Adolescent ; Child ; Child, Preschool ; Female ; Herpesvirus 4, Human ; Humans ; Infant ; Infectious Mononucleosis ; diagnosis ; pathology ; virology ; Liver ; pathology ; Male

Objective To explore the clinical and laboratory characteristics of langerhans cell histiocytosis (LCH) in children, so as to improve diagnosis level and decrease misdiagnosis rate.Methods Twenty-five cases of LCH from Jan.1996 to Feb.2006 were analyzed by retrospective study. The clinical data were collected and abstracted for information regarding clinical symptom, physical sign, laboratory examination, imaging,pathology,diagnosis and treatment.Results Some laboratory findings in hemogram, bone marrow examination and chest X-ray were non-specific.The X-ray characteristic of skeleton was osteolysis. Computerized tomography and magnetic resonance imaging were important in defining the extent of lesion in fundus cranii and sella.Seven cases were examined for anti-Epstein-Barr virus(EBV) IgM, 3 cases were positive;5 and 3 cases out of 10 cases showed humoral and cellular immunity abnormality,respectively. The misdiagnosis rate was 52%,1 case had been misdiagnosed for 7 years. Chemotherapy was effective in the future.Conclusions The clinical manifestations of LCH varies widely, leading to high rate of misdiagnosis.The etiology of LCH is unclear,and some of our patients show the evidence of EBV infection or immunity abnormality. Definitive diagnosis of LCH is based on pathology. Ultrastructure and immunophenotype should be done to improve diagnosis level.

Objective To Analyze the examination meaning of b-type brain natriuretic peptide precursor (NT-proBNP),homocysteine and coagulation-fibrinolysis indexes for patients with acute cerebral infarction.Methods Selected 40 patients with acute cerebral infarction (experimental group) to hospital from March 2014 to May 2015 and 40 healthy check-up cases (control group).Then,compared the indicators in blood between the two groups of patients,namely homocysteine (Hcy),NT-proBNP,activated clotting time live enzymes enzyme (APTT),original activator inhibitory factor (PAI-1) and tissuetype fibrinolytic enzyme original activator (tPA).Meanwhile,also compared these indicators for the experimental group before and after treatment.Results Before treatment,the levels of Hcy,t-PA,NT-proBNP,PAI-1 and ATPP for experiment group were 17.7±3.6 μmol/L,29.4±7.9 μmol/L,3 212.8±2 511.4 ng/L,130.1±17.8 μmol/L and 37.8±4.5 s,respectively.The levels of Hey,t-PA,NT-proBNP,PAI-1 and ATPP for control group were 7.2± 2.1 μmol/L,15.1 ± 3.7 μmol/ L,198.7 ± 1 14.8 ng/L,67.8 ± 7.9 μmol/L and 37.8 ± 4.5 s,respectively.After treatment,the levels of Hcy,t-PA,NT-proBNP,PAI-1 and ATPP for experiment group were 12.2±1.5 μmol/L,18.2±2.3 μmol/L,348.7±194.8 ng/L,78.6±9.8 μmol/L and 32.2±4.5 s,respectively.Before treatment,the indicator of APTT for experiment patients was significantly shorter than it after treatment and that of the control group.The other four indicators were significantly higher than them after treatment and those of the control group.The differences were statistically significant (P ＜0.05).Conclusion Hcy,NT-proBNP,APTT,PAI-1,and t-PA had closely relation with the occurrence of acute cerebral infarction development,and they can be helpful to evaluate disease progression and predict prognosis for patients with acute cerebral infarction.

OBJECTIVETo explore the effect of Shenxiong Huayu Capsule (SHC) on the cerebral ischemia-reperfusion (IR) injury and the expression of growth associated protein 43 (GAP43) after total cerebral IR in the hippocampal CA1 region of rats.

METHODSTotally 100 male adult SD rats were randomly divided into five groups, i.e., the control group, the model group, the group A (by taking SHC once daily), the group B (by taking SHC twice daily), and the group C (by taking SHC thrice daily), 20 in each group. The total IR model was prepared by improved Pulsinelli's 4-vessel occlusion method. Morphological changes of the hippocampal CA1 region were observed by HE staining at day 1, 3, 7, and 14. The expression of GAP43 in the hippocampal CA1 region was detected using immunohistochemical assay at day 1, 3, 7, and 14. Meanwhile, the behavioral score was determined. The expression of GAP43 in the hippocampal CA1 region was detected using Western blot at day 14.

RESULTSCompared with the control group, the expression of GAP43 increased in the model group, the behavioral score was elevated, degenerated neurons increased, and survival neurons decreased in the model group (all P < 0.05). Compared with the model group, the expression of GAP-43 increased (with the most significant difference seen in the group C, P < 0.01), the behavioral score significantly decreased, degenerated neurons decreased, and survival neurons increased in each HSC group (all P < 0.05). Survival neurons obviously increased at day 14, of which, most number of survival neurons and highest contents of GAP43 protein could be seen in the group C, showing statistical difference when compared with those of the group A and the group B (P < 0.01).

CONCLUSIONSHC had protective effect on total cerebral IR in the hippocampal CA1, which might be associated with increased expression of GAP43.

Animals ; Brain Ischemia ; metabolism ; CA1 Region, Hippocampal ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; GAP-43 Protein ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism

Objeceive To compare the expression of Ku70 and Bax in hippocampus CA1 between normal rats and diabetic rats following cerebral ischemia/reperfusion, so as to explore the roles of Ku70 and Bax in aggravating cerebral ischemial reperfusion mjury nn diabetes. Meehods Totally 72 male SD rats were divided into 3 groups randomly: sham operated (SO) group, normoglycemia global cerebral ischemia/reperfusion (NCI) group, and diabetic global cerebral ischemia/reperfusion (DCI) group. The rats in DCI group were treated by streptozodn (STZ) and improved Puliinelii's foue-vessel occlusion method to estabiish diabetic global cerebral ischemia/reperfusion modll. Andanimals in NCI group were not gvven STZ, and other treatments were iimllar to those in the DCI group. Animals in the SO group only had blood vessels exposed. Changes of neuron pathology in hippocampus CA1 were observed by H-E stammg under iight microscopy at 1, 6, 24, and 48 h after lschemial reperfusion; expresioon of Ku70 was detected by immunohistochemistry and Western blotting analyils, and expresioon of Bax was detected by immunohistochemistry. Resules The neuron structure in hippocampus CA1 of rats was damaged nnNCI group, and the density of survival neuronswas significanely lower than that nn the SO group at all studied time ponnts(P<0. 05); the neuron structure damage nn DCI group was more severe, and the demity of sunival neurons was signiticanely lower than that of the NCI group at all studied time points(P<0. 05). The expresioon of Ku70 at 1 and 6 h nn NCI group was signiticanely higher than that in the SO group (P<0. 05), and that at 24 and 48 h was signiticanely lower than that nn the SO group(P<0. 05); Ku70 expression nn DCI group was significanely lower than that nn the NCI group at all studied time ponnts(P<0. 05). Bax expresioon in NCI group was signiticanely higher than that in the SO group at all studied time points(P<0. 05), and that in DCI group was signiticanely higher than that in the NCI group at all studied time ponnts (P<0. 05). Conclusion Diabetes can aggravate global cerebral ischemia/reperfusion injury, which may be related to Ku70 Expression decrease and Bax Expression Increase.

BACKGROUND:There is lack of an effective measuring means to diagnose deep venous thrombosis (DVT) in clinic.KLF2 and KLF4 are down-expressed at prethrombotic state,which may be served as predictive molecular markers to diagnose DVT.OBJECTIVE:To explore the feasibility of KLF2 and KLF4 as molecular markers to prediagnose DVT in rats.METHODS:Totally 90 rats were obtained from 100 rats to establish traumatic DVT models and divided into the prethrombotic,thrombosis crest-time and non-thrombosis groups.The remained 10 rats served as control group.Rat blood was collected at each time point,and the expressions of KLF2 and KLF4 were detected by real-time PCR.RESULTS AND CONCLUSION:The KLF2 and KLF4 mRNA expressions in the prethrombotic group and thrombosis crest-time group were lower than that of the control group.However,the KLF2 and KLF4 mRNA expressions in the non-thrombosis group was higher than that of the control group.Therefore,KLF2 and KLF4 may be candidate molecular markers for prediagnosis of DVT in rats.

BACKGROUND: Deep venous thrombosis (DVT) always occurs after orthopedic surgery. At present, clinical diagnosis of DVT has been lack of an effective measuring means for a long time. Cathepsin may be an effective biological marker of DVT. OBJECTIVE: To study the expression change of cathepsin B and cathepsin C in the rat blood cells before and after DVT and to investigate the feasibility of cathepsin B and cathepsin C as candidate molecular markers for early diagnosis of DVT. METHODS: Totally 100 Sprague Dawley rats were randomly divided into normal control group (n=10) and model group (n=90). Rat traumatic deep vein thrombosis models were established by clamping the femoral vein and fixing the bilateral hind limbs. According to observation time points and the different situations of thrombosis, rat models were assigned to three subgroups: pre-thrombosis, intra-thrombosis, and non-thrombosis. Blood RNA of each group was extracted and reverse transcribed into cDNA. The expression of cathepsin B and cathepsin C in blood cells was detected using real-time fluorescence quantitative PCR. RESULTS AND CONCLUSUON: Expression of cathepsin B and cathepsin C in the blood cells was obviously expressed in the intra-thrombosis subgroup. There was no significant difference in cathepsin B and cathepsin C expression between pre-thrombosis, non-thrombosis groups and normal control group. These findings suggest that cathepsin B and cathepsin C are closely related to DVP and they can be used as the candidate molecular markers for early diagnosis of DVT.

BACKGROUND:The molecular mechanism of traumatic deep vein thrombosis is complex.Numerous studies focus on clinical observation and epidemiology,but its molecular mechanism has not been a new breakthrough.OBJECTIVE:By use of gene array technology,this study was aimed to study the expression changes of matrix metalloproteinases in rat models of traumatic deep vein thrombosis,and to explore the roles of matrix metalloproteinases in traumatic deep venous thrombosis.METHODS:A total of 150 SD rats,SPF grade,of 8-12 weeks old,body weight of 250-300 g,were divided at random into normal control group (n=10) and model group (n=140).Rat traumatic deep venous thrombosis models were set up by clamping the femoral vein and fixing the bilateral hind limbs,and the fixation of hip spica with plaster bandage was conducted in each group.Then rats were divided into 7 subgroups:post-traumatic 0.5 hours,post-traumatic 2.5 hours (initial period of thrombosis),post-traumatic 25 hours (thrombogenesis at thrombotic crest-time),post-traumatic 25 hours non-thrombogenesis at the thrombotic crest-time),post-traumatic 72 hours (thrombus resolution),post-traumatic 72 hours thrombus insolution) and post-traumatic 168 hours (nonthrombosis).At the corresponding phasess,the femoral vein tissues were incised,and total RNA of femoral vein was extracted using Trizol one-step method.Applying Genechip Rat Genome 430 2.0 genechips,the gene expressions in femoral vein were detected in different groups.The rate of traumatic deep venous thrombogenesis and non-thrombogenesis,the rate of thrombi solution and insolution were observed;the expressions of matrix metalloproteinases and tissue inhibitor of metalloproteinases at different time phases was detected by gene array data analysis.RESULTS AND CONCLUSION:Three model rats died and the remaining 147 rats were involved in the final analysis.At the post-traumatic 25 hours,the rate of thrombogenesis was 50.5% and nonthrombogenesis was 49.5%.To the post-traumatic 168 hours,the rate of thrombus solution was 56.7% and thrombus insolution was 43.3%.Both matrix metalloproteinases and tissue inhibitor of metalloproteinases exhibited differential expressions in the course of traumatic deep venous thrombosis.Under the thrombus insolution state,matrix metalloproteinases continued to show a high expression,tissue inhibitor of metalloproteinase expression was down-regulated in the thrombus formation,was significantly inhibited in the thrombus insoluUon process.In the process of traumatic deep vein thrombosis and insolution,matrix metalloproteinase was closely related to traumatic deep vein thrombosis,the matrix metalloproteinase/tissue inhibitor of metalloproteinases are likely to affect the biological state of thrombosis.

Objective To analyse MMACHC mutations for 45 pedigrees with combined methylmalonic aciduria and homocyctinuria by Sanger sequencing, and to discuss the utility of prenatal genetic diagnosis for these pedigrees.Method Peripheral blood was collected from 45 probands and their parents from 2012-2015 in Genetic Counselling Clinic of the First Affiliated Hospital of Zhengzhou University, and the DNA were extracted from the blood.Then the coding sequence of MMACHC gene was amplified by PCR, and the PCR products were further sequenced to detect mutations for each pedigree.For 12 families, chorionic villus sampling was performed on the pregnant women to make prenatal genetic diagnosis.Result There were 14 distinct mutations detected in the 45 pedigrees, and the most frequent mutations are c.609G>A(W203X),c.658-660delAAG(K220del)and c.80A>G (Q27A).Two of those mutations have not been reported before:one is a splicing site mutation c.81+1G>A;while the other is a missense mutation c.665A>G,p.Y222C.Most mutations were found in exon 4.Among the 12 pedigrees who received prenatal diagnosis, 2 fetuses were normal, 7 fetuses were carriers of heterozygous mutation, and the other 3 fetuses were patients with compound heterozygous mutation or homozygous mutation.The couples whose fetuses were normal or carriers continued the gestation, while the couples whose fetuses were patients decided to terminate the pregnancy.After delivery, the outcome of the fetuses was the same as the prenatal diagnose results.Conclusion Two novel mutations of MMACHC were identified and prenatal genetic diagnosis helps to avoid the delivery of combined methylmalonic aciduria and homocyctinuria patients.

Objective To study the distribution and related factors of curative care expenditure (CCE) of injury in Gansu Province in 2017. Methods Based on the "A System of Health Accounts 2011 (SHA 2011)", the curative care expenditure of injury in Gansu Province was calculated and analyzed. The five?stage stratified cluster sampling method was adopted to extract 149 medical and health institutions, 120 township hospitals (including community health service centers), 150 individual clinics and 600 village clinics (including community health service stations). The top?down allocation method was used to calculate the cost of injury treatment in Gansu Province, and the influencing factors were analyzed by multiple linear regression. Results In 2017, the CCE of injury in Gansu province was 3.831 billion yuan, and the expense in general hospitals was 2.708 billion yuan. Among them, the cost of lower limb injury and head injury were 1.090 and 0.847 billion yuan. People aged 40 to 69 years old spent 1.901 billion yuan on injury treatment, and the CCE of injury treatment for men and women were 2.422 and 1.409 billion yuan respectively. The results of multiple linear regression showed that hospitalization expenditure was significantly associated with length of stay, operation, hospital grade, age, payment method and gender (P<0.001). Conclusion The economic burden of injury in Gansu Province is relatively heavy, so it is necessary to focus on preventions for different groups and costly injury sites.