Adolescent ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Leukemia, Myeloid ; pathology ; physiopathology ; Male

Southern blotting with a labeled and linearized pUC 19 DNA containing a specific fragment of 0. 24 kb DNA of Plasmodium vivax asexual blood stages (kindly offered by Dr. C. Kidson )was used for further identification of blood samples showing positive reaction by dot-blot hybridization. The results showed that those with positive reaction from patients with P. vivax, with P. falciparum or with fever but with negative microscopic findings were also positive by Southern blotting. It was confirmed that some of those positive with P. falciparum were likely to infect P. vivax at the same time. So did a part of those with fever but negative in the blood films (Figs. 1,2).

Objective To investigate the changes in iNOS expression in brain injury induced by hepatic ischemia-reperfusion (IR) in rats.Methods Thirty-two male Wistar rats weighing 240-280 g were randomly divided into 2 groups: sham operation group (group S,n = 8) and group IB( n = 24).The hepatic IR was induced by clamping the hepatic artery and portal vein according te the method described by LONG et al.In group IR the rats were killed at 3,6 and 24 h of reperfusion after 40 min hepatic ischemia (8 rats at each time point).The rats in group S were also killed.The brains were removed for determination of NO content (by nitrate reductase assay),SOD activity (by xanthine oxidase method),MDA content(by colorimetric method),nitrotyrosine (NT) expression (by Western blot),and iNOS mRNA expression (by RT-PCR).Results Compared with group S,cerebral NO and MDA content were significantly increased at 6 and 24 h of reperfusion,expression of cerebral NT and iNOS mRNA up-regulated and SOD activity decreased at 6 h of reperfusion in group IR (P < 0.05 or 0.01).Cerebral NO and MDA content were significantly higher and SOD activity lower at 6 and 24 h of reperfusion than at 3 h of reperfusion in group IR (P < 0.05).Conclusion The expression of iNOS in brain tissues is up-regulated after hepatic IR and it produces a great amount of NO inducing brain injury through peroxynitrite (ONOO-).

Child, Preschool ; Heart Diseases ; physiopathology ; Humans ; Iliac Vein ; physiopathology ; Leukemia, Lymphoid ; complications ; Male ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; complications ; Thrombosis ; etiology ; physiopathology

·AIM: To investigate the effect of the dipeptide Arg-Glnon retinal neovascularization of retinopathy of prematurity(ROP) in the oxygen-induced retinopathy (OIR) animalmodel.·METHODS.- Forty-eight 7-day-old C57BL/6J mice were exposed to 750mL/L oxygen for 5 days and then to normal situation to produce the murine model of oxygen-induced retinopathy (OIR). All mice received twice daily intra- peritoneal injections of PBS or the dipeptide Arg-Gln(1.0, 3.0, 5.0g/kg per day), starting on postnatal day 12 and continuing till postnatal day 17. Experimental groups (36 mice, 12 in each group) received Arg-Gln, while the control group (12 mice) received PBS. All mice were executed at postnatal day 17. The changes of retinal vessels of mice were observed by ADPase histochemical technique and HE staining was used to count preretinal neovascular nuclei. RNA was isolated from retinas of 28 mice (7 in each group) selected at random and VEGF mRNA level of each group was measured by real-time RT-PCR.·RESULTS; Neovascularization reduced in retinas of the dipeptide Arg-Gln treated group in a dose-dependent manner. Compared with control group, experimental group had diminished non-perfusion area and neovascular tufts in retinal flatmount. The number of the endo-theliocyte nuclei of new vessels extending from retina to vitreous was significantly less in the eyes of the experimental group than in control group. Arg-Gln at 5g/kg per day reduced preretinal neovascularization by about 75% (P＜ 0.01). There was a significant reduction in VEGF mRNA at the 17th day in Arg-Gln treated group compared with control group(P＜0.01).·CONCLUSION; Arg-Gln dramatically inhibits retinal angiogenesis in OIR and this effect is associated with a reduction in retinal VEGF mRNA level. It appears to be a safe way to prevent and treat some neovascular retinal diseases including retinopathy of prematurity.

We have developed and characterised a mouse model of Japanese encephalitis virus (JEV) infection via footpad inoculation in order to better mimic viral transmission by mosquito bites. Two-week-old and 5-week-old mice consistently developed signs of infection such as ruffled fur, weight loss, hunchback posture, tremors, mask-like facies and occasionally, hindlimb paralysis at 4 days post infection (dpi) and 11-13 dpi, respectively. Most of the animals died within 24 to 48 hours following the onset of signs of infection, with mortalities of 100% and 33.3% in 2-week-old and 5-week-old mice, respectively. Mild meningitis and variable parenchymal inflammation with formation of microglial nodules, focal necrosis and neuronophagia, and perivascular cuffing by inflammatory cells were observed in the caudate nucleus, putamen, thalamus, cerebral cortex, brainstem, and spinal cord. Viral antigens/RNA were demonstrated by immunohistochemisty and in situ hybridization, respectively, in most of these areas as well as in the hippocampus and cerebellum, albeit more focally. The pathological findings in this mouse model were generally similar to human Japanese encephalitis (JE) and other established JE models but perhaps, compared to other JEV mouse models, it demonstrates lethal encephalitic infection more consistently. We believe that our mouse model should be useful to study the pathogenesis of JE, and for testing anti-viral drugs and vaccines

We have developed and characterised a mouse model of Japanese encephalitis virus (JEV) infection via footpad inoculation in order to better mimic viral transmission by mosquito bites. Two-week-old and 5-week-old mice consistently developed signs of infection such as ruffled fur, weight loss, hunchback posture, tremors, mask-like facies and occasionally, hindlimb paralysis at 4 days post infection (dpi) and 11-13 dpi, respectively. Most of the animals died within 24 to 48 hours following the onset of signs of infection, with mortalities of 100% and 33.3% in 2-week-old and 5-week-old mice, respectively. Mild meningitis and variable parenchymal inflammation with formation of microglial nodules, focal necrosis and neuronophagia, and perivascular cuffing by inflammatory cells were observed in the caudate nucleus, putamen, thalamus, cerebral cortex, brainstem, and spinal cord. Viral antigens/RNA were demonstrated by immunohistochemisty and in situ hybridization, respectively, in most of these areas as well as in the hippocampus and cerebellum, albeit more focally. The pathological findings in this mouse model were generally similar to human Japanese encephalitis (JE) and other established JE models but perhaps, compared to other JEV mouse models, it demonstrates lethal encephalitic infection more consistently. We believe that our mouse model should be useful to study the pathogenesis of JE, and for testing anti-viral drugs and vaccines
Encephalitis, Japanese ; Virus Diseases

Objective To investigate the effects of inhalation of isoflurane at different time points on hypoxic-ischemic brain injury in neonatal rats.Methods One hundred and eighty 7-day-old Sprague-Dawley rats,weighing 12-16 g,were randomly divided into 6 groups (n =30 each):sham operation group (group Ⅰ),cerebral hypoxia/ischemia (H/I) group (group Ⅱ),and inhalation of isoflurane at different time point groups (groups Ⅲ-Ⅵ).Brain ischemia was induced by double ligation of left common carotid artery followed by inhalation of 8 ％ O2 + 92 ％ N2 for 2 h at 37 ℃.In groups Ⅲ,Ⅳ,Ⅴ and Ⅵ 1.5 ％ isoflurane was inhaled for 30 min starting from 0,3,6,12 h after H/I respectively,while the rats were exposed to 30％ O2 and 70％ N2 only in groups Ⅰ and Ⅱ.The survival rate at 7 days after H/I was recorded.The animals were sacrificed at 7 days after H/I.The brains were removed and the right and left cerebral hemispheres (CH) were weighed separately.The ratio between left/right CH was calculated.The density of normal neurons in ventral posterior inferior thalamic nucleus and posterior cingulate cortex in left and right CH were measured and the ratio of the density of normal neurons in the left to right CH was calculated.Results Compared with group Ⅰ,the weight of left cerebral hemisphere,ratio between left/right CH,and ratio of the density of normal neurons in the left to right CH were significantly decreased in other five groups (P ＜ 0.05).Compared with group Ⅱ,the weight of left cerebral hemisphere,ratio between left/right CH,and ratio of the density of normal neurons in the left to right CH were significantly increased in groups Ⅲ,Ⅳand Ⅴ (P ＜ 0.05).There were no significant differences in the indices nentioned above among groups Ⅲ,Ⅳand Ⅴ (P ＞ 0.05).There was no significant difference in the survival rate among groups Ⅱ-Ⅵ (P ＞ 0.05).Conclusion Inhalation of 1.5％ isoflurane for 30 min within 6 h after cerebral H/I can reduce the cerebral injury in neonatal rats.

This article was aimed to study the physiological mechanisms in frozen storage to reduce early bolting of Angelica sinensis. By analyzing the root soluble sugar, soluble protein, MDA content changes before and after -10oC processing of the Angelica sinensis seedlings of different size from different sources , the physiological mechanisms in frozen storage reducing early bolting of A . sinensis had been studied. The results indicated that the greater seedlings , the higher content of soluble sugar , lower protein content and higher MDA . There were no obvious differences on the soluble sugar , soluble protein and MDA content of the same size seedlings from different sources . After -10oC freezing , the content of soluble sugar and protein in the seedlings with the same size were decreased. Meanwhile, the content of MDA was increased. It was concluded that the content of soluble sugar, soluble protein and MDA were obviously related to the size of Angelica sinensis seedlings from the same source before and after low temperature process .

Objective To investigate the clinical role of central venous pressure(CVP) to evaluate fluid responsiveness in septic shock patients. Methods 66 septic shock patients were studied, every patient was administered a volume challenge, before and after it, CVP, intrathoracic blood volume index (ITBVI),global end-diastolic volume index(GEDVI), cardiac index(CI), stroke volume index(SVI) were measured by PiCCO method. All the obtained values were analyzed by statistics method. Results Initial CVP in responders is significantly different from that in nonresponders; △ITBVI, △GEDVI, △CI, △SVI, △HR (△:changes) before and after volume challenge in responders were significantly different from those in nonresponders; the significance of △ITBVI, AGEDVI to predict volume responsiveness was strong indicated by high values of areas under the receiver operating characteristic curves (0.674 and 0.700, respectively).If patients were regrouped by CVP≤11 mm Hg(1 mm Hg=0.133 kPa) and CVP > 11 mm Hg, initial ITBVI and GEDVI in responders were not significantly different from that in nonresponders; △ITBVI,△GEDVI, △CI, △SVI before and after volume challenge in responders were significantly different from those in nom'esponders. Conclusion In septic shock patients, CVP play a guidance role to predict and evaluate volume responsiveness and when CVP was > 11 nun Hg, a positive response will be less likely. Initial volumetric parameters(intrathoracic blood volume and global end-diastolic volume) play a questionable role in predicting and evaluating volume responsiveness, changes before and after volume challenge maybe helpful.