[Objective] To investigate the molecular prevalence and genotype of human parvovirus B19(B19) among blood donors in Lanzhou, and provide data support for monitoring the positive rate of B19 DNA in local blood donors. [Methods] A total of 7 644 blood donor samples collected from January to September 2022 were randomly screened using real-time fluorescent PCR, resulting in 23 samples testing positive for B19 DNA. The characteristics of the B19 DNA reactive donors including gender, age, blood donation recruitment and promotion mode, and donation frequency were analyzed using SPSS 22.0. Additionally, the VP1 gene fragment of B19 DNA reactive samples was sequenced and an evolutionary tree was constructed by the N-J method. [Results] The results showed that the positive rate of B19 DNA in Lanzhou was 0.30%, and the positive population mainly consisted of female individuals aged 18-30 years old who were first-time blood donors; furthermore, genotype 1a was identified as predominant. [Conclusion] The positive rate of B19 DNA is low among blood donors in Lanzhou, with genotype 1a being predominant. It is recommended to periodically monitor the B19 prevalence in blood donors and enhance prevention and control measures, thus improving blood quality and safety.

ObjectiveTo explore the effects of different dosage forms of Kaixinsan （KXS） on the morphology and function of mitochondria in rat models of Alzheimer's disease （AD） and potential mechanisms of action. MethodsMale SD rats were randomly assigned to a sham group， model group， treatment groups receiving KXS decoction， powders， and granules （3.08 g·kg^-1）， as well as donepezil group （0.51×10^-3 g·kg^-1）， with 10 rats in each group. AD model was created using intracerebroventricular injection of streptozocin （STZ）. After 30 days of administration， behavioral assessments were conducted， and mitochondrial morphology was observed using transmission electron microscopy. Mitochondrial respiratory chain complex content was measured via enzyme-linked immunosorbent assay （ELISA）. Changes in mitochondrial membrane potential were measured via JC-1 staining， and superoxide dismutase （SOD） activity and reactive oxygen species （ROS） levels were measured via biochemical assays. The mRNA expression of adenosine 5'-monophosphate-activated protein kinase （AMPK）， peroxisome proliferator-activated receptor gamma coactivator-1α （PGC-1α）， and silent information regulator 3 （SIRT3） was detected by real-time fluorescent quantitative polymerase chain reaction （Real-time PCR）， and Western blot was used to examine the protein expression levels of optic atrophy protein1 （OPA1）， mitochondrial fission protein 1 （FIS1）， AMPK， p-AMPK， PGC-1α， and SIRT3. ResultsCompared with the sham group， rats in the model group had significantly lower recognition index， spontaneous alternation rate， escape latency， number of platform crossings， time spent in the target quadrant， and percentage of distance traveled in the target quadrant distance （P<0.05， P<0.01）. Significant mitochondrial damage was observed in the hippocampal tissue， with a marked decrease in mitochondrial respiratory chain complex content （P<0.01） and reduced mitochondrial membrane potential （P<0.05）. Additionally， the SOD activity was reduced， while ROS levels were elevated （P<0.01）. The mRNA expression of PGC-1α and SIRT3 was significantly downregulated （P<0.01）， along with decreased protein expression levels of OPA1， p-AMPK/AMPK， PGC-1α， and SIRT3， whereas FIS1 protein expression was significantly upregulated （P<0.05， P<0.01）. Compared with the model group， rats in KXS-treated groups （various dosage forms） showed significant improvement in behavioral indexes （P<0.05， P<0.01）， reduced hippocampal mitochondrial damage， and more organized mitochondrial cristae. Mitochondrial respiratory chain complex content was significantly increased （P<0.05， P<0.01）， and mitochondrial membrane potentials were elevated （P<0.05）. SOD activity was elevated， and ROS levels were significantly reduced （P<0.05， P<0.01）. Furthermore， the mRNA expression of PGC-1α and SIRT3 was upregulated， with increased protein levels of OPA1， p-AMPK/AMPK， PGC-1α， and SIRT3， while FIS1 protein expression levels were significantly reduced （P<0.05， P<0.01）. Across the KXS-treated groups， the granule group showed a higher spontaneous alternation rate than the decoction and powder groups （P<0.05）. ConclusionKXS decoction， powders， and granules can improve the learning and memory ability of rats， with granules being the most effective. The mechanism of action may involve activation of the AMPK/PGC-1α/SIRT3 signaling pathway， improvement of the mitochondrial function， and subsequent amelioration of the brain energy metabolism disorders.

ObjectiveTo explore the effects of different dosage forms of Kaixinsan （KXS） on the morphology and function of mitochondria in rat models of Alzheimer's disease （AD） and potential mechanisms of action. MethodsMale SD rats were randomly assigned to a sham group， model group， treatment groups receiving KXS decoction， powders， and granules （3.08 g·kg^-1）， as well as donepezil group （0.51×10^-3 g·kg^-1）， with 10 rats in each group. AD model was created using intracerebroventricular injection of streptozocin （STZ）. After 30 days of administration， behavioral assessments were conducted， and mitochondrial morphology was observed using transmission electron microscopy. Mitochondrial respiratory chain complex content was measured via enzyme-linked immunosorbent assay （ELISA）. Changes in mitochondrial membrane potential were measured via JC-1 staining， and superoxide dismutase （SOD） activity and reactive oxygen species （ROS） levels were measured via biochemical assays. The mRNA expression of adenosine 5'-monophosphate-activated protein kinase （AMPK）， peroxisome proliferator-activated receptor gamma coactivator-1α （PGC-1α）， and silent information regulator 3 （SIRT3） was detected by real-time fluorescent quantitative polymerase chain reaction （Real-time PCR）， and Western blot was used to examine the protein expression levels of optic atrophy protein1 （OPA1）， mitochondrial fission protein 1 （FIS1）， AMPK， p-AMPK， PGC-1α， and SIRT3. ResultsCompared with the sham group， rats in the model group had significantly lower recognition index， spontaneous alternation rate， escape latency， number of platform crossings， time spent in the target quadrant， and percentage of distance traveled in the target quadrant distance （P<0.05， P<0.01）. Significant mitochondrial damage was observed in the hippocampal tissue， with a marked decrease in mitochondrial respiratory chain complex content （P<0.01） and reduced mitochondrial membrane potential （P<0.05）. Additionally， the SOD activity was reduced， while ROS levels were elevated （P<0.01）. The mRNA expression of PGC-1α and SIRT3 was significantly downregulated （P<0.01）， along with decreased protein expression levels of OPA1， p-AMPK/AMPK， PGC-1α， and SIRT3， whereas FIS1 protein expression was significantly upregulated （P<0.05， P<0.01）. Compared with the model group， rats in KXS-treated groups （various dosage forms） showed significant improvement in behavioral indexes （P<0.05， P<0.01）， reduced hippocampal mitochondrial damage， and more organized mitochondrial cristae. Mitochondrial respiratory chain complex content was significantly increased （P<0.05， P<0.01）， and mitochondrial membrane potentials were elevated （P<0.05）. SOD activity was elevated， and ROS levels were significantly reduced （P<0.05， P<0.01）. Furthermore， the mRNA expression of PGC-1α and SIRT3 was upregulated， with increased protein levels of OPA1， p-AMPK/AMPK， PGC-1α， and SIRT3， while FIS1 protein expression levels were significantly reduced （P<0.05， P<0.01）. Across the KXS-treated groups， the granule group showed a higher spontaneous alternation rate than the decoction and powder groups （P<0.05）. ConclusionKXS decoction， powders， and granules can improve the learning and memory ability of rats， with granules being the most effective. The mechanism of action may involve activation of the AMPK/PGC-1α/SIRT3 signaling pathway， improvement of the mitochondrial function， and subsequent amelioration of the brain energy metabolism disorders.

Objective:To explore the curative efficacy of Dingke Decoction in the treatment of post infectious cough based on the the real-world clinical data.Methods:Retrospective cohort study was conducted. 245 patients with cough after infection in the hospital of Jingan Chinese Medical Hospital from July 2021 to July 2022 were set as study objects. The fact that whether the patients with Dingke Decoction or not were divided into control group (90 cases, without Dingke Decoction) and treatment group (155 cases, with Dingke Decoction). By using propensity nearest neighbor 1:1 matching to balance the confounding factors before treatment, 56 cases were successfully matched in both groups. The control group was treated symptomatically according to the actual clinical situation, while the treatment group was treated with modified Dingke Decoction on the basis of symptomatic treatment in the control group. The treatment for both groups lasted for 2 weeks. TCM symptom scores and cough severity score were evaluated using the Leicester Cough Quality of Life Questionnaire (LCQ) before and after treatment. Levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) were detected through ELISA; adverse reactions during the treatment were recorded, and the clinical efficacy was evaluated.Results:The total effective rate of the treatment group was 91.07% (51/56), while that of the control group was 76.79% (43/56), with a statistically significant difference between the two groups ( χ2=4.24, P=0.040). The daytime cough symptom score (1.03 ± 0.67 vs. 1.20 ± 0.66, t=7.40) and nighttime cough symptom score (0.74 ± 0.62 vs. 1.26 ± 0.54, t=6.27) in the treatment group were lower than those in the control group after treatment ( P<0.001). After treatment, the LCQ physiological (5.30 ± 0.79 vs. 4.78 ± 1.09, t=-2.44), psychological (5.33 ± 0.92 vs. 4.70 ± 1.12, t=-2.39), and social (5.23 ± 0.94 vs. 4.60 ± 0.81, t=-2.86) scores in the treatment group were higher than those in the control group ( P<0.05). After treatment, he treatment group serum IL-6 [(14.29 ± 3.94) ng/L vs. (19.99 ± 5.17) ng/L, t=4.80] and TNF-α [(36.23 ± 7.83) ng/L vs. (42.44 ± 7.63) ng/L, t=3.11] were lower than those in the control group ( P<0.01). The incidence of adverse reactions in the control group was 8.92% (5/56) and 5.36% (3/56), respectively, without statistical significance ( χ2=0.54, P=0.716). Conclusion:Based on the real-world research method, medicine Dingke Decoction can improve the clinical efficacy and the quality life of post infectious cough patients, and the mechanism may be related to reducing airway inflammation response.

Histone deacetylase 3(HDAC3)is an epigenetic modification enzyme,which participates in the occur-rence and development of atherosclerosis(As).It is significant to search for effective HDAC3 inhibitors for the treatment of atherosclerosis.This article reviews the relationship between HDAC3 and atherosclerosis,the latest research progress of HDAC3 inhibitors,and the therapeutic effects of some traditional Chinese medicine on cardiovascular diseases by inhibi-ting HDAC3.It aims to provide new ideas for developing anti-atherosclerotic drugs targeting HDAC3.

Hepatic stellate cell(HSC)activation is a key link in the development of liver fibrosis.The metabolic reprogramming of activated HSC has become a hot topic in current research,especially the change of glycolysis is an important factor in regulating HSC activation.Based on the metabolic reprogramming in the process of HSC activation,this paper expounds the mechanism of regulating HSC activation and liver fibrosis through glycolysis,and reviews the research progress of traditional Chinese medicine and its active ingredients in regulating HSC glycolysis to prevent and treat liver fibrosis.Liver fibrosis is a complex pathological process involving multiple factors and pathways.From the perspective of regulating the glycolysis of activated HSC,it can provide a new idea for the development of anti-liver fibrosis drugs.

Bronchiectasis has the characteristics of long course,gradual aggravation,easy recurrence and difficult to treat.The characteristics are similar to those arouse by incubative pathogenic factors.Based on the theory of incubative pathogenic factors,this disease is often related to the incubative pathogenic factors in the body's areas with deficient healthy qi,which occur at regular times.The etiology can be external,congenital,or internal.Treatment should focus on different characteristics of incubative pathogenic factors.Attention should be paid to clearing and dispersing in external pathogenic factors,while attention should be paid to supporting and promoting healthy qi in congenital pathogenic factors,and do not forget to remove internal pathogenic factors.

Objective:To analyze the genus, drug resistance/virulence and phylogenetic characteristics of Brucella strains isolated from brucellosis surveillance sentinels in Henan Province from 2013 to 2022, and provide baseline data for the surveillance, early warning and outbreak tracing of brucellosis. Methods:Blood samples were collected from patients with Brucella infection for strain isolation, culture and species identification, drug susceptibility test, whole genome sequencing, splicing and assembly, functional/virulence/resistance gene prediction analysis and phylogenetic tree drawing based on single nucleotide polymorphism (SNP). Results:In 36 brucellosis patients, the majority were men (86.11%, 31/36), young adults aged 18-50 (88.89%, 32/36) and farmers/herdsmen (72.22%, 26/36). A total of 36 strains of Brucella melitensis were isolated, and average 1 305 functional proteins of 21 categories were predicted by strain genome; all the strains carried four main virulence factors (pmm, VirB group, BtpA/BtpB, BvrS/BvrR). The drug sensitivity rate was 100.00% to six types of antibiotics including levofloxacin, rifampicin, doxycycline, streptomycin, tetracycline and gentamicin, they showed different resistances to three antibiotics including compound trimethoprim-sulfamethoxazole, ciprofloxacin and ampicillin. The strains carried four types of resistance genes and two clusters of resistance genes, with four combinations of genotypes, the resistance mechanisms included antibiotic degradation/modification enzymes, resistant nodular cell differentiation (RND) efflux pumps, 16S/23S ribosomal rRNA binding site mutations, etc. The number of SNP differed in the genomes of 36 Brucellamelitensis strains ranged from 0 to 454 and phylogenetic tree was divided into three major branches, with relative branch distances between 0.000 0 and 0.498 6 for each strain. Conclusions:Human Brucellamelitensis strains isolated from surveillance sentinels in Henan from 2013 to 2022 carried multiple virulence and antibiotic resistance genes and had different drug resistance phenotypes. Single nucleotide polymorphism analysis and phylogenetic tree analysis showed significant differences in phylogenetic relationships among different strains.

Signal transducer and activator of transcription 3(STAT3)is an intracellular signaling factor that plays a critical role in various cellular processes,including the growth,differentiation,apoptosis,and immune response of cells.Aberrant activation of T helper cell 17(Th17)is closely associated with the morbidity and progress of various autoimmune diseases.STAT3 participates in the pathogenesis of Sj?gren syndrome by inducing excessive proliferation and abnormal differentiation of Th17 cells and affecting lymphocyte infiltration into exocrine glands.Therefore,targeting the STAT3 signaling pathway represents a potential novel therapeutic approach for the treatment of Sj?gren syndrome.This review summarizes the research of STAT3 in the pathogenesis and progression of Sj?gren syndrome through regulating Th17 cells,focusing on current inhibitors targeting the STAT3 signaling pathway as potential therapeutic targets for Sj?gren syndrome.

Osteoporosis can be induced by various factors including prolonged glucocorticoid usage, diminished estrogen levels, secondary hyperparathyroidism, and alterations in the microenvironment of bone tissue. The bone metabolism imbalance(osteogenic-lipogenic imbalance) plays a crucial role in the development of osteoporosis. This imbalance is primarily driven by an increase in the differentiation of bone marrow mesenchymal stem cells into adipocytes and a decrease in their differentiation into osteoblasts, thus forming the core of the osteogenic-lipogenic imbalance observed in osteoporosis. The bone morphogenesis protein(BMP) plays a crucial role in the regulation of the osteogenic-lipid balance in osteoporosis. This regulatory function is accomplished through both the Smad-dependent and Smad-independent pathways. This review centers on the Smad-dependent and Smad-independent pathways facilitated by BMP, offering a comprehensive overview of the potential mechanisms through which BMP-2, 4, 6, 7, and 9 contribute to the regulation of osteogenesis and lipid metabolism in osteoporosis via these pathways. In order to present novel insights for the identification of efficacious targets for clinical anti-osteoporosis medications.