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Planning your mode of supply regarding twin child birth: A new web-based questionnaire.
Electrostatic interactions for the S1-S2 pair as well as the S1-S3 pair were relatively weak. Van der Waal interaction energies between adjacent segments were on average greater than that between diagonally opposite segments. Salt bridge interactions between S4-arginines and the negatively charged residues in other segments appear to contribute more to stabilizing the energy than the van der Waals interactions between nonpolar residues. The overall behavior of residue-residue contacts is similar among the transmembrane domains, reflecting the common inter- transmembrane interaction pattern in the VSD. In addition, analysis of the residue positions suggested that subtle differences in the orientation of the salt-bridges can be attributed to the difference in the inter-transmembrane interaction strengths inside the VSDs.Excitation functions of alpha-particle induced reactions on natNd up to 50 MeV were measured at the RIKEN AVF cyclotron. To derive cross sections activation method, stacked target technique and gamma-ray spectrometry were adopted. Formations of 153,145Sm, 151,150,149,148m,148g,144,143Pm, and 149,147Nd were investigated. The results were compared with the previous experimental data and the TENDL-2019 data. Discrepancies among most of them were found.This study determines the optimum temperature for the alkali fusion process used to effectively separate iodine from solidified radwaste attaining low-level 129I by neutron activation. The alkali fusion temperature was adjusted to 120, 200, and 400 °C to approach the optimum conditions associated with a good statistical distribution of the measured 129I data and high chemical recovery yield. Statistical analysis revealed that the optimum temperature of the alkali fusion process was 200 °C, displaying good central tendency and low variance of the measured 129I data, and the respective chemical recovery yields were higher than other temperatures. The optimum fusion condition provides more reliable scaling factors (129I/137Cs) of radwaste.
Secondary CNS involvement by systemic lymphomas (SCNSL) is uncommon, but when it occurs, is usually due to diffuse large B cell lymphoma (DLBCL). Three recent unusual cases serve to highlight diagnostic challenges.

To report SCNSL from DLBCL and two unusual lymphoma types follicular lymphoma with high-grade transformation to DLBCL and NK/T cell lymphoma, nasal type (ENKL), nasal type.

SCNSL in the DLBCL case occurred at 7-year interval from primary in a 54-year-old woman who presented with stroke-like symptoms and a right postcentral gyrus 2.6×2.9×2.6cm. mass. The follicular lymphoma occurred at 6-month interval in a 69-year-old woman with 1month of diplopia and 2weeks of cognitive decline; multifocal lesions involved temporal lobe, subependymal periventricular areas, brainstem, cerebellum, hypothalamus, corpus callosum and gyrus rectus. The ENKL occurred at 25-month interval from nasal biopsy in a 45-year-old man with 1week of altered mental status; multifocal cerebral and brainstem lesions were identified. Histological features in cases 1 and 3 were identical to the primary lymphoma, with high-grade transformation to DLBCL in the follicular lymphoma.

Unusual features in our series include longer interval from primary to relapse in case 1 with DLBCL (usually <2years of diagnosis), and SCNSL occurring from either follicular lymphoma or EKNL, nasal type (<6% of cases). Pathologists play an important role in excluding infectious, especially in cases with parenchymal lesions and characterizing the lymphoma type in SCNSL.
Unusual features in our series include longer interval from primary to relapse in case 1 with DLBCL (usually less then 2 years of diagnosis), and SCNSL occurring from either follicular lymphoma or EKNL, nasal type ( less then 6% of cases). Pathologists play an important role in excluding infectious, especially in cases with parenchymal lesions and characterizing the lymphoma type in SCNSL.
The diagnosis of combined hepatocellular-cholangiocarcinoma (cHCC-CCA) requires histomorphological detection of both hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (iCCA). However, these primary liver cancers (PLCs) have a wide variety of microscopic appearances resulting in difficulties and uncertainties in cHCC-CCA's diagnosis. This study aims to perform a clinicopathologic analysis on the diagnosis of PLCs at a tertiary referral hospital in Thailand using traditional morphologic studies.

A 5-year retrospective analysis of pathologically diagnosed PLCs was conducted. Pathological features and clinical characteristics of cHCC-CCA and other PLCs with the histopathologic resemblance to cHCC-CCA were studied. The pathological diagnosis was rendered based on histomorphological context rather than immunoreactivity. A literature review containing diagnostic pitfalls of cHCC-CCA was carried out.

PLCs from a total of 295 patients were retrieved, and cHCC-CCA accounted for 1.4% (n=4) of the should never be diagnosed as cHCC-CCA.
Cellular growth arrest, associated with 'senescence', helps to safeguard against the accumulation of DNA damage which is often recognized as the underlying mechanism of a wide variety of age-related pathologies including cancer. Cellular senescence has also been described as a 'double-edged sword'. In cancer, for example, the creation of an immune-suppressive milieu by senescent tumor cells through the senescence-associated secretory phenotype contributes toward carcinogenesis and cancer progression.

The potential for cellular senescence to confer multi-faceted effects on tissue fate has led to a rejuvenated interest in its landscape and targeting. Interestingly, redox pathways have been described as both triggers and propagators of cellular senescence, leading to intricate cross-links between both pathways.

In this review, we describe the mechanisms driving cellular senescence, the interface with cellular redox metabolism as well as the role that chemotherapy-induced senescence plays in secondary carcinogenesis. learn more Notably, the role that anti-apoptotic proteins of the Bcl-2 family play in inducing drug resistance via mechanisms that involve senescence induction.

Though the therapeutic targeting of senescent cells as cancer therapy remains in its infancy, we summarize the current development of senotherapeutics, including recognized senotherapies, as well as the repurposing of drugs as senomorphic/senolytic candidates.
Though the therapeutic targeting of senescent cells as cancer therapy remains in its infancy, we summarize the current development of senotherapeutics, including recognized senotherapies, as well as the repurposing of drugs as senomorphic/senolytic candidates.Parkinson's Disease (PD) is a neurodegenerative disorder affecting more than 10 million people worldwide. Currently, PD has no cure and no early diagnostics methods exist. Mitochondrial dysfunction is presented in the early stages of PD, and it is considered an important pathophysiology component. We have previously developed mitochondria-targeted hydroxycinnamic acid derivatives, presenting antioxidant and iron-chelating properties, and preventing oxidative stress in several biological models of disease. We have also demonstrated that skin fibroblasts from male sporadic PD patients (sPD) presented cellular and mitochondrial alterations, including increased oxidative stress, hyperpolarized and elongated mitochondria and decreased respiration and ATP levels. We also showed that forcing mitochondrial oxidative phosphorylation (OXPHOS) in sPD fibroblasts uncovers metabolic defects that were otherwise hidden. In this work, we tested the hypothesis that a lead mitochondria-targeted hydroxycinnamic acid derivative ts based on a polyphenol scaffold can be used as potential drug candidates for delaying PD progression, validating the use of fibroblasts from sPD patients with more active OXPHOS as platforms for mitochondria-based drug development.Potassium channels are important regulators of cellular homeostasis and targeting these proteins pharmacologically is unveiling important mechanisms in cancer cell biology. Here we demonstrate that pharmacological stimulation of the Kv11.1 potassium channel activity results in mitochondrial reactive oxygen species (ROS) production and fragmentation in breast cancer cell lines and patient-derived organoids independent of breast cancer subtype. mRNA expression profiling revealed that Kv11.1 activity significantly altered expression of genes controlling the production of ROS and endoplasmic-reticulum (ER) stress. Characterization of the transcriptional signature of breast cancer cells treated with Kv11.1 potassium channel activators strikingly revealed an adaptive response to the potentially lethal augmentation of ROS by increasing Nrf2-dependent transcription of antioxidant genes. Nrf2 in this context was shown to promote survival in breast cancer, whereas knockdown of Nrf2 lead to Kv11.1-induced cell death. In conclusion, we found that the Kv11.1 channel activity promotes oxidative stress in breast cancer cells and that suppression of the Nrf2-mediated anti-oxidant survival mechanism strongly sensitized breast cancer cells to a lethal effect of pharmacological activation of Kv11.1.Sirtuin 1 (SIRT1) has been described to modify immune responses by modulation of gene transcription. As transcriptional reprogramming is the molecular substrate of trained immunity, a de facto innate immune memory, we investigated the role of SIRT1 in the induction of trained immunity. We identified various SIRT1 genetic single nucleotide polymorphisms affecting innate and adaptive cytokine production of human peripheral blood mononuclear cells (PBMCs) in response to various stimuli on the one hand, and in vitro induction of trained immunity on the other hand. Furthermore, inhibition of SIRT1 upregulated pro-inflammatory innate cytokine production upon stimulation of PBMCs. However, inhibition of SIRT1 in vitro had no effect on cytokine responses upon induction of trained immunity, while activation of SIRT1 mildly modified trained immunity responses. In conclusion, SIRT1 modifies innate cytokine production by PBMCs in response to various microbes, but has only a secondary role for BCG and β-glucan-induced trained immunity responses.
We aimed to investigate the association between cerebral arteriosclerosis stenosis (CAS) and the short-term prognosis of non-valvular atrial fibrillation (NVAF) related cardioembolic stroke treated by reperfusion therapy.

The data of 195 consecutive NVAF related cardioembolic stroke patients were retrospectively collected. We defined poor functional outcome as a modified Rankin scale (mRS) score of >2 at 90 days.

Patients with CAS were more likely to be older (75.5±6.8 vs. 72.5±9.2 years, p=0.001), more current smokers (35.6% vs. 24.1%, p=0.018), with hypertension (88.1% vs. 65.6%, p<0.001), diabetes mellitus (50.0% vs. 20.0%, p=0.020), dyslipidemia (33.9% vs. 23.6%, p=0.029), previous history of stroke (30.5% vs. 19.5%, p=0.012), and congestive heart failure (32.2% vs. 22.6%, p=0.041). Patients with CAS had higher National Institutes of Health Stroke Scale (NIHSS) (18 [13, 22] vs. 15 [9, 19], p<0.001), and 90-day mRS scores (5 [3, 6] vs. 3[2, 5], p<0.001). Multivariate logistic regression analysis showed that CAS (odds ratio [OR] 3.
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