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Given the disadvantageous factors of the currently prevalent high-pressure hydrogen cylinder storage technology for providing hydrogen to proton exchange membrane fuel cell (PEMFC), such as bulky systems, significant energy losses, and high costs, this study adopts a novel and efficient solid-state hydrogen storage technology as the hydrogen supply method for PEMFC. Through the design of the topological structure of the metal hydride hydrogen storage system, a simulation model of the metal hydride hydrogen storage system is built on the MATLAB/Simulink platform based on this structure. The research focuses on designing corresponding control methods for the hydrogen release process of the solid-state hydrogen storage device. The simulation results demonstrate that the designed controller achieves rapid response within 15 seconds, exhibiting excellent dynamic performance, and effectively realizes the objective of supplying hydrogen to the fuel cell system rapidly and stably.

Objective: Protein kinase C (PKC) has been implicated in the increased contraction of human airway smooth muscle cells (HASMCs) in asthma. Using the three-dimensional collagen gel contraction system, the study aimed to determine the effects of LY333531, a specific inhibitor of the PKC-β isoform, on the contraction of tumor necrosis factor (TNF)-α-sensitized HASMCs. Methods: Cultured HASMCs were divided into five groups: the control group received no treatment, and the cells in the TNF-α group were sensitized with 10 ng/mL TNF-α for 48 h, while TNF-α was administered to sensitize HASMCs in the presence of 0.1, 0.2, and 0.5 μM LY333531 for 48 h in the 0.1LY, 0.2LY, and 0.5LY groups, respectively. Following this, HASMCs contraction was stimulated with 1 mM acetylcholine (ACh) for up to 24 h in each group and assessed using a three-dimensional collagen gel contraction assay. Furthermore, western blot and immunofluorescence analysis were performed. Results: The collagen gel contraction assay revealed that TNF-α increased the protein expression of phosphorylated PKC-β2, CPI-17, and MLC while exacerbating ACh-induced HASMCs contraction. LY333531 significantly attenuated HASMCs contraction and downregulated the protein expression of both p-CPI-17 and p-MLC. Conclusions: At least in part by regulating CPI-17 and MLC phosphorylation, LY333531 attenuates augmented contraction of TNF-α-sensitized HASMCs in a collagen gel contraction system. [ABSTRACT FROM AUTHOR]

To evaluate the health-related quality-of-life (QOL) outcomes in surgical breast cancer survivors who received breast conservation therapy (BCT) compared to mastectomy, we utilized a systematic review to conduct observational studies of QOL in patients with breast cancer following breast conservation therapy from their inception until October 2021. The PubMed, the Cochrane Library, and the Web of Science databases were systematically searched to retrieve the observational studies. The pooled odds ratios (ORs) with 95% confidence intervals (CIs) were applied as an effect estimate and calculated using Stata 15 software. Nine studies comprising 2301 patients were included. The results showed that no significant differences compared to mastectomy were detected for global health status (P = 0.971 and P = 0.613), physical function (P = 0.099), emotional function (P = 0.096), cognitive function (P = 0.377), social function (P = 0.602), sexual functioning (P = 0.072), and sexual enjoyment (P = 0.142), while role function (P = 0.036), body image (P = 0.000), and future perspective (P = 0.012) showed a significant difference for BCT when compared to mastectomy. When compared to breast reconstruction (BR), the BCT group was inferior at physical function (P = 0.002) and cognitive function (P = 0.040) but superior at body image (P = 0.001). When used the Functional Assessment of Cancer Therapy (FACT) tool, BCT has better results in physical function (P = 0.000), emotional function (P = 0.000), and social function (P = 0.000) than mastectomy. QOL outcomes after BCT were better than mastectomy in body image, future perspective, and role function. BCT may be an acceptable option in the study setting for breast cancer patients who pursue high QOL. [ABSTRACT FROM AUTHOR]

Objective. To use meta-analysis to systematically compare the efficacy and adverse reaction rates of albumin paclitaxel and docetaxel in the treatment of breast cancer. Methods. This study included Chinese and English literature studies on clinical controlled studies of albumin paclitaxel and docetaxel in the treatment of breast cancer by searching CNKI, Weipu, Wanfang, PubMed, Embase, and Cochrane Library. Two researchers participated in the screening of the literature, used the inclusion and exclusion criteria as reference indicators, extracted relevant data, and used the software RevMan5.3 to conduct quality evaluation and meta-analysis of the literature. Results. 4 literature stuides were retrieved that met the inclusion criteria, with 243 study subjects. The included literature had a lower risk of bias. Meta-analysis results showed that compared with the docetaxel group, the protein paclitaxel group had significant differences in objective effective rate (ORR) (OR = 1.56, 95% CI (0.80, 3.03), P = 0.19), complete remission (CR) (OR = 1.79, 95% CI (0.96, 3.35), P = 0.07), partial remission (PR) (OR = 0.88, 95% CI (0.53, 1.47), P = 0.62), nausea (OR = 0.87, 95% CI (0.51, 1.74), P = 0.84), and vomiting (OR = 0.62, 95% CI (0.45, 1.78) P = 0.76). The reason may be that the number of literatures included in this study is small or the sample size is insufficient. However, it had an advantage in the incidence of neutropenia (OR = 0.38, 95% CI (0.16, 0.88), P = 0.02), and the difference between the two groups was statistically significant. Conclusion. Albumin paclitaxel treatment can better reduce the incidence of neutropenia in breast cancer patients and is of great significance to the safety of breast cancer patients. [ABSTRACT FROM AUTHOR]

Background. Both apoptosis and necroptosis have been recognized to be involved in ischemia reperfusion-induced lung injury. We aimed to compare the efficacies of therapies targeting necroptosis and apoptosis and to determine if there is a synergistic effect between the two therapies in reducing lung ischemia reperfusion injury. Methods. Forty Sprague-Dawley rats were randomized into 5 groups: sham (SM) group, ischemia reperfusion (IR) group, necrostatin-1+ischemia reperfusion (NI) group, carbobenzoxy-Val-Ala-Asp-fluoromethylketone+ischemia reperfusion (ZI) group, and necrostatin-1+carbobenzoxy-Val-Ala-Asp-fluoromethylketone+ischemia reperfusion (NZ) group. The left lung hilum was exposed without being clamped in rats from the SM group, whereas the rats were subjected to lung ischemia reperfusion by clamping the left lung hilum for 1 hour, followed by reperfusion for 3 hours in the IR group. 1 mg/kg necrostatin-1 (Nec-1: a specific necroptosis inhibitor) and 3 mg/kg carbobenzoxy-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk: a pan caspase inhibitor) were intraperitoneally administrated prior to ischemia in NI and ZI groups, respectively, and the rats received combined administration of Nec-1 and z-VAD-fmk in the NZ group. Upon reperfusion, expressions of receptor-interacting protein 1 (RIP1), receptor-interacting protein 3 (RIP3), and caspase-8 were measured, and the flow cytometry analysis was used to assess the cell death patterns in the lung tissue. Moreover, inflammatory marker levels in the bronchoalveolar lavage fluid and pulmonary edema were evaluated. Results. Both Nec-1 and z-VAD-fmk, either alone or in combination, significantly reduced morphological damage, inflammatory markers, and edema in lung tissues following reperfusion, and cotreatment of z-VAD-fmk with Nec-1 produced the optimal effect. The rats treated with Nec-1 had lower levels of inflammatory markers in the bronchoalveolar lavage fluid than those receiving z-VAD-fmk alone (P < 0.05). Interestingly, the z-VAD-fmk administration upregulated RIP1 and RIP3 expressions in the lung tissue from the ZI group compared to those in the IR group (P < 0.05). Reperfusion significantly increased the percentages of necrotic and apoptotic cells in lung tissue single-cell suspension, which could be decreased by Nec-1 and z-VAD-fmk, respectively (P < 0.05). Conclusions. Nec-1 synergizes the pan caspase inhibitor to attenuate lung ischemia reperfusion injury in rats. Our data support the potential use of Nec-1 in lung transplantation-related disorders. [ABSTRACT FROM AUTHOR]

Acute lung injury (ALI) is characterized by tissue damage and inflammatory cytokine secretion; however, the therapeutic options available to treat ALI remain limited. Necrostatin-1 (Nec-1) has the ability to attenuate cell necroptosis in various inflammatory diseases. The present study evaluated the protective effects of Nec-1 on a mouse model of lipopolysaccharide-induced ALI. Histological alterations in the lungs were evaluated through hematoxylin and eosin staining, and the expression levels of cytokines in the bronchoalveolar lavage fluid and lung tissues were determined by ELISA. In addition, accumulated production of reactive oxygen species was determined by staining with DCFH-DA probes, western blotting and immunofluorescence. The results revealed that treatment with the necroptosis inhibitor, Nec-1, exerted significant protective effects on ALI-induced inflammation and necroptosis. The key proteins involved in necroptosis were markedly reduced, including receptor-interacting serine/threonine-protein kinase (RIP)1 and RIP3. Notably, antioxidant proteins were upregulated by Nec-1, which may attenuate oxidative stress. Furthermore, treatment with Nec-1 markedly suppressed necroptosis in the pulmonary alveoli RLE-6TN cell line. Taken together, these data revealed a novel association between ALI and necroptosis, and suggested that necroptosis inhibitors may be used as effective anti-inflammatory drugs to treat ALI. [ABSTRACT FROM AUTHOR]

Objective. This study was aimed to investigate the protective effect of methylene blue against lung injury induced by reperfusion of ischemic hindlimb in a rat model. Methods. Twenty-four healthy adult male Sprague-Dawley rats were equally randomized into three groups: sham (SM) group, ischemia reperfusion (IR) group, and methylene blue (MB) group. Rats in both IR and MB groups were subjected to 4 h of ischemia by clamping the left femoral artery and then followed by 4 h of reperfusion. Treatment with 1% methylene blue (50 mg/kg) was administrated intraperitoneally at 10 min prior to reperfusion in the MB group. After 4 h of reperfusion, malondialdehyde (MDA) level, myeloperoxidase (MPO), and superoxide dismutase (SOD) activities in lung tissue were detected; inflammatory cytokines, including IL-1β and IL-6, were measured in bronchoalveolar lavage fluid (BALF); correspondingly, the morphological changes and water content in both gastrocnemius muscle and lung samples were evaluated. Results. Hindlimb IR caused remarkable morphological abnormalities and edema in both muscle and lung tissues. SOD activity was decreased, both the MPO activity and MDA level in lung tissue, as well as IL-1β and IL-6 levels in BALF, were increased in the IR group (p<0.05). Compared with the IR group, SOD activity was increased, whereas MPO activity and MDA level in lung tissue and IL-1β and IL-6 levels in BALF were decreased in the MB group (p<0.05). Also, the histological damage and edema in both lung and muscle tissues were significantly attenuated by the treatment of methylene blue. Conclusion. Methylene blue attenuates lung injury induced by hindlimb IR in rats, at least in part, by inhibiting oxidative stress. [ABSTRACT FROM AUTHOR]

In this work, we develop a phase-field-based lattice Boltzmann (LB) method for a two-scalar model of the two-phase flows with interfacial mass or heat transfer. Through the Chapman-Enskog analysis, we show that the present LB method can correctly recover the governing equations for phase field, flow field, and concentration or temperature field. In particular, to derive the two-scalar equations for the mass or heat transfer, we propose a new LB model with an auxiliary source distribution function to describe the extra flux terms, and the discretizations of some derivative terms can be avoided. The accuracy and efficiency of the present LB method are also tested through several benchmark problems, and the influence of mass or heat transfer on the fluid viscosity is further considered by introducing an exponential relation. The numerical results show that the present LB method is suitable for the two-phase flows with interfacial mass or heat transfer.

High-temperature requirement factor A3 (HTRA3), a member of the HTRA protein family, is closely associated with apoptosis and plays a crucial role in controlling signal transmission and cancer development. However, the regulatory pathways of HTRA3 in tumors are not fully understood, necessitating a comprehensive analysis of HTRA3 in cancers. In this study, we conducted a multi-omics analysis of HTRA3 in pan-cancer using data from various databases including TCGA, cBioPortal, GeneMANIA, DAVID, TIMER2.0, SangerBox, and RNAactDrug. Our analysis included gene expression, survival prognosis, diagnostic value, mutation, gene-gene interaction, enrichment analysis, and drug sensitivity analysis. We found that HTRA3 is aberrantly expressed in a variety of cancers and significantly correlates with diagnosis, prognosis, TMB, MSI, immune checkpoint (ICP) genes, and drug sensitivity in various cancer types. HTRA3 is involved in a variety of cancer pathways, particularly extracellular matrix (ECM) alterations, and has a potential role in epithelial-mesenchymal transition (EMT). HTRA3 expression is positively correlated with the abundance of cancer-associated fibroblasts (CAFs) and endothelial cells in the tumor microenvironment, and is also positively correlated with immune scores, stromal scores, and ESTIMATE scores in multiple cancers. HTRA3 is often overexpressed in cancer and is associated with poor prognosis and regulation of the tumor's immune response. Therefore, it may serve as a novel biomarker for tumor diagnosis and treatment.

Gut functions, such as gastrointestinal motility, gastric secretion and pancreatic secretion, were reduced with age. Glucose tolerance is impaired, and the release of insulin and β-cell's sensitivity on glucose are reduced with age. However, a lot of controversial data have been reported as insulin concentrations after glucose ingestion are either higher or no different in elderly and young subjects. Thus, this study was aimed to investigate whether aging could affect pancreatic exocrine secretion and its action mechanisms. An isolated perfused rat pancreatic model was used to exclude the effects of external nerves or hormones. Pancreatic secretion was increased by CCK under 5.6 mM glucose background in the isolated perfused pancreas of young (3 months), 12 months and 18 months aged rats. There was no significant difference between young and aged rats. In 3 months old rats, CCK-stimulated pancreatic secretion was potentiated under 18 mM glucose background. However, the potentiation effects of endogenous insulin and CCK were not observed in 12 and 18 months old rats. Exogenous insulin also potentiated CCK-stimulated pancreatic secretion in 3 months old rats. Similarly, exogenous insulin failed to potentiate CCK-stimulated pancreatic secretion as that of 3 months old rats. Wet weight of pancreas and amylase content in pancreatic tissue were not changed with age. These results indicate that pancreatic exocrine secretion is reduced with age and endogenous insulin secretion and/or action is involved in this phenomenon.