Methods: Fifty patients who underwent UBE-TLIF and 50 patients who underwent W-TLIF, each with >2 years of follow-up, were retrospectively analyzed. Outcomes included operative parameters, time to postoperative mobilization, paravertebral muscle atrophy and fat infiltration rates, clinical scores (Visual Analog Scale [VAS], Oswestry Disability Index [ODI], Japanese Orthopaedic Association [JOA]), modified Macnab criteria, fusion rates, and complications. Results: Compared with W-TLIF, the UBE-TLIF group had significantly less intraoperative blood loss, shorter operative times, and lower postoperative drainage volumes (p <0.05). The UBE-TLIF group showed faster postoperative recovery and shorter hospital stays. At 6 months, 1 year, and 2 years, W-TLIF patients had higher multifidus and erector spinae atrophy, and greater paravertebral muscle fat infiltration (p <0.05). The UBE-TLIF group also had lower VAS and ODI scores at 1 year and 2 years (p <0.05) and fewer surgical complications (6% vs. 10%). Fusion rates (94% vs. 92%) and modified Macnab outcomes (88% vs. 86%) were comparable (p >0.05). Conclusions UBE-TLIF is associated with reduced intraoperative trauma, quicker recovery, and fewer complications. In the long-term, it better preserves paravertebral muscle integrity and provides superior pain and functional outcomes.

Diabetic nephropathy belongs to diabetic microvascular aseptic inflammation， which is the main cause of end-stage renal disease and can cause damage to the structure of glomeruli and tubulointerstitium. Pyroptosis is a potent pro-inflammatory model of programmed cell death mediated by gasdermin （GSDM） protein family， which is characterized by nuclear shrinkage， chromatin DNA fragmentation， plasma membrane rupture， cell swelling and deformation. Related studies have found that pyroptosis is closely related to the occurrence and development of diabetic nephropathy. Inhibition of pyroptosis to a certain extent can reduce diabetic renal injury， so the pathway of pyroptosis involved in the pathogenesis of diabetic nephropathy is the current research focus. The characteristics of multi-components， multi-targets and multi-pathways of traditional Chinese medicine have significant advantages in the treatment of diabetic nephropathy. Some components of traditional Chinese medicine， single traditional Chinese medicine and compound prescription of traditional Chinese medicine can improve diabetic renal injury by inhibiting pyroptosis pathway and related targets. Based on the molecular mechanism of pyroptosis， this paper clarifies the mechanism of pyroptosis in diabetic nephropathy by expounding the relationship between pyroptosis and its pathway targets and diabetic nephropathy. This paper summarizes the research status of traditional Chinese medicine in the treatment of diabetic nephropathy by interfering with related pyroptosis pathways in recent years， so as to provide perspectives and ideas for the prevention， early diagnosis， drug development and molecular treatment of diabetic nephropathy in the future.

The inference of tissue origin of body fluid stains is crucial for case investigation and court proceedings.However,traditional methods for identification of body fluid stains,such as morpho-logical,chemical,and immunoassay identifications have certain limitations,and there is an urgent need for more efficient methods for confirmatory experiments.In recent years,the rapid development of tran-scriptomics technology has provided new means for the identification of tissue origin of body fluid stains.Different types of RNA in the transcriptome have their own advantages.This paper elaborates in detail on the application of different types of RNA,such as mRNA,miRNA,circRNA,lncRNA,piRNA and microbial transcriptomics in body fluid identification,and summarizes their respective ad-vantages and limitations,in order to provide a reference for related research.

Objective:To investigate the biological role and molecular mechanism of checkpoint kinase 1 (CHK1) in delaying cardiac aging in mice.Methods:In vitro, a senescence model of H9C2 cells (a cardiomyocyte line) was induced using H 2O 2. A control group (without H 2O 2 treatment) and three H 2O 2-treated groups (at concentrations of 10, 30, and 50 μmol/L) were set up. The CCK-8 assay was used to evaluate the proliferative activity of cells in each group; Western blot analysis was employed to detect the expression level of CHK1; and quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to determine the messenger RNA (mRNA) expression levels of P16 and interleukin-1β (IL-1β). In vivo, C57BL/6 wild-type mice aged 2 months ( n=15) and 24 months ( n=40), as well as myocardial-specific CHK1-overexpressing (CHK1-TG) mice aged 2 months ( n=15) and 24 months ( n=40), were selected. The mice were divided into four groups based on age and genotype: 2-month-old wild-type (WT-2M), 24-month-old wild-type (WT-24M), 2-month-old CHK1-TG (CHK1-TG-2M), and 24-month-old CHK1-TG (CHK1-TG-24M). Echocardiography was used to evaluate cardiac function of mice in the WT-24M and CHK1-TG-24M groups. Western blot analysis was conducted to measure the protein expression levels of CHK1, total Ras-related protein 1 (Rap1), NADPH oxidase 4 (Nox4), and Rap1-guanosine triphosphate (Rap1-GTP, the active form of Rap1) in the cardiac tissue of mice in each group. qRT-PCR was used to detect the messenger RNA (mRNA) expression levels of CHK1, collagen type Ⅰ (Coll1), matrix metalloproteinase-2 (Mmp2), alpha-smooth muscle actin (α-SMA), P53, P21, P16, thioredoxin 1 (Trx1), thioredoxin reductase (TrxR), glutathione recluctase (GR), Rap1, and Nox4. Immunofluorescence staining was employed to determine the protein expression levels of P53, P21, and P16, as well as the proportion of histone H2AX phosphorylation-positive cells. Dihydroethidium (DHE) staining was used to detect the relative intensity of DHE. Wheat germ agglutinin staining, HE staining, Masson staining and Sirius red staining were applied to measure the cross-sectional area of cardiomyocytes, cardiac morphology, and myocardial fibrosis area. Mice in the WT-24M and CHK1-TG-24M groups were intraperitoneally injected with the Rap1 activity inhibitor GGTI298 (25 μmol/kg). After injection, the oxidative stress damage in the cardiac tissue of the mice was detected, along with the mRNA expression levels of fibrosis-related indicators (Coll1, Mmp2, and α-SMA) and cell cycle inhibitory proteins (P16, P21, and P53). Results:A concentration of 30 μmol/L was determined as the optimal concentration for establishing an H 2O 2-induced senescence model of myocardial cells in vitro. The expression level of CHK1 in H9C2 cells of the 30 μmol/L H 2O 2 group was lower than that in the control group ( P<0.05). Echocardiographic examination showed that the left ventricular ejection fraction ((61.08±1.13)% vs. (52.55±2.02)%) and fractional shortening ((31.80±1.27)% vs. (25.18±1.59)%) of mice in the CHK1-TG-24M group were higher than those in the WT-24M group (both P<0.05). qRT-PCR and Western blot analysis revealed that, compared with the WT-24M group, mice in CHK1-TG-24M group had higher expression levels of CHK1 and its mRNA, lower expression levels of Nox4 and its mRNA, and higher expression level of Rap1-guanosine triphosphate (Rap1-GTP) (all P<0.05). However, there were no statistically significant differences in the total expression level of Rap1 and its mRNA between the two groups (both P>0.05). In addition, the mRNA expression levels of Coll1, Mmp2, and α-SMA in myocardial tissue of mice in the CHK1-TG-24M group were lower than those in the WT-24M group (all P<0.05). Immunofluorescence staining results showed that the expression levels of P53, P21, and P16 proteins, as well as the proportion of phosphorylated histone H2AX-positive cells in myocardial tissue of mice in the WT-24M group were higher than those in the CHK1-TG-24M group (all P<0.05). qRT-PCR further confirmed that the mRNA expression levels of the above-mentioned proteins in cardiac tissue of mice in the WT-24M group were higher than those in the CHK1-TG-24M group (all P<0.05). DHE staining results indicated that the relative intensity of DHE in cardiac tissue of mice in the CHK1-TG-24M group was lower than that in the WT-24M group ( P<0.05). Meanwhile, the left ventricular internal diameter, cross-sectional area of cardiomyocytes, and myocardial fibrosis area of mice in the CHK1-TG-24M group were all smaller than those in the WT-24M group (all P<0.05). Furthermore, the degree of DNA damage in cardiac tissue as well as the mRNA levels of fibrosis-related indicators (Coll1, Mmp2, and α-SMA) and cell cycle inhibitory proteins (P53, P21, P16) in mice of the WT-24M+GGTI298 group were higher than those in the WT-24M group and the CHK1-TG-24M+GGTI298 group (all P<0.05). Conclusion:CHK1 alleviates oxidative stress-induced damage in mouse cardiomyocytes by activating the Rap1/Nox4 signaling pathway, thereby delaying cardiac aging in mice.

OBJECTIVE: To assess the independent and combined effects of air pollutants, meteorological factors, and greenspace exposure on new tuberculosis (TB) cases. METHODS: TB case data from Shanghai (2013-2018) were obtained from the Shanghai Center for Disease Control and Prevention. Environmental data on air pollutants, meteorological variables, and greenspace exposure were obtained from the National Tibetan Plateau Data Center. We employed a distributed-lag nonlinear model to assess the effects of these environmental factors on TB cases. RESULTS: Increased TB risk was linked to PM _2.5, PM ₁₀, and rainfall, whereas NO ₂, SO ₂, and air pressure were associated with a reduced risk. Specifically, the strongest cumulative effects occurred at various lags: PM _2.5 ( RR = 1.166, 95% CI: 1.026-1.325) at 0-19 weeks; PM ₁₀ ( RR = 1.167, 95% CI: 1.028-1.324) at 0-18 weeks; NO ₂ ( RR = 0.968, 95% CI: 0.938-0.999) at 0-1 weeks; SO ₂ ( RR = 0.945, 95% CI: 0.894-0.999) at 0-2 weeks; air pressure ( RR = 0.604, 95% CI: 0.447-0.816) at 0-8 weeks; and rainfall ( RR = 1.404, 95% CI: 1.076-1.833) at 0-22 weeks. Green space exposure did not significantly impact TB cases. Additionally, low temperatures amplified the effect of PM _2.5 on TB. CONCLUSION Exposure to PM _2.5, PM ₁₀, and rainfall increased the risk of TB, highlighting the need to address air pollutants for the prevention of TB in Shanghai.
China/epidemiology* ; Humans ; Air Pollutants/analysis* ; Tuberculosis/epidemiology* ; Incidence ; Meteorological Concepts ; Particulate Matter/adverse effects* ; Environmental Exposure ; Male ; Female ; Adult ; Air Pollution ; Middle Aged

Objective To investigate the effects of Sini Powder on serum hypothalamic-pituitary-adrenal(HPA)axis-related hormones and inflammatory factors in liver cancer mice with comorbid depression,and to evaluate its effect on depressive behavior and tumor proliferation activity.Methods Forty-eight specific pathogen-free female C57BL/6 mice were randomly assigned to either a blank(n=8)or model group(n=40).The modeling group was subjected to chronic unpredictable mild stress(CUMS)for six weeks.Both groups underwent orthotopically transplanted liver tumor surgery at the end of the fourth week of CUMS treatment.At the end of the sixth week of CUMS treatment,color Doppler ultrasonography was used to observe tumor formation in the orthotopic transplantation liver tumors,and the tail suspension test was used to assess depressive behavior.Non-tumor-bearing and deceased mice were excluded.The remaining model group mice were stratified by tail suspension immobility time and randomly assigned to the following groups:model group(distilled water),Fluoxetine group(5.0 mg/kg),and Sini Powder low-dose,medium-dose,and high-dose groups(5.2,10.4,and 20.8 g/kg,respectively),with six mice per group.The treatments were administered once daily for 21 consecutive days.After treatment,depressive behaviors were assessed using the open field,tail suspension,and forced swimming tests.The proliferation status of the orthotopic liver transplantation tumor was evaluated by measuring the size of the tumor,observing pathological changes in the tumor tissue through hematoxylin and eosin staining,and detecting the positive cell rate of proliferating cell nuclear antigen(Ki-67)in the tumor tissue using immunohistochemistry.The levels of HPA axis-related hormones in serum,such as corticotropin-releasing hormone(CRH),adrenocorticotropic hormone(ACTH),corticosterone(CORT),as well as inflammatory factors such as tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),and interleukin-6(IL-6)were measured using an enzyme-linked immunosorbent assay.Western blotting was used to assess mitogen-activated protein kinase(MAPKs)phosphorylation and the expression of nuclear factor-κB(NF-κB),NOD-like receptor family pyrin domain-containing receptor 3(NLRP3),and cysteine aspartic protease-1(Caspase-1)in orthotopic tumors.Results Compared with the blank group,the model group showed reduced total distance traveled in open field test,prolonged immobility times in the tail suspension and forced swimming tests(P<0.05,P<0.01),indicating successful establishment of the liver cancer with comorbid depression mice model.Also,the model group showed increased orthotopic tumor volume(P<0.01),and elevated serum CRH,ACTH,CORT,TNF-α,IL-1β,and IL-6 levels(P<0.01).The phosphorylation of MAPKs in tumor tissues was suppressed(P<0.01),while NF-κB,NLRP3,and Caspase-1 expression levels were downregulated(P<0.01).Compared with the model group,Sini Powder medium-and high-dose groups exhibited increased total distance traveled in the open field test(P<0.05),reduced forced swimming test and prolonged total distance traveled in open field test(P<0.01),while Sini Powder high-dose group showed reduced immobility times in the tail suspension test(P<0.05).Also,Sini Powder low-dose,medium-dose,and high-dose groups showed slower tumor growth,histological changes,including vacuolization and necrosis,decreased Ki-67 positive cell rate(P<0.01),and reduced serum CRH,ACTH,CORT,TNF-α,IL-1β,and IL-6 levels(P<0.05).Additionally,the phosphorylation of MAPKs in tumor tissues was suppressed(P<0.01),and NF-κB,NLRP3,and caspase-1 expression levels were downregulated(P<0.01).Conclusion Sini Powder may alleviate depressive behaviors and suppress tumor proliferation activity in liver cancer mice with comorbid depression by modulating MAPKs activation,inhibiting NF-κB,NLRP3,and Caspase-1 expressions,and reducing serum inflammatory factors and HPA axis-related hormones levels.

Objective:To investigate the biological role and molecular mechanism of checkpoint kinase 1 (CHK1) in delaying cardiac aging in mice.Methods:In vitro, a senescence model of H9C2 cells (a cardiomyocyte line) was induced using H 2O 2. A control group (without H 2O 2 treatment) and three H 2O 2-treated groups (at concentrations of 10, 30, and 50 μmol/L) were set up. The CCK-8 assay was used to evaluate the proliferative activity of cells in each group; Western blot analysis was employed to detect the expression level of CHK1; and quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to determine the messenger RNA (mRNA) expression levels of P16 and interleukin-1β (IL-1β). In vivo, C57BL/6 wild-type mice aged 2 months ( n=15) and 24 months ( n=40), as well as myocardial-specific CHK1-overexpressing (CHK1-TG) mice aged 2 months ( n=15) and 24 months ( n=40), were selected. The mice were divided into four groups based on age and genotype: 2-month-old wild-type (WT-2M), 24-month-old wild-type (WT-24M), 2-month-old CHK1-TG (CHK1-TG-2M), and 24-month-old CHK1-TG (CHK1-TG-24M). Echocardiography was used to evaluate cardiac function of mice in the WT-24M and CHK1-TG-24M groups. Western blot analysis was conducted to measure the protein expression levels of CHK1, total Ras-related protein 1 (Rap1), NADPH oxidase 4 (Nox4), and Rap1-guanosine triphosphate (Rap1-GTP, the active form of Rap1) in the cardiac tissue of mice in each group. qRT-PCR was used to detect the messenger RNA (mRNA) expression levels of CHK1, collagen type Ⅰ (Coll1), matrix metalloproteinase-2 (Mmp2), alpha-smooth muscle actin (α-SMA), P53, P21, P16, thioredoxin 1 (Trx1), thioredoxin reductase (TrxR), glutathione recluctase (GR), Rap1, and Nox4. Immunofluorescence staining was employed to determine the protein expression levels of P53, P21, and P16, as well as the proportion of histone H2AX phosphorylation-positive cells. Dihydroethidium (DHE) staining was used to detect the relative intensity of DHE. Wheat germ agglutinin staining, HE staining, Masson staining and Sirius red staining were applied to measure the cross-sectional area of cardiomyocytes, cardiac morphology, and myocardial fibrosis area. Mice in the WT-24M and CHK1-TG-24M groups were intraperitoneally injected with the Rap1 activity inhibitor GGTI298 (25 μmol/kg). After injection, the oxidative stress damage in the cardiac tissue of the mice was detected, along with the mRNA expression levels of fibrosis-related indicators (Coll1, Mmp2, and α-SMA) and cell cycle inhibitory proteins (P16, P21, and P53). Results:A concentration of 30 μmol/L was determined as the optimal concentration for establishing an H 2O 2-induced senescence model of myocardial cells in vitro. The expression level of CHK1 in H9C2 cells of the 30 μmol/L H 2O 2 group was lower than that in the control group ( P<0.05). Echocardiographic examination showed that the left ventricular ejection fraction ((61.08±1.13)% vs. (52.55±2.02)%) and fractional shortening ((31.80±1.27)% vs. (25.18±1.59)%) of mice in the CHK1-TG-24M group were higher than those in the WT-24M group (both P<0.05). qRT-PCR and Western blot analysis revealed that, compared with the WT-24M group, mice in CHK1-TG-24M group had higher expression levels of CHK1 and its mRNA, lower expression levels of Nox4 and its mRNA, and higher expression level of Rap1-guanosine triphosphate (Rap1-GTP) (all P<0.05). However, there were no statistically significant differences in the total expression level of Rap1 and its mRNA between the two groups (both P>0.05). In addition, the mRNA expression levels of Coll1, Mmp2, and α-SMA in myocardial tissue of mice in the CHK1-TG-24M group were lower than those in the WT-24M group (all P<0.05). Immunofluorescence staining results showed that the expression levels of P53, P21, and P16 proteins, as well as the proportion of phosphorylated histone H2AX-positive cells in myocardial tissue of mice in the WT-24M group were higher than those in the CHK1-TG-24M group (all P<0.05). qRT-PCR further confirmed that the mRNA expression levels of the above-mentioned proteins in cardiac tissue of mice in the WT-24M group were higher than those in the CHK1-TG-24M group (all P<0.05). DHE staining results indicated that the relative intensity of DHE in cardiac tissue of mice in the CHK1-TG-24M group was lower than that in the WT-24M group ( P<0.05). Meanwhile, the left ventricular internal diameter, cross-sectional area of cardiomyocytes, and myocardial fibrosis area of mice in the CHK1-TG-24M group were all smaller than those in the WT-24M group (all P<0.05). Furthermore, the degree of DNA damage in cardiac tissue as well as the mRNA levels of fibrosis-related indicators (Coll1, Mmp2, and α-SMA) and cell cycle inhibitory proteins (P53, P21, P16) in mice of the WT-24M+GGTI298 group were higher than those in the WT-24M group and the CHK1-TG-24M+GGTI298 group (all P<0.05). Conclusion:CHK1 alleviates oxidative stress-induced damage in mouse cardiomyocytes by activating the Rap1/Nox4 signaling pathway, thereby delaying cardiac aging in mice.

Objective:To explore the efficacy and safety of type A botulinum toxin (BTX-A) in alleviating pain and reducing capsular contracture after breast augmentation surgery.Methods:This single-center, double-blind, and randomized controlled trial included 212 female patients who underwent breast augmentation surgery at Changsha YaMei Medical Cosmetic Hospital from May 2020 to January 2021. Patients were divided into two groups according to whether BTX-A was injected into the pectoralis major during the augmentation: 106 in the BTX-A group, with an average age of (33.1±3.8) years; and 106 in the control group, with an average age of (33.3±3.5) years. The visual analogue scale (VAS) was used to assess pain on days 1, 3 and 7 post-operation. After two years of follow-up, the postoperative VAS scores, duration of pain, rates of capsular contracture, and incidence of adverse reactions were compared between the two groups.Results:One case was lost to follow-up in each group. On postoperative days 1 and 3, the VAS scores of the BTX-A group were (3.93±1.77) and (5.35±2.04) scores, respectively, lower than those of the control group, which were (5.93±2.17) and (7.34±1.75) scores (both P<0.001). On day 7, the scores were (1.96±1.71) and (2.26±1.90) scores, respectively, with no statistically significant difference ( P=0.225). The pain severity in both groups showed a trend of initial increase followed by a decrease, with a significant difference ( P<0.001). The duration of pain in the BTX-A group was (2.6±1.8) days, shorter than that in the control group (4.9±2.1) days, with a statistically significant difference ( P<0.001). The rate of capsular contracture in the BTX-A group was 0.95% (1/105), compared to 1.90% (2/105) in the control group, with no statistically significant difference ( P=1.000). The incidence of adverse reactions was 11.32% (12/106) in the BTX-A group and 10.38% (11/106) in the control group, with no statistically significant difference ( P=0.825). There were no severe adverse reactions such as respiratory or cardiovascular events or deaths in either group. Conclusion:BTX-A can alleviate pain after breast augmentation surgery with high safety. However, it does not have a significant advantage in preventing capsular contracture.

Objective:To study the risk factors of thyroid nodules in patients with type 2 diabetes.Methods:Data of patients with type 2 diabetes with normal thyroid function admitted to the Department of Endocrinology of Heze Municipal Hospital from January to June 2024 were collected. Binary logistic regression was used to analyze the influencing factors of thyroid nodules in patients with type 2 diabetes, and the receiver operating characteristic curve (ROC curve) was used to evaluate the diagnostic efficacy of each influencing factor.Results:Among 162 patients with type 2 diabetes, 96 had thyroid nodules, accounting for 59.3%. The incidence of thyroid nodules in women was significantly higher than that in men (χ 2 = 4.56, P = 0.034). Multivariate logistic regression analysis showed that age (≥50 years old), overweight and obesity [body mass index (BMI)≥24.0 kg/m 2], high glycated hemoglobin (≥10%), and high total cholesterol ( > 6.5 mmol/L) were independent risk factors for thyroid nodules in patients with type 2 diabetes ( OR = 1.83, 1.67, 1.08, 3.65, P < 0.05), and men was an independent protective factor ( OR = 0.63, P = 0.039). The ROC curve results showed that total cholesterol and total cholesterol combined with glycated hemoglobin could distinguish patients with thyroid nodules from those without thyroid nodules, with AUC = 0.64 and 0.68, respectively, and the differences were statistically significant ( P < 0.05). Conclusions:The incidence of thyroid nodules in patients with type 2 diabetes is relatively high. Age, overweight and obesity, high glycated hemoglobin, and high total cholesterol are independent risk factors for thyroid nodules in patients with type 2 diabetes, and total cholesterol has the ability to distinguish patients with thyroid nodules.