Objective To comparatively complete clinical effectiveness of laparoscopic and open-bifemoral bypass in the treatment of advanced atherosclerosis.Methods During January 2008 to January 2013,according to the treatment method,a total of 60 patients with advanced atherosclerosis patients were divided into group A and group B,and there were 30 cases in each group,and group A was treated with open master bifemoral bypass surgery,and group B was treated with laparoscopic totally master bifemoral bypass surgery,to compare the general information of the two groups,surgery related indicators,clinical efficacy and survival rate,and to analyze the effect of surgical treatment on the prognosis of patients by COX model.Results The operation time of patients in group B (365.3 ±41.3) min and aortic clamping time (59.5 ± 18.3) min were significantly higher than that of group A,(294.3 ±35.5) min and(26.5 ± 19.3) min (P ＜0.05),bleeding amount (400.0 ± 145.3) ml and length of hospital stay (10.5 ± 2.1) d of group B patients was significantly lower than that of group A (1 002.3 ± 324.3) ml and (16.4 ± 4.3) d (P ＜ 0.05);postoperative mortality,thrombosis rate and the incidence of serious complications of patients in group B were significantly lower than group A (P ＜ 0.05);survival rate at different time of group B was significantly higher than that of group A (P ＜ 0.05);COX model analysis show that the surgical methods affect the postoperative mortality,thrombosis and the occurrence of severe complications.Conclusions Completely laparoscopic master bifemoral bypass can significantly decreased advanced main iliac artery occlusion disease mortality,and has small surgical trauma,less postoperative complications,rapid recovery and other advantages,especially for elderly critically ill patients,and it was worthy of clinical application.

Juvenile idiopathic arthritis(JIA)is the most common rheumatology disease in childhood period with poor prognosis.The biological agents are newly developed drugs with features of clear therapeutic targets and fast effects.But its use in JIA is still limited,so this article focuses on the clinical use experience,timming and sideffects of the biological agents on JIA.

BACKGROUND:After spinal cord injury, endogenous neural stem cel s are activated to proliferate and migrate to repair damaged tissue. As a clinical medicine, methylprednisolone shows a lot of functions, but its effects on endogenous neural stem cel s are stil unknown.
OBJECTIVE:To explore the effects of methylprednisolone on the proliferation and migration of endogenous neural stem cel s after spinal cord injury.
METHODS:Seventy-five Sprague-Dawley rats were used to make animal models of T10 complete paraplegia using Al en’s method, and randomized into methylprednisolone, normal saline and model groups. Rats in these three groups were given intraperitoneal injection of 1 g/L methylprednisolone solution at a dose of 30 mg/kg for 10 minutes and at a dose of 5.4 mg/kg/h for 23 hours, given intraperitoneal injection of normal saline at the same dose and given no treatment, respectively. Neurological and motor functions were assessed by somatosensory evoked potential and Basso Beattie Bresnahan scores at 7, 14, 21, 28 days after spinal cord injury. BrdU and Nestin staining of the injured spinal cord segment was conducted.
RESULTS AND CONCLUSION:A large amount of BrdU-and Nestin-positive cel s were visible in al the groups, and the number of these cel s reached the peach at 14 days after spinal cord injury. Methylprednisolone was found to inhibit BrdU-, Nestin-or double-positive cel s, indicating methylprednisolone can inhibit the proliferation and migration of endogenous neural stem cel s. The results of Basso Beattie Bresnahan scores showed no notable improvement in the motor function of the limbs. Methylprednisolone also showed no significant effects on the motor evoked potential latency, but promoted nerve conduction recovery. Al these findings indicate that methylprednisolone has some hindering effects on spinal cord repair by inhibiting the proliferation and migration of endogenous neural stem cel s after spinal cord injury.

Objective To explore the mechanism of LMWH therapy for SAP.Methods 48 wistar rats were random divided into 3 groups,sham group(S group),severe acute pancreatitis group(SAP group)and LMWH therapy group(H group).Serum amylase,IL-6,acinar cell apoptosis and the activity of NF-κB were detected and compared.Results The expression of amylase and IL-6 in SAP group was significantly higher than that in H group(P＜0.01).The apoptosis index of acinar cell in SAP group wag significantly lower than that in H group(P＜0.01),while the activity of NF-κB in SAP groupwas stronger than that in H group.Conclusions LMWH therapy may ameliorate SAP by inducing acinar cell apoptosis through suppressing the activity of NF-κB.

Administration, Oral ; Adolescent ; Condylomata Acuminata ; drug therapy ; Cyclophosphamide ; administration & dosage ; therapeutic use ; Female ; Humans ; Male ; Middle Aged ; Penile Diseases ; drug therapy ; Vulvar Diseases ; drug therapy

Artemisinin is a key anti-malarial drug and few clinically meaningful resistant cases about its application have so far been reported. The World Health Organization (WHO) officially recommended the use of ACT (Artemisinin-based Combination Therapy) as the first line antimalarial application to increase its inhibitory efficacy and prevent the likely resistance development. Based on our current understanding of artemisinin, a set of compounds were selected to study their interaction with artemisinin by using the yeast (S. cerevisiae) model, in the hope that knowledge gained might provide some references for clinical investigations. In this research, yeast strain (BY4742) was cultured in the nonfermentable YPGE solid medium with 4 μmol · L(-1) artemisinin and one of the selected compounds for 48 hours, and the combined drug efficiency was evaluated by the inhibition of yeast growth. The compounds belong to the categories of oxygenants, antioxidants, metal ions, ion chelators and uncouplers. Among them, 0.2 mmol L(-1) FeCl3, 60 μmol · L(-1) BPS, 1 mmol · L(-1) CuCl2, 0.75 mmol · L(-1) VE and 1 mmol · L(-1) VC antagonized the action of artemisinin, while 40 μmol · L(-1) DNP, 0.1 μmol · L(-1) CCCP and 0.25 mmol · L(-1) H2O2 had synergistic effects. These results suggested that redox-active and mitochondria-dysfunctional compounds could affect artemisinin's potency, supporting our prior proposed mitochondrial model for artemisinin's action. This research in addition provided a convenient method to screen likely artemisinin-interacting compounds.
Artemisinins ; pharmacology ; Drugs, Chinese Herbal ; pharmacology ; Saccharomyces cerevisiae ; drug effects ; growth & development

Purpose To explore the value of 320 row dynamic volume CT angiography in the preoperative assessment of juvenile nasopharyngeal angiofibroma (JNA) and in determining feeding arteries.Materials and Methods The imaging data of 18 cases with JNA proved by surgery and pathology and examined by 320 row dynamic volume CT were analyzed retrospectively.The imaging staging and feeding artery of tumors were determined.Results Most tumors (17/18) showed heterogeneous enhancement in the early stage of enhancement.With the extension of time,the enhancement scope of lesions expended.The time-density curve (TDC) of 11 cases demonstrated rapid ascending and rapid descending after injecting contrast,while 7 cases showed continuous increasing.The blood supply of all tumors included the external carotid artery system of the affected side and showed a close relationship with tumor staging.With the increase of tumor stage,the number of feeding arteries increased (r=0.858,P＜0.05).The feeding arteries of stage Ⅱc and stage Ⅲ tumors included ipsilateral maxillary artery and ascending pharyngeal artery.Besides,the effective radiation dose of 320 row CT angiography for searching arteries [(3.30±0.08) mSv]was less than that of DSA [(7.62±2.39) mSv] (t=-7.98,P＜0.05).Conclusion The 320 row dynamic volume CT imaging of JNA has certain characteristics,which can display the blood supply artery and accurate staging of tumors,thus it has important value in preoperative evaluation of JNA.

AIM:To observed the protective effect of diminazene aceturate ( DIZE) , an angiotensin-converting enzyme 2 (ACE2) activator, on diabetic nephropathy (DN) rats.METHODS:Male Wistar rats (n=30) were randomly divided into normal control (NC) group, DN group and DIZE group (each group consisted of 10 rats).The rats in DN group and DIZE group were induced by intraperitoneal injection of streptozotocin at dose of 65 mg/kg.After 12 weeks, the rats in DIZE group and DN group received subcutaneous injection of DIZE (15 mg· kg -1 · d-1 ) or vehicle for 4 weeks. The samples of blood and urine were collected at week 16, and ratio of kidney weight to body weight (KW/BW), plasma glucose (GLU), 24 h urinary protein (24UP) and serum creatinine (SCr) were measured.The renal pathological changes in each group were observed by periodic acid-Schiff ( PAS) staining and immunohistochemistry .The levels of AngⅡ and Ang-(1-7) in the plasma, and TGF-β1 and VCAM-1 in the renal tissues were measured by ELISA .The mRNA and protein levels of collagen I and FN were determined by quantification real-time PCR and immunohistochemistry .The effects of DIZE on the expression of ACE2 in DN rats were determined by Western blot .RESULTS:DIZE remarkably increased the expression of ACE2 and Ang-(1-7) in DN rats.Compared with NC group , the GLU, KW/BW, 24UP, SCr, and the ex-pression of collagen I , FN, TGF-β1 and VCAM-1 in DN group and DIZE group were increased .However , after treatment of the DN rats with DIZE, these indicators were decreased except the KW/BW.The GLU showed no significant change . CONCLUSION:DIZE raised the activity of ACE2 and increased the expression of Ang-(1-7), thus alleviating fibrosis and inflammation in the kidney and having therapeutic potential for diabetic nephropathy .

Objective To study interleukin-1 receptor(IL-1R) and connexin(Cx36) gene expression following Mg 2+-free-induced seizures in cultured developing neuron. Methods Rat embryo cortical neurons cultured for 6 and 17 days were exposed to Mg 2+-free media to induce seizure. At different time after Mg 2+-free treatment, real-time RT-PCR was used to detect IL-1R and Cx36 mRNA expression. Results 1. IL-1R mRNA expression transiently decreased after Mg 2+-free treatment in neurons cultured for 6 and 17 days in vitro. Then the levels of IL-1R mRNA expression recovered in neurons cultured for 6 days, but IL-1R mRNA expression were increased in neurons cultured for 17 days compared with control group and the peak was at 24 hours. 2. In neurons cultured for 6 days in vitro, Cx36 mRNA expression increased after Mg 2+-free treatment compared with control group, the peak was at 24 hours. But in neurons cultured for 17 days in vitro, Cx36 mRNA expression decreased at 6 hours after Mg 2+-free treatment compared with control group, the peak was at 24 hours. Conclusions IL-1R mRNA and Cx36 mRNA expression following Mg 2+-free-induced seizures are different between the neurons cultured for 6 and 17 days in vitro. This is possibly related to the different neuron injury between 6 and 17 days in vitro following seizures.