Eriocalyxin B ameliorated experimental autoimmune prostatitis via modulation of macrophage polarization through gut microbiota-mediated vitamin D alteration.

Background: Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a often heterogeneous condition in urology. Accumulating evidence suggests that the autoimmune response against prostate antigens is related to CP/CPPS. The gut microbiota may be a possible cause of a number of autoimmune diseases.

[The Effect of VWF Propeptide on VWF Mutant in D1 Domain].

Objective: To investigate whether co-transfection of wild-type VWFpp with VWF mutant in D1 region is able to correct VWF defects in biosynthesis and secretion.

Methods: Four VWF mutant plasmids were single transfected into HEK 293 cells, or co-transfected into HEK 293 cells with the wild type VWFpp plasmids. The VWF in supernatant and lysate of transfected cells were analyzed by ELISA, vertical VWF multimer electrophoresis.

Clinical characteristics and outcomes of adult patients with acquired thrombotic thrombocytopenic purpura: a single center retrospective study.

Background: Thrombotic thrombocytopenic purpura (TTP) is a rare disease and a potentially life-threatening thrombotic microangiopathy. Although the diagnostic and therapeutic techniques have improved, it is still difficult for clinicians to identify early due to different initial clinical manifestations and the incidence and survival rate are reported inconsistently. This study investigated the clinical characteristics, treatment strategies, and treatment outcomes of adult patients with acquired TTP.

Effect of Eriocalyxin B on prostatic inflammation and pelvic pain in a mouse model of experimental autoimmune prostatitis.

Background: Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a common disease in males. Eriocalyxin B (EriB), a natural diterpenoid purified from Isodon eriocalyx var. laxiflora, was previously reported to have antitumor effects via multiple immune-related pathways.

CaMK4-dependent phosphorylation of Akt/mTOR underlies Th17 excessive activation in experimental autoimmune prostatitis.

Chronic prostatitis and chronic pelvic pain syndrome (CP/CPPS) is a complicated syndrome characterized by genitourinary pain in the absence of bacterial infection. Th17 cell-driven autoimmunity has been proposed as a cause of CP/CPPS. However, the factors that promote Th17-driven autoimmunity in experimental autoimmune prostatitis (EAP) and the molecular mechanisms are still largely unknown.

Microglial activation and neurobiological alterations in experimental autoimmune prostatitis-induced depressive-like behavior in mice.

Background: Patients with chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) frequently show depressive symptoms clinically and increasing evidence indicates a correlation between CP/CPPS and depression. However, the underlying mechanisms of CP/CPPS-related depression remain poorly understood. Here, we sought to determine the role of hippocampal microglial activation and neurobiological changes in a mouse model of experimental autoimmune prostatitis (EAP)-induced depression and the treatment efficacy of Chinese herb extract baicalein.

Development of acquired factor V inhibitor after treatment with ceftazidime: a case report and review of the literature.

We report the case of a 59-year-old Chinese man who showed an asymptomatic coagulation factor V deficiency pattern after second intravenous treatment with ceftazidime. Normal pooled plasma failed to correct the abnormalities in a mixing test, and the presence of factor V inhibitor was confirmed by the Bethesda method. The coagulopathy was not corrected by transfusion of fresh frozen plasma and prothrombin complex concentrate, but rather by treatment with prednisone and withdrawal of dubious drugs.

[Congenital afibrinogenemia caused by a novel insertion mutation in the FGB gene].

Objective: To investigate the genetic defect and its mechanism in a patient with congenital afibrinogenemia.

Methods: The plasma fibrinogen activity and antigen of the patient was determined using the Clauss method and immuno-nephelometric assay, respectively. Genomic DNA was isolated from peripheral blood of the proband and his related family members.

[Gene analysis and pathogenesis in 40 patients with hemophilia B].

Hemophilia B (HB) is a recessive X-linked inherited disorder, the pathogenesis of HB is deficiency or functional abnormalities of coagulation factor IX, which is caused by F9 gene mutations. To explore the mechanism of its molecular pathology, 40 patients with HB were studied with polymerase chain reaction (PCR) and direct sequencing. The diagnosis of HB patients were based on clinical manifestation and deficient factor IX activity in plasma.

Valproic acid-associated low fibrinogen and delayed intracranial hemorrhage: case report and mini literature review.

A 41-year-old male had suffered from gradual hearing loss in his right ear for 2 years. Head computed tomography and magnetic resonance imaging scans showed a neoplasm in the cerebellopontine angle region, which was confirmed by the diagnosis of acoustic neurilemmoma by pathological findings after surgery. Following surgery, he routinely received valproic acid (VPA) to prevent seizures.

[Identification and functional analysis of a novel missense mutation Ser250Phe underlying congenital coagulation factor Ⅶ deficiency].

Objective: To identify and characterize a missence mutation Ser250 Phe underlying coagulation factor Ⅶ (FⅦ) deficiency in a Chinese patient and his family.

Methods: The FⅦ gene (F7) was analyzed by DNA sequencing, and the FⅦ levels (including antigen and activity) in patient's plasma were determined with enzyme-linked immunoabsorbent assay (ELISA) and one stage prothrombin time based method. In addition, a FⅦ-250 Phe mutant corresponding to the identified mutation was expressed in HEK293 cells, and a subcellular localization experiment in CHO cells was performed to clarify the molecular mechanism of FⅦ deficiency caused by the FⅦ-250 Phe mutation.

Clinical, pathological, and genetic analysis of ten patients with MYH9-related disease.

MYH9-related disease (MYH9-RD) is an autosomal dominant disorder caused by mutations in the MYH9 gene. It is characterized by a triad of giant platelets, thrombocytopenia, and characteristic Döhle body-like granulocyte inclusions. In this study we report 10 unrelated patients with MYH9-RD in whom the following seven MYH9 gene mutations were found: W33R, p.

Clinical study of thalidomide combined with dexamethasone for the treatment of elderly patients with newly diagnosed multiple myeloma.

Objective: To investigate the relationship between the efficacy and safety of different doses of thalidomide (Thal) plus dexamethasone (Dex) as the initial therapy in elderly patients with newly diagnosed multiple myeloma (MM).

Methods: Clinical data of 28 elderly patients with newly diagnosed MM who underwent the TD regimen as the initial therapy were analyzed retrospectively. The patients were divided into two groups according to the maximal sustained dose of Thal: lower dose (group A) and higher dose (group B).

[Clinical features and gene analyses of six patients with MYH9-related disease].

Objective: To investigate clinical features and to identify gene mutations in six patients with nonmuscle myosin heavy chain 9 gene (MYH9)-related disease.

Methods: The platelet counts were measured using automated complete blood cell counter and manual manner. The size of platelets and inclusion bodies were observed under light microscopy.

[Prenatal diagnosis for two families of congenital factor V deficiency].

Objective: To provide genetic consulting and prenatal diagnosis for two families with congenital factor V deficiency based on the known mutations of factor V gene (G16088C and G69969T).

Methods: Chorionic DNA was obtained at 12 weeks of gestation and analyzed to exclude maternal cell contamination through microsatellite DNA analysis. It was then amplified with PCR and sequenced to determine the presence of mutations in exons 3 and 23.

[Relationship between factor VIII inhibitor development and polymorphisms of TNFα and CTLA-4 gene in Chinese Han patients with hemophilia A].

Objective: To investigate the potential association between factor VIII inhibitor development and polymorphisms of tumor necrosis factor-α (TNF-α)-308 and cytotoxic T-lymphocyte associated protein-4 gene in Chinese Han patients with hemophilia A (HA).

Methods: The single base change polymorphism in TNF-α and CTLA-4 gene was analyzed in 140 Chinese Han patients with hemophilia A who have been treated with plasma-derived FVIII concentrates and 108 normal controls by using PCR-restrictive fragment length polymorphism (RFLP). All of the HA patients' plasma samples were measured by modified-Nijmegen assay simultaneously.

[Genotype and phenotype analysis of congenital coagulator factor VII deficiency in four Chinese pedigrees].

Objective: To investigate the clinical manifestation and gene mutation in four Chinese pedigrees with the congenital coagulation factor VII deficiency.

Methods: Prothrombin time (PT), activated partial thromboplastin time, thrombin time and plasma fibrinogen were measured using STAGO STA-R automatic coagulation analyzer, and the coagulation activity of factor VII (FVII:C) was determined by a PT-based one stage method, and factor VII antigen (FVII:Ag) level by a sandwich enzyme-linked immunoabsorbsent assay. All exons, exon-intron boundaries and 3',5'untranslated regions of the FVII gene from the genomic DNA of the probands and their families were amplified by PCR, and then sequenced.

Treatment of vitamin K-dependent coagulation factor deficiency and subarachnoid hemorrhage.

Background: In adults, vitamin K-dependent coagulation factor deficiency (VKCFD) increases in the recent years. We treated a VKCFD patient with subarachnoid hemorrhage, with favorable outcomes.

Methods: A 19-year-old male student with VKCFD was treated at our hospital.

[Analysis of coagulation factor VIII inhibitor development related factors in hemophilia A patients.].

Objective: To analyze the clinical features of hemophilia A (HA), and the factors associated with the factor VIII (FVIII) inhibitor development.

Methods: One huandred and thirteen patients with HA were recruited in this retrospective study, among whom, 85 were treated with FVIII replacement therapy. The FVIII inhibitor levels and factors associated with the inhibitor development were correspondingly investigated in these 85 patients.

[Pathology, diagnosis and treatment of a patient with hemotidrosis.].

Objective: To investigate the pathology, diagnosis and treatment of a patient with hemotidrosis.

Methods: Coagulation tests, coagulation factor activities, von Willebrand factor concentration, bleeding time and platelet aggregation were measured. The bloody exudates from the skin was examined under light microscopy.

[Inherited dysfibrinogenemia caused by Arg16His mutation in alpha chain of fibrinogen.].

Objective: To analyze the phenotype and genotype of a family with inherited dysfibrinogenemia.

Methods: Assays of coagulation, including activated partial thromboplastin time (APTT), prothrombin time (PT) and thrombin time (TT), were carried out with Stago Compact in the proband and his family members. The activity and antigen of fibrinogen in plasma were determined by Clauss and immunoturbidimetry, respectively.