Development of a Simple Scoring System for Predicting Discharge Safety from the Medical ICU to Low-Acuity Wards: The Role of the Sequential Organ Failure Assessment Score, Albumin, and Red Blood Cell Distribution Width.

Despite advancements in artificial intelligence-based decision-making, transitioning patients from intensive care units (ICUs) to low-acuity wards is challenging, especially in resource-limited settings. This study aimed to develop a simple scoring system to predict ICU discharge safety. We retrospectively analyzed patients admitted to a tertiary hospital's medical ICU (MICU) between July 2016 and December 2021. This period was divided into two phases for model development and validation. We identified risk factors associated with unexpected death within 14 days of MICU discharge and developed a predictive scoring system that incorporated these factors. We verified the system's performance using validation data. In the development cohort, 522 patients were discharged from the MICU, and 42 (8.04%) died unexpectedly. In multivariate analysis, the Sequential Organ Failure Assessment (SOFA) score (odds ratio [OR] 1.26, 95% confidence interval [CI] 1.13-1.41), red blood cell distribution width (RDW) (OR 1.20, 95% CI 1.07-1.36), and albumin (OR 0.37, 95% CI 0.16-0.84) were predictors of unexpected death. Each variable was assigned a weighted point in the scoring system, and the area under the curve (AUC) was 0.788 (95% CI 0.714-0.855). The scoring system was performed using an AUC of 0.738 (95% CI 0.653-0.822) in the validation cohort of 343 patients with 9.62% of unexpected deaths. When a cut-off of 0.032 was applied, a sensitivity and a specificity of 81.8% and 55.2%, respectively, were achieved. This simple bedside predictive score for ICU discharge uses the SOFA score, albumin level, and RDW to aid in timely decision-making and optimize critical care facility allocation in resource-limited settings.

The N-Terminal Region of Cucumber Mosaic Virus 2a Protein Is Involved in the Systemic Infection in Brassica juncea.

Brassica juncea belongs to the Brassicaceae family and is used as both an oilseed and vegetable crop. As only a few studies have reported on the cucumber mosaic virus (CMV) in B. juncea, we conducted this study to provide a basic understanding of the B. juncea and CMV interactions. B. juncea-infecting CMV (CMV-Co6) and non-infecting CMV (CMV-Rs1) were used. To identify the determinants of systemic infection in B. juncea, we first constructed infectious clones of CMV-Co6 and CMV-Rs1 and used them as pseudo-recombinants. RNA2 of CMV was identified as an important determinant in B. juncea because B. juncea were systemically infected with RNA2-containing pseudo-recombinants; CMV-Co6, R/6/R, and R/6/6 were systemically infected B. juncea. Subsequently, the amino acids of the 2a and 2b proteins were compared, and a chimeric clone was constructed. The chimeric virus R/6Rns/R6cp, containing the C-terminal region of the 2a protein of CMV-Rs1, still infects B. juncea. It is the 2a protein that determines the systemic CMV infection in B. juncea, suggesting that conserved 160G and 214A may play a role in systemic CMV infection in B. juncea.

Inhibition of lysyl oxidase by pharmacological intervention and genetic manipulation alleviates epilepsy-associated cognitive disorder.

Epilepsy-associated cognitive disorder (ECD), a prevalent comorbidity in epilepsy patients, has so far uncharacterized etiological origins. Our prior work revealed that lysyl oxidase (Lox) acted as a novel contributor of ferroptosis, a recently discovered cell death mode in the regulation of brain function. However, the role of Lox-mediated ferroptosis in ECD remains unknown. ECD mouse model was established 2 months later following a single injection of kainic acid (KA) for. After chronic treatment with KA, mice were treated with different doses (30 mg/kg, 100 mg/kg and 300 mg/kg) of Lox inhibitor BAPN. Additionally, hippocampal-specific Lox knockout mice was also constructed and employed to validate the role of Lox in ECD. Cognitive functions were assessed using novel object recognition test (NOR) and Morris water maze test (MWM). Protein expression of phosphorylated cAMP-response element binding (CREB), a well-known molecular marker for evaluation of cognitive performance, was also detected by Western blot. The protein distribution of Lox was analyzed by immunofluorescence. In KA-induced ECD mouse model, ferroptosis process was activated according to upregulation of 4-HNE protein and a previously discovered ferroptosis in our group, namely, Lox was remarkably increased. Pharmacological inhibition of Lox by BAPN at the dose of 100 mg/kg significantly increased the discrimination index following NOR test and decreased escape latency as well as augmented passing times within 60 s following MWM test in ECD mouse model. Additionally, deficiency of Lox in hippocampus also led to pronounced improvement of deficits in ECD model. These findings indicate that the ferroptosis regulatory factor, Lox, is activated in ECD. Ablation of Lox by either pharmacological intervention or genetic manipulation ameliorates the impairment in ECD mouse model, which suggest that Lox serves as a promising therapeutic target for treating ECD in clinic.

Complete mitochondrial genome of the diving beetle, Cybister brevis Aubé, 1838 (Coleoptera, Dytiscidae) from Jeju Island.

The mitochondrial genome of Cybister brevis Aubé, 1838, is 16,198 bp long and includes 37 genes that are highly conserved in the family Dytiscidae. Phylogenetic analysis revealed that all genera in Dytiscidae, except Hydroporus and Oreodytes, are monophyletic. The Hydroporini tribe was found to be polyphyletic and closely associated with the Hygrotini, Bidessini, and Hyphydrini tribes. Dytiscinae was found to be a highly divergent polyphyletic group comprising three distinct clades. This study also revealed that C. brevis is closely related to Cybister japonicus and that the tribe Cybistrini diverged relatively early compared to other tribes in Hydroporinae. These findings are consistent with those of previous studies and provide new insights into the phylogeny of the Dytiscidae family, which has previously shown discrepancies between morphological characteristics and molecular data. The genome-level analyses conducted in this study serve as a valuable foundation for future investigations into the Dysticidae evolutionary history.

Quantitative and qualitative mutational impact of ionizing radiation on normal cells.

The comprehensive genomic impact of ionizing radiation (IR), a carcinogen, on healthy somatic cells remains unclear. Using large-scale whole-genome sequencing (WGS) of clones expanded from irradiated murine and human single cells, we revealed that IR induces a characteristic spectrum of short insertions or deletions (indels) and structural variations (SVs), including balanced inversions, translocations, composite SVs (deletion-insertion, deletion-inversion, and deletion-translocation composites), and complex genomic rearrangements (CGRs), including chromoplexy, chromothripsis, and SV by breakage-fusion-bridge cycles. Our findings suggest that 1 Gy IR exposure causes an average of 2.33 mutational events per Gb genome, comprising 2.15 indels, 0.17 SVs, and 0.01 CGRs, despite a high level of inter-cellular stochasticity. The mutational burden was dependent on total irradiation dose, regardless of dose rate or cell type. The findings were further validated in IR-induced secondary cancers and single cells without clonalization. Overall, our study highlights a comprehensive and clear picture of IR effects on normal mammalian genomes.

[Research Progress on Characteristics of Human Microplastic Pollution and Health Risks].

Microplastic pollution is not only an environmental problem but also a social problem. Many studies have been conducted on the sources, abundance, and distribution of microplastics in the environment, but an understanding of human exposure levels and potential health risks remains very limited. Based on the bibliometric methods, the present review systematically summarized the exposure pathways of microplastics in humans, and then the characteristics and potential adverse impacts on human health were expounded upon. Available literature showed that microplastics in human bodies were mainly concentrated on sizes smaller than 50 µm, and polyethylene (PE), polypropylene (PP), and polyethylene terephthalate (PET) were the main polymers. Microplastics in environments entered human bodies mainly through food and respiratory pathways, then accumulated in lung and gastrointestinal tissues. Most importantly, small-sized microplastics could distribute in tissues and organs via the circulatory system. The results from lab-based toxicological experiments showed that microplastics not only posed threats to cell membrane integrity, immune stress, gut microbiota, and energy metabolism but also had potentially adverse impacts on the reproductive system. To further understand the health risks of microplastic pollution, it is necessary to promote research on the toxicological effects of microplastics as well as the inner mechanisms and also to establish risk assessment frameworks for evaluating microplastic pollution. These works are crucial to preventing the risks of microplastic pollution with scientific evidence.

Orally Administrated Inflamed Colon-Targeted Nanotherapeutics for Inflammatory Bowel Disease Treatment by Oxidative Stress Level Modulation in Colitis.

Inflammatory bowel disease (IBD) is characterized by an inappropriate and persistent inflammatory immune response and is often accompanied by excessive reactive oxygen species (ROS) production. For effective IBD treatment, there is a high demand for safe and targeted therapy that can be orally administered. In this study, we aimed to propose the use of inflamed colon-targeted antioxidant nanotherapeutics (ICANs) for in situ oxidative stress level modulation in colitis. ICANs consist of mesoporous silica nanoparticles (MSNs) with surface-attached ROS-scavenging ceria nanoparticles (CeNPs), which are further coated with poly(acrylic acid) (PAA) to facilitate preferential adherence to inflamed colon tissues through electrostatic interaction. We achieved a high ROS-scavenging property that remained effective even after artificial gastrointestinal fluid incubation by optimization of the molecular weight and PAA-coating pH. The orally administered ICANs demonstrated enhanced adherence to inflamed colon tissues in an acute inflammation mouse model of IBD induced by dextran sulfate sodium. This targeted delivery resulted in gut microenvironment modulation by regulating redox balance and reducing inflammatory cell infiltration, thereby suppressing the colitis-associated immune response. These findings highlight the potential of noninvasive ICANs as a promising candidate for treating inflammatory intestinal diseases by oxidative stress level modulation in colitis.

Aspergillus Galactomannan Titer as a Diagnostic Marker of Invasive Pulmonary Aspergillosis in Lung Transplant Recipients: A Single-Center Retrospective Cohort Study.

Invasive pulmonary aspergillosis (IPA) can occur in immunocompromised patients, and an early detection and intensive treatment are crucial. We sought to determine the potential of Aspergillus galactomannan antigen titer (AGT) in serum and bronchoalveolar lavage fluid (BALF) and serum titers of beta-D-glucan (BDG) to predict IPA in lung transplantation recipients, as opposed to pneumonia unrelated to IPA. We retrospectively reviewed the medical records of 192 lung transplant recipients. Overall, 26 recipients had been diagnosed with proven IPA, 40 recipients with probable IPA, and 75 recipients with pneumonia unrelated to IPA. We analyzed AGT levels in IPA and non-IPA pneumonia patients and used ROC curves to determine the diagnostic cutoff value. The Serum AGT cutoff value was 0.560 (index level), with a sensitivity of 50%, specificity of 91%, and AUC of 0.724, and the BALF AGT cutoff value was 0.600, with a sensitivity of 85%, specificity of 85%, and AUC of 0.895. Revised EORTC suggests a diagnostic cutoff value of 1.0 in both serum and BALF AGT when IPA is highly suspicious. In our group, serum AGT of 1.0 showed a sensitivity of 27% and a specificity of 97%, and BALF AGT of 1.0 showed a sensitivity of 60% and a specificity of 95%. The result suggested that a lower cutoff could be beneficial in the lung transplant group. In multivariable analysis, serum and BALF AGT, with a minimal correlation between the two, showed a correlation with a history of diabetes mellitus.

GPX4 overexpressed non-small cell lung cancer cells are sensitive to RSL3-induced ferroptosis.

Ferroptosis can be induced by inhibiting antioxidant enzymes GPX4 or system Xc-, increased intracellular iron concentrations, and lipid peroxidation. Recently, it has been suggested that ferroptosis can be an effective way to induce cancer cell death, although the specific relevance and mechanism of ferroptosis have not been fully elucidated. Here, we investigated the anticancer effects of ferroptosis inducers erastin and RSL3 on non-small cell lung cancer (NSCLC) cells. RSL3 induced cell death more effectively in NSCLC cells than erastin, with limited cytotoxicity in BEAS-2B normal bronchial epithelial cells. The sensitivity of NSCLC cells to RSL3 induced death was dependent on GPX4 expression levels; the effect of RSL3 was reversed by ferrostatin-1 (a ferroptosis inhibitor) but not by Z-VAD-FMK, chloroquine, bafilomycin A1, or necrostatin-1. RSL3 induced ferroptosis by promoting lipid peroxidation, elevating intracellular LIP concentration and ROS level, and blocking GSH-to-GSSH conversion through the inhibition of GPX4 and induction of Nrf2/HO1. Furthermore, RSL3 induced autophagosomes but disrupted the formation of autolysosomes with lysosomal membrane destabilization. GPX4 knockdown had a similar effect on ferroptosis phenotypes as RSL3. Taken together, RSL3-induced ferroptosis depends on the regulation of GPX4-Nrf2/HO1 in NSCLC cells. These results may be useful in predicting the ferroptosis response in NSCLC as well as drug resistant cancer cells.

G-Protein ß-Subunit Gene TaGB1-B Enhances Drought and Salt Resistance in Wheat.

In the hexaploid wheat genome, there are three Gα genes, three Gß and twelve Gγ genes, but the function of Gß in wheat has not been explored. In this study, we obtained the overexpression of TaGB1 Arabidopsis plants through inflorescence infection, and the overexpression of wheat lines was obtained by gene bombardment. The results showed that under drought and NaCl treatment, the survival rate of Arabidopsis seedlings' overexpression of TaGB1-B was higher than that of the wild type, while the survival rate of the related mutant agb1-2 was lower than that of the wild type. The survival rate of wheat seedlings with TaGB1-B overexpression was higher than that of the control. In addition, under drought and salt stress, the levels of superoxide dismutase (SOD) and proline (Pro) in the wheat overexpression of TaGB1-B were higher than that of the control, and the concentration of malondialdehyde (MDA) was lower than that of the control. This indicates that TaGB1-B could improve the drought resistance and salt tolerance of Arabidopsis and wheat by scavenging active oxygen. Overall, this work provides a theoretical basis for wheat G-protein ß-subunits in a further study, and new genetic resources for the cultivation of drought-tolerant and salt-tolerant wheat varieties.

Cascading effects of seed-stem-individual spatial patterns along a grazing gradient.

Studying the seed trait-stem trait-individual spatial pattern system is helpful for understanding the developmental direction of plant dynamics and populations under grazing disturbance as well as the antagonistic relationship between animals and plants, but few systematic analyses of this spatial pattern system have been carried out. Kobresia humilis is the dominant species in alpine grasslands. We studied K. humilis seed traits and their relationship with K. humilis reproductive individuals, the relationship between reproductive and vegetative stems, and the weights and spatial patterns of reproductive and nonreproductive individuals under four grazing treatments: no grazing (control), light grazing, moderate grazing and heavy grazing. We explored the relationship among seed size and seed number with reproductive stems and vegetative stems along the grazing gradient and assessed the spatial pattern changes between reproductive and nonreproductive individuals. The results showed the following: (1) Seed size increased with increasing grazing intensity, and the coefficient of variation for seed size and seed number in the heavy grazing treatment was greater than 0.6. (2) The structural equation model showed that grazing treatment had a positive effect on seed number, seed size and reproductive stem number and a negative effect on reproductive stem weight. (3) Grazing treatment did not affect the resource allocation to reproductive stems and vegetative stems per unit length of reproductive K. humilis individuals. (4) Compared with the number of reproductive individuals in the no grazing treatment, the number in the heavy grazing treatment decreased significantly, and the negative correlation between reproductive individuals and nonreproductive individuals changed from a full-scale negative correlation to a small-scale negative correlation and a large-scale positive correlation. Our study showed that grazing could activate and change the resource allocation pattern of dominant species in a grassland and have significant positive effects on reproductive stem number, reproductive stem weight, seed number and seed size. Along a grazing intensity gradient, with the increase in distance between reproductive and nonreproductive individuals, the transformation of intraspecific relationships from a negative correlation to a positive correlation is an ecological strategy conducive to population survival.

Association of general and central obesity, and their changes with risk of knee osteoarthritis: a nationwide population-based cohort study.

In this study, we aimed to evaluate the association between general and central obesity, and their changes with risk of knee osteoarthritis (OA) using retrospective cohort data collected from the Korean National Health Insurance Service. We studied 1,139,463 people aged 50 and over who received a health examination in 2009. To evaluate the association between general and/or central obesity and knee OA risk, a Cox proportional hazard models were used. Additionally, we investigate knee OA risk according to the change in obesity status over 2 years for subjects who had undergone health examinations for 2 consecutive years. General obesity without central obesity (HR 1.281, 95% CI 1.270-1.292) and central obesity without general obesity (HR 1.167, 95% CI 1.150-1.184) were associated with increased knee OA risk than the comparison group. Individuals with both general with central obesity had the highest risk (HR 1.418, 95% CI 1.406-1.429). This association was more pronounced in women and younger age group. Remarkably, the remission of general or central obesity over two years was associated with decreased knee OA risk (HR 0.884; 95% CI 0.867-0.902; HR 0.900; 95% CI 0.884-0.916, respectively). The present study found that both general and central obesity were associated with increased risk of knee OA and the risk was highest when the two types of obesity were accompanied. Changes in obesity status have been confirmed to alter the risk of knee OA.

Association between knee osteoarthritis and the risk of cardiovascular disease and the synergistic adverse effects of lack of exercise.

We aimed to determine whether knee OA is associated with CVD risk and all-cause death and to evaluate whether the association differs by exercise behavior. We used Korea National Health Insurance Service (KNHIS) database and included 201,466 participants (7572 subjects diagnosed with knee OA) who underwent health screening between 2009 and 2015. Those who had been diagnosed with knee OA or CVD before the index year were excluded. Cox proportional hazard models were used after adjusting for sociodemographic and CVD risk factors to evaluate the association between knee OA and CVD risk and all-cause death. Stratification analysis was further performed to determine the effect of exercise behavior on this relationship. During a median follow-up of 7.06 ± 2.24 years, 8743 CVD (2510 MI and 6553 stroke) cases developed. Individuals with knee OA had increased risks of CVD [hazard ratio (HR) 1.26, 95% confidence interval (CI) 1.15-1.38], myocardial infarction (MI) (HR 1.20, 95% CI 1.00-1.44), and stroke (HR 1.29, 95% CI 1.16-1.43) compared with those without knee OA. Those with knee OA who did not exercise had an increased risk of CVD (HR 1.25, 95% CI 1.11-1.40), whereas no significant increased CVD risk was observed in those with knee OA who exercised at least once a week (HR 1.11, 95% CI 0.96-1.28). There was no association between knee osteoarthritis and all-cause death. Knee OA was independently associated with an increased risk of CVD. Lack of exercise might have a synergistic adverse effect on the association between knee OA and CVD.

Astrocytic lactate dehydrogenase A regulates neuronal excitability and depressive-like behaviors through lactate homeostasis in mice.

Alterations in energy metabolism are associated with depression. However, the role of glycolysis in the pathogenesis of depression and the underlying molecular mechanisms remain unexplored. Through an unbiased proteomic screen coupled with biochemical verifications, we show that the levels of glycolysis and lactate dehydrogenase A (LDHA), a glycolytic enzyme that catalyzes L-lactate production, are reduced in the dorsomedial prefrontal cortex (dmPFC) of stress-susceptible mice in chronic social defeat stress (CSDS) model. Conditional knockout of LDHA from the brain promotes depressive-like behaviors in both male and female mice, accompanied with reduced L-lactate levels and decreased neuronal excitability in the dmPFC. Moreover, these phenotypes could be duplicated by knockdown of LDHA in the dmPFC or specifically in astrocytes. In contrast, overexpression of LDHA reverses these phenotypic changes in CSDS-susceptible mice. Mechanistic studies demonstrate that L-lactate promotes neuronal excitability through monocarboxylic acid transporter 2 (MCT2) and by inhibiting large-conductance Ca2+-activated potassium (BK) channel. Together, these results reveal a role of LDHA in maintaining neuronal excitability to prevent depressive-like behaviors.

Foxtail millet MYB-like transcription factor SiMYB16 confers salt tolerance in transgenic rice by regulating phenylpropane pathway.

R2R3-MYB transcription factors play an important role in the synthesis of phenylpropanoid-derived compounds, which in turn provide salt tolerance in plant. In this study, we found that the expression of foxtail millet R2R3-MYB factor SiMYB16 can be induced by salt and drought. SiMYB16 is localized in the nucleus and acts as a transcriptional activator. Phylogenetic analysis indicates that SiMYB16 belongs to the R2R3-MYB transcription factor family subgroup 24. Transgenic rice expressing SiMYB16 (OX16) had a higher survival rate, lower malondialdehyde content, and heavier fresh weight compared with type (WT) under salt stress conditions. The transgenic plants also had a higher germination rate in salt treatment conditions and higher yield in the field compared with wild-type plants. Transcriptome analysis revealed that the up-regulated differential expression genes in the transgenic rice were mainly involved in phenylpropanoid biosynthesis, fatty acid elongation, phenylalanine metabolism, and flavonoid biosynthesis pathways. Quantitative real-time PCR analysis also showed that the genes encoding the major enzymes in the lignin and suberin biosynthesis pathways had higher expression level in SiMYB16 transgenic plants. Correspondingly, the content of flavonoid and lignin, and the activity of fatty acid synthase increased in SiMYB16 transgenic rice compared with wild-type plants under salt stress treatment. These results indicate that SiMYB16 gene can enhance plant salt tolerance by regulating the biosynthesis of lignin and suberin.

Synthesis and application of the methyl analogues of S-adenosyl-L-methionine / 生物工程学报

Methylation plays a vital role in biological systems. SAM (S-adenosyl-L-methionine), an abundant cofactor in life, acts as a methyl donor in most biological methylation reactions. SAM-dependent methyltransferases (MTase) transfer a methyl group from SAM to substrates, thereby altering their physicochemical properties or biological activities. In recent years, many SAM analogues with alternative methyl substituents have been synthesized and applied to methyltransferases that specifically transfer different groups to the substrates. These include functional groups for labeling experiments and novel alkyl modifications. This review summarizes the recent progress in the synthesis and application of SAM methyl analogues and prospects for future research directions in this field.

The Clinical Manifestation, Executive Dysfunction, and Caregiver Strain in Subthreshold Attention-Deficit/Hyperactivity Disorder

Objective@#Subthreshold attention-deficit/hyperactivity disorder (ADHD) has been suggested to be a “morbid condition” which also needs medical attention. @*Methods@#The present study recruited 89 children with subthreshold ADHD (sADHD), 115 children with diagnosed ADHD (cADHD), and 79 healthy controls (HC) to explore the clinical manifestation, executive functions (EFs) of sADHD, and the caregiver strain. The clinical manifestation was evaluated through clinical interviews and parent-reports. Executive functions were assessed both experimentally and ecologically. Caregiver strain was measured by a parent-reported questionnaire. @*Results@#For the clinical manifestation, both sADHD and cADHD indicated impairments when compared with HC. The comorbidities and the scaled symptoms indicated that the externalizing behaviors were relatively less serious in sADHD than cADHD, whereas the internalizing behaviors between two groups were comparable. For ecological EFs, sADHD scored between cADHD and HC in inhibition and working memory. For experimental EFs, sADHD was comparable to cADHD in inhibition, shifting, and was worse than cADHD in verbal working memory. For the caregiver strain, all scores of sADHD were between that in cADHD and that in HC. @*Conclusion@#Our present findings supported the suggestion of subthreshold ADHD as “morbid condition,” which should be treated with caution in clinical practice, especially for the internalizing behaviors and some key components of EFs.

Study on the mechanism of Taohong siwu decoction improving peripheral nerve injury induced by paclitaxel in rats / 中国药房

OBJECTIVE To explore the mechanism of Taohong siwu decoction （THD） improving peripheral nerve injury induced by paclitaxel （PTX） in rats. METHODS The effects of THD （1 g/mL drug-containing serum） and PTX （0.1 μmol/L） alone or in combination on the proliferation rate of Schwann cells line RSC96 as well as the expressions of lysosomal-associated membrane protein-2 （LAMP2）， autophagy marker protein yeast Atg 6 homolog （Beclin1）， phosphatidylinositol 3-kinase （PI3K）， protein kinase B （Akt）， and mammalian target of rapamycin （mTOR） were investigated， and then compared with autophagy promoter rapamycin and autophagy inhibitor 3-methyladenine （3-MA）. The effects of high-dose and low-dose THD on the expressions of myelin basic protein （MBP） and myelin protein zero （MPZ）， S100 calcium-binding protein （S100）， LAMP2， Beclin1， PI3K， Akt and mTOR were tested at the end of the experiment. RESULTS After treatment of THD+PTX， the proliferation rate of RSC96 cells was significantly higher than those treated with PTX alone. After treatment of THD+PTX or THD+ 3-MA， the protein expressions of LAMP2 and Beclin1 in RSC96 cells were significantly higher than those treated with PTX or 3- MA alone， while the protein expressions of PI3K， Akt and mTOR were significantly lower than those treated with PTX or 3-MA alone （P＜0.05）. Compared with model group， the protein expressions of MBP， MPZ， S100， LAMP2 and Beclin1 in sciatic nerve of rats were increased significantly in THD high-dose and low-dose groups， while the protein expressions of PI3K， Akt and mTOR were significantly decreased （P＜0.05）. CONCLUSIONS THD may activate Schwann cell autophagy by inhibiting the PI3K/Akt/ mTOR signaling pathway， thereby improving peripheral nerve injury caused by PTX.

Relationship among fasting plasma glacose coefficient of variation and macular morphology and microcirculation in patients with nonproliferative diabetic retinopathy / 国际眼科杂志(Guoji Yanke Zazhi)

AIM: To investigate the relationship among the fasting plasma glucose coefficient of variation(FPG-CV)and macular morphology and microcirculation in patients with nonproliferative diabetic retinopathy(NPDR).METHODS: A retrospective analysis of 82 cases(82 eyes)with NPDR admitted to our hospital from February 2018 to June 2022 was the research object, and another 82 cases(82 eyes)of non-diabetic retinopathy(NDR)patients during the same period were selected as the control group, and the clinical data of the two groups of patients were analyzed. Multivariate Logistic regression was used to analyze the risk factors affecting the incidence of NPDR, and the back propagation(BP)neural network model was established and evaluated. Pearson correlation was used to analyze the correlation among FPG-CV and macular morphology and microcirculation in patients. RESULTS: The results of multivariate Logistic regression analysis showed that the disease duration ≥7.2a, glycated hemoglobin A1c(HbA1c)≥7.7%, triglyceride(TG)≥1.9 mmol/L, microalbuminuria(MALB)≥24.5 mg/L, FPG-CV ≥9.8%, superficial capillary plexus-vessel density(SCP-VD)<27.6%, deep capillary plexus-vessel density(DCP-VD)<47.7%, foveal avascular zone(FAZ)area ≥0.38 mm2, central retinal thickness(CRT)≥197.7 μm and subfoveal choroidal thickness(SFCT)<227.7 μm were risk factors for NPDR(P<0.05). The number of hidden layer nodes is 5, and the receiver operating characteristic(ROC)curve, calibration curve and clinical decision curve show that the prediction model has good discrimination, accuracy and validity. The results of Pearson correlation analysis showed that FPG-CV was negatively correlated with SCP-VD, DCP-VD and SFCT(P<0.05); FPG-CV was positively correlated with FAZ area and CRT(P<0.05).CONCLUSION: The course of disease, HbA1c, TG, MALB, FPG-CV, SCP-VD, DCP-VD, FAZ area, CRT and SFCT are all related to the pathogenesis of NPDR. With the increase of FPG-CV, the indexes of macular morphology and microcirculation changed. FPG-CV was negatively correlated with SCP-VD, DCP-VD and SFCT and positively correlated with FAZ area and CRT.

Genome-Wide Analysis of the Peptidase M24 Superfamily in Triticum aestivum Demonstrates That TaM24-9 Is Involved in Abiotic Stress Response.

The peptidase M24 (Metallopeptidase 24, M24) superfamily is essential for plant growth, stress response, and pathogen defense. At present, there are few systematic reports on the identification and classification of members of the peptidase M24 proteins superfamily in wheat. In this work, we identified 53 putative candidate TaM24 genes. According to the protein sequences characteristics, these members can be roughly divided into three subfamilies: I, II, III. Most TaM24 genes are complex with multiple exons, and the motifs are relatively conserved in each sub-group. Through chromosome mapping analysis, we found that the 53 genes were unevenly distributed on 19 wheat chromosomes (except 3A and 3D), of which 68% were in triads. Analysis of gene duplication events showed that 62% of TaM24 genes in wheat came from fragment duplication events, and there were no tandem duplication events to amplify genes. Analysis of the promoter sequences of TaM24 genes revealed that cis-acting elements were rich in response elements to drought, osmotic stress, ABA, and MeJA. We also studied the expression of TaM24 in wheat tissues at developmental stages and abiotic stress. Then we selected TaM24-9 as the target for further analysis. The results showed that TaM24-9 genes strengthened the drought and salt tolerance of plants. Overall, our analysis showed that members of the peptidase M24 genes may participate in the abiotic stress response and provided potential gene resources for improving wheat resistance.