Miracle-dz/UniFAR-FTUs huggingface dataset:
The Presence of Eschars, but Not Greater Severity, in Portuguese Patients Infected with Israeli Spotted Fever

Abstract: In Portugal, Mediterranean spotted fever (MSF) is caused by R. conorii Malish and Israeli spotted fever (ISF) strains. It has been suggested that the ISF strain isolated from patients with MSF causes different clinical manifestations compared to those caused by Malish strain, namely the absence of eschar and greater severity. The aim of this study was to analyze the presence or absence of eschar and of fatality in Portuguese patients infected with either Malish or ISF strain. Of 94 patients with a clinical diagnosis of MSF between 1994 to 2004, 47 were infected with Malish strain and 47 with ISF strain. Eschars were reported in 20 patients (49%) infected with Malish strain, and in 17 (39%) with ISF strain. The presence of eschar is not statistically associated to a greater extent with either R. conorii strain (P= 0.346). A total of 22 patients died, 9 infected with Malish strain and 13 infected with ISF strain, and no statistically significant difference was found (P= 0.330). This study showed that the concepts of absence of the eschar and greater severity in Israeli spotted fever infection should be revised.
Sustained Endothelial Progenitor Cell Dysfunction After Chronic Hypoxia‐Induced Pulmonary Hypertension

Circulating endothelial progenitor cells (EPCs) contribute to neovascularization of ischemic tissues and repair of injured endothelium. The role of bone marrow‐derived progenitor cells in hypoxia‐induced pulmonary vascular remodeling and their tissue‐engineering potential in pulmonary hypertension (PH) remain largely unknown. We studied endogenous mobilization and homing of EPCs in green fluorescent protein bone marrow chimeric mice exposed to chronic hypoxia, a common hallmark of PH. Despite increased peripheral mobilization, as shown by flow cytometry and EPC culture, bone marrow‐derived endothelial cell recruitment in remodeling lung vessels was limited. Moreover, transfer of vascular endothelial growth factor receptor‐2+/Sca‐1+/CXCR‐4+‐cultured early‐outgrowth EPCs failed to reverse PH, suggesting hypoxia‐induced functional impairment of transferred EPCs. Chronic hypoxia decreased migration to stromal cell‐derived factor‐1α, adhesion to fibronectin, incorporation into a vascular network, and nitric oxide production (−41%, −29%, −30%, and −32%, respectively, vs. normoxic EPCs; p < .05 for all). The dysfunctional phenotype of hypoxic EPCs significantly impaired their neovascularization capacity in chronic hind limb ischemia, contrary to normoxic EPCs cultured in identical conditions. Mechanisms contributing to EPC dysfunction include reduced integrin αv and β1 expression, decreased mitochondrial membrane potential, and enhanced senescence. Novel insights from chronic hypoxia‐induced EPC dysfunction may provide important cues for improved future cell repair strategies.
Do carriers of POLG mutation W748S have disease manifestations?

Mitochondrial recessive ataxia syndrome (MIRAS) is a common cause of autosomal recessive juvenile‐ or adult‐onset ataxia, at least in Scandinavia. MIRAS patients are homozygous or compound heterozygous for POLG mutations W748S and A467T. Because many first‐degree relatives of MIRAS patients in the studied families have reported neurological symptoms and some recent studies have suggested dominant negative effect of these mutations, a careful family study of heterozygotes was needed. We investigated all available members of the original large MIRAS family with W748S mutation. Neurological symptoms and signs were present in a number of carriers, but clearly defined neurological diseases did not segregate consistently with the mutation. Sensory polyneuropathy as a subclinical finding was observed in the majority of carriers examined. By positron emission tomography, cerebral glucose metabolism was moderately reduced in two out of four heterozygotes compared with severe reduction in one MIRAS patient. In conclusion, W748S heterozygotes showed no clinically manifesting phenotype.
The Psychology Surrounding Legal Standards of Competency and Representation for Children in U.S. Immigration Court

In recent years, immigration detentions have spiked. Further, the Zero Tolerance Policy enacted by President Trump has separated thousands of children from their families. Because many children are without their parents, and immigration court is civil in nature, thousands of children are placed in deportation hearings without representation each year. Child psychological research is at odds with the current deportation practices as psychological research deems children unable to understand the complexities of the court system or the impacts of deportation proceedings. A minimum competency to stand trial must be enacted to protect young children’s due process rights, regardless of citizenship. Further, children should be protected through a guardian ad litem or other legal representatives as they are a vulnerable class. This paper examines the relationship between the current legal standards for immigration court, relevant child psychological research, and explores policy recommendations for immigration competency standards and representation requirements.
Diagnosis from scenarios [system diagnosis]

Diagnosis of a system consists in providing explanations to a supervisor from a partial observation of the system and a model of possible executions. This paper proposes a partial order diagnosis algorithm that recovers sets of scenarios which correspond to a given observation. The main difficulty is that some actions are unobservable but may still induce some causal ordering among observed events. We first give an offline centralized diagnosis algorithm, then we discuss a distributed version of this algorithm
Implant treatment in the edentulous mandible: a prospective study on Brånemark system implants over more than 20 years.

PURPOSE This prospective investigation studied the clinical and radiographic performance of mandibular fixed prostheses supported by osseointegrated implants over more than 20 years. MATERIALS AND METHODS A total of 273 standard Brånemark implants (10 mm long) were placed in 47 patients between 1978 and 1982. Clinical and radiographic data collected at several examinations over the 20-year observation period have been reported previously. This study presents the outcome of the latest follow-up after 20 to 23 years. RESULTS Thirty patients (64%; 75% of those still alive) attended the 20-year follow-up examination. Three implants were lost during the entire observation period, and the 20-year implant cumulative survival rate was 98.9%. All patients had continuous prosthesis function, but two had their mandibular prostheses remade during the 20 years. No implants or prostheses were lost or fractured during the last 5 years, and only a few prosthodontic complications were noted. The mean bone level was 1.6 mm (SD 0.90) below the reference point after 20 years, and mean bone loss was 0.2 mm (SD 0.22) between the 15- and 20-year follow-ups. Thirty-seven implants (24%) showed more than two exposed threads at the 15-year follow-up examination, but only four implants (3%) presented pain and/or bone loss exceeding one thread (0.6 mm) during the last 5 years. CONCLUSION The successful treatment result after 15 years continued up to more than 20 years in function. During the last 5 years, a majority of the implants with several exposed implant threads could be maintained without any complications, and the frequency of implants showing signs of ongoing peri-implantitis was less than 3%.
Three-level hysteresis current regulation for a three phase neutral point clamped inverter

This paper presents a new hysteresis current regulation strategy for a three-phase three-level neutral point clamped (NPC) inverter. The strategy uses the zero-crossing of the fundamental component of the phase leg switched voltage to select the output voltage level, with only one hysteresis comparator required per phase leg. The same average voltage is then used to vary the hysteresis band as the load back-emf changes in order to maintain a constant switching frequency. Next, the strategy is extended to a three-phase NPC inverter by subtracting the common mode interacting current from the total phase leg current error before making any switching decision. The three-phase leg current errors are also synchronized to a fixed clock frequency to further improve the frequency regulation and obtain a line to line harmonic performance that is close to open-loop phase disposition (PD) pulse width modulation.
Nickel and Extracellular Acidification Inhibit the Water Permeability of Human Aquaporin-3 in Lung Epithelial Cells*

Nickel is a common cause of pneumoconiosis. Here, we show that nickel inactivates aquaporin (AQP)-3, the water channel expressed apically in epithelial cells of human terminal airways. Human AQP3 was transiently transfected into human lung cells, and water permeability was measured in transfected and neighboring untransfected cells. Incubation with NiCl2 rapidly, dose-dependently, and reversibly decreased water permeability in AQP3-expressing cells. Acidification of the extracellular medium also caused rapid, dose-dependent, and reversible inhibition of AQP3. Sensitivity of AQP3 to nickel was lower at alkaline pH than at neutral and acidic pH. Cells transfected with human AQP4 and AQP5, which are also expressed in airway epithelia, were insensitive to nickel and extracellular acidification. Zinc and cadmium, other common causes of pneumoconiosis, had no effect on the water permeability of AQP3. Three extracellular residues, Trp128, Ser152, and His241, were responsible for the blocking effect of nickel on human AQP3. Ser152 was identified as a common site for nickel and pH sensitivity. His53, Tyr124, and His154 were also involved in regulation of AQP3 by extracellular pH. In addition, the aromatic side chain of His154 was shown to be important for the water permeability of AQP3. Our results imply that nickel and extracellular pH may modulate lung water clearance and that defective water clearance may be an early component of nickel-induced lung disease.
Melatonin inhibits apoptosis and improves the developmental potential of vitrified bovine oocytes

Vitrification of oocytes has been shown to be closely associated with increased levels of reactive oxygen species (ROS) and apoptotic events. However, little information is available the effect of melatonin on the ROS levels and apoptotic events in vitrified oocytes. Therefore, we studied the effect of melatonin on ROS and apoptotic events in vitrified bovine oocytes by supplementing vitrification solution or in vitro maturation (IVM) and vitrification solution with 10−9 m melatonin. We analyzed the ROS, mitochondrial Ca2+ (mCa2+) and membrane potential (ΔΨm), externalization of phosphatidylserine (PS), caspase‐3 activation, DNA fragmentation, mRNA expression levels of Bax and Bcl2 l1, and developmental potential of vitrified bovine oocytes. Vitrified bovine oocytes exhibited increased levels of ROS, mCa2+, Bax mRNA, and caspase‐3 protein and higher rates of PS externalization and DNA fragmentation, and decreased ΔΨm and Bcl2 l1 mRNA expression level. However, melatonin supplementation in vitrification solution or IVM and vitrification solution significantly decreased the levels of ROS, mCa2+, Bax mRNA expression, and caspase‐3 protein, and PS externalization and DNA fragmentation rates, and increased the ΔΨm and Bcl2 l1 mRNA expression level in vitrified oocytes, resulting in an increased developmental ability of vitrified bovine oocytes after parthenogenetic activation. The developmental ability of vitrified oocytes with melatonin supplementation in IVM and vitrification solution was similar to that of fresh ones. This study showed that supplementing the IVM and vitrification medium or vitrification medium with 10−9 m melatonin significantly decreased the ROS level and inhibited apoptotic events of vitrified bovine oocytes, consequently increasing their developmental potential.
Building Efficient Key-Value Stores via a Lightweight Compaction Tree

Log-Structure Merge tree (LSM-tree) has been one of the mainstream indexes in key-value systems supporting a variety of write-intensive Internet applications in today’s data centers. However, the performance of LSM-tree is seriously hampered by constantly occurring compaction procedures, which incur significant write amplification and degrade the write throughput. To alleviate the performance degradation caused by compactions, we introduce a lightweight compaction tree (LWC-tree), a variant of LSM-tree index optimized for minimizing the write amplification and maximizing the system throughput. The lightweight compaction drastically decreases write amplification by appending data in a table and only merging the metadata that have much smaller size. Using our proposed LWC-tree, we have implemented three key-value LWC-stores on different storage mediums including Shingled Magnetic Recording (SMR) drives, Solid State Drives (SSD), and conventional Hard Disk Drives (HDDs). The LWC-store is particularly optimized for SMR drives, as it eliminates the multiplicative I/O amplification from both LSM-trees and SMR drives. Due to the lightweight compaction procedure, LWC-store reduces the write amplification by a factor of up to 5× compared to the popular LevelDB key-value store. Moreover, the random write throughput of the LWC-tree on SMR drives is significantly improved by up to 467% even compared with LevelDB on conventional HDDs. Furthermore, LWC-tree has wide applicability and delivers impressive performance improvement in various conditions, including different storage mediums (i.e., SMR, HDD, SSD) and various value sizes and access patterns (i.e., uniform and Zipfian).
Effect of community based management in failure to thrive: randomised controlled trial

Abstract Objective : To evaluate the effectiveness of a health visitor led intervention for failure to thrive in children under 2 years old. Design : Controlled trial, randomised by primary care practice. Setting : Newcastle upon Tyne health district. Intervention : Structured health visitor management, with dietetic, paediatric, and social work input as required. Subjects : 229 children (120 in intervention practices and 109 in control practices) were identified as failing to thrive by population screening during the first 2 years of life. Follow up was by home visit of a research nurse and review of the childrens' records at age 3 years. Main outcome measures : Follow up weight and height and number of routinely collected weights. Results : 95 of the 97 families offered intervention completed at least the initial assessment. At follow up, 187 (82%) records were reviewed, and these suggested that 15 (16%) controls were lost to follow up immediately after the screening weight was taken compared with only one child in the intervention group. In the 134 (58%) families who consented to home visits, children in the intervention group were significantly heavier and taller and were reported to have better appetites than childen in the control group, although both groups were equally satisfied by the services they had received. When the children were last weighed, 91 (76%) in the intervention group had recovered from their failure to thrive compared with 60 (55%) in the control group (P<0.001). Conclusion : In failure to thrive, health visitor intervention, with limited specialist support, can significantly improve growth compared with conventional management.
Role of de novo protein synthesis and calmodulin in rapid activation of Na(+)‐H+ exchange of aldosterone in frog diluting segment.

1. In the amphibian early distal tubule aldosterone activates the Na(+)‐H+ exchangers, resulting in an increase in intracellular pH (pHi). Since this activation is rapid (within 30 min), it may be mediated by either a genomic or non‐genomic pathway. 2. pHi was measured in single microperfused early distal tubule segments using the fluorescent probe 2',7'‐bis(carboxyethyl)‐5,6‐carboxyfluorescein (BCECF). 3. A 30 min incubation in aldosterone increased both resting pHi and the setpoint of the Na(+‐H+ exchanger. These changes were prevented by the mineralocorticoid receptor antagonist, spironolactone. 4. Actinomycin D and cycloheximide, inhibitors of transcription and translation, respectively, were without effect on resting pHi, but inhibited activation of the Na(+)‐H+ exchanger by aldosterone. 5. The effect of aldosterone upon pHi and setpoint was also prevented by the calcium‐calmodulin antagonist, W‐7. 6. These results indicate that, although the response to aldosterone is rapid, aldosterone binds to a specific mineralocorticoid receptor which then triggers gene activation followed by de novo protein synthesis. Furthermore, since calmodulin is a known activator of the Na(+)‐H+ exchanger, and the response is inhibited by W‐7, it is suggested that this protein may be calmodulin.
Human Papillomavirus 16-Positive Uterine Cervical Squamous Cell Carcinoma with Coinfection with Human Papillomavirus 34 Has a Lower Incidence in Lymph Node Metastasis than That without Coinfection with Human Papillomavirus 34

Our earlier study demonstrated high prevalence of multiple human papillomavirus (HPV) infection in patients with invasive uterine cervical cancer, including squamous cell carcinoma (SCC). HPV 16 is the most predominant genotype related to SCC of the uterine cervix. The aim of this study was to reveal the biological significance of multiple HPV infection concerning the tumor progression of invasive uterine cervical SCC. In the present study, the effects of coinfection with genotypes other than HPV 16 on tumor growth and lymph node metastasis of invasive uterine cervical SCC with HPV 16 infection were examined. Although coinfection with most genotypes did not influence tumor progression, the clinical stage of patients coinfected with HPV 16 and HPV 34 was significantly lower than that of those without HPV 34 coinfection (p = 0.0038). Moreover, no patient coinfected with HPV 16 and HPV 34 manifested lymph node metastasis, but about half of the patient population without HPV 34 coinfection did (p = 0.0299). These findings suggested that coinfection with HPV 34 could prevent the tumor progression of invasive uterine cervical SCC with HPV 16 infection.
Causes of late failure after heart transplantation: a ten-year survey.

BACKGROUND Little is known about the causes of death of heart transplant recipients who survive long-term. METHODS The pathologic and clinical records of 97 patients who underwent heart transplantation in Italy from 1985 to 1995 and died (85 of 97) or underwent retransplantation (12 of 97) at least 2 years after transplantation were surveyed. Graft failures were classified as late (occurring between 2 and 5 years after transplantation) and belated (more than 5 years). RESULTS Graft vasculopathy was the single most common cause of death (40.0%) and the only cause of late retransplantation. Tumors ranked second (23.5% of deaths), but the expected non-Hodgkin's lymphomas and Kaposi's sarcoma were accompanied by a high number of lung cancers (especially metastasizing adenocarcinomas). They were followed by the emergence or recurrence of pretransplantation diseases (9.4%), fatal infections (exclusively bacterial) (4.7%), the development of transmissible diseases (viral hepatitis and acquired immunodeficiency syndrome, 4.7%), and late acute rejection (2.3%). The distribution of failures differed in the late and belated periods: death and organ loss proportions for graft vasculopathy, respectively, fell and rose from the late to the belated period; some types of malignancy and fatal acute rejection were never observed in the belated period, whereas the emergence of pretransplantation diseases prevailed in the belated period. Graft vasculopathy was more frequent and tumors were less frequent among patients undergoing transplantation for ischemic heart disease. CONCLUSIONS The reasons why heart transplant recipients die or undergo retransplantation, respectively, in the late and belated periods slightly differ from one another and are widely different than in short-term survivors.
THE SHORT‐TERM EFFECT OF WHOLE‐BODY VIBRATION TRAINING ON VERTICAL JUMP,SPRINT, AND AGILITY PERFORMANCE

Previous studies have suggested that short-term whole-body vibration (WBV) training produces neuromuscular improvement similar to that of power and strength training. However, it is yet to be determined whether short-term WBV exposure produces neurogenic enhancement for power, speed, and agility. The purpose of this study was to investigate the effect short-term WBV training had on vertical jump, sprint, and agility performance in nonelite athletes. Twenty-four sport science students (16 men and 8 women) were randomly assigned to 2 groups: WBV training or control. Each group included 8 men and 4 women. Countermovement jump (CMJ) height, squat jump (SJ) height, sprint speed over 5, 10, and 20 m, and agility (505, up and back) were performed by each participant before and after 9 days of either no training (control) or WBV training. Perceived discomfort of every participant was recorded after daily WBV exposure and nonexposure. There were no significant differences between WBV and control groups for CMJ, SJ, sprints, and agility. Perceived discomfort differed between the first and subsequent days of WBV training (p < 0.05); however, there was no difference between the WBV and control groups. It is concluded that short-term WBV training did not enhance performance in nonelite athletes.
Oral anticoagulants vs aspirin in nonvalvular atrial fibrillation: an individual patient meta-analysis.

CONTEXT Patients with nonvalvular atrial fibrillation (AF) have an increased risk of stroke and other vascular events. OBJECTIVE To compare the risk of vascular and bleeding events in patients with nonvalvular AF treated with vitamin K -inhibiting oral anticoagulants or acetylsalicylic acid (aspirin). DESIGN Pooled analysis of patient-level data from 6 published, randomized clinical trials. PATIENTS A total of 4052 patients with AF randomly assigned to receive therapeutic doses of oral anticoagulant or aspirin with or without low-dose oral anticoagulants. MAIN OUTCOME MEASURES Ischemic and hemorrhagic stroke, other cardiovascular events, all-cause death, and major bleeding events. Person-year incidence rates were calculated to provide crude comparisons. Relative efficacy was assessed using proportional hazards modeling stratified by study. The variation of the oral anticoagulant's relative effect by pertinent patient factors was explored with interaction terms. All analyses were conducted using the intention-to-treat principle. RESULTS Patients receiving oral anticoagulant and aspirin were balanced for important prognostic factors. There was no significant heterogeneity between trials in the relative efficacy of oral anticoagulant vs aspirin for any outcome. Patients receiving oral anticoagulant were significantly less likely to experience any stroke (2.4 vs 4.5 events per 100 patient-years; hazard ratio [HR], 0.55; 95% confidence interval [CI], 0.43-0.71), ischemic stroke (HR, 0.48; 95% CI, 0.37-0.63), or cardiovascular events (HR, 0.71; 95% CI, 0.59-0.85) but were more likely to experience major bleeding (2.2 vs 1.3 events per 100 patient-years; HR, 1.71; 95% CI, 1.21-2.41). The reduction in ischemic stroke risk was similar in patients with paroxysmal AF (1.5 vs 4.7 events per 100 patient-years; HR, 0.32; 95% CI, 0.16-0.61; P<.001). Treating 1000 patients with AF for 1 year with oral anticoagulant rather than aspirin would prevent 23 ischemic strokes while causing 9 additional major bleeds. Overall all-cause survival did not differ but appeared to improve for oral anticoagulant patients 3 years after therapy was started. CONCLUSIONS Compared with aspirin, oral anticoagulant significantly decreases the risk of all strokes, ischemic strokes, and cardiovascular events for patients with nonvalvular chronic or paroxysmal AF but modestly increases the absolute risk of major bleeding. The balance of benefits and risks varies by patient subgroup.