Aim To study the inhibitory effect of gast-rodin (GSTD) on oleic acid (OA)-induced fat accu-mulation in HL-7702 cells and explore possible cellular signaling pathways. Methods The MTT method was used to study the impact of GSTD on cell viability in HL-7702 cells. Cellular steatosis was induced by 1 mmol·L-1 of OA administration for 24 h, and differ-ent concentrations of GSTD were added at the same time. Oil red O ( ORO) staining was used to determine fat accumulation in cells, and intracellular triglyceride ( TG) contents were assayed. Western blot was used to determine the phosphorylation levels of AMPKα and ACC in cells after GSTD administration. Compound C was used to treat the cells in order to study its influ-ence on the efficacies of GSTD. Results GSTD had no obvious toxicity in HL-7702 cells when its concen-tration was≤3 386. 5 μmol · L-1 . After 24 h of OA administration, there were large amounts of lipid drop-lets accumulated in HL-7702 cells, and intracellular TG contents greatly increased as well. However, when 169. 3 or 338. 7 μmol · L-1 of GSTD was added to-gether with OA, fat accumulation in cells was greatly inhibited, and intracellular TG contents were reduced averagely by 35% and 43 . 6%, respectively ( P<0. 01 vs OA alone ) . After administration, GSTD could in-crease the levels of p-AMPKα and p-ACC in HL-7702 cells time and dose dependently. Compound C could completely abolish the stimulating activity of GSTD on AMPK pathway and block its reducing effect on hepatic TG accumulation. Conclusions GSTD greatly inhibits OA-induced fat accumulation and reduces intracellular TG contents in HL-7702 cells;the efficacy of GSTD is dependent on the activation of cellular AMPK pathway.

Objective To investigate the resident performance on preoperative anesthetist visit in Beijing hospitals,thereby providing introduction for further training.Methods A self-designed questionnaire was distributed among the anesthesia residents who were receiving anesthesia residency training in Beijing through WeChat.The questionnaire covers geographic data of the residents,information on preoperative visit and existing training program.Results160 questionnaires were reclaimed.History-taking and physical examination were not comprehensive in many residents,the nature of surgery was not evaluated by most residents.The capacity of risk assessment and risk informing were not competent in many residents.The most desired training methods for preoperative visit were scenario simulation and bedside observation.Conclusions Scenario simulation with standard patient may have a promising prospect in preoperative anesthetist visit training.

Objective To investigate the effect of deltaNp63(ΔNp63) silencing on the proliferation of pancreatic cancer PANC1 cells.Methods ΔNp63 mRNA level in 23 pairs of pancreatic cancer and adjacent tissue specimen was detected by real-time PCR, andΔNp63 protein in human normal pancreatic ductal cell line HPDE6-C7 and pancreatic cancer cell line PANC1, CFPAC1 and BXPC3 was detected by Western blot. PANC1 cells were transfectedΔNp63 specific siRNA (ΔNp63-siRNA ) and scramble siRNA ( Con-siRNA ) using liposome, and untransfected cells served as control.ΔNp63 mRNA and protein was detected by real-time PCR and Western blot to validate the silencing ofΔNp63 expression.MTT assay and BrdU method were used to detect the proliferation and DNA synthesis of transfected PANC1 cells.Results TheΔNp63 mRNA expression in pancreatic cancer tissues and matched adjacent normal tissues was 0.99 ± 0.07 and 0.70 ±0.07, respectively.ΔNp63 mRNA expression in pancreatic cancer tissue was significantly up-regulated compared with that in the normal tissue (P=0.0034).TheΔNp63 protein expression in HPDE6-C7, PANC1, CFPAC-1 and BxPC3 cells was 0.97 ±0.09,3.06 ±0.16,2.57 ±0.11 and 2.45 ±0.08, respectively.TheΔNp63 protein level in pancreatic cancer cells were higher than that in HPDE6-C7 cells (P<0.001).ΔNp63 mRNA level in control, Con-siRNA and ΔNp63-siRNA group was 0.97 ±0.07,0.97 ±0.07 and 0.28 ±0.03, respectively, andΔNp63 protein expression level was 0.97 ±0.06,1.00 ±0.10 and 0.26 ±0.03.The expression ofΔNp63 mRNA and protein inΔNp63-siRNA group were significantly down-regulated comparing with those in Con-siRNA group (P<0.01).Significant inhibition on cell proliferation was observed in ΔNp63-siRNA group, which was statistically different from that in control and Con-siRNA group.The A490 value (DNA synthesis) of control, Con-siRNA andΔNp63-siRNA group was 0.55 ±0.04, 0.56 ±0.01 and 0.55 ±0.00 at 24 h after transfection, and 0.84 ±0.05,0.87 ±0.07 and 0.71 ±0.05 at 48 h after transfection.The DNA synthesis inΔNp63-siRNA group was significantly down-regulated compared with that in control and Con-siRNA group (P<0.05).Conclusions Knockdown ofΔNp63 could greatly inhibit the proliferation and DNA synthesis of pancreatic cancer PANC1 cells.

AIM: To explore the properties of the acetylcholine(ACh)-sensitive potassium channel in type Ⅱ vestibular hair cells(VHCs Ⅱ) in mice saccular macula and the modulation effect of calcium ions.METHODS: Under the whole-cell patch mode,the pharmacology properties of ACh-sensitive potassium channel and the modulation of calcium ions on ACh-sensitive potassium channel were investigated.RESULTS: Following extracellular perfusion of ACh,VHCs Ⅱ displayed a slow and sustained outward current,which was sensitive to tetraethylammonium(TEA,5 mmol/L) and charybdotoxin(CTX,100 nmol/L),but not sensitive to 4-aminopyride(4-AP,15 ?mol/L).ACh-sensitive potassium current was inhibited by intracellular application of ethylene glycol-bis(B-aminoethylether)-N,N,N',N'-tetraacetic-acid(EGTA,5 mmol/L) and extracellular perfusion of Cd2+ and Ni2+,respectively.Intracellular application of heparin(8 g/L) failed to inhibit ACh-sensitive potassium current.CONCLUSION: Extracellular application of ACh activates the big conductance,calcium-dependent potassium current(BK) in VHCs Ⅱ of mice,which is potently modulated by extracellular Ca2+ ions.However,intracellular IP3-dependent Ca2+ ions release mechanism is not involved in the activation of the ACh-sensitive BK channel.

0.05). However,the expression level of TKTL1 gene was significantly downregulated in the CNE cells transfected with siRNA TKTL1 construct compared with the cells transfected with control vector. Cancer cells were arrested in G0/G1 phase,and cancer cell proliferation was significantly inhibited in the CNE cells transfected with siRNA TKTL1 construct. CONCLUSION:TKTL1 plays an important role in the total transketolase activity and cell proliferation of human nasopharyngeal carcinoma. TKTL1 may be considered as a potential target for novel anti-cancer therapy.

OBJECTIVE: To study the clinical features, diagnosis and treatments of primary nasopharyngeal tuberculosis. METHOD: A case report was presented, and meanwhile etiopathogenesis and differential diagnosis were also reviewed. RESULT: A biopsy was taken and the histopathological examination showed tuberculosis granuloma with caseous necrosis. After anti-tuberculosis therapy, the symptoms disappeared. CONCLUSION Not only otologic disorders but also nasopharyngeal diseases need to be considered when aural fullness exists. More importantly, primary nasopharyngeal tuberculosis should be taken as one of the differential diagnosis.
Adult ; Female ; Humans ; Nasopharyngeal Diseases ; diagnosis ; microbiology ; Tuberculosis ; diagnosis

E-cadherin is a key epithelial protein and adhesive molecule. This study detected the E-cadherin expression in patients with chronic rhinosinusitis with nasal polyps (CRSwNP) and controls, and analyzed its possible role in the pathogenesis of CRSwNP. The expression of E-cadherin was detected by using Western blotting and immunohistochemistry in controls and patients with CRSwNP. Computed tomography (CT) scan findings were scored. The results showed that the E-cadherin expression was up-regulated in patients with CRSwNP as compared with controls (P=0.039) and the positive staining was predominantly localized on the epithelial cell membrane. E-cadherin level was correlated negatively with Lund-Mackay scores in patients with CRSwNP (r=-0.604, P=0.005). It is suggested that E-cadherin may be involved in the pathogenesis of CRSwNP and correlated with disease severity.

The protective roles of alpha-lipoic acid in the rat model of mitochondrial DNA (mtDNA) 4834bp deletion in inner ear were investigated. Forty female Wistar rats at 4 weeks of age were divided into four groups: group A (D-galactose group, n=10), group B (D-galactose+alpha-lipoic acid group, n=10), group C (alpha-lipoic acid group, n=10), and group D (control group, n=10). Auditory brainstem response (ABR) was used to detect the hearing threshold. Colorimetry was used to analyze activity of superoxide dismutase (SOD) and concentration of malondialdehyde (MDA). The percentage of mtDNA4834bp deletion in inner ear was identified by real-time PCR. There was no significant difference in ABR threshold shift among all groups. The percentage of mtDNA4834bp deletion in group A was higher than that in other groups, but there was no significant difference in percentage of mtDNA4834bp deletion among groups B, C, and D. The activity of SOD in group A was lower than that in other groups. The concentration of MDA in group A was higher than that in other groups. It was concluded that there was no significant hearing loss when the percentage of mtDNA4834bp deletion was lower than 12.5%. alpha-Lipoic acid could prevent the reactive oxygen species (ROS)-induced mtDNA4834bp deletion in inner ear of rats.

Objective To introduce treatment of old scaphoid fractures by internal fixation with common screws which have been modified into compression-like ones.Methods Twenty-five patients with old scaphoid fracture were admitted to our department from January,1995 to December,2002.They were 17 cases of delayed union,and eight cases of non-union and pseudoarticulation formation.All the patients were treated with open re- duction anti internal fixation by modified common cortical bone screws,some threads of which bad been erased so that they could act somewhat like compression ones.The modified screws were driven into the reduced scaphoid by simple surgical instruments to fix and compress the fracture ends.Results Nineteen cases were followed up for one to six years (mean,3 years).Fourteen cases of fracture healed,with an average healing time of 7 months.The mean extension-flexion arc of the injured wrists was between 106 degrees and 128 degrees.Three cases failed to heal,and two cases experienced deformed and sunken proximal scaphoid.Conclusions Common cortical bone screws can be easily changed into compression-like ones to treat old scaphoid fractures and result in satisfactory,clinic outcome.In addition,they are easily available,can be inserted through joint facet with limited negative effect on the joint,and play a double role of compression and fixation.

Objective To analyze mutations in the ATP2A2 gene in a Kazakh family with Darier's disease.Methods Clinical data were collected from 49 members from a family with Darier's disease,and peripheral blood samples were obtained from 44 family members and 100 unrelated healthy people.Genomic DNA was extracted from these blood samples.PCR and DNA sequencing were performed to detect mutations in the ATP2A2 gene.Results Darier's disease was inherited in an autosomal dominant manner in this family.A G→A heterozygous mutation (1288-1G→A) was identified at position 1288-1 at the splice site in exon 12 of the ATP2A2 gene in 11 patients in this family,but not in 33 healthy members or 100 healthy controls.Conclusion Darier's disease in this family may be caused by the heterozygous mutation (1288-1G→A)at the splice site in exon 12 of the ATP2A2 gene.