are described. The implications of designing and implementing preventive interventions for children undergoing school transitions are discussed.
Amniotic fluid cytokines (interleukin-6, tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-8) and the risk for the development of bronchopulmonary dysplasia.

OBJECTIVE Our purpose was to test the hypothesis that neonates who develop bronchopulmonary dysplasia have higher amniotic fluid concentrations of proinflammatory cytokines than those who do not develop bronchopulmonary dysplasia. STUDY DESIGN The relationship between amniotic fluid concentrations of interleukin-6, tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-8 and the occurrence of bronchopulmonary dysplasia in the neonate was examined in 69 patients who were delivered of preterm neonates (< or = 33 weeks) within 5 days of amniocentesis. Cytokines were measured by specific immunoassays. RESULTS Bronchopulmonary dysplasia was diagnosed in 19% (13/69) of newborns. Median amniotic fluid concentrations of interleukin-6, tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-8 concentrations were significantly higher in mothers whose infants had bronchopulmonary dysplasia than in mothers whose infants did not have bronchopulmonary dysplasia (p < 0.05 for each). Neonates who had bronchopulmonary dysplasia were delivered at earlier gestational ages and had lower birth weights than those without bronchopulmonary dysplasia. The differences in median amniotic fluid interleukin-6, interleukin-1 beta, and interleukin-8 between these two groups remained significant after we adjusted for the effect of gestational age at birth (p < 0.05 for each). CONCLUSIONS (1) Antenatal exposure to proinflammatory cytokines is a risk factor for the development of bronchopulmonary dysplasia; (2) the injury responsible for bronchopulmonary dysplasia in a subset of neonates may begin before birth.
Presynaptic Ca2+-Activated K+ Channels in Glutamatergic Hippocampal Terminals and Their Role in Spike Repolarization and Regulation of Transmitter Release

Large-conductance Ca2+-activated K+ channels (BK, also called Maxi-K orSlo channels) are widespread in the vertebrate nervous system, but their functional roles in synaptic transmission in the mammalian brain are largely unknown. By combining electrophysiology and immunogold cytochemistry, we demonstrate the existence of functional BK channels in presynaptic terminals in the hippocampus and compare their functional roles in somata and terminals of CA3 pyramidal cells. Double-labeling immunogold analysis with BK channel and glutamate receptor antibodies indicated that BK channels are targeted to the presynaptic membrane facing the synaptic cleft in terminals of Schaffer collaterals in stratum radiatum. Whole-cell, intracellular, and field-potential recordings from CA1 pyramidal cells showed that the presynaptic BK channels are activated by calcium influx and can contribute to repolarization of the presynaptic action potential (AP) and negative feedback control of Ca2+ influx and transmitter release. This was observed in the presence of 4-aminopyridine (4-AP, 40–100 μm), which broadened the presynaptic compound action potential. In contrast, the presynaptic BK channels did not contribute significantly to regulation of action potentials or transmitter release under basal experimental conditions, i.e., without 4-AP, even at high stimulation frequencies. This is unlike the situation in the parent cell bodies (CA3 pyramidal cells), where BK channels contribute strongly to action potential repolarization. These results indicate that the functional role of BK channels depends on their subcellular localization.
Feature evaluation based Fuzzy C-Mean classification

Fuzzy C-Means Clustering, FCM, is an iterative algorithm whose aim is to find the center or centroid of data clusters that minimize an assigned dissimilarity function. The degree of being in a certain cluster can be defined in terms of the distance to the cluster-centroid. The domain knowledge is used to formulate an appropriate measure. However the Euclidean distance is considered as a general measure for such value. The calculation of the Euclidean distance doesn't take into consideration the degree of relevance of each feature to the classification model. In this paper, scoring methods like ChiMerge and Mutual information are used in the FCM model to improve the calculation of the Euclidean distance. Experimental results demonstrate the better performances of the improved FCM on UCI benchmark data sets rather than the ordinary FCM, where the ordinary FCM uses in classification either all features or the most important features while the improved FCM uses all the features but the Euclidean Distance will be calculated according to the relevance degree of each feature.
Attenuation of Brain Reward Thresholds during Acute Opioid Withdrawal by Antagonism of CRF Receptors in the Extended Amygdala

Increased release of the stress neurotransmitter corticotropin-releasing factor (CRF) in regions of the extended amygdala has been shown to mediate drug withdrawal behavior. These symptoms of withdrawal have been characterized by dysphoria-like signs that can be measured by assessing levels of brain reward deficits using intracranial self stimulation (ICSS). In an initial study, the dose-response curve for naloxone-precipitated elevations in brain reward thresholds following an acute or repeated (4x at daily intervals) daily injections of 10 mg/kg of morphine was determined. Using a discrete-trial brain stimulation reward procedure, male Wistar rats implanted with stimulating electrodes aimed at the medial forebrain bundle received either repeat- or acute- treatment of morphine (10 mg/kg) 4 hr prior to one of several doses of naloxone (0.01, 0.033, 0.33. 1.0 mg/kg); naloxone was administered just prior to a test session. Naloxone dose-dependently increased thresholds after acute and repeat morphine, and its potency was greater after repeated morphine treatments. Selecting an optimal dose of naloxone (1.0 mg/kg) under acute morphine pretreatment conditions, a second study examined the effects of bilateral infusion of the CRF-R1 antagonist, antalarmin (1.0, 3.3 nmol), into the CeA and NAC shell. Results suggest that 4 h after an acute morphine (10 mg/kg) pretreatment, the highest dose of antalarmin tested (3.3 nmol) in both brain regions significantly attenuated naloxone-induced elevations in reward thresholds. The data indicate that preventing endogenous CRF in the CeA and the shell of the NAC from binding to CRF-R1 receptors can significantly blunt the brain reward deficits that result from precipitated opioid withdrawal
This Paper Is Included in the Proceedings of the 12th Usenix Symposium on Operating Systems Design and Implementation (osdi '16). Correlated Crash Vulnerabilities Correlated Crash Vulnerabilities

Modern distributed storage systems employ complex protocols to update replicated data. In this paper, we study whether such update protocols work correctly in the presence of correlated crashes. We find that the correctness of such protocols hinges on how local file-system state is updated by each replica in the system. We build PACE, a framework that systematically generates and explores persistent states that can occur in a distributed execution. PACE uses a set of generic rules to effectively prune the state space, reducing checking time from days to hours in some cases. We apply PACE to eight widely used distributed storage systems to find correlated crash vulnerabilities, i.e., problems in the update protocol that lead to user-level guarantee violations. PACE finds a total of 26 vulnerabilities across eight systems , many of which lead to severe consequences such as data loss, corrupted data, or unavailable clusters.
Redundancy, Self-Motion, and Motor Control

Outside the laboratory, human movement typically involves redundant effector systems. How the nervous system selects among the task-equivalent solutions may provide insights into how movement is controlled. We propose a process model of movement generation that accounts for the kinematics of goal-directed pointing movements performed with a redundant arm. The key element is a neuronal dynamics that generates a virtual joint trajectory. This dynamics receives input from a neuronal timer that paces end-effector motion along its path. Within this dynamics, virtual joint velocity vectors that move the end effector are dynamically decoupled from velocity vectors that do not. Moreover, the sensed real joint configuration is coupled back into this neuronal dynamics, updating the virtual trajectory so that it yields to task-equivalent deviations from the dynamic movement plan. Experimental data from participants who perform in the same task setting as the model are compared in detail to the model predictions. We discover that joint velocities contain a substantial amount of self-motion that does not move the end effector. This is caused by the low impedance of muscle joint systems and by coupling among muscle joint systems due to multiarticulatory muscles. Back-coupling amplifies the induced control errors. We establish a link between the amount of self-motion and how curved the end-effector path is. We show that models in which an inverse dynamics cancels interaction torques predict too little self-motion and too straight end-effector paths.
Helminth species richness in wild wood mice, Apodemus sylvaticus, is enhanced by the presence of the intestinal nematode Heligmosomoides polygyrus

SUMMARY We analysed 3 independently collected datasets of fully censused helminth burdens in wood mice, Apodemus sylvaticus, testing the a priori hypothesis of Behnke et al. (2005) that the presence of the intestinal nematode Heligmosomoides polygyrus predisposes wood mice to carrying other species of helminths. In Portugal, mice carrying H. polygyrus showed a higher prevalence of other helminths but the magnitude of the effect was seasonal. In Egham, mice with H. polygyrus showed a higher prevalence of other helminth species, not confounded by other factors. In Malham Tarn, mice carrying H. polygyrus were more likely to be infected with other species, but only among older mice. Allowing for other factors, heavy residual H. polygyrus infections carried more species of other helminths in both the Portugal and Egham data; species richness in Malham was too low to conduct a similar analysis, but as H. polygyrus worm burdens increased, so the prevalence of other helminths also increased. Our results support those of Behnke et al. (2005), providing firm evidence that at the level of species richness a highly predictable element of co-infections in wood mice has now been defined: infection with H. polygyrus has detectable consequences for the susceptibility of wood mice to other intestinal helminth species.
Vpu Directs the Degradation of the Human Immunodeficiency Virus Restriction Factor BST-2/Tetherin via a βTrCP-Dependent Mechanism

ABSTRACT The primary roles attributed to the human immunodeficiency virus type 1 (HIV-1) Vpu protein are the degradation of the viral receptor CD4 and the enhancement of virion release. With regard to CD4 downregulation, Vpu has been shown to act as an adapter linking CD4 with the ubiquitin-proteasome machinery via interaction with the F-box protein βTrCP. To identify additional cellular βTrCP-dependent Vpu targets, we performed quantitative proteomics analyses using the plasma membrane fraction of HeLa cells expressing either wild-type Vpu or a Vpu mutant (S52N/S56N) that does not bind βTrCP. One cellular protein, BST-2 (CD317), was consistently underrepresented in the membrane proteome of cells expressing wild-type Vpu compared to the proteome of cells expressing the Vpu mutant. To verify the biological relevance of this phenotype for HIV pathogenesis, we showed that in T cells infected with HIV-1, BST-2 downregulation occurred in a Vpu-dependent manner. Recently, BST-2 has been identified as the interferon-inducible cellular factor Tetherin, which restricts HIV virion release in the absence of Vpu. We address here the unresolved mechanism of Vpu-mediated BST-2 downregulation. Our data show that the presence of wild-type Vpu reduced cell surface and total steady-state BST-2 levels, whereas that of the mutant Vpu had no effect. In addition, treatment of cells with the lysosome acidification inhibitor concanamycin A, but not treatment with the proteasome inhibitor MG132, reduced BST-2 downregulation by wild-type Vpu, thereby suggesting that the presence of Vpu leads to the degradation of BST-2 via an endosome-lysosome degradation pathway. The importance of βTrCP in this process was confirmed by demonstrating that in the absence of βTrCP, BST-2 levels were restored despite the presence of Vpu. Taken together, these data support the hypothesis that, in similarity to its role in CD4 degradation, Vpu acts as an adapter molecule linking BST-2 to the cellular ubiquitination machinery via βTrCP. However, in contrast to the proteasome-dependent degradation of CD4, which occurs in the endoplasmic reticulum, Vpu appears to interact with BST-2 in the trans-Golgi network or in early endosomes, leading to lysosomal degradation of BST-2. Via this action, Vpu could counter the tethering function of BST-2, resulting in enhanced HIV-1 virion release. Interestingly, although HIV-2 does not express Vpu, an isolate known to exhibit enhanced viral egress can downregulate surface BST-2 by an as-yet-unknown mechanism that does not appear to involve degradation. Understanding the molecular mechanisms of both Vpu-dependent and -independent mediated antagonism of BST-2 will be critical for therapeutic strategies that exploit this novel viral function.