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β-Thalassemia has been shown to be associated with adverse short-term perinatal outcomes including low birth weight and preterm labor. The aim of this study was to assess whether in-utero exposure of maternal β-thalassemia minor is a risk factor for offspring hematological morbidity.

A population-based retrospective cohort study was conducted, including all infants born between the years 1991-2014 at a tertiary medical center. Long-term hospitalizations with hematologic morbidities were compared between offspring of mothers with or without β-thalassemia minor. Multiple gestations, perinatal mortality, chromosomal disorders and congenital malformations were excluded. Both study groups were followed until 18years of age for hospitalization with hematological morbidities. Kaplan-Meier survival curve was used to compare the cumulative hematological morbidity incidence between both groups, and a Cox proportional hazard model was used to control for confounders.

During the study period, 243,682 deliveries met the inclusion criteria, of them 0.3% (n=677) were of mothers with β-thalassemia minor. Among offspring to thalassemic versus non-thalassemic mothers, hospitalization rates involving hematological morbidity, were higher (3.3% vs. 0.7%, p<0.001) a finding that was consistent with the Kaplan-Meier survival curve (log rank p<0.001). Using Cox regression model, which adjusted for maternal age, SGA, gestational age and birth weight, maternal β-thalassemia minor was found to be an independent risk factor for long-term offspring hematological (aHR=5.54; 95% CI 3.63-8.44, p<0.001, 5.56; 95% CI 3.65-8.47, p<0.001, and 5.49; 95% CI 3.60-8.36, p<0.001, respectively).

Prenatal maternal β-thalassemia minor is independently associated with offspring long-term hematological morbidity.

Prenatal maternal β-thalassemia minor is independently associated with offspring long-term hematological morbidity.Colonoscopy is the gold standard for pre-cancerous polyps screening and treatment. The polyp detection rate is highly tied to the percentage of surveyed colonic surface. However, current colonoscopy technique cannot guarantee that all the colonic surface is well examined because of incomplete camera orientations and of occlusions. The missing regions can hardly be noticed in a continuous first-person perspective. Therefore, a useful contribution would be an automatic system that can compute missing regions from an endoscopic video in real-time and alert the endoscopists when a large missing region is detected. We present a novel method that reconstructs dense chunks of a 3D colon in real time, leaving the unsurveyed part unreconstructed. The method combines a standard SLAM system with a depth and pose prediction network to achieve much more robust tracking and less drift. It addresses the difficulties for colonoscopic images of existing simultaneous localization and mapping (SLAM) systems and end-to-end deep learning methods.Chest computed tomography (CT) based analysis and diagnosis of the Coronavirus Disease 2019 (COVID-19) plays a key role in combating the outbreak of the pandemic that has rapidly spread worldwide. To date, the disease has infected more than 18 million people with over 690k deaths reported. Reverse transcription polymerase chain reaction (RT-PCR) is the current gold standard for clinical diagnosis but may produce false positives; thus, chest CT based diagnosis is considered more viable. However, accurate screening is challenging due to the difficulty in annotation of infected areas, curation of large datasets, and the slight discrepancies between COVID-19 and other viral pneumonia. In this study, we propose an attention-based end-to-end weakly supervised framework for the rapid diagnosis of COVID-19 and bacterial pneumonia based on multiple instance learning (MIL). We further incorporate unsupervised contrastive learning for improved accuracy with attention applied both in spatial and latent contexts, herein we propose Dual Attention Contrastive based MIL (DA-CMIL). DA-CMIL takes as input several patient CT slices (considered as bag of instances) and outputs a single label. Attention based pooling is applied to implicitly select key slices in the latent space, whereas spatial attention learns slice spatial context for interpretable diagnosis. A contrastive loss is applied at the instance level to encode similarity of features from the same patient against representative pooled patient features. Empirical results show that our algorithm achieves an overall accuracy of 98.6% and an AUC of 98.4%. Moreover, ablation studies show the benefit of contrastive learning with MIL.

This retrospective study investigated the midterm results of medial opening wedge high tibia osteotomy, with a monoplanar or a biplanar osteotomy using two types of implant system.

Osteotomies were performed on 241 knees (231 patients). The mean follow-up period was 6.0years (SD 3.0, range 0.2-12.8years). Two types of implant system were used, a precountered non-locking plate (PP) (n=74) and a precountered locking plate (LP) (n=167). A Kaplan-Meier cumulative survival curve and a Cox regression model were used to analyse and revise survival and risk factors.

Cumulative survival estimates for LP were 80% at 5years, and 64% at 10years (SE=0.4, CI 95% 9.0-10.5), and for PP, they were 68% at 5years and 49% at 10years (SE=0.5, CI 95% 6.3-8.2) (p=0.024). The revision rate was 26% (44/167) for the LP group, and 47% (35/74) for the PP group (p=0.001). Reoperations on LP osteotomies occurred for the tibial monoplanar cut and biplanar cut groups, in 19/52 (37%) and 25/167 (16%) osteotomies, respectively (p=0.04). Our Cox regression model showed that PP had a higher risks (RR=1.7; CI 95% 1.1-2.6) of revision, when compared with LP (p=0.026).

The risk of revision for any reason and that of early conversion to total knee arthroplasty (TKA) after high tibia osteotomy were significantly increased for PP, when compared with LP.

The risk of revision for any reason and that of early conversion to total knee arthroplasty (TKA) after high tibia osteotomy were significantly increased for PP, when compared with LP.Amphibians such as Xenopus tropicalis exhibit a remarkable capacity for tissue regeneration after traumatic injury. see more Although transforming growth factor-β (TGF-β) receptor signaling is known to be essential for tissue regeneration in fish and amphibians, the role of TGF-β ligands in this process is not well understood. Here, we show that inhibition of TGF-β1 function prevents tail regeneration in Xenopus tropicalis tadpoles. We found that expression of tgfb1 is present before tail amputation and is sustained throughout the regeneration process. CRISPR-mediated knock-out (KO) of tgfb1 retards tail regeneration; the phenotype of tgfb1 KO tadpoles can be rescued by injection of tgfb1 mRNA. Cell proliferation, a critical event for the success of tissue regeneration, is downregulated in tgfb1 KO tadpoles. In addition, tgfb1 KO reduces the expression of phosphorylated Smad2/3 (pSmad2/3) which is important for TGF-β signal-mediated cell proliferation. Collectively, our results show that TGF-β1 regulates cell proliferation through the activation of Smad2/3. We therefore propose that TGF-β1 plays a critical role in TGF-β receptor-dependent tadpole tail regeneration in Xenopus.GTP-bound forms of Ras proteins (Ras•GTP) assume two interconverting conformations, "inactive" state 1 and "active" state 2. Our previous study on the crystal structure of the state 1 conformation of H-Ras in complex with guanosine 5'-(β, γ-imido)triphosphate (GppNHp) indicated that state 1 is stabilized by intramolecular hydrogen-bonding interactions formed by Gln61. Since Ras are constitutively activated by substitution mutations of Gln61, here we determine crystal structures of the state 1 conformation of H-Ras•GppNHp carrying representative mutations Q61L and Q61H to observe the effect of the mutations. The results show that these mutations alter the mode of hydrogen-bonding interactions of the residue 61 with Switch II residues and induce conformational destabilization of the neighboring regions. In particular, Q61L mutation results in acquirement of state 2-like structural features. Moreover, the mutations are likely to impair an intramolecular structural communication between Switch I and Switch II. Molecular dynamics simulations starting from these structures support the above observations. These findings may give a new insight into the molecular mechanism underlying the aberrant activation of the Gln61 mutants.

The Epworth Sleepiness Scale (ESS) is the most common instrument for measuring subjective sleep propensity in people with epilepsy but has not yet been validated in this population.

We aimed to systematically assess the validity, performance, and internal consistency of the ESS, as well as correlations between the ESS and disease-specific variables and patient-reported outcome measures in a cohort of adults with epilepsy (AWE).

Ninety-five AWE completed sleep and seizure diaries, in-laboratory polysomnography (PSG) and patient-reported outcome measures, including the ESS, Insomnia Severity Index (ISI), and the Beck Depression Inventory (BDI). Demographic information and data from 95 matched controls referred for PSG for suspected obstructive sleep apnea (OSA) was taken from the electronic medical record. Frequencies of high ESS item ratings (item score ≥2) were calculated for each group. Cronbach's α and factor analysis were performed to assess the internal consistency and validity of the ESS within casssociated with greater insomnia scores on the ISI (p = 0.024) and depressive symptoms on the BDI (p = 0.018).

This study provides validity for the use of the ESS in adult populations with epilepsy.

This study provides validity for the use of the ESS in adult populations with epilepsy.

To explore the role of several genetic polymorphisms (APOE ε4, BDNF Met, and COMT Val) in executive functioning performance in patients with pharmacoresistant temporal lobe epilepsy (TLE).

Ninety-three adults (51 female, mean age = 39 years) with TLE completed executive functioning measures as part of a comprehensive preoperative neuropsychological evaluation, including Trail Making Test (Part B), Wisconsin Card Sorting Test (Conceptual Level Responses and Perseverative Errors), Color Word Interference from the Delis Kaplan Executive Function System, and measures of phonemic and semantic verbal fluency. Genotyping of the APOE, BDNF, and COMT genes was conducted using DNA extracted from peripheral blood or brain tissue (from epilepsy surgery).

After adjustment for general cognitive ability, COMT Val carriers showed poorer performance on semantic verbal fluency and color word interference than non-carriers, and BDNF Met carriers showed poorer performance on phonemic verbal fluency than those without a Met allele.

Results suggest that COMT and BDNF polymorphisms are associated with performance on several EF measures in patients with TLE, including tasks assessing verbal fluency and response inhibition and account for up to 16% of the variance in test performance. The APOE polymorphism was not significantly associated with any of the executive function measures analyzed.

Results suggest that COMT and BDNF polymorphisms are associated with performance on several EF measures in patients with TLE, including tasks assessing verbal fluency and response inhibition and account for up to 16% of the variance in test performance. The APOE polymorphism was not significantly associated with any of the executive function measures analyzed.

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