Aortopulmonary Septal Defect ; therapy ; Catheterization ; Female ; Humans ; Infant

BackgroundResearches demonstrated that the levels of soluble CD44 (sCD44)molecule in aqueous is significantly higher in primary open-angle glaucomous(POAG) eye than normal eye,but how the sCD44 would affect the expression of apoptosis protein in trabecular meshwork cells is below understanding.Objective The present study was to investigate the effect of sCD44 on the expression of regulatory proteins bcl-2 associated death factor bad in trabecular meshwork cells in the patients with POAG.MethodsHuman scleral tissue with trabecular meshwork were obtained from POAG patients during the surgery.The trabecular meshwork cells were primarily cultured by explant culture method and identified by immunochemistry.The third generation of cells were incubated with free-serum DMEM/F12 medium added differnt dosages of sCD44 (0,1,5,10,25,50 mg/L) for 48 hours.The expression of bad protein in cultured cells was detected using cell counting kit-8 (CCK-8) as the absorbance values at 490 nm(A,90 value),and the bad protein level in cultured cells was assayed by ELISA.ResultsThe cultured cells showed the positive response for laminin ( LM ),neuron specific enolase ( NSE ),fibronectin ( FN ) monoclonal antibodies.The CCK-8 assay showed that the A490 values of the trabecular meshwork cells in 0,1,5,10,25,50 μg/L of sCD44 groups were 0.2460±0.0019,0.1874±0.0015,0.1570±0.0016,0.1302±0.0019,0.1084±0.0018,0.0940±0.0020 respectively with a statistically significant difference among the 6 groups( F =14.922,P =0.000 ),and the A490 values in various dosages of sCD44 groups were significantly lower than the 0 μg/L sCD44 group (P=0.013,0.008,0.011,0.005,0.004).The ELISA assay showed that bad protein levels in 0,1,5,10,25,50 μg/L of sCD44 groups were ( 114.8461 ± 2.9560 ),( 137.8270 ± 2.4259 ),( 161.4194 ± 3.7381 ),( 170.9453 ± 3.2006 ),( 221.2252 ±4.3738 ),( 324.6167±4.4220) ng/L,showing a total difference among them ( F =16.610,P =0.000 ),and the bad protein levels in various dosages of sCD44 groups were significantly lower than the 0 μg/L sCD44 group( P =0.017,0.013,0.008,0.007,0.006).ConclusionssCD44 can contribute to the apoptosis of the trabecular meshwork cells in patients with POAG in certain dose range by regulating the apoptosis regulatory proteins bcl-2 associated death factor bad.

Objective To discuss the diagnosis and treatment of cerebral sparganosis. Methods To summary four cases of cerebral sparganosis, focusing on the clinical course and imaging findings, with the goal of better diagnostic skills. Results All 4 cases had some kind of misdiagnosis and improvement after surgery or parasiticidal pharmacotherapy. Cerebral MRI and CT scans revealed relatively extensive white matter degeneration and focal enhancements. Subsequent scans showed changes in shape and location of the enhanced foci, indicating the migration of sparganum. Pathologic findings of 3 patients who had undergone surgery showed granuloma and sparganum. Conclusions Cerebral sparganosis has relatively special manifestions on imaging, which are of diagnostic value. The spaganum should be as completely removed as possible during surgery.

BACKGROUND:Mesenchymal stem celltransplantation promoted skin repair in trauma via various regulatory mechanisms and inhibited scar formation. At present, many scholars believed that bioactive factors secreted by mesenchymal stem cells played an important role.
OBJECTIVE:To investigate the effects of bone marrow mesenchymal stem cellconditioned medium on the proliferation and col agen synthesis of hypertrophic scar fibroblasts.
METHODS:Human bone marrow mesenchymal stem cells and hypertrophic scar fibroblasts were isolated and cultured, and bone marrow mesenchymal stem cellconditioned medium was prepared. Hypertrophic scar fibroblasts were cultured in vitro with 12, 24, and 48 hour-col ected conditioned medium for 24 hours, which was compared with blank control group. The proliferation of cells was determined by CCK-8. Type I and type III col agen expression in hypertrophic scar fibroblasts was detected using real-time PCR.
RESULTS AND CONCLUSION:Compared with the blank control group, 24 and 48 hour-col ected conditioned medium significantly inhibited the proliferation of hypertrophic scar fibroblasts (P<0.01), and also suppressed col agen synthesis of hypertrophic scar fibroblasts (P<0.01). Results suggested that bone marrow mesenchymal stem cellconditioned medium inhibited the proliferation and col agen synthesis of hypertrophic scar fibroblasts by secreting anti-fibrotic bioactive factors, which may provide new theoretical supports for celltherapy to reduce cutaneous scarring.

OBJECTIVETo investigate the effect of peroxisiome proliferator activated receptor-α (PPAR-α) on the regulation of cardiomyocyte hypertrophy and the relationship between the effect of PPAR-α with PI3K/Akt//mTOR signal pathway.

METHODSCardiomyocyte hypertrophy was induced by isoproterenol (ISO). The cell surface area was measured by image analysis system (Leica). The expressions of atrial natriuretic peptide (ANP), β-myosin heavy chain (β-MHC) and PPAR-α mRNA were detected by qRT-PCR. The protein expressions of Akt, mTOR and P70S6K were detected by Western blot. The expression of PPAR-α was suppressed by RNAi.

RESULTS(1) The expression of PPAR-α was significantly reduced in cardiomyocyte hypertrophy. PPAR-α activator Fenofibrate (Feno) increased the expression of PPAR-α and suppressed cardiomyocyte hypertrophy. The inhibitory effect of Feno on cardiomyocyte hypertrophy was reversed by PPAR-α RNAi. (2) Feno significantly inhibited the increase of the protein expressions of p-Akt, p-mTOR and p-p70S6K in ISO induced cardiomyocyte hypertrophy, which could be blocked by PPAR-α RNAi. (3) PI3K antagonist LY294002 (LY) or mTOR antagonist rapamycin (RAPA) markedly-inhibited cardiomyocyte hypertrophy. The inhibitory effects of LY or RAPA on cardiomyocyte hypertrophy were reversed by PPAR-α RNAi.

CONCLUSIONPPAR-α can negatively regulate cardiomyocyte hypertrophy. The effect might be associated with PPAR-α inhiting PI3K/ Akt/mTOR signal pathway.

Atrial Natriuretic Factor ; metabolism ; Cardiomegaly ; metabolism ; Cells, Cultured ; Fenofibrate ; pharmacology ; Humans ; Isoproterenol ; adverse effects ; Myocytes, Cardiac ; drug effects ; metabolism ; Myosin Heavy Chains ; metabolism ; PPAR alpha ; metabolism ; Phosphatidylinositol 3-Kinases ; metabolism ; Proto-Oncogene Proteins c-akt ; metabolism ; RNA, Messenger ; Ribosomal Protein S6 Kinases, 70-kDa ; metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases ; metabolism

Abnormalities, Multiple ; genetics ; pathology ; Child, Preschool ; Chromosome Aberrations ; Diagnosis, Differential ; Diarrhea ; diagnosis ; etiology ; therapy ; Exocrine Pancreatic Insufficiency ; complications ; Fever ; diagnosis ; etiology ; Fingers ; abnormalities ; Humans ; Male ; Pancreatic Diseases ; etiology ; Syndrome

Animals ; Animals, Newborn ; Brain ; blood supply ; metabolism ; pathology ; Carrier Proteins ; genetics ; DNA-(Apurinic or Apyrimidinic Site) Lyase ; genetics ; Gene Expression ; Hypoxia-Ischemia, Brain ; genetics ; pathology ; In Situ Hybridization ; Protein Tyrosine Phosphatase, Non-Receptor Type 13 ; Protein Tyrosine Phosphatases ; genetics ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Wistar

Objective To examine whether the marginal division of the striatum(MrD)is involved in the associative learning and memory function of human brain with the help of functional magnetic resonance imaging(fMRI)technique.Methods Sixteen right-handed normal volunteers participated in a test of paired-word associative learning and memory,while the fMRI data were recorded.Control tasks were performed for the block-design.Statistcs parameter mapping 99 was used to analyze the data and to obtain the activated brain regions.Results When the threshold was set as P＜0.005.using a one-sample T-test,the left occipital lobe and the superior and middle gyrus of the left frontal lobe were activated remarkably during the encoding process of the paired-word associative learning and memory task,with the maximum intensity T value being 13.87 and 9.36.respectively.The left MrD was also obviously activated during this stage(T value was 5.46).But during the retrieval process,the left parietal lobe was prominently activated(T value was 8.73).Conclusion The resuhs of this study reveal that the subcortical structures such as MrD as well as the cerebral cortex are involved in the associative learning and memory of paired-word in human brain.

Objective To observe the incidence of ischemic J wave before and post percutaneous coronary intervention (PCI) in patients with coronary heart disease (CHD). Methods CHD patients ( n =117 ) underwent percutaneous coronary intervention (PCI) in Shanxi cardiovascular hospital were included in this study. The 12-lead ECC s were recorded within 24 hours before and after PCI. The ischemic J waves of five lead-groups ( Ⅱ, Ⅲ ,aVF group: V1, V2 group; V3, V4 group; V5, V6 group; Ⅰ ,aVL group) were analyzed and the number of lead-groups with J waves ( 0 - 5 ) were obtained in each patient. According to time course or wave amplitude, J waves were classified into three grades: small (time course between 0.02 -0.03 s or wave amplitude between 0.05 -0.09 mV), large ( time course between 0.04 -0.06 s or wave amplitude between 0.10 -0.20 mV) and enormous (time course ＞0.06 s or wave amplitude ＞0.20 mV) J waves. Results The number of lead-groups with ischemic J waves (0 -5 ) in each patient was similar between pre and post PCI in the 117 patients (χ2 =6.23,P=0.285). The numbers of small, large and enormous J waves were 157, 36 and 9 respectively before PCI and 163, 20 and 5 after PCI. The incidence of small J waves increased (77.72% vs. 86.70% ) while large and enormous J waves decreased ( 17.82%, 4.46% vs. 10.64%, 2.66% ) post PCI ( χ2 = 5.28, P ＜ 0.05 ). Conclusions The numbers of lead-groups with ischemic J waves were similar before and post PCI. However, the amplitude of ischemic J waves decreased after PCI suggesting PCI could improve ischemic J waves in CHD patients.

Objective: To observe the effects of microwave on the activity of SOD and the contents of MDA in renal cortex and testis of mice. Methods: Microwave generator(2 450 MHz, 10 mW/cm2) was used to expose mice; NBT,DTNB and TBA were used to mearure the activity of SOD and the contents of MDA in renal cortex and testis of the mice after microwave exposure.Results: The content of MDA in renal cortex and testis of the mice increased progressively on days 1,6,12 and reached the highest level on day 24 after the microwave exposure (P<0.01). The activity of SOD in renal cortex and testis of the mice decreased progressively on days 1, 6, 12 and reached the lowest level on day 24 after the microwave exposure (P<0.01). Conclusions: Microwave exposure can produce reactive oxygen free radicals and lead to depress SOD activity.