Objective:To study the effect of tertiary lymphoid structures(TLS)on the pathological response and prognosis of patients with non-small cell lung cancer(NSCLC)receiving neoadjuvant therapy.Methods:We retrospectively collected the data of 132 patients with NSCLC who underwent neoadjuvant therapy and surgery at Tianjin Chest Hospital between January 2019 and December 2023,including 40 in the neoadjuvant chemotherapy(NC)group and 92 in the NC plus immunotherapy(NCI)group.The percentage of residual viable tumor(RVT)and tumor infiltrating lymphocyte(TIL)counts were evaluated by hematoxylin and eosin(H&E)staining,while TLS number and matur-ity were assessed by H&E and immunohistochemical staining.The differences in TLS number and maturity and effects on patient pathologic-al response and prognosis were compared between groups.Results:TIL count,total TLS number,pathological complete response and major pathological response rates were significantly higher in the NCI versus NC group(P<0.001).Moreover,a multivariate Logistic analysis sho-wed that TLS number and maturity and TIL count affected pathological response in the NCI group(P<0.05).A multiple linear regression ana-lysis indicated that a low TIL count was a risk factor for a high RVT in the NC group,while a low number of mature TLS,low TIL count,and N stage were independent risk factors for a high RVT in the NCI group(all P<0.05).In the NCI group,a multivariate Cox regression analysis showed that a low number of mature TLS(P=0.001)and low TIL count(P=0.009)were independent predictors of disease-free survival(DFS),while a survival analysis showed that patients in the NCI group with high(vs.low)numbers of mature TLS and a high(vs.low)TIL count had significantly longer DFS(all P<0.001).Conclusions:A low number of mature TLS and low TIL count were associated with an adverse patholo-gical response and short DFS in patients with NSCLC.Thus,TLS maturity and TIL count can predict the pathological response and prognosis of patients with NSCLC treated with NCI.

Objective:To investigate the prevalence of cataracts, the surgical coverage, and postoperative visual acuity of adults in Ningxia.Methods:A cross-sectional study using multistage cluster random sampling was conducted.Ten survey sites in Ningxia were selected and the population aged 18 years and over was surveyed with questionnaire, height and weight measurements, visual acuity, intraocular pressure, fundus photography and slit-lamp examinations.Cataract prevalence and its influencing factors were analyzed.Cataract prevalence, surgical coverage and presenting visual acuity (PVA) and best corrected visual acuity (BCVA) after surgery were investigated in different age groups of the examined population.The study adhered to the Declaration of Helsinki and was approved by the Ethics Committee of the People's Hospital of Ningxia Hui Autonomous Region (No.[2023]-LL-010).Participants signed informed consent prior to the examination.Results:A total of 6 145 people should be examined, and 5 721 people were actually examined, with an examination rate of 93.10%.The study population consisted of 2 558 males, accounting for 44.71%, and 3 163 females, accounting for 55.28%, with ages ranging from 18 to 93 years old and an average age of (64.27±13.48) years.Among them, 1 180 patients diagnosed with cataract, with a cataract prevalence of 20.62%.The prevalence of cataract increased with age and decreased with education level, showing statistically significant differences ( χ2=1 091.32, 581.92; both at P<0.01).The prevalence of cataract was significantly higher among people with hypertension, diabetes mellitus, hyperlipidemia, and coronary heart disease than those without these diseases ( χ2=274.65, 118.15, 78.05, 182.71; all at P<0.01).Cataract surgery was performed in 245 cases in the cataract patient population, with a surgical coverage rate of 20.76%.Of the 245 cases, 229 cases were implanted with IOLs, with an implantation rate of 93.40%.The social burden rate of cataract blindness was 2.29%, and increased with age.Of the 339 eyes that underwent cataract surgery, 241 had a PVA≥0.3, accounting for 71.09%, and 272 had a BCVA≥0.3, accounting for 80.24%. Conclusions:In Ningxia, cataracts are still the main cause of vision impairment and blindness in the elderly, and the social burden rate of cataract blindness is high.Moreover, the coverage rate of cataract surgery is low, so both the coverage and quality of surgery need improvement.

Objective The current study aims to investigate the protective effect and mechanisms of baicalin on pathological left ventricular remodeling.Methods Angiotensin Ⅱ(Ang Ⅱ)infusion mouse model was adopted to evaluate the impact of baicalin on pathological left ventricular remodeling in vivo.C57BL/6J mice were randomly allocated to 5 experimental groups,including sham controls,model group(Ang Ⅱ-infusion controls),as well as low-,medium-,and high-dose baicalin treatment groups.Except for the sham controls,C57/BL6 mice were subjected to AngⅡ infusion for 2 weeks.The mice from the baicalin treatment groups received baicalin via gavage at the indicated doses for 2 weeks.The blood pressure,body weight,heart weight and tibia length were measured at the end of the indicated treatments.Immunohistochemistry of wheat germ agglutinin(WGA)was performed to examine the cross-sectional area of cardiomyocytes.Immunohistochemistry was also performed to assess the expression of atrial natriuretic peptide(ANP)in cardiomyocytes.Hematoxylin/eosin(HE)staining and Masson's trichrome staining were performed to evaluate the cardiac pathologies.In vitro experiments were as follows.Ang Ⅱ was adopted to induce cardiomyocyte hypertrophy in H9C2 cells in order to determine if baicalin is able to directly suppress cardiomyocyte hypertrophy.H9C2 cells were divided into vehicle control group(VC group),model group(Ang Ⅱ group)and baicalin group(Bai group).The morphology and size of cardiomyocytes were examined by rhodamine phalloidin staining.The intracellular level of ANP was analyze by immunofluorescence staining.Mitochondrial superoxide(Mito-SOX)was assessed to evaluate oxidative stress.The mitochondrial membrane potential(ΔΨm)was analyzed by JC-1 staining.The opening of mitochondrial permeability transition pore(mPTP)was evaluated by calcein acetyl methyl ester(Calcein AM)staining.Results The in vivo findings:Baicalin significantly antagonized Ang Ⅱ-induced elevation of systolic blood pressure(P<0.05)when administered at the medium and high doses.Meanwhile,baicalin treatment resulted in lower ratios of heart weight to tibia length(HW/TL)and heart weight to body weight(HW/BW)in Ang Ⅱ-infused mice.Baicalin treatment mitigated cardiomyocyte hypertrophy(P<0.05)and lowered the level of cardiomyocyte ANP(P<0.05)in Ang Ⅱ-infused mice.Furthermore,baicalin treatment significantly alleviated cardiac inflammation and fibrosis in Ang Ⅱ-infused mice(P<0.05).In vitro findings:Baicalin suppressed Ang Ⅱ-stimulated enlargement of cardiomyocytes and elevation of the intracellular ANP in H9C2 cells.Moreover,baicalin alleviated Ang Ⅱ-induced mitochondrial oxidative stress,mitochondrial ΔΨm impairment and mPTP opening(P<0.05).Conclusion Our current findings demonstrate that baicalin is effective at mitigating Ang Ⅱ-mediated left ventricular pathological remodeling.Baicalin is pharmacologically active at antagonizing Ang Ⅱ-induced hypertrophic responses and mitochondrial dysfunction in cardiomyocytes,which may in part account for its therapeutic effects against pathological left ventricular remodeling.

Objective The current study aims to investigate the protective effect and mechanisms of baicalin on pathological left ventricular remodeling.Methods Angiotensin Ⅱ(Ang Ⅱ)infusion mouse model was adopted to evaluate the impact of baicalin on pathological left ventricular remodeling in vivo.C57BL/6J mice were randomly allocated to 5 experimental groups,including sham controls,model group(Ang Ⅱ-infusion controls),as well as low-,medium-,and high-dose baicalin treatment groups.Except for the sham controls,C57/BL6 mice were subjected to AngⅡ infusion for 2 weeks.The mice from the baicalin treatment groups received baicalin via gavage at the indicated doses for 2 weeks.The blood pressure,body weight,heart weight and tibia length were measured at the end of the indicated treatments.Immunohistochemistry of wheat germ agglutinin(WGA)was performed to examine the cross-sectional area of cardiomyocytes.Immunohistochemistry was also performed to assess the expression of atrial natriuretic peptide(ANP)in cardiomyocytes.Hematoxylin/eosin(HE)staining and Masson's trichrome staining were performed to evaluate the cardiac pathologies.In vitro experiments were as follows.Ang Ⅱ was adopted to induce cardiomyocyte hypertrophy in H9C2 cells in order to determine if baicalin is able to directly suppress cardiomyocyte hypertrophy.H9C2 cells were divided into vehicle control group(VC group),model group(Ang Ⅱ group)and baicalin group(Bai group).The morphology and size of cardiomyocytes were examined by rhodamine phalloidin staining.The intracellular level of ANP was analyze by immunofluorescence staining.Mitochondrial superoxide(Mito-SOX)was assessed to evaluate oxidative stress.The mitochondrial membrane potential(ΔΨm)was analyzed by JC-1 staining.The opening of mitochondrial permeability transition pore(mPTP)was evaluated by calcein acetyl methyl ester(Calcein AM)staining.Results The in vivo findings:Baicalin significantly antagonized Ang Ⅱ-induced elevation of systolic blood pressure(P<0.05)when administered at the medium and high doses.Meanwhile,baicalin treatment resulted in lower ratios of heart weight to tibia length(HW/TL)and heart weight to body weight(HW/BW)in Ang Ⅱ-infused mice.Baicalin treatment mitigated cardiomyocyte hypertrophy(P<0.05)and lowered the level of cardiomyocyte ANP(P<0.05)in Ang Ⅱ-infused mice.Furthermore,baicalin treatment significantly alleviated cardiac inflammation and fibrosis in Ang Ⅱ-infused mice(P<0.05).In vitro findings:Baicalin suppressed Ang Ⅱ-stimulated enlargement of cardiomyocytes and elevation of the intracellular ANP in H9C2 cells.Moreover,baicalin alleviated Ang Ⅱ-induced mitochondrial oxidative stress,mitochondrial ΔΨm impairment and mPTP opening(P<0.05).Conclusion Our current findings demonstrate that baicalin is effective at mitigating Ang Ⅱ-mediated left ventricular pathological remodeling.Baicalin is pharmacologically active at antagonizing Ang Ⅱ-induced hypertrophic responses and mitochondrial dysfunction in cardiomyocytes,which may in part account for its therapeutic effects against pathological left ventricular remodeling.

OBJECTIVE: To explore the molecular reasons of weak expression of B antigen on the red cell. METHODS: Serological test for blood group was carried out, including red cell and plasma grouping, and anti-A1 and anti-H testing, and confirming weak A or B antigens by adsorption and elution. Exons 1-7 were sequenced directly, and one of them was cloned and sequenced. RESULTS: All of the 23 samples showed the weak B antigen by serological method. The alleles of the subgroups were identified by DNA sequencing, including 2 Bel subgroup, 4 B3 subgroup, 14 Bw subgroup, 2 CisAB subgroup and a novel allele. The novel allele showed a nucleotide substitution 662G>A in the exon 7, and the sequence was submitted to Blood Group Antigen Gene Mutation Database, and the novel allele was named Bel10. CONCLUSION Nucleotide substitution in exon results in blood subgroup, which showed that the antigens were weakened, and Bw phenotype was the most frequently subgroup.
ABO Blood-Group System/genetics* ; Alleles ; Exons ; Genotype ; Humans ; Nucleotides ; Phenotype