OBJECTIVETo define the anatomical approach, anatomical planes and related vessels and nerves to create a safe and reproducible combined sublingual and bi-vestibular access for trans-oral video-assisted thyroidectomy.

METHODSFrom November 2009 to May 2011, twenty-five embalmed human specimens were dissected for anatomical information of the cervical region, the mandible region and the supra-hyoid muscles. On twenty fresh frozen human specimens after an experimental trans-oral endoscopic thyroidectomy, the related vascular, neural structures and muscles were evaluated.

RESULTSThe optical access port was placed in the midline sublingual. The geniohyoid muscle, mylohyoid muscle and the anterior belly of the digastric muscle were divided in the midline in order to reach the plane under the platysma muscle. The mucosa was sagittal incised bilaterally in the vestibular of oral cavity for working trocar, at the level of the first molar of the mandible. The working trocar reached directly the periosteum of the mandible, under the facial vessel and the marginal branch of facial nerve, and then passed below the platysma muscle into the infra-laryngeal working area. The distance from mental nerve to mandibular midline and between mental nerve and facial artery were (25.8 ± 0.9) mm and (29.4 ± 0.9) mm respectively. Anatomical dissections showed that after an experimental trans-oral combined sublingual and bi-vestibular access, all muscles of the floor of the oral cavity as well as the related vascular and neural structures are intact. The maximum nodule size of the resected specimens in the totally trans-oral approach was up to 50 mm.

CONCLUSIONThe combined sublingual and bi-vestibular access of trans-oral video-assisted thyroidectomy is safe and reproducible.

Adolescent ; Adult ; Female ; Humans ; Male ; Mandible ; anatomy & histology ; Middle Aged ; Mouth ; anatomy & histology ; Mouth Floor ; anatomy & histology ; Thyroidectomy ; methods ; Young Adult

Objective To mvesugate the Tate of YMDD mutation accompamed with pre-core(region and core promotor region mutation and the clinical significance.Methods YMDD mutation and pre-core(at 1896 nu- cleotide)region and core promotor region(at 1762.1764 nucleotide)mutation were detected from the 122 patients with chronic hepatitis B virus after receiving lamivudine treatment above 6 months.Results 40 cases were tested for YMDI)mutations in 122 HBV patients with lamivudine treatment,and the positive rate of YMDD mutation was 32.8 %.After YMDD mutation,ALT,AST and HBV DNA of the patients significantly increased(P0.05).Conclusion The patients with YMDD mutation had higher rate of pre-core region(at 1896 nucleotide)and basal core promotor region(at 1762, 1764 nucleotide)mutation than those without YMDD mutation,but there was no correlation between the mutation and the deterioration of disease condition and the bad prognosis.

OBJECTIVETo investigate whether the CD4+CD25+Foxp3+ regulatory T cells are associated with serum TGF beta 1 in patients with hepatitis B.

METHODSPatients with chronic hepatitis B (CHB), chronic asymptomatic carriers (AsC), normal subjects (NS) and the resolved from HBV infection (Resolved) were recruited in this study. Flow cytometric analysis was used to detect the frequency and phenotype of peripheral CD4+CD25+Foxp3+ T cells, and Foxp3 gene expression were examined by real time PCR. Serum TGF beta 1 levels were measured by ELISA (enzyme-linked immunosorbent assay).

RESULTSPatients with CHB or AsC exhibited significantly higher frequency of CD4+CD25+Foxp3+ T cells compared to healthy controls. CD4+CD25+ T cells derived from patients with CHB and AsC expressed higher level of Foxp3-mRNA. Furthermore, the frequency of CD4+CD25+Foxp3+ regulatory T cells was correlated with serum HBV DNA copy numbers in patients with CHB and AsC. Our results indicated that the serum TGF beta was increased in CHB and AsC patients compared to control patients, and that serum TGF beta was correlated with the expression of Foxp3-mRNA and the frequency of CD4+CD25+Foxp3+ regulatory T cells in patients with CHB and AsC.

CONCLUSIONSThe findings have important implication in the understanding of the role and mechanism of aberrant CD4+CD25+Foxp3+ regulatory T cells in the maintenance of chronicity in hepatitis B patients.

Adolescent ; Adult ; CD4 Antigens ; immunology ; metabolism ; Carrier State ; blood ; immunology ; Female ; Flow Cytometry ; Forkhead Transcription Factors ; immunology ; metabolism ; Hepatitis B Surface Antigens ; blood ; immunology ; Hepatitis B, Chronic ; blood ; immunology ; Humans ; Interleukin-2 Receptor alpha Subunit ; immunology ; metabolism ; Male ; Phenotype ; Polymerase Chain Reaction ; RNA, Messenger ; genetics ; metabolism ; T-Lymphocytes, Regulatory ; immunology ; virology ; Transforming Growth Factor beta ; blood ; Viral Load ; Young Adult

Aim To identify the molecular target of gabapentin in the treatment of postherpetic neuralgia(PHN). Methods The molecular target of gabapentin for PHN was analyzed by network pharmacology and molecular docking and confirmed by coprecipitation test. Rats were randomly divided into control group, model group, model+50 mg·kg-1 gabapentin group, model+100 mg·kg-1 gabapentin group, and model+200 mg·kg-1 gabapentin group, with nine rats in each group. The pain-related behaviors of the rats were measured at different time points. The mRNA and protein expressions of CACNA2D1, Bax, and Bcl-2 in rat spinal cord were determined by immunofluorescence, Western blot, and qPCR. Results CACNA2D1 was the target gene of gabapentin that determined via network pharmacology, molecular docking, and co-precipitation tests. After modeling, mechanical pain threshold and thermal pain threshold significantly decreased, and the number of apoptotic GABA cells significantly increased. However, after intraperitoneal injection of 50, 100, and 200 mg·kg-1 gabapentin, mechanical pain threshold and thermal pain threshold significantly increased(P<0.05), and the number of apoptotic GABA cells significantly decreased(P<0.01). Immunofluorescence and Western blot results showed that compared with the model group, with the increase of gabapentin concentration, the positive expression rate of Bax significantly decreased, and the positive expression rate of Bcl-2 and CACNA2D1 significantly increased. The mRNA expression levels of Bax, Bcl-2 and CACNA2D1 detected by qPCR were consistent with the results of immunofluorescence and Western blot. Conclusions Gabapentin up-regulates the expression of target protein CACNA2D1, inhibits the proapoptotic protein Bax, and promotes the expression of apoptotic inhibitor Bcl-2.