Objective To investigate the expression of 5-lipoxygenase activating protein gene (ALOX5AP) polymorphism in the patients with cerebral infarction,and explore its relationship with cerebral infarction susceptibility.Methods Patients with cerebral infarction and healthy volunteers were selected for this study,whose venous blood was extracted and detected with polymerase chain reaction/restriction fragment length polymorphism (PCR-RFLP).Haplotype A (SG13S114T,SG13S89G,SG13S32A,SG13S25G),haplotype B (SG13S377A,SG13S114A,SG13S41A,SG13S35G),and their nucleotide polymorphism loci were observed.Results Single nucleotide polymorphism (SNP)-SG13S114,SNP-SG13S32 and HapA carrying rate were significantly different between patients with cerebral infarction and healthy volunteers (P ＜0.05).SNP-SG13S114 and SNP-SG13S32 were independent risk factors of cerebral infarction (OR ＞ 1.0,P ＜ 0.05).Conclusions The morbidity of cerebral infarction in Wenling City was influenced by SNP-SG13S114,SNP-SG13S32,and HapA carrying rate.

Objective:To observe the expression of Th1 versus Th2 type cytokines in primary hepatic cancer(PHC)and its adjacent liver tissues.Methods:The gene expression of Th1/Th2 cytokines was detected by RT-PCR using IFN-?and IL-2 as Th1 type cytokine genes,IL-4 and IL-10 as Th2 type cytokine genes.Results:Thl type cytokines were expressed in 7 and 9 cases,while Th0 type cytokines in 4 and 2 among 11 PHC and their adjacent liver tissues,respectively.Conclusion:Th1 type cytokines are expressed predominantly in primary hepatic cancer and its adjacent liver tissue.

Objective To evaluate atrial septal defect (ASD) occlusion employing a small right anterior thoracotomy approach. Methods A total of 21 patients with ASD underwent general anesthesia and 2 -3 cm incision was made in the fourth right intercostal space. Utilizing transesophageal or transthoracic echocardiography, the occluder was released using a monotube unit. Results All patients were occluded successfully. No patient required open surgery utilizing extracorporeal circulation. There were no major complications and no evidence of residual atrial shunt. Conclusion ASD occlusion via a minimal surgical incision is safe, less invasive, and has excellent outcomes.

eEF1A2 might be a putative oncoprotein in HCC .eEF1A2 over-expression has noticeable effects on the HCC cell prolifera-tion enhancement , differentiation inhibition , and cell cycle acceleration through the G 0/G1 phase to S phase and G 2/M phases.

Abstract: Objective　To investigate the clinical characteristics and diagnosis key points of brain abscess caused by Nocardia asiatica, and provide a clinical basis for diagnosing and treating intracranial infection caused by Nocardia. Methods　A case of pulmonary Nocardia asiatica complicated with brain abscess diagnosed at the Second Affiliated Hospital of Hainan Medical University was selected to analyze the clinical manifestations, cerebrospinal fluid characteristics, pulmonary and cranial imaging features, and treatment plan, and to summarize the diagnosis and treatment experience. Results　The patient was an elderly woman with a history of diabetes, dry cough was the first symptom without fever or headache. At the beginning of the course, it was diagnosed as pulmonary infection and tuberculosis in the local hospital, and received conventional antimicrobial and anti-tuberculosis therapies, but showed no improvement. The patient developed progressive limb weakness, followed by consciousness disorders, and coma. Cerebrospinal fluid (CSF) adenosine deaminase and lactate dehydrogenase were not abnormal, CSF pressure, protein and white blood cells were high, mainly with multiple nuclear cells. CSF glucose and chloride were normal in the early stage of the disease, but decreased significantly in the later stage. Metagenomic analysis of cerebrospinal fluid indicated Nocardia asiatica with a specific sequence number of 537. Lung CT showed exudation, abscess, and cavity in the right lung. Skull MRI scan + enhancement suggested multiple scattered abscesses in both cerebral hemispheres. The abscesses were of different sizes and showed ring enhancement, with extensive surrounding edema, and ventricular compression. After treatment with meropenem, linezolid, and compound sulfamethoxazole tablets, the cerebrospinal fluid recovered, and the lesions in the lungs and intracranial structures improved. Conclusions　Brain abscess caused by Nocardia asiatica is similar to the tuberculous brain in clinical symptoms, cerebrospinal fluid examination, craniocerebral imaging, so we should be alert to the possibility of Nocardia infection in patients with diabetes. At the same time, metagenomic testing of the cerebrospinal fluid can help confirm the diagnosis. The mortality and disability rates of brain abscess caused by Nocardia are high. Early diagnosis and treatment can improve the prognosis.

Follicle-stimulating hormone (FSH) is synthesized and secreted by the anterior pituitary, which binds to its receptors expressed on the membrane of Sertoli cells in the testis to bring about spermatogenesis. With the development of DNA sequencing technology, FSH SNPs rs10835638 and FSHR SNPs rs6165, rs6166, and rs1394205 were detected, which might directly affect the expression of FSH and activity of FSHR, resulting in male spermatogenic dysfunction. This review focuses on the relationship of FSH and FSHR gene polymorphisms with male infertility.
Follicle Stimulating Hormone ; genetics ; Humans ; Infertility, Male ; genetics ; Male ; Polymorphism, Single Nucleotide ; Receptors, FSH ; genetics ; Sertoli Cells ; Spermatogenesis ; Testis

Antibodies, Monoclonal ; metabolism ; CD79 Antigens ; metabolism ; Epstein-Barr Virus Infections ; Herpesvirus 4, Human ; isolation & purification ; Humans ; Immunoglobulin G ; metabolism ; Male ; Middle Aged ; Nose Neoplasms ; metabolism ; pathology ; therapy ; virology ; Paranasal Sinus Neoplasms ; metabolism ; pathology ; therapy ; virology ; Plasmacytoma ; metabolism ; pathology ; therapy ; virology

An 81-year-old male presented with an 8-year history of recurrent ulcer on the left dorsal foot which gradually spread to involve both lower limbs. Physical examination revealed no abnormality of any organ systems and no palpable superficial lymph nodes. Skin examination showed erythematous swelling of the left dorsal foot with an ulcer sized 7 cm × 10 cm on the surface. Tendon was visible at the base of the ulcer, and the ulcer margin was elevated giving a dyke-like appearance. The perilesional skin was purple-brown. There were several millet-like papuloid lesions circularly arranged at the inner side of the right foot as well as dark erythematous or brown nodules and pigmented patches with tenderness on both lower limbs. Histopathology of the ulcer of the left dorsal foot and papuloid lesions on the right foot revealed a visible epidermotropic infiltrate in the epidermis as well as an infiltration throughout the entire dermis with medium-sized atypical lymphoid cells with obvious mitoses. Immunohistochemical examination showed the coexpression of both T cell markers (including CD3, CD45RO, CD43) and B cell marker (CD20), with scatted positive staining for PAX-5and negative staining for CD79α or CD1 9. PCR confirmed the rearrangement of T cell receptor (TCR)-γgene. A diagnosis of peripheral T cell lymphoma unspecified was made in view of the rearrangement of TCR-γgene and above findings. The patient was treated with the following modified CHOP regimen: intravenous cyclophosphamide 0.8 g, leurocristine 2 mg and epirubicin hydrochloride 60 mg, as well as oral prednisone 15 mg twice daily for 5 days every 3 weeks (one treatment session). After 3 treatment sessions, the lesions improved markedly.

ObjectiveTo explore the procedures and methods for genetic diagnosis in one nonsyndromic variants of congenital neutropenia (NSVCN) patient and its pathogenic mutation.Methods Genomic DNA was prepared from one NSVCN patient who had progressed to chronic myelomonocytic leukemia and ELA2,HAX1,WASp and GFI1 genes were amplified and sequenced.Results A novel compound heterogeneous mutation consisting of two frame-shift mutations (c.430-1insG and c.655- 9del5bp) was found in HAX1 gene.ConclusionA practically genetic diagnosis procedure for NSVCN has been established,and the novel HAX1 gene mutation may contribute to the etiology of NSVCN.