Miracle-dz/UniFAR-FTUs huggingface dataset:
Intraoperative Rise of Surface Temperature Monitors Success of Sympathectomy in Palmoaxillary Hyperhidrosis

Objectives: Patients with hyperhidrosis suffer from an extreme perspiration that cannot be aligned with natural or situational standards. Endoscopic sympathectomy is a meaningful option for palmar and axillary hyperhidrosis. A standardized method of monitoring the immediate intraoperative success has not been established yet. The presented investigation shows one proposed sollution by monitoring skin surface temperature. The main aspect is to demonstrate a significant rise in temperature with utility for monitoring the immediate success of surgery. Methods: Twenty patients with primary hyperhidrosis were observed and treated in a standardized setting against a control group (n = 10). We obtained diverse data that permit determination of a point of time of measurement of surface temperature and definition of a degree of temperature variance. Results: After 5 minutes a significant change of 0.5? Celcius was noted on the palms; after 10 minutes on average 1.2? Celcius. Axillary temperature had significantly changed after 10 minutes with a mean temperature variation of 0.8? Celcius on the right side and 0.6? Celcius on the left side. Conclusions: Under consideration of appropriate time intervals of measurement and determined changes in surface temperature an early control of correct clip application in ETS is possible. In the palmar aspect an increase of 0.5? Celcius at an 5 minutes interval, and more than 1? Celcius at 10 minutes after placement of the clip as compared to basic values before application of the clip can be proposed.
β2-Adrenergic Receptor Polymorphisms Affect Airway Responsiveness to Salbutamol in Asthmatics

We examined the β-adrenergic receptor (β2AR) polymorphisms (Arg16 → Gly, Gln27 → Glu) and clinical status for 117 asthmatics. Airway responsiveness to methacholine and β2-agonists was evaluated with Astograph®. The atopic factors, pulmonary function test, and airway responsiveness to methacholine did not differ significantly among the different β2AR genotypes. Asthmatics homozygous for Glyl 6 showed significantly lower airway responsiveness to inhaled salbutamol than those heterozygous for Arg/Gly16 or homozygous for Arg16. Asthmatics heterozygous for Gln/Glu27 had significantly later asthma onsets than those homozygous for Gln27. These results suggest that β2AR polymorphisms play an important role in the airway responsiveness to inhaled β2- agonist and the initial asthma onset.
Synchronous Change of Atmospheric CO2 and Antarctic Temperature During the Last Deglacial Warming

No Leader to Follow Changes in the concentration of atmospheric CO2 and surface air temperature are closely related. However, temperature can influence atmospheric CO2 as well as be influenced by it. Studies of polar ice cores have concluded that temperature increases during periods of rapid warming have preceded increases in CO2 by hundreds of years. Parrenin et al. (p. 1060; see the Perspective by Brook) present a revised age scale for the atmospheric component of Antarctic ice cores, based on the isotopic composition of the N2 that they contain, and suggest that temperature and CO2 changed synchronously over four intervals of rapid warming during the last deglaciation. Rising air temperature did not lead the increase of atmospheric carbon dioxide concentration during the last deglaciation. [Also see Perspective by Brook] Understanding the role of atmospheric CO2 during past climate changes requires clear knowledge of how it varies in time relative to temperature. Antarctic ice cores preserve highly resolved records of atmospheric CO2 and Antarctic temperature for the past 800,000 years. Here we propose a revised relative age scale for the concentration of atmospheric CO2 and Antarctic temperature for the last deglacial warming, using data from five Antarctic ice cores. We infer the phasing between CO2 concentration and Antarctic temperature at four times when their trends change abruptly. We find no significant asynchrony between them, indicating that Antarctic temperature did not begin to rise hundreds of years before the concentration of atmospheric CO2, as has been suggested by earlier studies.
Traffic-related air pollution and pregnancy outcomes in the Dutch ABCD birth cohort study

Objectives There is growing evidence for an adverse effect of maternal exposure to air pollution on pregnancy outcomes. As European data on this topic are limited, the aim of this study was to evaluate the impact of maternal exposure to traffic-related air pollution during different periods of pregnancy on preterm birth and fetal growth. Methods We estimated maternal residential exposure to NO2 during pregnancy (entire pregnancy and trimesters) for 7600 singleton births participating in the Amsterdam Born Children and their Development (ABCD) prospective birth cohort study by means of a temporally adjusted land-use regression model. Associations between air pollution concentrations and preterm birth and fetal growth (expressed as small for gestational age and term birth weight) were analysed by means of logistic and linear regression models with and without adjustment for maternal physiological, lifestyle and sociodemographic characteristics. Results There was no indication of an increase in preterm birth among highly exposed women. Children of mothers with NO2 levels in the highest exposure category on average had the highest term birth weight of all children and were among those with the lowest risk of being small for gestational age with little indication of a dose–response relationship. Conclusions In this study, there is no evidence for a harmful effect of estimated maternal exposure to traffic-related air pollution during pregnancy on pregnancy outcomes such as preterm birth, small for gestational age and term birth weight.
Comparison of Sensitivities of Two Commercial Gamma Interferon Release Assays for Pulmonary Tuberculosis

ABSTRACT There are few head-to-head comparisons of the commercial gamma interferon release assays (GIRAs). We compared the performance of the T-SPOT.TB and QuantiFERON-TB Gold In-Tube (QFT-IT) assays in patients with culture-proven pulmonary tuberculosis. Blood was drawn for both assays within 14 days of starting antituberculosis treatment. The QFT-IT indeterminate rate was 3.5%; the T-SPOT.TB failure rate was 1.4%. There was poor agreement between the GIRAs (κ = 0.257) among the 270 patients with valid results for both tests. The sensitivities of the T-SPOT.TB and QFT-IT assays were 94.1 and 83.0%, respectively, with a significant difference in the performance of the assays (P = 0.001 [McNemar test]). Factors independently associated with indeterminate QFT-IT results were an age of ≥60 years (odds ratio [OR] 11.18, 95% confidence interval [CI] = 1.841 to 67.823, P = 0.009), female sex (OR = 7.47, 95% CI = 1.517 to 36.733, P = 0.013) and non-Chinese (i.e., Indian or Malay) race (OR = 7.89, 95% CI = 1.585 to 39.267, P = 0.012). The QFT-IT assay was significantly less sensitive in patients ≥60 years old (OR = 0.41, 95% CI = 0.181 to 0.918, P = 0.030) and in Indian compared to Chinese patients (OR = 0.27, 95% CI = 0.073 to 0.990, P = 0.048). The T-SPOT.TB assay was significantly less sensitive in Malay (OR = 0.23, 95% CI = 0.063 to 0.815, P = 0.023) and Indian patients (OR = 0.09, 95% CI = 0.017 to 0.429, P = 0.003) compared to Chinese patients. The performance of both assays was not significantly altered in diabetics. The diminished sensitivity of the GIRAs in persons of Malay and Indian race merits further study.
Exogenous Estrogen Does Not Attenuate the Association Between Rofecoxib and Myocardial Infarction in Perimenopausal Women

Rofecoxib has been proposed to increase the risk of myocardial infarction (MI) through suppression of cyclooxygenase 2-mediated prostacyclin. Estrogen may have protective effects through augmenting cyclooxygenase 2 expression and subsequently increasing prostacyclin. Estrogen may attenuate the association between rofecoxib and MI. We used 1999-2002 Medicaid claims data to measure the MI hazard ratio (HR) attributed to rofecoxib exposure in estrogen-exposed and unexposed 45- to 65-year-old women. We identified 184,169 female rofecoxib users who contributed 309,504 person-years and experienced 1217 first MIs. Estrogen exposure seemed protective [MI-HR 0.72; 95% confidence interval (CI), 0.62-0.84] in this cohort. Rofecoxib was associated with an elevated MI-HR in both estrogen-exposed (2.01; 95% CI, 1.60-2.54) and estrogen-unexposed women (1.69; 95% CI, 1.43-1.99). The rofecoxib-estrogen interaction ratio was not significantly different from 1 (1.19; 95% CI, 0.91-1.57). Although estrogen use was associated with a lower risk of MI, it did not seem to attenuate the association between rofecoxib and MI.
Sudden Death of Cardiac Origin and Psychotropic Drugs

Mortality rate is high in psychiatric patients versus general population. An important cause of this increased mortality is sudden cardiac death (SCD) as a major side-effect of psychotropic drugs. These SCDs generally result from arrhythmias occurring when the posology is high and may attain a toxic threshold but also at dosages within therapeutic range, in the presence of risk factors. There are three kinds of risk factors: physiological (e.g., low cardiac rate of sportsmen), physiopathological (e.g., hepatic insufficiency, hypothyroidism) and “therapeutic” (due to interactions between psychotropic drugs and other medicines). Association of pharmacological agents may increase the likelihood of SCDs either by (i) a pharmacokinetic mechanism (e.g., increased torsadogenic potential of a psychotropic drug when its destruction and/or elimination are compromised) or (ii) a pharmacodynamical mechanism (e.g., mutual potentiation of proarrhythmic properties of two drugs). In addition, some psychotropic drugs may induce sudden death in cases of pre-existing congenital cardiopathies such as (i) congenital long QT syndrome, predisposing to torsade de pointes that eventually cause syncope and sudden death. (ii) A Brugada syndrome, that may directly cause ventricular fibrillation due to reduced sodium current through Nav1.5 channels. Moreover, psychotropic drugs may be a direct cause of cardiac lesions also leading to SCD. This is the case, for example, of phenothiazines responsible for ischemic coronaropathies and of clozapine that is involved in the occurrence of myocarditis. The aims of this work are to delineate: (i) the risk of SCD related to the use of psychotropic drugs; (ii) mechanisms involved in the occurrence of such SCD; (iii) preventive actions of psychotropic drugs side effects, on the basis of the knowledge of patient-specific risk factors, documented from clinical history, ionic balance, and ECG investigation by the psychiatrist.
Molecular Characterization of an Arabidopsis Gene Encoding a Phospholipid-Specific Inositol Polyphosphate 5-Phosphatase1[w]

Phosphoinositides are important molecules that serve as second messengers and bind to a complex array of proteins modulating their subcellular location and activity. The enzymes that metabolize phosphoinositides can in some cases serve to terminate the signaling actions of phosphoinositides. The inositol polyphosphate 5-phosphatases (5PTases) comprise a large protein family that hydrolyzes 5-phosphates from a variety of inositol phosphate and phosphoinositide substrates. We previously reported the identification of 15 putative 5PTase genes in Arabidopsis and have shown that overexpression of the At5PTase1 gene can alter abscisic acid signaling. At5PTase1 and At5PTase2 have been shown to hydrolyze the 5-phosphate from inositol phosphate substrates. We have examined the substrate specificity of the At5PTase11 protein, which is one of the smallest predicted 5PTases found in any organism. We report here that the At5PTase11 gene encodes an active 5PTase enzyme that can only dephosphorylate phosphoinositide substrates containing a 5-phosphate. In addition to hydrolyzing known substrates of 5PTase enzymes, At5PTase11 also hydrolyzes the 5-phosphate from phosphatidylinositol (3,5) bisphosphate. We also show that the At5PTase11 gene is regulated by abscisic acid, jasmonic acid, and auxin, suggesting a role for phosphoinositide action in these signal transduction pathways.
Assembly of the MreB‐associated cytoskeletal ring of Escherichia coli

The Escherichia coli actin homologue MreB is part of a helical cytoskeletal structure that winds around the cell between the two poles. It has been shown that MreB redistributes during the cell cycle to form circumferential ring structures that flank the cytokinetic FtsZ ring and appear to be associated with division and segregation of the helical cytoskeleton. We show here that the MreB cytoskeletal ring also contains the MreC, MreD, Pbp2 and RodA proteins. Assembly of MreB, MreC, MreD and Pbp2 into the ring structure required the FtsZ ring but no other known components of the cell division machinery, whereas assembly of RodA into the cytoskeletal ring required one or more additional septasomal components. Strikingly, MreB, MreC, MreD and RodA were each able to independently assemble into the cytoskeletal ring and coiled cytoskeletal structures in the absence of any of the other ring components. This excludes the possibility that one or more of these proteins acts as a scaffold for incorporation of the other proteins into these structures. In contrast, incorporation of Pbp2 required the presence of MreC, which may provide a docking site for Pbp2 entry.
Relapse of childhood acute lymphoblastic leukemia and outcomes at a reference center in Latin America: organomegaly at diagnosis is a significant clinical predictor

ABSTRACT Objective: Relapse is the major cause of treatment failure in acute lymphoblastic leukemia (ALL) of childhood; it is more frequent among high-risk patients from low-middle income than from high-income countries. The frequency, sites and outcome of relapsed ALL in children of northeast Mexico over a decade was documented. Methods: A retrospective analysis of 246 children belonging to a low-income group <16 years with de novo ALL during 2004–2015 was performed. Five-year overall survival (OS) and event-free survival was estimated by Kaplan–Meier analysis. Data on time, site, response to therapy and final outcome of relapse were analyzed. Hazard ratios (HRs) of relapse and death were estimated by the Cox regression model. Very early relapse was defined as that occurring in <18 months, early relapse between 18 and 36 months, and late relapse >36 months from diagnosis, respectively. Results: Eighty-seven (35.4%) children relapsed. Five-year OS was 82.6% in children without relapse vs. 42% for relapsed patients. Bone marrow (BM) was the most frequent site of relapse (51.72%). Isolated central nervous system (CNS) relapses occurred in 29.9%. Five-year OS was 11.2% for BM and 15.5% for early relapse. HR of relapse for organomegaly was 3.683, 2.247 for an initial white blood cell count >50 000 × 109/l and 1.169 for positive minimal residual disease status. Conclusion: A high rate of very early, CNS, and BM relapse with a considerably low 5-year OS requiring reassessment of therapy was documented. Organomegaly at diagnosis was a highly significant clinical predictor for relapse.
Identification of a common helper provirus integration site in Abelson murine leukemia virus-induced lymphoma DNA

Abelson murine leukemia virus induces oligoclonal pre-B lymphoma in mice. The expression of the v-abl oncogene in target cells does not appear to be sufficient for tumor induction in several mouse strains, and additional genetic events are thought to be required. We postulated that the helper Moloney murine leukemia virus might induce these events, and its potential role as an insertional mutagen was assessed by the search of a common helper provirus integration site in Abelson murine leukemia virus lymphomas. Molecular cloning of cellular sequences adjacent to Moloney proviruses enabled us to identify a cellular region, designated Ahi-1, which was found occupied by the helper proviruses in 16% of Abelson pre-B-cell lymphomas. All proviruses for which the precise integration site within Ahi-1 could be mapped were found to be in the same orientation. Ahi-1 has been mapped to mouse chromosome 10 and represents a new common proviral integration site. These data suggest that the helper virus contributes to the induction of secondary genetic events which may be important for the development of Abelson murine leukemia virus-induced pre-B-cell lymphoma.
Detection of complement C3 and factor B gene expression in normal colorectal mucosa, adenomas and carcinomas

Local secretion of complement components in the human intestine has been previously reported. However, the cellular source has not been identified. In this study, we demonstrate complement C3 and factor B mRNA expression in the normal colonic mucosa by in situ hybridization analysis. C3 and factor B genes were found to be expressed at high levels in the epithelial cells of the lower parts of the crypts in colonic mucosa, and this expression decreased gradually from the crypt base to the luminal surface. At the upper crypt and the luminal surface, these genes almost disappeared. C3 and factor B genes were expressed in all crypts at the same level. Furthermore, C3 and factor B gene expression was also identified in adenomas and carcinomas. In these neoplastic tissues, C3 and factor B genes were expressed uniformly, and the polarized distribution observed in the normal crypts was not detected. It is likely that complement components are locally synthesized in the intestine, and that these complement components may actively participate in normal immune and inflammatory responses over the enormous surface area of the intestinal mucosa.
Increased cardiac output contributes to the development of chronic intermittent hypoxia‐induced hypertension

What is the central question of this study? Chronic intermittent hypoxia (CIH)‐induced hypertension is commonly believed to be a consequence of sympathetic nervous system hyperactivity, but direct recordings of chronic vasoconstriction have never been performed hitherto. We determined whether chronic vasoconstriction contributes to the development of hypertension in CIH‐exposed animals. What is the main finding and its importance? We found no evidence of chronic vasoconstriction in CIH‐exposed rats; instead, the development of hypertension was due to an increase in cardiac output. This attempt to increase O2 flow may lead to the initial development of hypertension. Increased in cardiac output has never been previously reported and could be an important parameter to measure in sleep apnoea patients.
MEG dual scanning: a procedure to study real-time auditory interaction between two persons

Social interactions fill our everyday life and put strong demands on our brain function. However, the possibilities for studying the brain basis of social interaction are still technically limited, and even modern brain imaging studies of social cognition typically monitor just one participant at a time. We present here a method to connect and synchronize two faraway neuromagnetometers. With this method, two participants at two separate sites can interact with each other through a stable real-time audio connection with minimal delay and jitter. The magnetoencephalographic (MEG) and audio recordings of both laboratories are accurately synchronized for joint offline analysis. The concept can be extended to connecting multiple MEG devices around the world. As a proof of concept of the MEG-to-MEG link, we report the results of time-sensitive recordings of cortical evoked responses to sounds delivered at laboratories separated by 5 km.
Macronutrient Intake and Cancer: How Does Dietary Restriction Influence Tumor Growth and Why Should We Care?

This perspective on the report by Rogozina and colleagues (beginning on page 712 in this issue of the journal) reviews mechanisms that may underlie inhibitory effects of dietary restriction on tumor growth in the mouse mammary tumor virus transforming growth factor alpha (MMTV-TGF-alpha) breast cancer model and comments on the potential clinical relevance of these mechanisms. The inhibitory effect of caloric restriction on carcinogenesis and tumor growth in rodent models is a classic finding that is receiving increasing attention. In some experimental models, the magnitude of the effect is significant, rivaling what can be achieved by pharmacologic approaches to cancer prevention or treatment. Major challenges include defining the underlying mechanisms and determining the clinical relevance of laboratory models of caloric restriction.
Changes in Leydig Cell Gene Expression During Development in the Mouse1

Abstract Developmental changes in the expression of 18 Leydig cell-specific mRNA species were measured by real-time polymerase chain reaction to partially characterize the developmental phenotype of the cells in the mouse and to identify markers of adult Leydig cell differentiation. Testicular interstitial webs were isolated from mice between birth and adulthood. Five developmental patterns of gene expression were observed. Group 1 contained mRNA species encoding P450 side chain cleavage (P450scc), P450c17, relaxin-like factor (RLF), glutathione S-transferase 5-5 (GST5-5), StAR protein, LH receptor, and epoxide hydrolase (EH); group 2 contained 3β-hydroxysteroid dehydrogenase (3β-HSD) VI, 17β-hydroxysteroid dehydrogenase (17β-HSD) III, vascular cell adhesion molecule 1, estrogen sulfotransferase, and prostaglandin D (PGD)-synthetase; group 3 contained patched and thrombospondin 2 (TSP2); group 4 contained 5α-reductase 1 and 3α-hydroxysteroid dehydrogenase; group 5 contained sulfonylurea receptor 2 and 3β-HSD I. Group 1 contained genes that were expressed in fetal and adult Leydig cells and which increased in expression around puberty toward a maximum in the adult. Group 2 contained genes expressed only in the adult Leydig cell population. Group 3 contained genes with predominant fetal/neonatal expression in the interstitial tissue. Group 4 contained genes with a peak of expression around puberty, whereas genes in group 5 show little developmental change in expression. Highest mRNA levels in descending order were RLF, P450c17, EH, 17β-HSD III, PGD-synthetase, GST5-5, and P450scc. Results identify five genes expressed in the mouse adult Leydig cell population, but not in the fetal population, and one gene (TSP2) that may be expressed only in the fetal Leydig cell population. The developmental pattern of gene expression suggests that three distinct phases of adult Leydig cell differentiation occur.