Association between high-density lipoprotein cholesterol and lumbar bone mineral density in Chinese: a large cross-sectional study.

BACKGROUND: The association between lipid and bone metabolism, particularly the role of high-density lipoprotein cholesterol (HDL-C) in regulating bone mineral density (BMD), is of significant interest. Despite numerous studies, findings on this relationship remain inconclusive, especially since evidence from large, sexually diverse Chinese populations is sparse. This study, therefore, investigates the correlation between HDL-C and lumbar BMD in people of different genders using extensive population-based data from physical examinations conducted in China. METHODS: Data from a cross-sectional survey involving 20,351 individuals aged > = 20 years drawn from medical records of health check-ups at the Health Management Centre of the Henan Provincial People's Hospital formed the basis of this study. The primary objective was to determine the correlation between HDL-C levels and lumbar BMD across genders. The analysis methodology included demographic data analysis, one-way ANOVA, subgroup analyses, multifactorial regression equations, smoothed curve fitting, and threshold and saturation effect analyses. RESULTS: Multifactorial regression analysis revealed a significant inverse relationship between HDL-C levels and lumbar BMD in both sexes, controlling for potential confounders (Male: ß = -8.77, 95% CI -11.65 to -5.88, P < 0.001; Female: ß = -4.77, 95% CI -8.63 to -0.90, P = 0.015). Subgroup and threshold saturation effect analyses indicated a stronger association in males, showing that increased HDL-C correlates with reduced lumbar BMD irrespective of age and body mass index (BMI). The most significant effect was observed in males with BMI > 28 kg/m2 and HDL-C > 1.45 mmol/L and in females with a BMI between 24 and 28 kg/m2. CONCLUSION: Elevated HDL-C is associated with decreased bone mass, particularly in obese males. These findings indicate that individuals with high HDL-C levels should receive careful clinical monitoring to mitigate osteoporosis risk. TRIAL REGISTRATION: The research protocol received ethics approval from the Ethics Committee at Beijing Jishuitan Hospital, in conformity with the Declaration of Helsinki guidelines (No. 2015-12-02). These data are a contribution of the China Health Quantitative CT Big Data Research team, registered at clinicaltrials.gov (code: NCT03699228).

The Role of eIF5A1 in LPS-Induced Neuronal Remodeling of the Nucleus Accumbens in the Depression.

BACKGROUND: The pathogenesis of depression is complex, with the brain's reward system likely to play an important role. The nucleus accumbens (NAc) is a key region in the brain that integrates reward signals. Lipopolysaccharides (LPS) can induce depressive-like behaviors and enhance neuroplasticity in NAc, but the underlying mechanism is still unknown. We previously found that eukaryotic translation initiation factor A1 (eIF5A1) acts as a ribosome-binding protein to regulate protein translation and to promote neuroplasticity. METHODS: In the present study, LPS was administered intraperitoneally to rats and the expression and cellular location of eIF5A1 was then investigated by RT-PCR, Western blotting and immunofluorescence. Subsequently, a neuron-specific lentivirus was used to regulate eIF5A1 expression in vivo and in vitro. Neuroplasticity was then examined by Golgi staining and by measurement of neuronal processes. Finally, proteomic analysis was used to identify proteins regulated by eIF5A1. RESULTS: The results showed that eIF5A1 expression was significantly increased in the NAc neurons of LPS rats. Following the knockdown of eIF5A1 in NAc neurons, the LPS-induced increases in neuronal arbors and spine density were significantly attenuated. Depression-like behaviors were also reduced. Neurite outgrowth of NAc neurons in vitro also increased or decreased in parallel with the increase or decrease in eIF5A1 expression, respectively. The proteomic results showed that eIF5A1 regulates the expression of many neuroplasticity-related proteins in neurons. CONCLUSIONS: These results confirm that eIF5A1 is involved in LPS-induced depression-like behavior by increasing neuroplasticity in the NAc. Our study also suggests the brain's reward system may play an important role in the pathogenesis of depression.

NLRP3 inflammasome contributes to endothelial dysfunction in angiotensin II-induced hypertension in mice.

AIMS: Inflammation is a key feature of endothelial dysfunction induced by angiotensin (Ang) II. The purpose of this study was to explore the role of Nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome in endothelial dysfunction in Ang II-induced hypertension. MATERIALS AND METHODS: We analyzed blood pressure and vascular function of wild-type (WT) and Nlrp3 knockout (Nlrp3-/-) mice, treated with Ang II. In vitro, we mainly tested the endothelial nitric oxide synthase (eNOS) phosphorylation expression of human umbilical vein endothelial cells (HUVECs). KEY FINDINGS: Here we showed that 14-day Ang II infusion into mice resulted in the elevation of blood pressure, NLRP3 expression, serum interleukin (IL)-1ß level, and the decline of endothelium-dependent relaxation function, p-eNOS-Ser1177 expression in aortas. Nlrp3 deficiency reduced Ang II-induced blood pressure elevation and endothelial dysfunction. In vitro, NLRP3 was involved in the effect of Ang II on reducing p-eNOS-Ser1177 expression. Moreover, the direct effect of IL-1ß on vascular endothelial injury could be observed in both vivo and vitro. SIGNIFICANCE: Our result demonstrates that the NLRP3 inflammasome is critically involved in the detrimental effects of Ang II on vascular endothelium in hypertension via the activation of IL-1ß, placing NLRP3 as a potential target for therapeutic interventions in conditions with endothelial dysfunction in hypertension.

Stress conditions induced circRNAs profile of extracellular vesicles in brain microvascular endothelial cells.

Cerebral ischemia causes hypoxic injury and inflammation, and brain microvascular endothelial cells (BMVECs) dysfunction is an initial stage of blood-brain barrier disruption. Endothelial cells secrete extracellular vesicles (EVs) that are involved in intercellular signal transduction. EVs contain a variety of RNAs, proteins, and metabolites. Circular RNA (circRNA) is a member of the non-coding RNA. The expression profile and potential function of circRNAs in BMVECs are unknown. Here, human BMVECs have undergone hypoxia or TNF-α induction, and the changes in circRNAs were measured by RNA sequencing. A total of 70 circRNAs showed differential expression, including 43 previously unrecorded circRNAs and 27 recorded circRNAs. Since astrocyte end-feet encircle endothelial cells, they are considered the main targets of the EVs from BMVEC. The miRNA sequence data and bioinformatics were used to predict the circRNA-miRNA-mRNA networks in astrocytes. The gene ontology (GO) analysis showed the main downstream targets of circRNAs are DNA transcription regulation and protein kinase-related signaling pathways. These results suggest that altering circRNAs may be a potential therapeutic target for cerebral ischemia induced hypoxic injury and inflammation.

Leonurine Attenuates Myocardial Fibrosis Through Upregulation of miR-29a-3p in Mice Post-myocardial Infarction.

ABSTRACT: Myocardial fibrosis (MF) is a pathological process that accelerates cardiac remodeling in myocardial infarction (MI), and miR-29 has become one of the foci of research into MF. As an alkaloid extracted from Herba leonuri, leonurine (LE) has been found to be an effective natural active ingredient for inhibiting fibrosis in many preclinical experiments. However, whether LE protects against MF after MI through modifying miR-29 remains unclear. The present study aimed to investigate the therapeutic effects of LE on MF, and to elucidate the underlying mechanisms involved. A mouse model of MI was established, followed by administration of LE for 4 weeks. We found that LE effectively improved cardiac function, and attenuated fibrosis and cardiac remodeling in mice post-MI. In vitro, LE simultaneously inhibited proliferation and migration of neonatal mouse cardiac fibroblasts (CFs) exposed to angiotensin II (Ang II), and the activation of collagen synthesis and myofibroblast generation was markedly suppressed by LE. Notably, we found that all mature miR-29 family members were downregulated in the myocardial tissues of mice post-MI, whereas LE significantly upregulated miR-29a-3p expression, and such upregulation was also detected in LE-treated CFs under Ang II stimulation. Knockdown of miR-29a-3p by a specific miRNA inhibitor upregulated the protein levels of TGF-ß, collagen III, and collagen I in CFs, and completely reversed the antifibrotic effects of LE on CFs. Our study suggests that LE exerts cardioprotective effects against MF, possibly through the upregulation of miR-29a-3p.

Broad and dynamic neurochemical alterations in the brain of alcoholic rats.

Ethanol is the active ingredient in alcoholic beverages. As ethanol consumption increases from zero to very high, it is still unknown which metabolites are present at different times and which are essential to normal functioning. In this article, we used an intermittent-access 20% ethanol drinking paradigm to make Wistar male rats voluntarily drink large amounts of ethanol for 10, 20, 30, and 50 days, respectively. A hydrogen-1 nuclear magnetic resonance approach was used to investigate the time-dependent neurochemical metabolites spectra in the hippocampus, striatum, nucleus accumbens and prefrontal cortex. Multivariate pattern recognition techniques were used to analyze the hydrogen-1 nuclear magnetic resonance spectra data. Metabolic profiling was obtained, differentiating the ethanol-treated and control rats. The ethanol-affected metabolites disrupted processes associated with neurotransmitters, oxidative stress, energy metabolism and amino acids. Together, our findings demonstrate broad, dynamic, and time-dependent endogenous metabolic alterations in rats treated with ethanol.

Progesterone promotes endothelial nitric oxide synthase expression through enhancing nuclear progesterone receptor-SP-1 formation.

Progesterone exerts antihypertensive actions partially by modulating endothelial nitric oxide synthase (eNOS) activity. Here, we aimed to investigate the effects and mechanisms of progesterone on eNOS expression. First, human umbilical vein endothelial cells (HUVECs) were exposed to progesterone and then the eNOS transcription factor specificity protein-1 (SP-1) and progesterone receptor (PRA/B) expression were assessed by Western blotting and qRT-PCR. The interaction between SP-1 and PRA/B was next determined through coimmunoprecipitation assay. The chromatin immunoprecipitation assay and luciferase assay were used to investigate the relationship of PRA/B, SP-1, and eNOS promoter. At last, rats were intraperitoneally injected with progesterone receptor antagonist RU-486, and then the expression of eNOS and vasodilation function in thoracic aorta and mesenteric artery were measured. The results showed that progesterone could increase eNOS expression in HUVECs. Further study showed that progesterone increased PRA-SP-1 complex formation and facilitated PRA/B and SP-1 binding to eNOS promoter. Mutating SP-1 or PR-binding motif on eNOS promoter abolished the effect of progesterone on eNOS gene transcription. We also observed that progesterone receptor antagonist RU-486 reduced eNOS expression and impaired vasodilation in rats. Those results suggest that progesterone modulates eNOS expression through promoting PRA-SP-1 complex formation, and progesterone antagonist attenuates eNOS expression, leading to the loss of vascular relaxation.NEW & NOTEWORTHY Progesterone directly upregulated endothelial nitric oxide synthase (eNOS) expression in human endothelial cells. Progesterone augmented eNOS promoter activity through a progesterone receptor A- and specificity protein-1-dependent manner. Antagonism of the progesterone receptor reduced eNOS expression and impaired vasodilation in rats.

N-Glycosylation at Asn695 might suppress inducible nitric oxide synthase activity by disturbing electron transfer.

Inducible nitric oxide synthase (iNOS) plays critical roles in the inflammatory response and host defense. Previous research on iNOS regulation mainly focused on its gene expression level, and much less is known about the regulation of iNOS function by N-glycosylation. In this study, we report for the first time that iNOS is N-glycosylated in vitro and in vivo. Mass spectrometry studies identified Asn695 as an N-glycosylation site of murine iNOS. Mutating Asn695 to Gln695 yields an iNOS that exhibits greater enzyme activity. The essence of nitric oxide synthase catalytic reaction is electron transfer process, which involves a series of conformational changes, and the linker between the flavin mononucleotide-binding domain and the flavin adenine dinucleotide-binding domain plays vital roles in the conformational changes. Asn695 is part of the linker, so we speculated that attachment of N-glycan to the Asn695 residue might inhibit activity by disturbing electron transfer. Indeed, our NADPH consumption results demonstrated that N-glycosylated iNOS consumes NADPH more slowly. Taken together, our results indicate that iNOS is N-glycosylated at its Asn695 residue and N-glycosylation of Asn695 might suppress iNOS activity by disturbing electron transfer.

Modulation of VDR and Cell Cycle-Related Proteins by Vitamin D in Normal Pancreatic Cells and Poorly Differentiated Metastatic Pancreatic Cancer Cells.

Many in vitro studies support the general idea that vitamin D plays a protective role against cancer. Increased doses of vitamin D dietary supplements have been widely used for the potential anticancer benefits of vitamin D. However, despite substantial epidemiological research, there are no clear conclusive data to support the use of vitamin D as a cancer preventive or treatment agent. In the, herein, reported study, we checked the effects of 1,25-dihydroxyvitamin D3 concentrations on the expression level of the vitamin D receptor (VDR) and cell cycle-related proteins CDKN1A (p21) and CDK1 in pancreatic cells and Panc-1 pancreatic cancer (PC) cells. We found that VDR, CDKN1A, and CDK1 were upregulated by an increase in 1,25-dihydroxyvitamin D3 concentration in normal pancreatic cells but not in the advanced cancer cell line Panc-1 from poorly differentiated metastatic PC cells. A further increase in 1,25-dihydroxyvitamin D3 concentration above the physiological range significantly downregulated the expression of VDR, indicating that VDR is modulated by VDR levels to maintain normal functioning during dramatic variations in vitamin D concentration. By increasing the level of cell cycle inhibitory and promoting proteins p21 and CDK1, vitamin D theoretically has both preventive and promoting effects on pancreatic cell division.

Alterations of circular RNAs in hyperglycemic human endothelial cells.

Circular RNA (circRNA), a family of RNA generated by RNA circularization, is ubiquitously expressed in tissues and possesses increasingly important biological functions. Hyperglycemia-induced endothelial dysfunction is an initiating event in the pathogenesis of diabetes-associated cardiovascular complications. How high glucose may affect circRNAs is unknown. To address this issue, human endothelial cells were exposed to high glucose treatment and the changes of circRNAs were measured by RNA sequencing. A total 3686 circRNAs, including 1040 previously unrecorded circRNAs, were detected; and 95 different expression (DE) circRNAs were observed. The host genes of these DE circRNAs were further studied by function enrichment analyses. These analyses revealed genes of phosphoproteins, transferases, and zine finger proteins. Since circRNAs can function as a microRNA (miRNA) sponge, circRNAs-miRNAs interaction networks were explored by bioinformatics. These analyses identified a number of miRNAs, which might interact with DE circRNAs and play roles in the actions of high glucose on endothelial cells. These results demonstrate that high glucose exposure profoundly changes circRNA expression in endothelial cells. Altered circRNA expression may contribute to the effects of high glucose on endothelial function in diabetes.

Blended learning in medical physiology improves nursing students' study efficiency.

The rapid development of mobile phones and communication networks is profoundly changing the lives of people in China. With the gradual growth of Wi-Fi on college and university campuses, Chinese schools are setting off a wave of teaching reform combining online material with traditional classroom instruction. We adapted a Chinese University massive open online course physiology course into a private university online course, specifically designed for second-semester bachelor's level nursing students at Taishan Medical University. This online course blended with classroom teaching was offered to 108 freshmen from two parallel reform classes. A third class of 55 students was offered the traditional classroom lecture-based course as a control. Impressive teaching effects were achieved in reform classes, as indicated by significant improvement in student performance on the final examination and positive student feedback. The student surveys showed that 68% of students preferred the blended course over traditional classroom courses. The most highly rated advantages of the blended course were flexible learning time (84%) and improvement of independent study skills (75%). As higher education enters the internet era, exploiting the high-quality cyber resources may be the fastest and most economical way to improve teaching efficiency and enhance students' study experience.

Effects of Alpha-Synuclein on Primary Spinal Cord Neurons Associated with Apoptosis and CNTF Expression.

Spinal cord injury (SCI) often causes neurological deficits with poor recovery; the treatment, however, is far from satisfaction, and the mechanisms remain unclear. Using immunohistochemistry and western blotting analysis, we found α-synuclein (SNCA) was significantly up-regulated in the spinal caudal segment of rats subjected to spinal cord transection at 3 days post-operation. Moreover, the role of SNCA on neuronal growth and apoptosis in vitro was determined by using overexpressing and interfering SNCA recombined plasmid vectors, and the underlying mechanism was detected by QRT-PCR and western blotting. Spinal neurons transfected with SNCA-shRNA lentivirus gave rise to an optimal neuronal survival, while it results in cell apoptosis in SNCA-ORF group. In molecular level, SNCA silence induced the up-regulation of CNTF and down-regulation of Caspase7/9. Together, endogenous SNCA plays a crucial role in spinal neuronal survival, in which the underlying mechanism may be linked to the regulation both apoptotic genes (Caspase7/9) and CNTF. The present findings therefore provide novel insights into the role of SNCA in spinal cord and associated mechanism, which may provide novel cue for the treatment of SCI in future clinic trials.

Role of vitamin D receptor gene polymorphisms in pancreatic cancer: a case-control study in China.

The study was conducted to investigate the relationship between vitamin D receptor (VDR) gene rs2228570 and rs1544410 polymorphisms and pancreatic cancer (PC). Two hundred fifty-eight PC patients and 385 healthy controls were enrolled in this study. The genotypes of rs2228570 and rs1544410 were assayed using the polymerase chain reaction/restriction fragment length polymorphism (PCR-RFLP) method. Univariate and multivariate logistic regression analyses were applied to determine the association between PC-onset risk and VDR gene polymorphisms. Contingency table analysis was performed to evaluate the relationship between the gene polymorphisms and clinicopathological tumor features such as location, pathological differentiation, and the TNM classification of PC. In rs2228570, the T loci and genotypes with T allele could increase the risk of PC; in rs1544410, the G loci and genotypes AG + GG could decrease the onset risk of PC significantly. The contingency table analysis indicated that the rs2228570 polymorphisms were correlated with the pathological differentiation of PC significantly, and the rs1544410 polymorphisms were correlated with the TNM classification of PC significantly. In conclusion, the VDR gene polymorphisms were correlated with incidence, pathological differentiation, and the TNM classification of PC significantly in our study population. So, the VDR polymorphisms have important implications in the incident rate and survival rate of PC.

Transplantation of olfactory ensheathing cells promotes the recovery of neurological functions in rats with traumatic brain injury associated with downregulation of Bad.

BACKGROUND AIMS: The neuroprotective effects of olfactory ensheathing cells (OECs) after transplantation have largely been known in the injured nervous system. However, the underlying mechanisms still must be further elucidated. We explored the effects of OEC transplantation on the recovery of neurophysiologic function and the related anti-apoptosis mechanism in acute traumatic brain injury. METHODS: The OECs from neonatal Sprague-Dawley rats were isolated, identified and labeled and then were immediately transplanted into the regions surrounding the injured brain site that is resulted from free-weight drop injury. RESULTS: Nerve growth factor and it's recepor, p75 was expressed in cultured OECs. Transplanted OECs survived, migrated around the injury site and significantly improved the neurological severe scores compared with the control group (P < 0.05). OEC transplantation significantly increased the number of GAP-43-immunopositive fibers and synaptophysin-positive vesicles (P < 0.05) but significantly decreased the number of apoptotic cells (P < 0.05). On the molecular level, the expression of Bad in the OEC transplantation group was significantly downregulated (P < 0.05). CONCLUSIONS: OEC transplantation could effectively improve neurological deficits in TBI rats; the underlying mechanism may be related with their effects on neuroprotection and regeneration induction, which is associated with the downregulation of the apoptotic molecule Bad.

The Role of EGG in Identifying Prevocalic Glottal Stop.

OBJECTIVE: The aim of the study is to investigate the use of incidences and characteristics of Prevocalic Electroglottographic Signal (PVES) derived from electroglottography (EGG) in characterizing glottal stops (GS) in cleft palate speech. METHODS: Mandarin nonaspirated monosyllabic first-tone words were used for the speech sampling procedure. A total of 1680 utterances (from 83 patients with repaired cleft palates) were divided into three categories based on the results of auditory-perceptual evaluation of recorded speech sounds by three independent reviewers: [Category A (absence of GS agreed by all three reviewers) (n = 1192 tokens), Category B (two out of three reviewers agreed on the presence of a GS) (n = 181 tokens) and Category C (all three reviewers agreed on the presence of a GS) (n = 307 tokens)]. The EGG signals of the 1680 utterances were analyzed using a MATLAB program to automatically mark the instances of PVES (amplitude and time-interval) in the GS utterances. RESULTS: The result showed that the incidence of EGG PVES presented good positive correlation with auditory-perceptual evaluation (r = 0.703, P＜0.000). Statistical analysis revealed a significant difference in mean PVES amplitude among different groups (P＜0.05). There was a significant distinction in the time interval between groups A and B, as well as in groups A and C (P＜0.05). CONCLUSIONS: The study suggests PVES can be an objective means of identifying GS in cleft palate speech. It also indicates that proportion of amplitude and time interval of PVES tend to be positively correlate with subjective assessment.

Galactooligosaccharides in infant formulas: Maillard reaction characteristics and influence on formation of advanced glycation end products.

As prebiotics supplemented in infant formulas (IFs), galactooligosaccharides (GOSs) also have many other biological activities; however, their Maillard reaction characteristics are still unclear. We investigated the Maillard reactivity of GOSs and their effects on advanced glycation end product (AGE) formation during IF processing. The results showed that AGE and HMF formation was temperature-dependent and reached the maximum at pH 9.0 in the Maillard reaction system of GOSs and Nα-acetyl-L-lysine. Acidic conditions accelerated HMF formation; however, protein cross-linking was more likely to occur under alkaline conditions. The degree of polymerization (DP) of GOSs had no significant effect on AGEs formation (except pyrraline); however, the greater the DP, the higher the concentration of HMF and pyrraline. Besides, compared with arginine and casein, lysine and whey protein were more prone to Maillard reaction with GOSs. GOSs promoted AGEs formation in a dose-dependent manner during the processing of IFs. These results provide a reliable theoretical basis for application of GOSs in IFs.

Comparative effects of pectin and hydrolyzed pectin coating as pre-frying treatments on acrylamide formation in potato chips.

This study aimed to compare the effects of pectin and hydrolyzed pectin coating as pre-frying treatments on acrylamide content and quality characteristics of fried potato chips. The hydrolyzed pectin with molecular weight (Mw) of 8.81 ± 0.49 kDa was obtained through partial degradation of pectin (Mw: 747.57 ± 6.73 kDa) using pectinase. Results showed that both pectin and hydrolyzed pectin coating significantly inhibited acrylamide formation and inhibition rates exceeded 90 %. Hydrolyzed pectin had stronger inhibitory activity against acrylamide formation than pectin, especially when the concentration of hydrolyzed pectin was >2 %, its inhibitory rate exceeded 95 %. Compared to pectin coating, hydrolyzed pectin coating endow fried potato chips with smaller browning, higher crispness, less moisture but higher oil content. Overall, hydrolyzed pectin had better application prospects than pectin in inhibiting acrylamide formation of fried potato chips.

Association between liver fat level and risk of hypertension: evidence from a Chinese health examination dataset.

BACKGROUND: Hypertension development is predominantly influenced by inflammation, excessive fat deposition, and metabolic irregularities. Among these factors, liver fat accumulation is a critical metabolic disorder. However, the quantification of liver fat levels and its associated risk for hypertension incidence remain ambiguous. This project is designed to explore the association between liver fat levels and the risk of hypertension in a healthy population. METHODS: This cross-sectional study involved 4955 participants from the Health Management Center at Henan Provincial People's Hospital who were surveyed between February 2020 and February 2023. Participants were categorized into four groups based on liver fat quartiles. Subgroup analyses, restricted cubic spline regression models, and logistic regression were utilized to assess the association between liver fat levels and hypertension risk. The relationships between liver fat levels and inflammatory markers were examined using multiple linear regression models. Additionally, a mediation analysis was conducted to explore the role of inflammatory factors in the relationship between liver fat and hypertension risk. RESULTS: Participants with hypertension exhibited greater liver fat levels than did those without hypertension. An increased risk of hypertension was associated with elevated liver fat levels, even after adjusting for other covariates [Q4 vs. Q1 in model II: odds ratio (OR = 1.28), 95% confidence interval (CI) = 1.04-1.59, P = 0.022; P for trend = 0.039]. A nonlinear relationship was observed between liver fat level and hypertension risk, with a notable increase in hypertension risk occurring at liver fat levels greater than 8.65%. Additionally, a positive correlation was found between inflammatory markers and liver fat levels. A mediation effect of 4.76% was noted, linking hypertension risk and liver fat levels through neutrophils. CONCLUSION: Liver fat levels exceeding 8.65% significantly elevated the risk of hypertension. Inflammatory factors serve as crucial mediators of the relationship between liver fat and hypertension.

Antifungal Activity and Mechanism of Electron Beam Irradiation Against Rhizopus oryzae.

Electron beam irradiation is a physical fungicidal technique that has emerged as a potential application in China. However, its antifungal activity and mechanism against Rhizopus oryzae have not been reported. Thus, this study aimed to investigate the antifungal activity and mechanism of electron beam irradiation of R. oryzae. The antifungal activity analysis showed that the D10 value and complete elimination dose of R. oryzae irradiated by electron beam were 1.73 kGy and 8.08 kGy, respectively. Electron beam irradiation has a strong inhibitory effect on the filamentous biomass of R. oryzae. To reveal the antifungal mechanism of electron beam against R. oryzae, this study analyzed the dynamic changes in the cell wall, cell membrane, and oxidative stress induced by different irradiation doses. The results showed that electron beam irradiation destroyed the cell wall structure of R. oryzae, increasing chitinase activity and decreasing chitin content. Cell membrane integrity is disrupted, increasing relative conductivity, decreasing pH values, and decreasing soluble protein content. Electron beam irradiation causes oxidative stress in cells, increasing H2O2 content, decreasing antisuperoxide anion activity, decreasing DPPH free radical scavenging activity, and inhibiting defense enzyme (CAT and SOD) activity. This phenomenon indicates that electron beams can cause structural damage to and metabolic dysfunction of cells and disorders of redox homeostasis, which may be the main cause of growth inhibition and cell death in R. oryzae.

SPOP regulates the expression profiles and alternative splicing events in human hepatocytes.

Speckle type BTB/POZ protein (SPOP) may have cancer promoting or inhibiting effects. At present, the role of SPOP in hepatocellular carcinoma (HCC) has rarely been studied. In this study, to investigate the effects of SPOP in HCC and elucidate the underlying molecular mechanisms of its relationship with genes, differentially expressed genes (DEGs) were classified through RNA sequencing. The gene ontology analysis and Kyoto Encyclopedia of Genes and Genomes functional pathway analysis were used to further predict the function of DEGs after the overexpression of SPOP. The biological function of SPOP-regulated alternative splicing events in cells is comprehensively assessed. The Cancer Genome Atlas database and Gene Expression Omnibus dataset were performed to evaluate the correlation between SPOP and HCC progression. Due to SPOP overexpression, 56 DEGs in the HCC related pathway were further identified. The results showed that SPOP overexpression facilitated the cell proliferation and changed the gene expression profiles of human normal hepatocytes. SPOP-regulated alternative splicing events were involved in pathways associated with cellular processes, metabolism, environmental information procession, organismal systems, and so on. In conclusion, SPOP may potentially exhibit tumor-promoting effects, necessitating further investigations to unveil its molecular mechanisms comprehensively.