Role of autophagy in acute myeloid leukemia therapy / 癌症

Despite its dual role in determining cell fate in a wide array of solid cancer cell lines, autophagy has been robustly shown to suppress or kill acute myeloid leukemia cells via degradation of the oncogenic fusion protein that drives leukemogenesis. However, autophagy also induces the demise of acute leukemia cells that do not express the known fusion protein, though the molecular mechanism remains elusive. Nevertheless, since it can induce cooperation with apoptosis and differentiation in response to autophagic signals, autophagy can be manipulated for a better therapy on acute myeloid leukemia.

Aquaporin-4 and traumatic brain edema / 中华创伤杂志(英文版)

Brain edema leading to an expansion of brain volume has a crucial impact on morbidity and mortality following traumatic brain injury as it increases intracranial pressure, impairs cerebral perfusion and oxygenation, and contributes to additional ischemic injuries. Classically, two major types of traumatic brain edema exist: "vasogenic" and "cytotoxic/cellular". However, the cellular and molecular mechanisms contributing to the development/resolution of traumatic brain edema are poorly understood and no effective drugs can be used now. Aquaporin-4 (AQP4) is a water-channel protein expressed strongly in the brain, predominantly in astrocyte foot processes at the borders between the brain parenchyma and major fluid compartments, including cerebrospinal fluid and blood. This distribution suggests that AQP4 controls water fluxes into and out of the brain parenchyma. In cytotoxic edema, AQP4 deletion slows the rate of water entry into brain, whereas in vasogenic edema, AQP4 deletion reduces the rate of water outflow from brain parenchyma. AQP4 has been proposed as a novel drug target in brain edema. These findings suggest that modulation of AQP4 expression or function may be beneficial in traumatic brain edema.

Effect of Xingnaojing injection on cerebral edema and blood-brain barrier in rats following traumatic brain injury / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To explore the effects of Xingnaojing injection on cerebral edema and blood-brain barrier (BBB) in rats following traumatic brain injury (TBI).</p><p><b>METHODS</b>A total of 108 adult male Sprague-Dawley rats were used as subjects and randomly assigned to three groups: sham-operation, TBI and Xingnaojing injection groups (10 ml/kg/d, intraperitoneal injection). TBI in rats was set up by the improved device of Feeney's weight-dropping model with the impact of 600 g.cm. Brain water content and BBB permeability expressed as Evans blue content were measured at 1, 3, 5 and 7 days after surgery.</p><p><b>RESULTS</b>In sham-operation group, brain water content and Evans blue content in brain tissue were 78.97%+/-1.22% and 5.13 microgram+/-0.71 microgram. Following TBI, water content in brain tissue was increased significantly at 1, 3, 5 and 7 days (83.49%+/-0.54%, 82.74%+/-0.72%, 80.22%+/-0.68%, 79.21%+/-0.60%), being significantly higher than that in sham operation group (P less than 0.05). Evans blue content was increased in TBI group (16.54 microgram+/-0.60 microgram, 14.92 microgram+/-0.71 microgram, 12.44 microgram+/-0.92 microgram, 10.14 microgram+/-0.52 microgram) as compared with sham-operation group(P less than 0.05). After treatment with Xingnaojing injection, brain water content decreased as compared with TBI group (81.91%+/-1.04%, 80.38%+/-0.72%, 79.54%+/-0.58%, 78.60%+/-0.77%, P less than 0.05). Xingnaojing injection also reduced the leakage of BBB as compared with TBI group (15.11 microgram+/-0.63 microgram, 13.62 microgram+/-0.85 microgram, 10.06microgram+/-0.67 microgram, 9.54 microgram+/-0.41 microgram, P less than 0.05).</p><p><b>CONCLUSION</b>Xingnaojing injection could alleviate cerebral edema following TBI via reducing permeability of BBB.</p>

Diagnosis and treatment of organotin poisoned patients / 世界急诊医学杂志（英文）

BACKGROUND:With the development of industry and agriculture, organotin compounds have been widely used in China. Organotin compounds cause a common occupational poisoning. The toxicity of organotin was reported in animal studies; however the reports about human organotin intoxication are very rare. In this study we retrospectively analyzed the clinical manifestations of 15 organotin-poisoned patients who had been treated at our hospital from 2002 through 2007. METHODS:Fifteen patients with organotin poisoning were admitted to Sir Run Run Shaw Hospital Affiliated to Zhejiang University School of Medicine from 2002 to 2007. They were 9 males and 6 females, aged from 25 to 52 years. Clinical manifestations and Glasgow Coma Scales showed that the poisoning was mild in 4 patients, moderate in 6 and severe in 5. The severe patients were given glucocorticoid after hospitalization by intravenous guttae of 500 mg methylprednisolone for the first day, followed by 160 mg methylprednisolone per day for three days, and then 80 mg methylprednisolone per day for another three days. Potassium glutamate and sodium glutamate were intravenously dripped to reduce blood ammonia; intravenous guttae plus oral administration of potassium 9 g/day was used to correct intractable hypokalemia; sodium bicarbonate was used to correct metabolic acidosis, and sedatives were used to control spasm and twitch; mechanical ventilators were used in 4 patients with dyspnea. RESULTS:Most of the patients showed elevated level of blood ammonia, decreased level of blood potassium and metabolic acidosis, but some had demyelination changes shown by CT and MRI. Treatments included correction of metabolic acids, blood potassium and ammonia, and mechanical ventilation when necessary. For patients with injuries of the nervous system, glucocorticoids were given immediately after hospitalization. These patients showed intractable hypokalemia and metabolic acidosis during the treatment. Forteen patients recovered completely without long-term side-effect. One patient in the aphasiac stage restored the linguistic capacity during a 6-month follow-up. CONCLUSIONS:Elevated level of blood ammonia, decresed level of blood potassium, and metabolic acidosis are common in patients with organotin poisoning. Demyelination can be observed in patients with severe poisoning. The abnormalities of the patients are reversible after suitable treatments.

Double filtration plasmapheresis in treatment of hyperlipidemic acute pancreatitis / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the therapeutic effects of double filtration plasmapheresis(DFPP) in treatment of hyperlipidemic acute pancreatitis.</p><p><b>METHODS</b>Nine patients with acute hyperlipidemic pancreatitis were treated with DFPP in addition to the conventional therapeutic measures. The clinical symptoms,serum levels of triglyceride (TG) and APACHE II scores were observed before and after DFPP.</p><p><b>RESULT</b>After DFPP the clinical symptoms of patients were improved greatly; serum levels of TG decreased from (83.48 +/-2.54)mmol/L to (4.09 +/-0.65)mmol/L(P<0.01) and APACHE II scores decreased from 12.2 +/- 2.3 to 6.2 +/- 1.3(P <0.05). There were no significant side effects during and after DFPP.</p><p><b>CONCLUSION</b>DFPP can be effectively and safely applied in patients with acute hyperlipidemic pancreatitis.</p>

Protective effects of edaravone on renal ischemia-reperfusion injury in rats / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the effect of edaravone on renal ischemia-reperfusion injury in rats.</p><p><b>METHODS</b>Fifty rats were randomly divided into five groups: sham operation group (Group A), renal ischemia-reperfusion group (Group B) and edaravone treated groups (Group C1, Group C2 and Group C3 with different drug dosages). Serum maleic dialdehyde (MDA) and superoxide dismutase (SOD), renal MDA and SOD, serum creatinine (Cr), blood urea nitrogen (BUN) were measured after the rat kidney was ischemia-reperfused for 24 hours. Renal ultrastructure was observed.</p><p><b>RESULT</b>Compared with Group A, serum and renal MDA, serum Cr, BUN of Group B were significant increased (P <0.01), serum and renal SOD of Group B were significant decreased (P <0.01). After edaravone treatment, serum MDA, Cr and renal MDA of Group C were lower than those in Group B (P<0.01); Serum and renal SOD of group C were higher than those in Group B (P <0.01); Compared with Group B, BUN level of Group C had no significant change (P >0.05). The renal ultrastructure was greatly injured in Group B, meanwhile it was obviously ameliorated in Group C.</p><p><b>CONCLUSION</b>Edaravone has protective effects on renal ischemia-reperfusion injury in rats.</p>

Effect of AVP on brain edema following traumatic brain injury / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To evaluate plasma arginine vasopressin (AVP) level in patients with traumatic brain injury and investigate the role of AVP in the process of brain edema.</p><p><b>METHODS</b>A total of 30 patients with traumatic brain injury were involved in our study. They were divided into two groups by Glasgow Coma Scale: severe traumatic brain injury group (STBI, GCS less than or equal to 8) and moderate traumatic brain injury group (MTBI, GCS larger than 8). Samples of venous blood were collected in the morning at rest from 15 healthy volunteers (control group)and within 24 h after traumatic brain injury from these patients for AVP determinations by radioimmunoassay. The severity and duration of the brain edema were estimated by head CT scan.</p><p><b>RESULTS</b>Plasma AVP levels (ng/L) were (mean+/-SD): control, 3.06+/-1.49; MTBI, 38.12+/-7.25; and STBI, 66.61+/-17.10. The plasma level of AVP was significantly increased within 24 h after traumatic brain injury and followed by the reduction of GCS, suggesting the deterioration of cerebral injury (P less than 0.01). And the AVP level was correlated with the severity (STBI r equal to 0.919, P less than 0.01; MTBI r equal to 0.724, P less than 0.01) and the duration of brain edema (STBI r equal to 0.790, P less than 0.01; MTBI r equal to 0.712, P less than 0.01).</p><p><b>CONCLUSIONS</b>The plasma AVP level is closely associated with the severity of traumatic brain injury. AVP may play an important role in pathogenesis of brain edema after traumatic brain injury.</p>

Effect of salvianolic acid B on neural cells damage and neurogenesis after brain ischemia-reperfusion in rats / 药学学报

This study is to observe the effect of salvianolic acid B (Sal B) on neural cells damage and neurogenesis in sub-granular zone (SGZ) and sub-ventricular zone (SVZ) after brain ischemia-reperfusion (I/R) in rats. A modified middle cerebral artery occlusion (MCAO) model of focal cerebral ischemia-reperfusion was used. The rats were divided into four groups: sham control group, ischemia-reperfusion group, Sal B 1 and 10 mg x kg(-1) groups. Sal B was consecutively administrated once a day by ip injection after MCAO. The neurogenesis in SGZ and SVZ was investigated by BrdU method 7 days after MCAO. The Nissl staining for neurons in the hippocampal CA1 and cerebral cortex was performed 14 days after MCAO. A beam-walking test was used to monitor the motor function recovery. We found that brain ischemia resulted in an increase of BrdU positive cells both in ipsilateral SGZ and SVZ at 7th day after MCAO. Sal B (10 mg x kg(-1)) significantly increased further the number of BrdU positive cells both in SGZ and SVZ (P < 0.01). Ipsilateral hippocampal neuron damage occurred and CA1 almost lost 14 days after MCAO. Sal B (10 mg x kg(-1)) obviously attenuated the neuron damage and increased the number of neuron both in ipsilateral CA1 and cerebral cortex (P < 0.01). We also observed an obvious improvement of motor function recovery when Sal B (10 mg x kg(-1)) administrated. From the results above we concluded that Sal B stimulated neurogenesis process both in SGZ and SVZ after brain ischemia, and also alleviated neural cells loss and improved motor function recovery after brain ischemia in rats.

Effect of congsheng capsule on intracellular calcium concentration in mice after ischemic cerebral injury / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To investigate the effect of Congsheng Capsule (CSC) in intracellular Ca2+ concentration in cerebral intra-synaptosomes of ischemia/reperfusion mice and analogous ischemic injured neurons to estimate the mechanism of CSC in antagonizing ischemic cerebral injury.</p><p><b>METHODS</b>The concentration of Ca2+ in cerebral intra-synaptosomes of mice and in neurocyte suspension of fetal mice were determined using Fura-2/AM double wavelength fluorescence spectrophotometer.</p><p><b>RESULTS</b>CSC 3 g/kg and 9 g/kg through gastrogavage could relieve the degree of calcium overloading of intra-synaptosomes in mice after cerebral ischemia/reperfusion. The CSC containing serum could inhibit the elevation of Ca2+ content in neurocytes induced by 1 hour hypoxia and glutamate of high concentration (200 mumol/L).</p><p><b>CONCLUSION</b>CSC plays a role in antagonizing ischemic injury through relieving the calcium overloading after cerebral ischemia.</p>

Protective effect of 3,4-oxo-isopropylidene-shikimic acid on vascular endothelial cell injured by hydrogen peroxide / 药学学报

<p><b>AIM</b>To study the effect of 3,4-oxo-isopropylidene-shikimic acid (ISA) on H2O2 (200 mol.L-1, 4 h) injured human umbilical vein endothelial cells (HUVEC).</p><p><b>METHODS</b>Morphological change was observed under microscop. Cell viability was assessed by MTT assay. The release of intracellular lactate dehydrogenase (LDH) and NO was assessed by colorimetry. Radioimmunoassay was used to assess 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha).</p><p><b>RESULTS</b>Pretreatment with ISA for 6 h alleviated the morphological damage of H2O2 induced HUVECs. At the concentration of 1-100 mumol.L-1, ISA prevented the inhibitory effect on cell viability induced by H2O2 in dose-dependent manner, but increased the ratio of cell viability from 60.4% to 84.3%. ISA reduced LDH release and increased the level of NO and 6-keto-PGF1 alpha in H2O2 induced HUVECs.</p><p><b>CONCLUSION</b>ISA exerted protective effect on H2O2 injured HUVEC.</p>

Experimental studies on the anti-thrombosis effect of 3,4-oxo-isopropylidene-shikimic acid / 药学学报

<p><b>AIM</b>To study the effect of 3,4-oxo-isopropylidene-shikimic acid (ISA) against arteriovenous shunt and middle cerebral artery thrombosis (MCAT) in rats.</p><p><b>METHODS</b>Arteriovenous shunt model was adopted to measure thrombus weight; The neurologic deficit (ND) and the infarct size (IS) of the middle cerebral thrombosis (MCAT) model induced by FeCl3 were observed; The effect of ISA on platelet aggregation rate of rat and rabbit by giving ISA in vivo and in vitro was studied.</p><p><b>RESULTS</b>ISA 25, 50, 100 and 200 mg.kg-1 ig was shown to reduced the weight of thrombus in arteriovenous shunt model; ISA 50, 100 and 200 mg.kg-1 ig for 2 times in 24 hours, attenuated the ND of rats subjected to MCAT; ISA 100 and 200 mg.kg-1 reduced IS of rats after MCAT by 27.8% and 31.6%, respectively; ISA 50, 100 and 200 mg.kg-1 ig inhibited platelet aggregation of normal rats; ISA 10(-3)-10(-5) mol.L-1, inhibited rabbit platelet aggregation in vitro.</p><p><b>CONCLUSION</b>ISA inhibited thrombosis by anti-platelet-aggregation.</p>