Objective To evaluate the diagnostic value of ultrasonography on thyroid microcarcinoma ,and to find out its sono-graphic characteristics .Methods Ultrasound performance of 206 thyroid microcarcinoma nodules in 150 patients confirmed by sur-gery and pathology were retrospectively analyzed ,nodules internal echo ,boundary ,the shape ,the blood flow and internal calcifica-tion and calcification size ,distribution and type were observed and compared with 82 benign nodules(diameter ≤1 cm) .Results In terms of solid low echo ,minicalcification ,aspect ratio≥1 ,rich blood flow and neck lymph node enlargement ,thyroid microcarcinoma were significantly higher than that of thyroid benign nodules (P<0 .05) .Ultrasonographic performance of thyroid microcarcinoma often presented as solid low echo ,irregular form ,aspect ratio ≥1 ,internal mostly small calcification ,edge blur and the surrounding small burrs .Color doppler blood flow showed that ,blood supply was rich in patients with strong nodules ,distribution was irregular , smaller nodules blood flow was not rich .Conclusion The two-dimensional and color doppler flow imaging(cdfi) might be has a im-portand value on thyroid microcarcinoma diagnosis .

Objective:To determine expression levels of ubiquitin C-terminal hydrolase-L1 (UCH-L1) and serum glial fibrillary acidic protein (GFAP) in patients with acute cerebral infarction and their clinical significance.Methods:A total of 80 patients with acute cerebral infarction in Chongqing Cancer Hospital from January 2014 to February 2016 were enrolled as an observation group.Another 80 healthy people served as a control group.The expression levels of UCH-L1 and GFAP in the 2 groups were detected.Results:Sensibility and specificity for UCH-L1 and GFAP were 75.0％,87.5％ and 81.3％,90.0％,respectively.Receiver operating characteristic curve areas of UCH-L1 and GFAP were 0.670 and 0.757,respectively.There were no significant significance in age,gender,drinking,smoke,diabetes,and hyperlipidemia in the 2 groups (P＞0.05).High blood pressure rate in the observation group was higher than that in the control group (P＜0.05).Spearson/Pearson analysis showed that serum UCH-L1 and GFAP levels were positively correlated with hypertension,but they were negatively correlated with sex,age,diabetes,hyperlipidemia,alcohol consumption,smoking,and other factors.General data at different time in the observation group was not statistically different (P＞0.05).The expression levels of UCH-L1 and GFAP in the observation group was higher than that in the control group (P＜0.05).UCH-L1 and GFAP levels at different time in the 2 groups were not statistically different (P＞0.05).UCH-L1 and GFAP levels in the light,medium,and heavy groups were higher than those in the control group (P＜0.05),while UCH-L1 and GFAP levels in the medium and heavy groups were higher than those in the light group (P＜0.05).There was significant difference between levels of UCH-L1 or GFAP and infarction size at different time in the observation group (P＜0.05).The results of Pearson correlation analysis showed that the levels of serum UCH-L1 and GFAP were positively correlated (r=0.634,P=0.001).Conclusion:The levels of serum UCH-L1 and GFAP are significantly increased at the early stage of acute cerebral infarction,and they have a certain correlation with the severity of cerebral infarction,which can provide a basis for early clinical diagnosis and treatment.

The effects of Sonic hedgehog (Shh) signaling pathway activation on S-type neuroblastoma (NB) cell lines and its role in NB tumorigenesis were investigated. Immunohistochemistry was used to detect the expression of Shh pathway components-Patched1 (PTCH1) and Gli1 in 40 human primary NB samples. Western blotting and RT-PCR were used to examine the protein expression and mRNA levels of PTCH1 and Gli1 in three kinds of S-type NB cell lines (SK-N-AS, SK-N-SH and SHEP1), respectively. Exogenous Shh was administrated to activate Shh signaling pathway while cyclopamine was used as a selective antagonist of Shh pathway. S-type NB cell lines were treated with different concentrations of Shh or/and cyclopamine for different durations. Cell viability was measured by using MTT method. Apoptosis rate and cell cycle were assayed by flow cytometry. The xenograft experiments were used to evaluate the role of Shh pathway in tumor growth in immunodeficient mice. High-level expression of PTCH1 and Gli1 was detected in both NB samples and S-type NB cell lines. Cyclopamine decreased the survival rate of the three cell lines while Shh increased it, and the inhibition effects of cyclopamine could be partially reversed by shh pre-treatment. Cyclopamine induced the cell apoptosis and the cell cycle arrest in G(0)/G(1) phase, while Shh induced the reverse effects and could partially prevent effects of cyclopamine. Cyclopamine could also inhibit the growth of NB in vivo. Our studies revealed that activation of the Shh pathway is important for survival and proliferation of S-type NB cells in vivo and in vitro through affecting cell apoptosis and cell cycle, suggesting a new therapeutic approach to NB.

BACKGROUNDPrevious studies have showed that photooxidative stress can lead to down-modulation of nuclear factor-kappa B (NF-kappaB) activity causing apoptosis of cultured photoreceptor cells. This study aimed at investigating whether NF-kappaB was involved in photoreceptor cells apoptosis induced by N-methyl-N-nitrosourea (MNU) in rats.

METHODSA single intraperitoneal injection of 60 mg/kg MNU was given to 50-day-old female rats. At different intervals after MNU treatment, the animals were sacrificed. Retinal damage was examined by a light microscope. The apoptotic index of the photoreceptor cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL). NF-kappaB was analysed by Western blot and Transcriptin Factor Assay Kits.

RESULTSThe pyknosis of the photoreceptor nuclei and the disorientation of the outer segment of the photoreceptor layer was seen after MNU treatment for 24 hours. The outer nuclear layer and photoreceptor layer were almost completely lost at 7 days. Photoreceptor cells apoptosis reached the peaked value at 24 hours. In apoptotic cascade, the protein levels of NF-kappaB p65 were only detected after MNU treatment for 12 and 24 hours in the nucleus. Conversely, the amounts of IkappaBalpha were markedly increased in the cytoplasm as well as in the nucleus. The activity of NF-kappaB p65 in the nucleus was down-modulated in the end.

CONCLUSIONSMNU-induced photoreceptor cell destruction was attributed to the apoptotic process by down-regulating the activation of NF-kappaB p65.

Animals ; Apoptosis ; drug effects ; Cell Nucleus ; metabolism ; Female ; I-kappa B Proteins ; analysis ; physiology ; Methylnitrosourea ; toxicity ; NF-KappaB Inhibitor alpha ; NF-kappa B ; analysis ; physiology ; Photoreceptor Cells ; chemistry ; drug effects ; pathology ; Rats ; Rats, Sprague-Dawley ; Retina ; drug effects ; pathology

OBJECTIVETo observe the changes of nuclear factor-kappa B (NF-kappaB) in the course of N-methyl-N-nitrosourea (MNU)-induced apoptosis of rat retinal photoreceptor cells and investigate the mechanism of MNU-induced retinal damage.

METHODSA single intraperitoneal injection of 60 mg/kg MNU was given to 50-day-old female rats, which were sacrificed at different intervals after MNU treatment. The retinal damage was examined with optical microscopy and photoreceptor cell apoptosis detected by TUNEL assay. Western blotting was performed to analyze the changes in NF-kappaB.

RESULTSPyknosis of the photoreceptor cell nuclei and disorientation of the outer segment of the photoreceptor layer was observed 24 h after MNU treatment, and the outer nuclear layer and photoreceptor layer were almost completely lost on day 7. Photoreceptor cell apoptosis peaked at 24 h, and in the apoptotic cascade, NF-kappaB p65 protein was only detected 12 and 24 h after MNU treatment, whereas the amount of I kappa B alpha, in contrast, markedly increased in the cytoplasm as well as in the nuclei.

CONCLUSIONMNU-induced retinal damage might be mediated through the signaling pathway of NF-kappaB/I kappa B alpha.

Animals ; Apoptosis ; drug effects ; Blotting, Western ; Female ; I-kappa B Proteins ; metabolism ; In Situ Nick-End Labeling ; Methylnitrosourea ; toxicity ; NF-kappa B ; metabolism ; Rats ; Rats, Sprague-Dawley ; Retinal Diseases ; chemically induced ; metabolism ; pathology

Objective To investigate the neuroprotective mechanism of sevoflurane in rats resuscitated from cardiac arrest (CA).Methods A ventricular fibrillation-induced CA model was established.Forty Wistar rats were randomly divided into the sham group,sevoflurane group and control group.Apoptosis-related proteins were measured by Western blot at 24 h after restoration of spontaneous circulation (ROSC).The status of mitochondrial permeability transition pore (MPTP) were measured using a spectrophotometer,and the mitochondrial membrane potential (MMP) were measured with JC-1 fluorescent probe.At 72 h after ROSC,the apoptotic index of neurons in hippocampal CA1 region was counted by TUNEL staining.Results The protein expression of Bax,Bak,cleaved-caspase 9,cleavedcaspase 3 and cytosolic cytochrome c were lower in the sevoflurane group (all P＜0.05),the protein expression of Bcl-2 was higher in the sevoflurane group compared with the control group (P＜0.05).The sevoflurane group had a less opening status of MPTP and a higher MMP compared with the control group (all P＜0.05).The sevoflurane group had less apoptotic neurons compared with the control group (P＜0.05).Conclusion By up-regulating the expression of Bcl-2,down-regulating Bax and Bak,sevoflurane could reduce the apoptosis of neurons and decrease the opening of MPTP,eventually reduce cerebral injuries.

The effects of Sonic hedgehog (Shh) signaling pathway activation on S-type neuroblastoma (NB) cell lines and its role in NB tumorigenesis were investigated. Immunohistochemistry was used to detect the expression of Shh pathway components-- Patchedl (PTCH1) and Glil in 40 human primary NB samples. Western blotting and RT-PCR were used to examine the protein expression and mRNA levels of PTCH1 and Glil in three kinds of S-type NB cell lines (SK-N-AS, SK-N-SH and SHEPI), re-spectively. Exogenous Shh was administrated to activate Shh signaling pathway while cyclopamine was used as a selective antagonist of Shh pathway. S-type NB cell lines were treated with different concen-trations of Shh or/and cyclopamine for different durations. Cell viability was measured by using MTT method. Apoptosis rate and cell cycle were assayed by flow cytometry. The xenograft experiments were used to evaluate the role of Shh pathway in tumor growth in immunodeficient mice. High-level expres-sion of PTCH1 and Gill was detected in both NB samples and S-type NB cell lines. Cyclopamine de-creased the survival rate of the three cell lines while Shh increased it, and the inhibition effects of cyclopaminc could be partially reversed by shh pre-treatment. Cyclopamine induced the cell apoptosis and the cell cycle arrest in G0/G1 phase, while Shh induced the reverse effects and could partially pre-vent effects of cyclopamine. Cyclopamine could also inhibit the growth of NB in vivo. Our studies re-vealed that activation of the Shh pathway is important for survival and proliferation of S-type NB cells in vivo and in vitro through affecting cell apoptosis and cell cycle, suggesting a new therapeutic ap-proach to NB.

Background Traditional Chinese medicine (TCM), especially herbal medicine, has been widely used in China and now is also being increasingly used in other countries for the treatment of cardiovascular diseases. Although many studies have demonstrated that certain Chinese herbal products are effective and safe for the treatment of cardiovascular diseases, most of these lack sufficient quality. Therefore, large randomized clinical trials and further scientific research to determine its safety, effectiveness are necessary.QiShen YiQi Dripping Pills (QSYQDP) is a herbal preparation clinically used in the treatment and prevention of coronary artery disease. Preliminary observations have shown its safety and effectiveness. Methods/Design This randomized, controlled trial will recruit 3600 patients with a history of myocardial infarction. Patients will be randomized into two groups by a Centr-Randomized System. One group receives QSYQDP, the other group receive aspirin. This trial protocol will describe eligibility criteria, detailed information on the treatment definition, blinding, endpoints, statistical methods, sample size determination, data management, legal aspects, and the current status of the trial. Discussion This trial is one of the first randomized, controlled clinical trial to evaluate the efficacy and safety of traditional Chinese herbal medicine in the treatment and secondary prevention of coronary artery disease. The results of this study should help to define the role of TCM in modern medical care, as well as to provide the management strategy for CAD patients in China and other countries.

OBJECTIVETo investigate the types and frequency of gene mutations in children with thalassemia in Kunming, Yunan Province.

METHODSA biochemical screening for thalassemia was performed by testing RBC fragility, MCV and hemoglobin electrophoresis on 1338 children from Kunming, Yunnan Province. Genetic diagnosis was performed on the children with α-thalassemia by gap-PCR and on the children with β-thalassemia by PCR-RDB.

RESULTSThe positive rate of the biochemical screening for thalassemia was 11.36% (152 cases). The positive rate of genetic diagnosis was 8.59% (115 cases). Of the 115 cases, α-thalassemia was found in 43 cases, β-thalassemia in 68 cases and α-combined-β thalassemia in 4 cases.--SEA/αα accounted for 47%, -α4.2/αα accounted for 21%, and HbH disease accounted for 14%. Six genotypes were found in 68 cases of β-thalassemia and the mutation frequency of βE was the highest (32%), followed by CD41-42 (24%), CD17 (23%), IVS-II654 (10%), CD71-72 (10%), and -28 (1%).

CONCLUSIONSThe frequency of gene mutations for thalassemia is high in children from Kunming, Yunnan Province. Premarital and prenatal screenings and genetic diagnosis for thalassemia should be carried out in this area.

Adolescent ; Child ; Child, Preschool ; Female ; Genetic Testing ; Humans ; Infant ; Infant, Newborn ; Male ; Mutation ; Thalassemia ; blood ; diagnosis ; genetics

Objective To determine the factors that influence the development of abnormal thyrotropin (TSH) level in an euthyroid population.Methods We conducted a follow-up study in 3 communities with different iodine status.Of the 3403 euthyroid subjects at baseline screened in 1999,80.1% ( n = 2727 ) was visited and sampled in 2004 for measuring TSH,thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TgAb).Results Iodine status in the 3 communities were stable.Decreased TSH level( <0.3 mU/L) developed in 2.5% (n =68) of sampled subjects,while raised TSH level( > 4.8 mU/L) in 2.4% (n = 64).A logistic analysis showed that risk factors for developing decreased TSH level included positive conversion of TPOAb (OR = 5.5 ),positive TPOAb both in 1999 and in 2004 ( OR = 4.0),positive TgAb in 2004 ( OR = 3.7) and TSH < 1.0 mU/L in 1999 ( OR = 2.6).Risk factors involved in developing raised TSH level included iodine status of Zhangwu community ( OR = 4.1 ),iodine status of Huanghua community ( OR = 3.9),positive TgAb in 2004 ( OR = 3.7 ),positive TPOAb both in 1999 and 2004 (OR =3.6),positive conversion of TPOAb (OR =2.7) and TSH > 1.9 mU/L in 1999 (OR = 2.6 ).Conclusions Exposure to long-term iodine excess imposes danger of developing hypothyroidism.The risk will be even higher when exposing to iodine adequacy after correction of iodine deficiency.An interval between 1.0 and 1.9 mU/L of TSH level was optimul with the least probability of developing abnormal TSH level.