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Background and Aims: Testicular atrophy is a common clinical manifestation of NOA, with a rate of 79.1%. The results of sperm retrieval using the mTESE method in a special NOA for testicular atrophy with volume [Formula: see text]5ml are currently inconsistent. As a result, we present the results of sperm retrieval using the mTESE method to patient NOA, who has a bilateral testicular volume [Formula: see text]5ml. Methods: A case series report of NOA with bilateral testicular volume [Formula: see text]5ml that indicated mTESE surgery to collect sperm at the assisted reproductive technology center of Tam Anh Ha Noi General Hospital between January 2022 and December 2022. Results: Four of seven NOA patients (57.1%) had successful sperm retrieval using the mTESE method, with bilateral testicular volume [Formula: see text]5 ml and a mean FSH level of 40,5 ± 21,9 (24,1-87,6) mIU/mL. In which case, 3/4 of patients simply require surgery on the monolateral testicular is sufficient sperm. Conclusions: Testicular atrophy does not appear to impair sperm retrieval results by the mTESE method, even the sperm retrieval rate tends to be higher in NOA patients with bilateral testicular volume [Formula: see text] 5ml.

Graphical AbstractCardiac fibrosis developed from fibrotic remodelling due to hypertension leads to heart failure. Immune cells are abundantly accumulated in fibrotic regions, but exact mechanisms how they contributed to cardiac fibrosis are not clear. Here we demonstrated that CD8 T cells are major contributor to cardiac fibrosis in hypertensive hearts. Stressed cardiomyocytes express STING-dependent RAE-1 that activates NKG2D + CD8 T cells to induce apoptosis of stressed cardiomyocytes. Preventing STING signalling in stressed cardiomyocytes attenuates cardiac fibrosis. Pharmacologically inhibiting cardiomyocayte-RAE-1 and CD8+ T cell-NKG2D axis may be a potential therapeutic strategy to prevent cardiac fibrosis in HFpEF patients.

Interaction between B and CD4 T cells is crucial for their optimal responses in adaptive immunity. Immune responses augmented by their partnership promote chronic inflammation. Here we report that interaction between B and CD4 T cells augments their atherogenicity to promote lipid-induced atherosclerosis. Genetic deletion of the gene encoding immunoglobulin mu (μ) heavy chain (μMT) in ApoE−/− mice resulted in global loss of B cells including those in atherosclerotic plaques, undetectable immunoglobulins and impaired germinal center formation. Despite unaffected numbers in the circulation and peripheral lymph nodes, CD4 T cells were also reduced in spleens as were activated and memory CD4 T cells. In hyperlipidemic μMT−/− ApoE−/− mice, B cell deficiency decreased atherosclerotic lesions, accompanied by absence of immunoglobulins and reduced CD4 T cell accumulation in lesions. Adoptive transfer of B cells deficient in either MHCII or co-stimulatory molecule CD40, molecules required for B and CD4 T cell interaction, into B cell-deficient μMT−/− ApoE−/− mice failed to increase atherosclerosis. In contrast, wildtype B cells transferred into μMT−/− ApoE−/− mice increased atherosclerosis and increased CD4 T cells in lesions including activated and memory CD4 T cells. Transferred B cells also increased their expression of atherogenic cytokines IL-1β, TGF-β, MCP-1, M-CSF, and MIF, with partial restoration of germinal centers and plasma immunoglobulins. Our study demonstrates that interaction between B and CD4 T cells utilizing MHCII and CD40 is essential to augment their function to increase atherosclerosis in hyperlipidemic mice. These findings suggest that targeting B cell and CD4 T cell interaction may be a therapeutic strategy to limit atherosclerosis progression.

The galectin family of secreted lectins are important regulators of immune cell function; however, their role in B cell responses is poorly understood. Here, the authors identify IgM-BCR as a ligand for galectin-9. In resting naive cells, they show that galectin-9 mediates a close association between IgM and CD22.

In this article, a multi-objective optimization of turning process study is presented. Two output parameters of the turning process taken into consideration are surface roughness and Material Removal Rate (MRR). Taguchi method has been applied to design the experimental matrix with four input parameters including nose radius, cutting velocity, feed rate and cutting depth. Copras method has been employed to solve the multi-objective optimization problem. Finally, the optimal values of the input parameters have been determined to simultaneously ensure the two criteria of the minimum surface roughness and the maximum MRR.

Background Peritoneal B1a cells attenuate atherosclerosis by secreting natural polyclonal immunoglobulin M (IgM). Regulatory B cells expressing T‐cell immunoglobulin mucin domain‐1 (TIM‐1) expanded through TIM‐1 ligation by anti‐TIM‐1 monoclonal antibody (RMT1‐10) induces immune tolerance. Methods and Results We examined the capacity of RMT1‐10 to expand peritoneal B1a cells to prevent atherosclerosis development and retard progression of established atherosclerosis. RMT1‐10 treatment selectively doubled peritoneal B1a cells, tripled TIM‐1+ B1a cells and increased TIM‐1+IgM+interleukin (IL)‐10+ by 3‐fold and TIM‐1+IgM+IL‐10− B1a cells by 2.5‐fold. Similar expansion of B1a B cells was observed in spleens. These effects reduced atherosclerotic lesion size, increased plasma IgM and lesion IgM deposits, and decreased oxidatively modified low‐density lipoproteins in lesions. Lesion CD4+ and CD8+ T cells, macrophages and monocyte chemoattractant protein‐1, vascular cell adhesion molecule‐1, expression of proinflammatory cytokines monocyte chemoattractant protein‐1, vascular cell adhesion molecule‐1, IL1β, apoptotic cell numbers and necrotic cores were also reduced. RMT1‐10 treatment failed to expand peritoneal B1a cells and reduce atherosclerosis after splenectomy that reduces B1a cells, indicating that these effects are B1a cell‐dependent. Apolipoprotein E‐KO mice fed a high‐fat diet for 6 weeks before treatment with RMT1‐10 also increased TIM‐1+IgM+IL‐10+ and TIM‐1+IgM+IL‐10− B1a cells and IgM levels and attenuated progression of established atherosclerosis. Conclusions RMT1‐10 treatment attenuates atherosclerosis development and progression by selectively expanding IgM producing atheroprotective B1a cells. Antibody‐based in vivo expansion of B1a cells could be an attractive approach for treating atherosclerosis.

BackgroundWe previously identified peritoneal B1a cells that secrete natural IgM as a key atheroprotective B cell subset. However, the molecules that activate atheroprotective B1a cells are unknown. Here, we investigated whether Toll‐like receptors (TLRs) TLR2, TLR4, and TLR9 expressed by B1a cells are required for IgM‐mediated atheroprotection. Methods and ResultsWe adoptively transferred B1a cells from wild‐type mice or from mice deficient in TLR2, TLR4, TLR9, or myeloid differentiation primary response 88 (MyD88) into ApoE−/− mice depleted of peritoneal B1a cells by splenectomy and fed a high‐fat diet for 8 weeks. Elevations in plasma total, anti‐oxLDL (oxidized low‐density lipoprotein), anti‐leukocyte, anti‐CD3, anti‐CD8, and anti‐CD4 IgMs in atherosclerotic mice required B1a cells expressing TLR4 and MyD88, indicating a critical role for TLR4‐MyD88 signaling for IgM secretion. Suppression of atherosclerosis was also critically dependent on B1a cells expressing TLR4‐MyD88. Atherosclerosis suppression was associated not only with reductions in lesion apoptotic cells, necrotic cores, and oxLDL, but also with reduced lesion CD4+ and CD8+ T cells. Transforming growth factor beta 1 (TGF‐β1) expression, including macrophages expressing TGF‐β1, was increased, consistent with increased IgM‐mediated phagocytosis of apoptotic cells by macrophages. Reductions in lesion inflammatory cytokines tumor necrosis factor alpha (TNF‐α), interleukin (IL) 1β, and IL‐18 were consistent with augmented TGF‐β1 expression. ConclusionsTLR4‐MyD88 expression on B1a cells is critical for their IgM‐dependent atheroprotection that not only reduced lesion apoptotic cells and necrotic cores, but also decreased CD4 and CD8 T‐cell infiltrates and augmented TGF‐β1 expression accompanied by reduced lesion inflammatory cytokines TNF‐α, IL‐1β, and IL‐18.

Radix bupleuri is traditionally used in Vietnam for its hepatoprotective activity. The herb was mainly imported from China, until it was recently introduced Vietnam. The plant is found mainly in the Northern region of Vietnam. The aim of this research was to isolate and characterize anti-inflammatory compounds from Radix bupleuri. The ethanol (EtOH) extract of Radix bupleuri was phytochemical investigation and the structure of five isolated known compounds was identified by 1D and 2D NMR data as well as by comparison with data reported in literature. The isolatd compounds were evaluated for their inhibitory effect on NO production in RAW 264.7 cells and the compounds showed moderate activity. Therefore, Radix bupleuri could serve as a potential therapeutic herb for the treatment of diseases related to inflammation. [ABSTRACT FROM AUTHOR]

In this study, Fe3O4/GO nanocomposite was synthesized by hydrothermal method and tested for its efficiency in removing methylene blue (MB) and congo red (CR) from water. The synthesized nanocomposite was characterized using Fourier-transform infrared spectroscopy (FTIR), X-ray diffraction (XRD), and scanning electron microscopy (SEM). The optimal values for MB and CR removal were determined to be pH 6.0, an adsorbent weight of 50.0 mg, and a contact time of 10 min. The adsorption isotherms of the contaminants on the nanocomposite were analyzed using the Freundlich model, indicating a heterogeneous distribution of active sites on the adsorbent surface. The highest adsorption capacity of MB and CR is 135.1 and 285.7 mg.g-1, respectively. Moreover, Fe3O4/GO nanocomposite recycled five cycles with proper adsorption capacity. Overall, the Fe3O4/GO nanocomposite holds great promise for efficient and sustainable water treatment, providing safe and clean water globally. [ABSTRACT FROM AUTHOR]