Objective To construct three models, SARIMA, XGBoost, and LightGBM, to predict the future trend of human brucellosis in mainland China, and to provide a basis for formulating policies for the prevention and control of brucellosis. Methods Monthly case data of human brucellosis in mainland China from 2014 to 2023 were collected. The SARIMA model was constructed using R 4.4.1. The XGBoost and LightGBM models were constructed using Python 3.8. Results From 2014 to 2023, a total of 536,443 cases of human brucellosis were reported in mainland China. The incidence rate first decreased and then increased. The average annual incidence was 3.82 per 100,000 people. The LightGBM model effectively captured the complex time‑series characteristics of human brucellosis. It had good performance while accurately predicting the trend. Based on the optimal LightGBM model, a short‑term prediction was made for the trend of human brucellosis in 2024. The results showed that in 2024, the disease would still have a clear seasonal pattern in China. The peak months were from April to June. The highest number of cases was in June (8,733.48 cases). The lowest number was in October (3,260.69 cases). The predicted total number of cases for the year was about 70,260. Overall, the incidence remained high. Conclusion China remains in a high-incidence phase of human brucellosis, necessitating further implementation of prevention and control measures and enhanced supervision and monitoring in key regions.

One of the main pathological features of airway inflammatory diseases is hypersecretion of airway mucus, which is manifested by goblet cell hyperplasia and mucociliary clearance dysfunction. In recent years, it has been found that the molecular structure of calcium activated chloride ion channels, transmenbrane protein 16A（TMEM16A）, is closely related to airway mucus hypersecretion.TMEM16A not only mediates ion transepithelial transport and hydration, but also participates in the regulation of mucin secretion. TMEM16A is highly expressed in airway epithelium of a variety of inflammatory diseases of upper and lower airway, such as asthma, cystic fibrosis, allergic rhinitis, chronic sinusitis and so on. Understanding the expression level and regulation mechanism of TMEM16A in different airway diseases and revealing its physiological function and pathological mechanism is critical for targeted disease treatment. This paper summarizes the research status of the discovery process, structural characteristics and regulatory mechanism of TMEM16A, and then summarizes the expression level of TMEM16A in asthma, cystic fibrosis, allergic rhinitis and chronic sinusitis ant related pathological mechanisms, clarifies the potential value of TMEM16A as a therapeutic target for the above four diseases, in order to guide treatment of airway inflammatory diseases.
Humans ; Asthma/metabolism* ; Anoctamin-1 ; Cystic Fibrosis/metabolism* ; Neoplasm Proteins/metabolism* ; Sinusitis/metabolism* ; Chloride Channels/metabolism* ; Rhinitis, Allergic/metabolism* ; Inflammation

A 64-year-old male patient with hemophilia A was scheduled for the surgical removal of a pulmonary mass. Preoperative evaluation revealed that the coagulation factor Ⅷ (FⅧ) activity was 0.5%, with an F Ⅷ inhibitor level of 32 BU/ml; the R value could not be detected on the thromboelastogram. Thoracoscopic lobectomy was successfully completed. On the day of the operation and the first day after the operation, 6 mg of recombinant activated coagulation factor Ⅶ (rFⅦa) was intravenously administered every 6 h. On postoperative day 1, the patient’s blood pressure dropped and the HGB gradually declined from 102 g/L to 65 g/L. Chest X-ray revealed a large amount of pleural effusion on the left side, and urgent thoracoscopic thoracic exploration was performed. A total of 3200 mL fresh blood was cleared, and a thoracic drainage tube was placed. On postoperative day 2, the rFⅦa dose was increased to 6 mg, which was intravenously administered every 4 h, and concentrated red cells were intermittently infused to correct anemia. Four days later, due to the inability to obtain rFⅦa, PCC (50 IU/kg every 8 hours) was administered. Additionally, treatment with methylprednisolone (40 mg/d) and cyclophosphamide (200 mg, every 2 weeks) was initiated to remove FⅧ inhibitors. The thoracic drainage tube was removed on postoperative day 9, and the patient was successfully discharged 3 weeks later.

Congenital coagulation factor Ⅶ deficiency is a rare autosomal incomplete recessive disorder caused by a defect in the coagulation factor Ⅶ (FⅦ) gene, with an incidence of approximately 1 in 500 000. Antiphospholipid antibody syndrome is relatively common and is a common cause of acquired thrombosis. However, the combination of the latter and the former is extremely rare in clinical practice, which brings difficulties to diagnosis and treatment. This article reported the laboratory examination, diagnosis and treatment of a patient with congenital coagulation factor Ⅶ deficiency and antiphospholipid syndrome after portal vein thrombosis, and reviewed the relevant literature.

A 64-year-old male patient with hemophilia A was scheduled for the surgical removal of a pulmonary mass. Preoperative evaluation revealed that the coagulation factor Ⅷ (FⅧ) activity was 0.5%, with an F Ⅷ inhibitor level of 32 BU/ml; the R value could not be detected on the thromboelastogram. Thoracoscopic lobectomy was successfully completed. On the day of the operation and the first day after the operation, 6 mg of recombinant activated coagulation factor Ⅶ (rFⅦa) was intravenously administered every 6 h. On postoperative day 1, the patient’s blood pressure dropped and the HGB gradually declined from 102 g/L to 65 g/L. Chest X-ray revealed a large amount of pleural effusion on the left side, and urgent thoracoscopic thoracic exploration was performed. A total of 3200 mL fresh blood was cleared, and a thoracic drainage tube was placed. On postoperative day 2, the rFⅦa dose was increased to 6 mg, which was intravenously administered every 4 h, and concentrated red cells were intermittently infused to correct anemia. Four days later, due to the inability to obtain rFⅦa, PCC (50 IU/kg every 8 hours) was administered. Additionally, treatment with methylprednisolone (40 mg/d) and cyclophosphamide (200 mg, every 2 weeks) was initiated to remove FⅧ inhibitors. The thoracic drainage tube was removed on postoperative day 9, and the patient was successfully discharged 3 weeks later.

Congenital coagulation factor Ⅶ deficiency is a rare autosomal incomplete recessive disorder caused by a defect in the coagulation factor Ⅶ (FⅦ) gene, with an incidence of approximately 1 in 500 000. Antiphospholipid antibody syndrome is relatively common and is a common cause of acquired thrombosis. However, the combination of the latter and the former is extremely rare in clinical practice, which brings difficulties to diagnosis and treatment. This article reported the laboratory examination, diagnosis and treatment of a patient with congenital coagulation factor Ⅶ deficiency and antiphospholipid syndrome after portal vein thrombosis, and reviewed the relevant literature.

ObjectiveTo explore the possible mechanism of Bimin Formula （鼻敏方） in treating lung-spleen qi deficiency syndrome of allergic rhinitis （AR） with high mucin secretion. MethodsThirty-four SD rats were randomly divided into a blank group （8 rats）， a model group （8 rats）， a low-dose Bimin Formula group （8 rats）， and a high-dose Bimin Formula group （10 rats）. Except for the blank group， the other groups were subjected to AR lung-spleen qi deficiency rat models induced by smoking， gavage of Ginkgo biloba leaf extract， and ovalbumin. After modeling， rats in the low- and high-dose Bimin Formula groups were given Bimin Formula concentrate （concentration of 2.16 g/ml） by gavage at doses of 1.08 g/100 g and 2.16 g/100 g， respectively， while rats in the model group were given 0.5 ml/100 g of normal saline by gavage， once daily for 28 days； the blank group was not intervened. Behavioral assessments were performed after intervention. ELISA was used to detect the levels of peripheral blood total immunoglobulin E （IgE）. HE staining was used to observe the pathological changes of nasal mucosa epithelium in rats， while immunohistochemistry was used to detect the expression of transmembrane protein 16A （TMEM16A） and mucin 5AC （MUC5AC） protein in nasal mucosa. Western Blot was used to detect the expression of nuclear factor kappa B （NF-κB） protein， and RT-PCR was used to detect the expression of TMEM16A， MUC5AC， and NF-κB mRNA in nasal mucosa. ResultsHE staining showed that the nasal mucosa epithelial cell structure in the blank group was intact without shedding， swelling， or necrosis； the nasal mucosa epithelial tissue of rats in the model group was thickened and partially shed， with infiltration of eosinophils and lymphocytes visible； the pathological changes in nasal mucosa tissue of rats in the high- and low-dose Bimin Formulagroups were improved， and more improvement was showen in the high-dose group. Compared with those in the blank group， the behavioral scores and peripheral blood total IgE levels of rats in the model group significantly increased， as well as the expression of TMEM16A， MUC5AC， and NF-κB proteins and mRNA in nasal mucosa （P＜0.05 or P＜0.01）. Compared with those in the model group， the behavioral scores and peripheral blood total IgE levels of rats in the high-dose Bimin Formula group decreased， and the expression of TMEM16A， MUC5AC， and NF-κB proteins and mRNA in nasal mucosaalso decreased （P＜0.05 or P＜0.01）； the behavioral scores and peripheral blood total IgE levels of rats in the low-dose Bimin Formula group were reduced， and the expression of TMEM16A and MUC5AC proteins and mRNA in nasal mucosa， as well as the expression of NF-κB protein decreased （P＜0.05 or P＜0.01）， but the difference in NF-κB mRNA expression was not statistically significant （P＞0.05）. Compared with the low-dose Bimin Formula group， the expression of NF-κB protein in the high-dose group decreased （P＜0.01）. ConclusionBimin Formula may improve the symptoms and high mucus secretion of AR lung-spleen qi deficiency by regulating the TMEM16A/NF-κB/MUC5AC signaling pathway in nasalmucosa.

Objective To investigate the influence factors of serum CA125 level in patients with ovarian chocolate cysts,and to study the effect on serum CA125 level of interventional therapy.Methods A total of 103 patients with single unilateral chocolate cyst of ovary underwent interventional treatment.According the serum CA125 level before interventional therapy,the patients were divided into normal group (CA125≤35 U/ml) and abnormal group (35 U/ml＜CA125≤200 U/ml).The clinical indexes of patients and ultrasound characteristics of cyst were compared between the two groups.The changes of serum CA125 levels before and after interventional therapy were analyzed.Results The difference of the course of diseases,dysmenorrhea history,diameter of cysts had statistical difference between the two groups (all P＜0.05).There were no statistical differences of age,history of dilivery,abortion history,history of pelvic surgery,cyst location between the two groups (all P＞0.05).In abnormal group,the mean serum level of CA125 reduced at 3 months (P＜0.000 1) and 6 months (P ＜0.000 1) after interventional therapy.In the normal group,there was no significant difference of the mean serum level of CA125 before and after interventional therapy (all P＞0.05).Conclusion Serum CA125 level is influenced by dysmenorrhea history,course of disease,diameter of cysts.Ultrasound-guided interventional therapy has intervention effect on patients with abnormal serum CA125 level before interventional therapy.

OBJECTIVETo perform phenotypic diagnosis, genetic diagnosis and prenatal diagnosis of inherited coagulation factor XIII (FXIII)deficiency in a Chinese family also provide a review of inherited coagulation F XIII deficiency.

METHODSThe activity levels of F XIII (F XIII:C) of proband and family members were measured by clot solubility test and REA-chrom F XIII kit. The antigen levels of F XIII(FXIII:Ag) were measured by enzyme-linked immunosorbent assay. Thrombelastography (TEG) test was used to make a comprehensive evaluation of coagulation status in the proband. All 15 exons and exon-intron boundaries of the F13A1 gene were amplified by PCR, and DNA sequencing was performed then. The mutation identified in the proband was screened in the family members. Furthermore, the related literatures were reviewed to provide a profile of clinical manifestation, gene mutations, the relationship between the mutations and phenotype, and treatments of inherited coagulation F XIII deficient cases.

RESULTSThe clot solubility test was positive in the proband. The FXIII:Ag level of the proband was less than 1% and the FXIII:C level was below the lower limit of detection (<3%). Two compound heterozygous missense mutations (p.Arg662* and p.Trp665*) were identified in the proband. Family study showed that the two mutations were both inherited from the parents. The fetus also carried two compound heterozygous mutations, the same as the proband, and was diagnosed with severe F XIII deficiency. As reported in the literatures, most mutations were missense mutations and nonsense mutations, and no hot spot was found. The clinical pattern of F XIII deficiency varied among patients, with potentially fatal consequences from severe bleeding complications.

CONCLUSIONBetter understanding of F XIII biochemical properties and function and developing of FXIII laboratory assays and genetic detection could prevent missed diagnosis, and patients moght benefit from better care.

Asian Continental Ancestry Group ; Base Sequence ; DNA Mutational Analysis ; Enzyme-Linked Immunosorbent Assay ; Exons ; Factor XIII ; genetics ; Factor XIII Deficiency ; genetics ; Female ; Heterozygote ; Humans ; Introns ; Mutation, Missense ; Pedigree ; Phenotype ; Polymerase Chain Reaction ; Pregnancy ; Prenatal Diagnosis

Aim Toinvestigatetheanalgesiceffectsof epidural osthole application on the mechanical allodyn-ia and the ERK/MAPK signaling pathway and the expression of COX-2 mRNA in the spinal dorsal horn.Methods 125adultmaleSDratswererandomizedin-to five groups( n=25 each) :Blank, Sham, NP, Ost and vehicle. At postoperative day 6, 1mg/rat osthole 50 μl was injected epidurally into group Ost and the same volume of vehicle was given into group vehicle. The mechanical pain threshold was measured by 50%MWT at 1 day before operation and the 3 rd,6 th,7 th, 14 th,21 st day after operation. After the measurement of pain threshold on postoperative day 14 , the L4-6 segment of spinal dorsal horn was removed for determi-nation of the expression of ERK, pERK and COX-2 mRNAbyWesternblotandRT-PCR.Results Com-pared with blank group, the mechanical pain threshold was only down-regulated at day 1 after operation in sham group, the expression of pERK and COX-2 mR-NA in sham group showed no significant difference ( P>0. 05 ); the mechanical pain threshold was signifi-cantly down-regulated after operation in NP, Ost and vehicle groups( P<0. 05 ) and the expression of pERK and COX-2 mRNA was significantly increased ( P <0. 05). Compared with vehicle group, the pain thresh-old in Ost group was significantly increased after drug administration( P<0. 05 ) and the expression of pERK and COX-2 mRNA was significantly reduced ( P <0. 05 ) . The expression of ERK showed no significant difference among each group(P>0. 05). The correla-tion analysis on pERK1/2 and COX-2 mRNA revealed the Pearson correlation coefficient was 0 . 878 and 0 . 910 , suggesting a strong positive correlation between pERKandCOX-2mRNA.Conclusions Ostholead-ministrated in the early stage after surgery can alleviate the nucleus pulposus-induced radicular inflammatory pain probably by inhibiting the expression of pERK and COX-2 mRNA in spinal dorsal horn.