Objective To investigate the allergic reaction of Shuanghuanglian Injection(SI)and chlorogenic acid.Meth- ods The sensitization of SI was evaluated by observed the systemic active allergic reaction on guinea pigs.The homogeneous and heterogenic passive skin allergic reactions in rats,mice and guinea pigs were observed to compare the sensitationz of SI and chlorogenic acid.Results The possibility of SI causing allergic reaction was higher than that of chlorogenic acid.Con- clusion It is suggested that the possibility of SI as a compound arising adverse reactions be higher than that of chlorogenic acid.

Child ; Epiphyses ; Fracture Fixation, Internal ; Humans ; Lower Extremity

Objective To compare the efficiency and safety of aspirin-dipyridamole and warfarin in the prevention of thromboembolism in patients with nonvalvular atrial fibrillation(NVAF)and high risk factors.Methods One hundred and forty NVAF patients with high risk factors were randomly divided into two groups.Warfarin group[78 cases international normalized ratio(INR)2.0-3.0,for the patients older than 75 years,INR ranging from 1.6 to 2.5]and combination group(62 cases received aspirin 160 mg once every day plus dipyridamole 160 mg 3 times every day).The incidence of death,thromboembolism(including stroke and peripheral arteries embolism)and hemorrhage events were observed.Results Followed-up 12-28 months.In warfarin group,3 cases lost,2 cages had stroke,2 cases suffered from serious bleeding events,6 cases had minor bleeding events.In combination group,2 cases lost,6 cases had stroke,and 2 cases suffered from peripheral arteries embolism events,3 cases had minor bleeding events,but no serious bleeding events occurred.The incidence of thromboembolism in warfarin group wag,lower than that in combination group[2.7%(2/75)vs 13.3%(8/60),P<0.05].There was no significant difference of the bleeding rate between the two groups[10.7%(8/75)vs 5.0%(3/60),P>0.05].Conclusions Warfarin anticoagulative therapy is more effective than aspirin and dipyridamole antiplatelet dual therapy for the prevention of thromboembolism events in patients with NVAF and high risk factors.The major bleeding events in warfarin group occurs in patients with INR>3.0,so under intensive monitoring(INR 2.0-3.0),warfarin therapy is effective and safety.

OBJECTIVETo evaluate computed tomography (CT) and magnetic resonance imaging (MRI) findings in patients with autoimmune pancreatitis (AIP).

METHODSThe imaging findings of pancreas and extra-pancreas in 24 patients with AIP were retrospectively reviewed. Among them, CT scan was performed in 18 patients, MRI in 11, and bGth CT and MRI in 10.

RESULTSThe pancreas showed diffuse enlargement (25%, 6/24), focal enlargement (37. 5%, 9/24), combined enlargement (25%, 6/24) ,and no enlargement (12. 5%, 9/24). Unenhanced CT showed hypoattenuation in AIP area (n = 2) . After intravenous injection of contrast medium, 17 patients showed abnormal contrast enhancement in the affected pancreatic parenchyma, including hypoattenuation during the arterial phase (50%, 9/18) and hyper attenuation during the delayed phase (94. 4%, 17/18). Precontrast MRI showed abnormal signal intense (n =9), including hypointense on T1-weight images (T1 WI) (n = 7), hyperintense (n = 7) and hypointense (n = 2) on T2-weight images (TIWI). Enhanced MRI demonstrated abnormal contrast enhancement within lesions (n = 11), including hypoattenuation during the arterial phase (81. 8%, 9/11) and good enhancement during the delayed phase (100%, 11111). A capsule-like rim was seen around pancreas (37. 5%, 9/24), among which CT detected in 6 out of 18 patients and MRI found in 7 out of 11 patients.The main pancreatic duct lumen within lesions has no visualization (100%, 24/24) and upstream dilation of the main pancreatic duct (n = 8) , ranging from 2. 2 to 4. 5 mm(mean 3. 1 0. 47 mm) in diameter. Narrowing of the common bile duct was shown in 14 patients. Miscellaneous findings were: infiltration of extrapancreatic vein (n = 9) and artery (n = 1); mild fluid collection around pancreas (n = 2); pseudocysts (n = 3). Fourteen patients also presented one or more of the following extrapancreatic imaging findings: narrowing of the intra-hepatic bile duct or hilar duct (n = 5); thickening of gallbladder wall (n = 5); fibrosis in mesenteric (n = 2), in retroperitoneal (n = 2) and in ligamentum teres hepatis (n = 1); renal involvement (n = 3); peri-pancreatic or para-aortic lymphadenopathy (n = 10); and ulcerative colitis (n = 3).

CONCLUSIONAIP display some characteristic CT and MRI imaging features: sausage-like change of the pancreas; capsule-like rims around lesions; delayed contrast enhancement in the affected pancreatic parenchyma; segment or diffuse pancreatic duct stenosis but mild upstream dilation and extrapancreatic organs involvement. CT and MRI findings combining with serological tests and pancreas biopsy can assist physicians to make accurate and timely diagnosis.

Adult ; Aged ; Autoimmune Diseases ; diagnosis ; Female ; Humans ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Pancreas ; diagnostic imaging ; pathology ; Pancreatitis ; diagnosis ; Retrospective Studies ; Tomography, X-Ray Computed

BACKGROUND: Progress of lung infection after kidney transplantation is rapid, and the adjustment of immunosuppressive drugs is critical, which related to the prognosis of pneumonia and the maintenance of renal function. Therefore, an accurate diagnosis for the pneumonitis post-kidney transplantation is of great significance for choosing the appropriate treatment scheme. OBJECTIVE: To summarize the diagnosis and treatment of pulmonary infection at different periods after kidney transplantation, and then to explore the proper treatment scheme. METHODS: A retrospective analysis of 178 cases of pulmonary infection at different periods after kidney transplantation was performed. According to the progress of patients with lung inflammation, the lung infection was divided into three phases: early, advanced, and phases, and then given different immunosuppressive treatments combined with glucocorticoids; for those with unclear pathogens, given broad-spectrum antibiotics, antiviral, anti-fungal and other drugs, and targeted anti-infective treatment was underwent once pathogen was confirmed. RESULTS AND CONCLUSION: (1) There were 178 patients with pulmonary infection after kidney transplantation, 90 cases occurred at postoperative 1-6 months (78 cases at postoperative 2-4 months), 16 cases occurred at postoperative 6-12 months, 14 cases occurred at postoperative 12-24 months, 12 cases occurred at postoperative 24-36 months, and 46 cases occurred at postoperative more than 36 months. (2) The clinical symptoms of pulmonary infection at the early stage were not obvious, fever was the earliest or primary symptom, and sometimes it was the only symptom. In some cases, the patients appeared with dry cough, expectoration with white mucous sputum, and the amount of sputum increased if infected with mixed bacteria or fungus. But the pulmonary signs are unobvious, and the main imageology feature of lung tissues showed interstitial inflammation. (3) Totally 173 patients were cured, the recovery rate reached to 97.2% and the curative efficacy was satisfactory. (4) Among five patients who dead from pulmonary infection, three were died from acute respiratory failure, and two were for multiple organ failure. Three patients presented with acute rejection to transplant kidney and were cured, and six patients suffered impaired renal function. (5) These results suggest that there is potential risk for pulmonary infection after renal transplantation and it develops rapidly. Based on the situation of pulmonary infection, the physicians can adjust the dose of immunosuppressor and hormone in time, so as to improve the immunosuppressive state and clarify the pathogen for pulmonary infection, then corresponding treatment for anti-infection will be offered, which is beneficial to increase the recovery rate of pulmonary infection and improve the stability of transplanted renal functions.

Objective To analyze the outcomes of the surgery repair for total anomalous pulmonary venous connection(TAPVC),and to investigate the risk factors which influence the mortality of the operation.Methods Comparative analysis was performed in the children with TAPVC who were treated operatively from Sep.2001 to Sep.2011 in the Third Affiliated Hospital of Zhengzhou University,Henan Diagnosis & Treatment Center of Congenital Heart Disease.The children included 37 male and 20 female,aged from 15 days to 6.5 years[(4.27 ± 8.63) months],with body weight 4.0-21.0 (6.33 ± 2.70) kg,and the clinical records in hospital including echocardiogram operation records were collected.The clinical data including the age on operation,body weight,diagnosis,anatomic type of TAPVC,the emergency event before operation,cardiopulmonary bypass time,aortic crossclamping time,were analyzed by chisquared test and Logistic multivariable regression analysis.The risk factors influencing the early mortality of TAPVC were analyzed.Results Fifty-seven children underwent the operation,and 7 (12.2％)cases died during the operation.The univariate analysis on outcomes indicated that the risk factors influencing the mortality of the operation included body weight(P =0.035),anatomic type of TAPVC (P =0.037),the emergency event before operation (P =0.021),and aortic crossclamping time(P =0.046).The Logistic multivariable regression analysis indicated that the emergency events before operation was the independent risk factor for the mortality of TAPVC(P =0.003).Conclusion TAPVC children with preoperative emergency events have higher postoperative mortality.

Alzheimer's disease (AD) has become one of the most important and most interesting focuses in the field of medical and scientific research. Up to now, the pathogenesis of AD has not been completely clarified. However, the high-density of amyloid β-protein (Aβ) in senile plaques of AD brain and the neurotoxicity of Aβ have been indisputable facts. The mechanisms underlying Aβ neurotoxicity are very complicated, involving calcium overload, inflammation, ion channel dysfunction, oxidative stress and so on. Among all of those, the mechanism of oxidative stress in Aβ neurotoxicity and the experimental progress of antioxidants in AD treatment have been widely reported in recent years. This review mainly discussed current research progresses on the oxidative stress of Aβ, so as to provide readers with some clues to the antioxidant therapy of AD.
Alzheimer Disease ; etiology ; metabolism ; physiopathology ; Amyloid beta-Peptides ; adverse effects ; metabolism ; Animals ; Antioxidants ; pharmacology ; Humans ; Oxidative Stress ; drug effects ; physiology

The accumulation of amyloid β-protein (Aβ) plaques is identified as a major pathological feature of Alzheimer's disease (AD). Recent studies show that soluble species of Aβ are involved in the early memory dysfunction long before neurodegenerative changes. However, the mechanism underlying the neurotoxicity of soluble Aβ is still unclear. Long-term potentiation (LTP) has been thought as an important cellular model of synaptic plasticity for many years. The studies on the hippocampal LTP and Aβ, especially those using AD transgenic models, provided more evidence for the Aβ-induced dysfunction of learning and memory. Based on the recent researches on AD, this article reviewed the effects of Aβ, especially soluble Aβ and its active fragments, on the hippocampal LTP. The possible mechanisms by which Aβ impairs hippocampal LTP are also discussed.
Alzheimer Disease ; physiopathology ; Amyloid beta-Peptides ; physiology ; Animals ; Hippocampus ; physiology ; Humans ; Learning Disorders ; physiopathology ; Long-Term Potentiation ; physiology ; Memory Disorders ; physiopathology ; Neuronal Plasticity ; Synapses ; physiology

There is a close correlation between type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD) in the course of pathophysiological processes. The neuroprotective action of glucagon-like peptide 1 (GLP-1), a latest drug for clinical treatment of T2DM, is being more deeply investigated at present, and a novel therapeutic strategy for AD with GLP-1 has been proposed boldly. This review mainly discussed the correlation of pathogenesis between T2DM and AD, the synthesis and secretion of GLP-1, the distribution and physiological effects of GLP-1 receptor in the brain, and the progresses on the study of GLP-1 in the treatment of AD.
Alzheimer Disease ; drug therapy ; physiopathology ; Amyloid beta-Peptides ; drug effects ; metabolism ; Animals ; Brain ; metabolism ; Diabetes Mellitus, Type 2 ; physiopathology ; Glucagon-Like Peptide 1 ; pharmacology ; therapeutic use ; Glucagon-Like Peptide-1 Receptor ; Humans ; Neuroprotective Agents ; pharmacology ; therapeutic use ; Receptors, Glucagon ; metabolism

OBJECTIVETo explore the effects of brain-derived neurotrophic factor (BDNF) pretreatment on beta amyloid protein (Abeta) induced impairment of in vivo hippocampal long-term potentiation (LTP) in the CA1 region of rats.

METHODSThirty-six adult male SD rats were randomly divided into six groups (n = 6): control, Abeta25-35, BDNF, (0.02 microg, 0.1 microg, 0.5 microg) BDNF + Abeta25-35. A self-made hippocampal local drug delivery catheter and a parallel bound stimulating/recording electrode were used to deliver drugs/stimulation and record field excitatory post-synaptic potentials (fEPSPs) in the hippocampal CA1 region of rats. High-frequency stimulation (HFS) was used to induce in vivo LTP.

RESULTS(1) Abeta25-35 (2 nmol) injection into CA1 region of rats did not affect the baseline fEPSPs, but inhibited the HFS-induced LTP significantly (P < 0.01). (2) Hippocampal CA1 injection of BDNF (0.1 microg) alone did not affect the baseline fEPSPs and HFS-induced LTP. (3) Compared with Abeta25-35 alone group, the averaged amplitude of LTP in BDNF (0.1 microg and 0.5 microg) plus Abeta25-35 groups significantly increased at 0 min, 30 min, and 60 min after HFS (P < 0.01), indicating that pretreatment with BDNF effectively protected against the Abeta,25-35 induced depression of LTP in a dose-dependent manner.

CONCLUSIONIntrahippocampal injection of BDNF can protect against the Abeta25-35-induced LTP impairment, suggesting that the up-regulation of BDNF in the brain could maintain the normal hippocampal synaptic plasticity and may contribute to the improvement of learning and memory in Alzheimer's (AD) disease patients.

Amyloid beta-Peptides ; antagonists & inhibitors ; Animals ; Brain-Derived Neurotrophic Factor ; pharmacology ; CA1 Region, Hippocampal ; drug effects ; physiology ; Excitatory Postsynaptic Potentials ; physiology ; Long-Term Potentiation ; physiology ; Male ; Peptide Fragments ; antagonists & inhibitors ; Rats ; Rats, Sprague-Dawley