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

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.

Objective To evaluate the application of M-mode echocardiography and Doppler echocardiography in diagnosing complete atrioventricular block (CAVB) in fetus. Methods M-mode and Doppler echocardiography were used to screen the fetuses and bradycadia was established as CAVB in 10 cases. Atrial and ventricular rhythm was measured by M-mode echocardiography. Flow of mitral valve, left ventricular in-flow and out-flow tract, venous duct was measured by Doppler echocardiography. The characteristics and prognoses of CAVB fetus were compared and analyzed. Results CAVB was established as independence in rhythm of atrium and ventricle. The rhythm of atrium could be in normal range, while the rhythm of ventricle should be slower than normal. Enlarged chambers were observed in 6 cases, cardiac dysfunction in 5 cases, and pericardial effusion in 7 cases. Tricuspid regurgitation and mitral regurgitation existed in 5 and 1 case, respectively. All of the CAVB fetus in this study underwent abortions. Conclusions Fetal echocardiography is proven to be a useful tool to diagnose CAVB, which greatly influenced the cardiac function in fetuses. Clear diagnosis as early as possible is crucial to the treatment of CAVB fetus.

Objective To explore the association between the infection of human cytomegalovirus(HCMV),herpes simplex virus typeⅠ(HSV-Ⅰ),HSV-Ⅱ,toxoplasma(TOX) and serum hepatitis B virus(HBV)these 5 pathogens and low body weight and pneumonia,and explore the clinical value of nested polymerase chain reaction (PCR) examining newborns infected with pathogens.Methods Forty-six newborn infants with low weight and 66 newborn infants with pneumonia were selected.And 1 mL pripheral blood of every newborn infant was drawn.Classic phenol-chloroform-isoamyl alcohol-protease digested,after neonatal serum extraction of DNA in peripheral blood through 2 pairs of pri-mers,the outer primer amplified larger DNA fragments and the inner primer amplified small fragments,in the amplified products.HCMV,HSV-Ⅰ,HSV-Ⅱ,TOX and HBV of the viral DNA in highly conservative district to design primer respectively and amplify its viral DNA,nested PCR was used to detect of these pathogens DNA in infants of low body weight and pneumonia,and to detect positive rate of infection.Screening for birth defects in infants in these virus infection.SPSS 10.0 software was used to analyze the relationship between infection of 5 pathogens.Results The infective rate of HCMV in 46 infants with low body quality was 91.3%,the infective rate of HSV-Ⅰwas 8.7%,the infective rate of HSV-Ⅱwas 15.2%,the infective rate of TOX was 8.7%,and the infective rate of HBV was 15.2%.Among 66 infants with pneumonia,the infective rate of HCMV was 83.3%,the infective rate of HSV-Ⅰwas 6.1%,the infective rate of HSV-Ⅱwas 16.7%,the infective rate of TOX was 6.1%,and the infective rate of HBV was 7.6%.The infective rate of HCMV was higher than that of other 4 pathogens,these infection rates were different statistically in these 5 kinds of pathogens(Pa=0).Conclusions Five kinds of pathogens both low pathosens screening is necessary newborns infants with low body weight and pneumonia,and for the early diagnosis and prevention of these pathogens.

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.

BACKGROUND: Edaravone can alleviate brain injury and improve neurological functions and symptoms. This study aimed to investigate the effect of edaravone on the p38Mitogen-activated protein kinases/Caspase-3 (p38MAPK /Caspase-3) pathway after diffuse brain injury (DBI) in rats. METHODS: DBI models were established according to the description of Marmarou's method. A total of 250 rats were divided (random number) into four groups: control group (CG, n=45), model group (MG, n=77), low-dose edaravone group (n=67, dosage 5 mg/kg) and high-dose edaravone group (n=61, dosage 10 mg/kg). After 1, 6, 24, 48, and 72 hours after injury, brain tissues were collected. The changes of neuron morphous in the hippocampal region were observed through Nissl staining. The expression levels of phosphorylated p38MAPK and caspase-3 were detected by immunohistochemistry and Western blotting respectively. Learning and memory function were tested with Morris water maze from the 3rd to 7th day after injury. RESULTS: Some neurons had histopathologic changes of necrosis and apoptosis in the model group compared with the control group. The phosphorylated p38MAPK expressions increased at 1, 6, 4, and 48 hours (P<0.05), but no significant difference was observed at 72 hours (0.54±0.19 vs. 0.40±0.14, P>0.05). Caspase-3 expressions increased at 6, 24, 48, and 72 hours respectively (P<0.05), but there was no significant difference at 1 hour (0.59±0.29 vs. 0.40±0.17, P>0.05). From the 3rd to 6th day during the Morris water maze test, the latency to find the platform was significantly prolonged (P<0.05) and times of rats crossing the platform was decreased on the 7th day (2.28±1.18 vs. 8.20±1.52, P<0.05). The phosphorylated p38MAPK expressions decreased at 6, 24 and 48 hours respectively in the low dose edaravone group compared with the model group (P<0.05), whereas no significant difference was seen at 1 hour (1.66±0.80 vs. 1.85±0.86, P>0.05). Caspase-3 expression decreased at 6, 24, 48, and 72 hours (P<0.05). The latency to find the platform was significantly shortened (P<0.05), and times of rats crossing the platform increased (4.17±1.15 vs. 2.28±1.18, P<0.05). The above mentioned parameters changed more significantly in the high-dose edaravone group than in the low-dose edaravone group. CONCLUSION: Edaravone can alleviate brain tissue damage after DBI, inhibit p38MAP signal activation after early injury, reduce the expression of caspase-3, and promote the recovery of neurological function in the late period.