Dynein-dependent collection of membranes defines the architecture and position of microtubule asters in isolated, geometrically confined volumes of cell-free extracts.

It is well established that changes in the underlying architecture of the cell's microtubule (MT) network can affect organelle organization within the cytoplasm, but it remains unclear whether the spatial arrangement of organelles reciprocally influences the MT network. Here we use a combination of cell-free extracts and hydrogel microenclosures to characterize the relationship between membranes and MTs during MT aster centration. We found that initially disperse ER membranes are collected by the aster and compacted near its nucleating center, all while the whole ensemble moves toward the geometric center of its confining enclosure.

Transfer Learning for Sentiment Analysis Using BERT Based Supervised Fine-Tuning.

The growth of the Internet has expanded the amount of data expressed by users across multiple platforms. The availability of these different worldviews and individuals' emotions empowers sentiment analysis. However, sentiment analysis becomes even more challenging due to a scarcity of standardized labeled data in the Bangla NLP domain.

Microtubule-dependent pushing forces contribute to long-distance aster movement and centration in egg extracts.

During interphase of the eukaryotic cell cycle, the microtubule (MT) cytoskeleton serves as both a supportive scaffold for organelles and an arborized system of tracks for intracellular transport. At the onset of mitosis, the position of the astral MT network, specifically its center, determines the eventual location of the spindle apparatus and ultimately the cytokinetic furrow. Positioning of the MT aster often results in its movement to the center of a cell, even in large blastomeres hundreds of microns in diameter.

Effect of Anti-TGF-β Treatment in a Mouse Model of Severe Osteogenesis Imperfecta.

Osteogenesis imperfecta (OI) is a heritable bone fragility disorder that is usually caused by mutations affecting collagen type I encoding genes. Recent studies in mouse models of recessive OI, Crtap mice, and dominant OI, +/G610C mice, found that application of a transforming growth factor beta (TGF-β) neutralizing antibody 1D11 rescues the bone phenotype. In the present study, we investigated TGF-β signaling in a mouse model of severe dominant OI with a high incidence of spontaneous fractures, Col1a1 mice, and the effect of TGF-β neutralizing antibody 1D11 on bone phenotype in 8-week-old mice.

Bacterial etiology of bloodstream infections and antimicrobial resistance in Dhaka, Bangladesh, 2005-2014.

Background: Bloodstream infections due to bacterial pathogens are a major cause of morbidity and mortality in Bangladesh and other developing countries. In these countries, most patients are treated empirically based on their clinical symptoms. Therefore, up to date etiological data for major pathogens causing bloodstream infections may play a positive role in better healthcare management.

The use of Quantiferon-TB gold in-tube test in screening latent tuberculosis among Saudi Arabia dialysis patients.

Background And Aim: Screening for tuberculosis (TB) is a key strategy for controlling infection. This study aimed to detect latent TB among dialysis patients.

Methods: This is a prospective study conducted in King Saud University, Riyadh involving hemodialysis (HD) and peritoneal dialysis (PD) patients aged ≥18 years.

Behavioral signs of pain and functional impairment in a mouse model of osteogenesis imperfecta.

Osteogenesis imperfecta (OI) is a congenital disorder caused most often by dominant mutations in the COL1A1 or COL1A2 genes that encode the alpha chains of type I collagen. Severe forms of OI are associated with skeletal deformities and frequent fractures. Skeletal pain can occur acutely after fracture, but also arises chronically without preceding fractures.

Effect of sclerostin antibody treatment in a mouse model of severe osteogenesis imperfecta.

Osteogenesis imperfecta (OI) is a heritable bone fragility disorder that is usually caused by mutations affecting collagen type I production in osteoblasts. Stimulation of bone formation through sclerostin antibody treatment (Sost-ab) has shown promising results in mouse models of relatively mild OI. We assessed the effect of once-weekly intravenous Sost-ab injections for 4weeks in male Col1a1(Jrt)/+mice, a model of severe dominant OI, starting either at 4weeks (growing mice) or at 20weeks (adult mice) of age.