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The valved linear compressor (VLC) is an essential part of the Joule-Thompson (J-T) throttling cryocooler in the liquid helium temperature region. The pressure pulsation may cause the fluctuation of the temperature and cooling capacity of the cryocooler, thus affecting its temperature stability. To measure the pressure pulsation of the VLC's pipe system, the mathematical model of pressure pulsation in the buffer tank of the VLC was established with the transfer matrix method based on the plane wave theory. The quantitative representation of the pulsating mass flow of the VLC was obtained with the linear damping based on the plane wave theory. Then, a test bench was set up to measure the pressure pulsation. The influence of the VLC's operating frequency and the suction and discharge buffer tank volume on the pressure pulsation was discussed. Results show that the pressure pulsation of the pipe system is related to the VLC's operating frequency. The pressure pulsation of the pipe system increases with the increase of the VLC's operating frequency. Both the inlet and outlet buffer tanks can effectively inhibit the pressure pulsation, but their capability is independent of each other. The pressure pulsation inhibition effect is better with the increase of the buffer tank volume. With the increase of the buffer tank volume, the pressure inhomogeneity at the inlet of the inlet buffer tank decreases to 164 over 423, but the pressure inhomogeneity at the outlet of the outlet buffer tank decreases to 8 over 23.

Beiging of white adipose tissue (WAT) is a particularly appealing target for therapeutics in the treatment of metabolic diseases through norepinephrine (NE)-mediated signaling pathways. Although previous studies report NE clearance mechanisms via SLC6A2 on sympathetic neurons or proinflammatory macrophages in adipose tissues (ATs), the low catecholamine clearance capacity of SLC6A2 may limit the cleaning efficiency. Here, we report that mouse organic cation transporter 3 (Oct3; Slc22a3) is highly expressed in WAT and displays the greatest uptake rate of NE as a selective non-neural route of NE clearance in white adipocytes, which differs from other known routes such as adjacent neurons or macrophages. We further show that adipocytes express high levels of NE degradation enzymes Maoa, Maob, and Comt, providing the molecular basis on NE clearance by adipocytes together with its reuptake transporter Oct3. Under NE administration, ablation of Oct3 induces higher body temperature, thermogenesis, and lipolysis compared with littermate controls. After prolonged cold challenge, inguinal WAT (ingWAT) in adipose-specific Oct3-deficient mice shows much stronger browning characteristics and significantly elevated expression of thermogenic and mitochondrial biogenesis genes than in littermate controls, and this response involves enhanced β-adrenergic receptor (β-AR)/protein kinase A (PKA)/cyclic adenosine monophosphate (cAMP)-responsive element binding protein (Creb) pathway activation. Glycolytic genes are reprogrammed to significantly higher levels to compensate for the loss of ATP production in adipose-specific Oct3 knockout (KO) mice, indicating the fundamental role of glucose metabolism during beiging. Inhibition of β-AR largely abolishes the higher lipolytic and thermogenic activities in Oct3-deficient ingWAT, indicating the NE overload in the vicinity of adipocytes in Oct3 KO adipocytes. Of note, reduced functional alleles in human OCT3 are also identified to be associated with increased basal metabolic rate (BMR). Collectively, our results demonstrate that Oct3 governs β-AR activity as a NE recycling transporter in white adipocytes, offering potential therapeutic applications for metabolic disorders.

Diabetes is a significant global public health issue with implications for vascular endothelial cells (ECs) dysfunction and the subsequent development and advancement of diabetes complications. This study aims to compare the cellular and molecular properties of the aorta in normal and streptozotocin (STZ)-induced diabetic mice, with a focus on elucidating potential mechanism underlying EC dysfunction. Here, we performed a single-cell RNA sequencing survey of 32,573 cells from the aorta of normal and STZ-induced diabetic mice. We found a compendium of 10 distinct cell types, mainly ECs, smooth muscle cells, fibroblast, pericyte, immune cells, and stromal cells. As the diabetes condition progressed, we observed a subpopulation of aortic ECs that exhibited significantly elevated expression of complement (C) molecule C1qa compared with their healthy counterparts. This increased expression of C1qa was found to induce reactive oxygen species (ROS) production, facilitate EC migration and increased permeability, and impair the vasodilation within the aortic segment of mice. Furthermore, AAV-Tie2-shRNA-C1qa was administered into diabetic mice by tail vein injection, showing that inhibition of C1qa in the endothelium led to a reduction in ROS production, decreased vascular permeability, and improved vasodilation. Collectively, these findings highlight the crucial involvement of C1qa in endothelial dysfunction associated with diabetes. Article Highlights: The molecular mechanisms and cellular heterogeneity of C1q in endothelial cells, which regulate vascular function, remain unclear. C1q is involved in the regulation of vascular function. C1q in vascular endothelial cells can regulate vascular function, including permeability, immunity, and diastolic function. C1q represents a promising therapeutic target for the treatment of endothelial dysfunction associated with diabetes. [ABSTRACT FROM AUTHOR]

Trauma-induced complete lead fracture is a rare complication of pacemaker implantation. Only a few cases have been previously reported. Common treatment included replacement of pacemaker and/or extraction of fractured lead. In this report, however, we describe this unique case of complete traumatic pacemaker lead fracture. The patient had her right-ventricular lead fractured after a bicycle accident and had lived with the fractured lead for 8 months prior to her hospitalization. After examinations, she was treated with a relatively conservative strategy. The pacemaker and fractured lead were left for further observation and follow-up.