Objective To analyse the distribution characteristics of negative pattern of hepatitis B virus Markers (HBV‐M ) in healthy population in Hangzhou district in 2014 ,and provide strategy for the prevention and control of HBV infection in HBV‐M negative population .Methods The HBV‐M (HBsAg ,HBsAb ,HBeAg ,HBeAb and HBcAb) in blood specimens of health examina‐tion population were tested by using ELISA .For 300 cases preserved HBV‐M negative specimens ,HBsAg and HBsAb were detec‐ted by using chemiluminescence immunoassay and HBV‐DNA was detected by using PROCLEIX ULTRIO? Assay .The viral load of HBV‐DNA reactive sample was quantitatively determined .Results Among 9 143 blood samples ,2 213 samples were HBV‐M negative ,and the negative rate was 24 .20% .The negative rate of male to female was 1∶1 .21 .Using chemiluminescence immunoas‐says and PROCLEIX ULTRIO? Assay simultaneously ,we found one case of low concentration of HBsAg(both HBsAb and HBV DNA nonreactive) ,four cases of low concentration of HBsAb(both HBsAg and HBV DNA nonreactive) ,two cases of HBV‐DNA reactive(HBV‐M negative) .One HBV‐DNA reactive sample could be quantified as 560 IU/mL .Conclusion In HBV‐M (ELISA) negative population of health examination of Hangzhou district ,a few subjects had low concentrations of HBsAg or HBsAb or HBV‐DNA .For HBV‐M negative population ,quantitative detection of HBV‐M and HBV‐DNA before HBV vaccination is recom‐mended to determine w hether they need HBV vaccine and the HBV vaccination plan .

BACKGROUND: Hyperhomocysteinemia has been suggested to be a possible independent risk factor for stroke.OBJECTIVE: To explore the relationship between hyperhomocysteinemia and cerebral infarction and hemorrhage, and analyze the factors that affect plasma homocysteine level.DESIGN: Case-controlled clinical trial.SETTING: Department of Neurology, Second Hospital Affiliated to Medical College of Zhejiang University.PARTICIPANTS: Totally 57 patients including 21 with cerebral hemorthage and 36 with brain infarction were treated in the Department of Neurology, Second Hospital Affiliated to Medical College of Zhejiang University Between January and November 2003. Twenty-eight healthy volunteers were also recruited from the subjects coming for routine physical examination.METHODS: Two milliliters of fasting venous blood was collected from all subjects in the morning for detecting the contents of plasma homocysteine,vitamin B12, folic acid, creatinine and so on. All patients were scored for clinical neurological impairment, with the hematoma volume calculated in patients with brain hemorrhage determined on the basis of CT scanning.acid, vitamin B12, clinical neurological impairment score and hematoma volume.RESULTS: Valid results were obtained from all the 57 stroke patients and in male and female patients of both cerebral infarction group and cerebral hemorrhage group than that of the subjects of the same gender in the control group [(25.2±21.4), (18.3±10.9), (11.5±2.9) μmol/L for male subjects;(22.8±18.9), (14.7±7.4), (10.8±2.6) μmol/L for female subjects, P＜ 0.05-0.01].The level of homocysteine was similar between cerebral infarction group and cerebral hemorrhage group, homocysteic acid level showed obvious inverse correlation with folic acid level (r=-0.442, -0.531, P ＜ 0.05), but without relation to vitamin B12 level (r=-0.086, -0.111, P ＞ 0.05). Homocysteine level was not obviously correlated to the neurological impairment scores in cerebral infarction group (r=-0.139, P ＞ 0.05), nor was it related to the scores or hematoma volume in cerebral hemorrhage group (r=0.225,0.425, P ＞ 0.05).CONCLUSION: Hyperhomocysteinemia is risk factor for cerebral infarction and hemorrhage. Plasma homocysteine level is inversely correlated with folic acid level, but not obviously related to vitamin B12, clinical neurologicla impairment score or hematoma volume.

Objective To study the influence of the measurement of the platelet-monocyte aggregates (PMAs) by using of flow cytometry (FCM).Methods Anticoagulated peripheral venous bloods from nine healthy donors were incubated with a PE-CD14 MAb (monocyte marker) and a FITC-CD42a MAb (platelet marker) for 20 min and the formations of PMAs were measured by use of FCM.The factors such as fixative, anticoagulant, storage time and temperature were analyzed.Results The PMAs of citrated whole blood increased with the time elapsed in 6 h after blood drawing when they were stored in the room temperature.The PMAs of each time point showed significant difference (P

The incidence of cutaneous squamous cell carcinoma (CSCC) is increasing rapidly. This study discussed the effects of artesunate (ART) on CSCC cell proliferation and migration via the solute carrier family 7 member 11 (SLC7A11)-glutathione peroxidase 4 (GPX4) pathway. MTT assessed cell viability and analyzed the IC50 value (69.26 μM). Accordingly, human CSCC cells (A431) were cultured in vitro, and treated with 70 μM ART, Ferrostatin-1, oe-SLC7A11, and C646, with cell biological behavior assessed.The potential targets of ART were predicted. p53 acetylation and protein stability and ART-p300 binding were examined. Thymusless nude mice were subcutaneously inoculated with A431 cells, and treated with ART and C646. ART-treated A431 cells showed weakened proliferation, migration, lactate dehydrogenase levels, oxidized glutathione/glutathione ratio, reactive oxygen species, malondialdehyde, and active Fe2+ levels, which could be reversed by suppressing ferroptosis. ART promoted p53 acetylation and protein stability and curbed the SLC7A11-GPX4 pathway by targeting p300. ART stimulated ferroptosis via the SLC7A11-GPX4 pathway, thereby repressing CSCC cell proliferation and migration, which were counteracted by p300 inhibition. ART regulated the SLC7A11-GPX4 pathway by up-regulating the p300-p53 axis, thereby hindering tumor growth in vivo. Collectively, ART inhibits CSCC proliferation and migration by modulating the SLC7A11-GPX4 pathway through the p300-p53 axis.

The incidence of cutaneous squamous cell carcinoma (CSCC) is increasing rapidly. This study discussed the effects of artesunate (ART) on CSCC cell proliferation and migration via the solute carrier family 7 member 11 (SLC7A11)-glutathione peroxidase 4 (GPX4) pathway. MTT assessed cell viability and analyzed the IC50 value (69.26 μM). Accordingly, human CSCC cells (A431) were cultured in vitro, and treated with 70 μM ART, Ferrostatin-1, oe-SLC7A11, and C646, with cell biological behavior assessed.The potential targets of ART were predicted. p53 acetylation and protein stability and ART-p300 binding were examined. Thymusless nude mice were subcutaneously inoculated with A431 cells, and treated with ART and C646. ART-treated A431 cells showed weakened proliferation, migration, lactate dehydrogenase levels, oxidized glutathione/glutathione ratio, reactive oxygen species, malondialdehyde, and active Fe2+ levels, which could be reversed by suppressing ferroptosis. ART promoted p53 acetylation and protein stability and curbed the SLC7A11-GPX4 pathway by targeting p300. ART stimulated ferroptosis via the SLC7A11-GPX4 pathway, thereby repressing CSCC cell proliferation and migration, which were counteracted by p300 inhibition. ART regulated the SLC7A11-GPX4 pathway by up-regulating the p300-p53 axis, thereby hindering tumor growth in vivo. Collectively, ART inhibits CSCC proliferation and migration by modulating the SLC7A11-GPX4 pathway through the p300-p53 axis.

The incidence of cutaneous squamous cell carcinoma (CSCC) is increasing rapidly. This study discussed the effects of artesunate (ART) on CSCC cell proliferation and migration via the solute carrier family 7 member 11 (SLC7A11)-glutathione peroxidase 4 (GPX4) pathway. MTT assessed cell viability and analyzed the IC50 value (69.26 μM). Accordingly, human CSCC cells (A431) were cultured in vitro, and treated with 70 μM ART, Ferrostatin-1, oe-SLC7A11, and C646, with cell biological behavior assessed.The potential targets of ART were predicted. p53 acetylation and protein stability and ART-p300 binding were examined. Thymusless nude mice were subcutaneously inoculated with A431 cells, and treated with ART and C646. ART-treated A431 cells showed weakened proliferation, migration, lactate dehydrogenase levels, oxidized glutathione/glutathione ratio, reactive oxygen species, malondialdehyde, and active Fe2+ levels, which could be reversed by suppressing ferroptosis. ART promoted p53 acetylation and protein stability and curbed the SLC7A11-GPX4 pathway by targeting p300. ART stimulated ferroptosis via the SLC7A11-GPX4 pathway, thereby repressing CSCC cell proliferation and migration, which were counteracted by p300 inhibition. ART regulated the SLC7A11-GPX4 pathway by up-regulating the p300-p53 axis, thereby hindering tumor growth in vivo. Collectively, ART inhibits CSCC proliferation and migration by modulating the SLC7A11-GPX4 pathway through the p300-p53 axis.

Hereditary angioedema (HAE) is an autosomal dominant inherited disease characterized by recurrent and unpredictable episodes of subcutaneous or submucosal edema. These attacks could induce fatal risk when larynx is involved. The estimated prevalence of HAE is about 1 in 50 000. Due to its rarity and the diversity of clinical manifestations, HAE is known little by related physicians and misdiagnosis and mistreatment happens very often. Therefore, it is crucial to improve physicians′ understanding of HAE. To address this, a comprehensive management approach for the diagnosis and treatment of HAE have developed in our hospital. This approach includes intra-hospital multi-disciplinary treatment (MDT), collaboration with provincial network hospitals, patient education online and offline interacting with media propaganda. By implementing this approach, the diagnostic precision was significantly improved, the diagnostic time was significantly shortened, and the frequency of emergency interventions for severe laryngeal edema was significantly reduced. Additionally, the collection of data from HAE patients has provided valuable clinical insights for the diagnosis and treatment of HAE in China.

Hereditary angioedema (HAE) is an autosomal dominant inherited disease characterized by recurrent and unpredictable episodes of subcutaneous or submucosal edema. These attacks could induce fatal risk when larynx is involved. The estimated prevalence of HAE is about 1 in 50 000. Due to its rarity and the diversity of clinical manifestations, HAE is known little by related physicians and misdiagnosis and mistreatment happens very often. Therefore, it is crucial to improve physicians′ understanding of HAE. To address this, a comprehensive management approach for the diagnosis and treatment of HAE have developed in our hospital. This approach includes intra-hospital multi-disciplinary treatment (MDT), collaboration with provincial network hospitals, patient education online and offline interacting with media propaganda. By implementing this approach, the diagnostic precision was significantly improved, the diagnostic time was significantly shortened, and the frequency of emergency interventions for severe laryngeal edema was significantly reduced. Additionally, the collection of data from HAE patients has provided valuable clinical insights for the diagnosis and treatment of HAE in China.

OBJECTIVETo assess the impact of metabolic syndrome(MS) on Framingham risk score(FRS) in patients with type 2 diabetes mellitus (T2DM).

METHODSThe anthropometric and biochemical data of 1708 patients with T2DM admitted in hospital from May 2008 to April 2013 were retrospectively analyzed, including 902 males and 806 females with a mean age of 57.1±11.8 years (20-79 years). Diagnosis of MS was made according to the criteria of the Adult Treatment Panel Ⅲ Criteria modified for Asians.

RESULTSCompared to non-MS/T2DM patients, MS/T2DM patients had higher waist circumference, body weight, body mass index, systolic and diastolic blood pressure, fasting C peptide, total cholesterol, triglyceride, and LDL-C (P<0.05), while lower HDL-C (P<0.01). Both FRS [13.0(10.0, 15.0) vs 11.0(9.0, 13.0) in male,15.0(12.0, 18.0) vs 12.0(6.0, 14.8) in female,P<0.01)] and 10-year cardiovascular risk [12.0%(6.0%, 20.0%) vs 8.0%(5.0%,12.0%) in male,3.0%(1.0%, 6.0%) vs 1.0%(0.0%, 2.8%) in female,P<0.01] were higher in MS/T2DM patients than those in non-MS/T2DM patients.Both FRS and 10-year cardiovascular risk were increased with the components of MS.

CONCLUSIONT2DM patients with MS have more cardiovascular risk factors, higher FRS and 10-year cardiovascular risk.