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By constructing a correlation network between global sea surface temperature anomalies (SSTAs) and summer precipitation anomalies in the Yunnan–Guizhou Plateau, key SST regions influencing summer precipitation anomalies in the Yunnan–Guizhou Plateau were selected. It was found that spring SSTAs in the Bay of Bengal, southwestern Atlantic, and eastern Pacific are crucial for influencing summer precipitation anomalies in the Yunnan–Guizhou Plateau. Setting SSTAs from these three regions as predictor variables 3 months in advance, we constructed multiple linear regression (MLR), ridge regression (RR), and lasso regression (LR) models to predict summer precipitation anomalies over the Yunnan–Guizhou region. The training phase involved data spanning from 1961 to 2005, which aimed to predict precipitation anomalies in the Yunnan–Guizhou Plateau for the period extending from 2006 to 2022. Based on MLR, RR, and LR models, the correlations between predicted values and observed summer precipitation anomalies in Yunnan–Guizhou were 0.48, 0.46, and 0.46, respectively. These values were all higher than the correlation coefficients of the NCC_CSM model’s predicted and observed values. Additionally, its performance in predicting summer precipitation anomalies over the Yunnan–Guizhou region, based on key SST regions, was assessed using performance metrics such as anomaly correlation coefficient (ACC), anomaly sign consistency rate (PC), and trend anomaly comprehensive score (PS score). The average ACC of MLR, RR, and LR models was higher than that of the NCC_CSM model’s predictions. For MLR, RR, LR, and NCC_CSM models, the PCs exceeding 50% of the year were 14, 14, 11, and 10, respectively. Furthermore, the average PS score for predicting summer precipitation anomalies over the Yunnan–Guizhou region using MLR, RR, and LR was approximately 73 points; 8 higher than the average PS score of the NCC_CSM model. Therefore, predicting summer precipitation anomalies over the Yunnan–Guizhou region based on key SST regions is of great significance for improving the prediction skills of precipitation anomalies in this region.

The PANK2 gene, which encodes mitochondrial pantothenate kinase 2 protein, is the disease-causing gene for pantothenate kinase-associated neurodegeneration (PKAN). We report a case of atypical PKAN with autism-like symptoms presenting with speech difficulties, psychiatric symptoms, and mild developmental retardation. Magnetic resonance imaging (MRI) of the brain showed the typical “eye-of-the-tiger” sign. Whole-exon sequencing revealed PANK2 p.Ile501Asn/p.Thr498Ser compound heterozygous variants. Our study highlights the phenotypic heterogeneity of PKAN, which can be confused with autism spectrum disorder (ASD) and attention-deficit hyperactivity disorder (ADHD) and requires careful clinical identification.

It is important to determine the cause of death in the case of asphyxia. However, it is difficult to conclude death by asphyxia, especially when the deceased has underlying heart disease, because there are often no specific and representative corpse signs for both asphyxia and sudden cardiac death (SCD). The aim of the present work was to investigate the potential of metabolomics to discriminate asphyxia from SCD as the cause of death. A total of thirty male Sprague–Dawley rats were used to construct models of asphyxia, SCD (interfering cause of death), and cervical dislocation (control). Untargeted and widely targeted metabolomics approaches were used to obtain rat pulmonary metabolic profiles in this study. First, the metabolic alterations resulting from asphyxia were explored. There were significant changes found in carbohydrate metabolism, the endocrine system, and the sensory system. Second, we screened potential biomarkers and built classification models to determine the cause of death. Moreover, some biomarkers remained differentiated at 24 h and 48 h postmortem, so the cause of death could still be determined after death. This study showed the application potential of metabolomics to investigate the metabolic changes occurring in the process of death, as well as to determine the cause of death on the basis of metabolic differences even after death.

Long non-coding RNA (LncRNA) emerges as a regulator in various diseases, including endometriosis (EM). This study aims to uncover the role of long non-coding RNA BRAF-activated non-protein coding RNA (lncRNA BANCR)-mediated competing endogenous RNA mechanism in endometrial stromal cell (ESC) proliferation and invasion in EM by regulating miR-15a-5p/TRIM59. ESCs were isolated from eutopic and ectopic endometrial tissues, followed by the determination of Cytokeratin 19 and Vimentin expressions in cells. Then, expressions of lncRNA BANCR, microRNA (miR)-15a-5p, and tripartite motif-containing 59 (TRIM59) in tissues and cells were determined by real-time quantitative polymerase chain reaction or Western blot assay, and cell proliferation and invasion were evaluated by cell counting kit-8 and transwell assays. After that, the subcellular localization of lncRNA BANCR and binding of miR-15a-5p to lncRNA BANCR or TRIM59 were analyzed. LncRNA BANCR was upregulated in ectopic endometrial tissues and ectopic ESCs (Ect-ESCs). Silencing lncRNA BANCR suppressed Ect-ESC proliferation and invasion. LncRNA BANCR inhibited miR-15a-5p to promote TRIM59 expression. miR-15a-5p downregulation or TRIM59 overexpression both reversed the effects of silencing lncRNA BANCR on Ect-ESC proliferation and invasion. In summary, our findings suggested that lncRNA BANCR facilitated Ect-ESC proliferation and invasion by inhibiting miR-15a-5p and promoting TRIM59.

This paper focuses on the influencing factors of MICP solidification of soil–rock mixture. After selecting the best soil–rock ratio through screening, the MICP process is tested from two aspects of rock content and particle size. The results show that the soil–rock mixture is not a uniform carrier of the medium, and the force on the surface of the sample is not uniform. With the increase in stress load, the stress–strain curve shows a sawtooth upward trend and peak value. The microbial cemented soil–rock mixture had a particle size of 0.2–0.4 cm and 0.4–0.6 cm under the rock block proportion of 50%. The unconfined compressive strength of the microbial cemented soil–rock mixture with a rock particle size of 0.6–0.9 cm reaches the highest at 60% rock block proportion. When the rock content is 20–50%, the unconfined compressive strength decreases with the increase in particle size. When the rock content is 60%, the value of unconfined compressive strength first decreases and then increases with the increase in particle size; both SEM and XRD test results proved that Sporosarcina pasteurii could effectively induce the formation of calcium carbonate and crystallizes at the pores of the particles to improve the mechanical properties of the soil.

Abstract Estimation of the postmortem interval (PMI) is a complicated task in forensic medicine, especially during homicide and unwitnessed death investigations. Many biological, chemical, and physical indicators can be used to determine the postmortem interval, but most are not accurate. Here, we present a novel matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) method that can be used for the estimation of PMI using molecular images and multivariate analyses. In this study, we demonstrate that both rat and human liver tissues of various PMIs (0, 2, 4, and 6days) can be discriminated using MALDI imaging and principal component analysis (PCA). Using genetic algorithm (GA), supervised neural network (SNN), and quick classifier (QC) methods, we built 6 classification models, which showed high recognition capability and good cross-validation. The histological changes in all the samples at different time points were also consistent with the changes seen in MALDI imaging. Our work suggests that MALDI-TOF MS, along with multivariate analysis, can be used to determine intermediate PMIs.

Objective. To estimate the additive interaction of body mass index (BMI) and family history of hypertension (FHH) on hypertension and explore whether the interaction could be influenced by behavioural risk factors. Methods. The cross-sectional data on 5791 participants were from the China National Health Survey in Gansu province in 2016. We assessed the additive interaction by calculating the relative excess risk due to interaction (RERI), the attributable proportion due to interaction (AP), and the synergy index (SI). Results. ORs for hypertension were highest in Han (13.52, 95% CI: 9.45 to 19.34) and Yugur (13.85, 95% CI: 8.48 to 22.63) with the combination of obesity and FHH. The interaction of BMI and FHH was significant in Han people, with the RERI, AP, and SI and their 95% CIs being 2.48 (1.13 to 3.82), 0.33 (0.19 to 0.47), and 1.61 (1.26 to 2.07) for overweight and FHH and 6.32 (1.91 to 10.73), 0.47 (0.27 to 0.67), and 2.02 (1.33 to 3.07) for obesity and FHH, respectively. The interaction of BMI and FHH was not significant in Yugur people. Adjustment for behavioural risk factors had little influence on the interactions, and risks of hypertension remained increased. Conclusions. BMI and FHH were associated with hypertension, and the interaction of BMI and FHH on hypertension was significant in Han but not in Yugur people. Behavioural risk factors had little influence on the associations and interactions. The exacerbation of hypertension risks by overweight or obesity in hypertension families deserves attention in weight control and community care.

Abstract Background There is increasing evidence to suggest an immunomodulation function both within the intestines and systemically upon consuming probiotic species. We recently isolated a novel LAB, Lactobacillus caseiZhang (LcZhang) from koumiss. LcZhang exhibited favorable probiotic properties, such as acid resistance, bile resistance, gastrointestinal (GI) colonization ability, etc. In order to examine the immunomodulatory qualities of LcZhang, we administered LcZhang to healthy mice with varying doses of either live or heat-killed LcZhang and measured various parameters of the host immune response. Results The study was performed in four separate experiments via oral administration of live and heat-killed LcZhang to BALB/c mice for several consecutive days. We investigated the immunomodulating capacity of LcZhang in vivo by analyzing the profile of cytokines, T cell subpopulations, and immunoglobulin concentrations induced in blood serum and intestinal fluid in BALB/c mice. Only live bacteria elicited a wide range of immune responses, which include the increased production of interferon-γ (IFN-γ), and depression of tumor necrosis factor-α (TNF-α) levels. In addition, interleukin-2 (IL-2) and IL-2 receptor gene transcription increased significantly, but the proportion of T cell subsets appeared to be unaffected. We also observed that LcZhang was capable of inducing gut mucosal responses by enhancing the production of secretory Immunoglobulin A (sIgA) as well influencing the systemic immunity via the cytokines released to the circulating blood. Conclusion The present work shows that the dose-dependent administration of LcZhang is capable of influencing immune responses, implying that it may be a valuable strain for probiotic use in humans.

Obesity with excessive levels of circulating free fatty acids (FFAs) is tightly linked to the incidence of type 2 diabetes. Insulin resistance of peripheral tissues and pancreatic β-cell dysfunction are two major pathological changes in diabetes and both are facilitated by excessive levels of FFAs and/or glucose. To gain insight into the mitochondrial-mediated mechanisms by which long-term exposure of INS-1 cells to excess FFAs causes β-cell dysfunction, the effects of the unsaturated FFA linoleic acid (C 18:2, n-6) on rat insulinoma INS-1 β cells was investigated. INS-1 cells were incubated with 0, 50, 250 or 500 μM linoleic acid/0.5% (w/v) BSA for 48 h under culture conditions of normal (11.1 mM) or high (25 mM) glucose in serum-free RPMI-1640 medium. Cell viability, apoptosis, glucose-stimulated insulin secretion, Bcl-2, and Bax gene expression levels, mitochondrial membrane potential and cytochrome c release were examined. Linoleic acid 500 μM significantly suppressed cell viability and induced apoptosis when administered in 11.1 and 25 mM glucose culture medium. Compared with control, linoleic acid 500 μM significantly increased Bax expression in 25 mM glucose culture medium but not in 11.1 mM glucose culture medium. Linoleic acid also dose-dependently reduced mitochondrial membrane potential (ΔΨm) and significantly promoted cytochrome c release from mitochondria in both 11.1 mM glucose and 25 mM glucose culture medium, further reducing glucose-stimulated insulin secretion, which is dependent on normal mitochondrial function. With the increase in glucose levels in culture medium, INS-1 β-cell insulin secretion function was deteriorated further. The results of this study indicate that chronic exposure to linoleic acid-induced β-cell dysfunction and apoptosis, which involved a mitochondrial-mediated signal pathway, and increased glucose levels enhanced linoleic acid-induced β-cell dysfunction. [ABSTRACT FROM AUTHOR]

Hyperglycemia-associated glucotoxicity induces β-cell apoptosis but the underlying mechanisms are unknown. Interestingly, prolonged exposure to high glucose upregulates the expression and function of the renin-angiotensin system (RAS). We hypothesize that the voltagegated outward potassium (Kv) current, which governs β-cell membrane potential and insulin secretion, has a role in glucotoxicity. In this study, we investigated the effects of prolonged exposure to high glucose on mouse pancreatic β-cells and concurrent effects on the RAS by examining changes in expression of angiotensin II (ANG II) receptors and changes in the expression and activity of Kv channels. β-Cells were incubated in high glucose medium for 1-7 days and then were examined with electrophysiological and molecular biology techniques. Prolonged exposure to high glucose produced a marked increase in β-cell primary Kv channel subunit, Kv2. 1, expression and Kv current amplitude. Enhanced expression of ANG II type 1 receptor (AT1R) was also observed under high glucose conditions, whereas blockade of AT1R by losartan did not alter Kv channel expression. External application of ANG II reduced Kv current amplitude under normal, but not high, glucose conditions. The effect of ANG II on IL channel gating was abolished by ANG H type 2 receptor (AT2R) antagonism. These data suggest that hyperglycemia alters β-cell function through modification of the IL channel which may be associated with the RAS. [ABSTRACT FROM AUTHOR]

Abstract  Reduction of pancreatic β-cell mass is a key element leading to type 2 diabetes. Obesity and overweight with high levels of lipids including cholesterol are tightly linked to type 2 diabetes. The direct impact of cholesterol on pancreatic β-cells, however, has not been extensively studied. In this study, MIN6 mouse β-cell line was used to test the effect of cholesterol on pancreatic β-cell apoptosis over different doses and durations. It was found that cholesterol dose- and time-dependently induced cell death of MIN6 cells above 160 μM after 6 h treatment in vitro. Annexin-V staining revealed that cholesterol treatment significantly induced apoptosis in MIN6 cells. Cholesterol treatment resulted in the loss of the ability to retain Rhodamine 123, indicating mitochondrial damage in MIN6 cells. Cholesterol-induced cell apoptosis and mitochondrial damage were blocked by low-temperature condition. In addition, glutathione also protected MIN6 cells from cholesterol-induced cell death. It is concluded that high level of cholesterol induces cell apoptosis in MIN6 cells, which is in part due to mitochondrial dysfunction. We suggest that excessive uptake of cholesterol in β-cells may contribute to β-cell apoptosis and dysfunction and the deterioration of type 2 diabetes. [ABSTRACT FROM AUTHOR]

Patients with diabetes mellitus, particularly those with cardiovascular complications, have increased risk of mortality when subject to anesthetics and surgery, compared with non-diabetic patients. Anesthetics may exert pressure on the cardiovascular system of diabetic patients, directly or by aggravating pre-existing cardiovascular complications. Advanced glycation end products (AGEs) are extremely accumulated in diabetes mellitus, and are confirmed to play an important role in the pathogenesis of diabetic microvascular and macrovascular complications. The purpose of the present study was to investigate the regulatory role of etomidate, which is widely used as intravenous general anesthetics, on the viability and apoptosis of human endothelial Eahy926 cells, in the presence of AGEs. The results demonstrated that etomidate and Glu-BSA (one type of AGE) synergistically reduced the human endothelial Eahy926 cell viability and induced cell apoptosis. In addition, western blot assay of apoptosis-associated molecules indicated that both agents synergistically upregulated the cytochrome c release, activated the apoptosis executor, caspase 3, and promoted the poly-ADP-ribose polymerase (PARP) lysis. Further results confirmed that the two agents synergistically promoted oxidative stress by decreasing mitochon-drial respiratory chain complex IV and mitochondrial membrane potential (MMP), while upregulating reactive oxygen species (ROS) and mitochondrial superoxide. In conclusion, the results presented in this study offer a novel insight into the mechanisms of endothelial cell apoptosis in response to etomidate in the presence of AGEs. These results suggest that oxidative stress has important role in the synergistic promotion of apoptosis by etomidate and AGEs in endothelial Eahy926 cells. [ABSTRACT FROM AUTHOR]