Objectve To optimize the synthesis process of phacolysin 1 for industrial production.Methods Phacolysin as the target product was synthesized with a total yield of 40.7% by condensation reaction of O-phenylenediamine and sulfonation reaction.The yield reported in literature was 24.8%.Results Such factors as the ratio of the raw materials,the catalyst,and the reaction time were inveatigated and optimized to make the reaction conditions mild and easy to control with less side effect.Conclusion The structure is confirmed by 1HNMR and MS,and the optimized process is more suitable for industrial production.

Adenoma ; genetics ; metabolism ; pathology ; surgery ; Adult ; Carcinoma, Renal Cell ; genetics ; metabolism ; pathology ; Chromosomes, Human, Pair 3 ; genetics ; Chromosomes, Human, Pair 7 ; genetics ; Diagnosis, Differential ; Diploidy ; Female ; Follow-Up Studies ; Humans ; Kidney Neoplasms ; genetics ; metabolism ; pathology ; surgery ; Male ; Middle Aged ; Retrospective Studies ; S100 Proteins ; metabolism ; Vimentin ; metabolism ; WT1 Proteins ; metabolism ; Wilms Tumor ; metabolism ; pathology

OBJECTIVEAccording to bone regeneration under the membrane and the bone regeneration deep fascia composite autologous red bone marrow transplantation applied in the treatment of fracture nonunion, in order to find a simple and effective clinical treatment of nonunion.

METHODSSince March 2006 to March 2009,17 patients of fracture nonunion were treated by the deep fascia composite autologous bone marrow transplantation,included 10 males and 7 females, aged from 7 to 52 years old (means 32 years). There were 10 cases of tibia, 5 cases of radius, 2 cases of clavicle. Injured to admission time was from 7 to 36 months (means 12 months). Ten cases underwent operation for 1 time,5 cases for twice and 2 cases for 3 times. The position of nonunion were all at bone shaft and the condition of the skin and soft tissue was good. X-ray film showed 11 cases of hyperplasia nonunion, 6 cases of shrinking. The original fixation were removed and the intramedullary nail or plate fixation were re-used, and fracture ends were sutured closed by autogenous deep fascia and implanted with autologous red bone marrow.

RESULTSSeventeen patients were followed-up for from 5 months to 2 years with an average of 1 year. Fracture healing time was from 12 to 20 weeks (means 16 weeks). According to the criteria of fracture healing to assess efficacy, the results were excellent in 14 cases, good in 2 cases and poor in 1 case.

CONCLUSIONDeep fascia composite autologous autologous red bone marrow transplantation for the treatment of fracture nonunion is suitable at the bone shaft and good condition of skin and soft tissue. The method has been observed that the fracture healing time is short.

Adolescent ; Adult ; Bone Marrow Transplantation ; Child ; Fascia ; Female ; Follow-Up Studies ; Fracture Healing ; Fractures, Bone ; diagnostic imaging ; physiopathology ; surgery ; Humans ; Male ; Middle Aged ; Time Factors ; Tomography, X-Ray Computed ; Transplantation, Autologous ; Young Adult

OBJECTIVEThis review discusses the experimental and clinical studies those show the expression of connexin 36 in the central nervous system and the possible role of connexin 36 in epileptic seizure.

DATA SOURCESAll articles used in this review were mainly searched from PubMed published in English from 1996 to 2012.

STUDY SELECTIONOriginal articles and reviews were selected if they were related to the expression of connexin 36 in the central nervous system and its role in epilepsy.

RESULTSThe distribution of connexin 36 is developmentally regulated, cell-specific and region-specific. Connexin 36 is involved in some neuronal functions and epileptic synchronization. Changes in the connexin 36 gene and protein were accompanied by seizures. Selective gap junction blockers have exerted anticonvulsant actions in a variety of experiments examined in both humans and experimental animals.

CONCLUSIONSConnexin 36 plays an important role in both physiological and pathological conditions in the central nervous system. A better understanding of the role of connexin 36 in seizure activity may contribute to the development of new therapeutic approaches to treating epilepsy.

Animals ; Central Nervous System ; metabolism ; Connexins ; metabolism ; Gap Junctions ; metabolism ; Humans ; Seizures ; metabolism

Objective:To investigate the effect of TPF-DM on blood glucose levels and immune function in severe traumatic brain injury (STBI) patients.Methods:We consecutively included 60 STBI patients who were randomly divided into control and experimental groups.The two groups of patients were treated with TPF and TPF-DM as the main energy supply,respectively.Total protein,albumin,prealbumin,procalcitonin (PCT),immunoglobulinM (IgM),immunoglobulinG (IgG),immunoglobulinA (IgA) and blood glucose of all patients were detected on day 1,7 and 14.Immune function related indicators,serum protein and blood glucose were statistically analyzed.Results In the first week,the mean blood glucose level and incidence of hypoglycemia were not significantly different between the two groups (P ＞ 0.05).However,the blood glucose variability (BGV) was significantly different (P ＜ 0.05).In the second week,both the blood glucose level and BGV were in normal range with no significant difference between two groups (P ＞ 0.05).At dayl,the total protein,albumin,prealbumin,IgM,IgG and IgA of all the patients were below the normal level,while the PCT was exact opposite,but with no significant difference between the two groups (P ＞ 0.05).At day7,PCT decreased compared to dayl in both the control and experimental groups,while the total protein,albumin,prealbumin,IgM,IgG and IgA increased,but the experimental group increased much more compare to the control group (P ＜ 0.05).At dayl4,all these indexes returned to normal levels with no significant difference between the two groups (P ＞ 0.05).Conclusion:TPF-DM is significantly better than TPF to control the blood glucose level.TPF-DM may have a positive effect on the control of early excessive inflammation and infection,and then improve the immune function.Yet the potential physiopathologic mechanism needs further study.

OBJECTIVETo study the effect of angiotensin II on phosphoinositide-3 kinase/Akt cascade in cultured fibroblasts derived from patients with hypertrophic scars.

METHODSThe expression of AT1 and AT2 receptor was detected by immunofluorescence staining. Cultured human skin fibroblasts were treated with Ang II (10(-9) - 10(-7) mol/L), with or without an AT1 receptor blocker, valsartan or an AT2 receptor antagonist, PD123319. The phosphorylation of Akt was detected by western blotting, and PI3K activity was measured by Assay of PI3-K activity.

RESULTSImmunofluorescence staining showed that cultured fibroblasts derived from hypertrophic scars expressed both AT1 and AT2 receptors. Ang II increased Akt phosphorylation and PI3K activity in cultured hypertrophic scar fibroblasts in a dose- and time-dependent manner. Additionally, Ang II-induced Akt phosphorylation was blocked by wortmannin, a PI3-K inhibitor. This Ang II-activated PI3-K/Akt cascade was significantly inhibited by valsartan, an AT1 receptor specific blocker (P<0.05), whereas enhanced by PD123319, an AT2 receptor antagonist (P<0.05).

CONCLUSIONThese results indicate that Ang II receptors regulates PI3-K/Akt cascade of hypertrophic scars fibroblasts via AT1 and AT2.

Angiotensin II ; pharmacology ; Angiotensin II Type 1 Receptor Blockers ; pharmacology ; Angiotensin II Type 2 Receptor Blockers ; Cells, Cultured ; Cicatrix, Hypertrophic ; metabolism ; pathology ; Fibroblasts ; cytology ; drug effects ; metabolism ; Humans ; Imidazoles ; pharmacology ; Phosphatidylinositol 3-Kinases ; metabolism ; Proto-Oncogene Proteins c-akt ; metabolism ; Pyridines ; pharmacology ; Receptor, Angiotensin, Type 1 ; Signal Transduction ; Tetrazoles ; pharmacology ; Valine ; analogs & derivatives ; pharmacology ; Valsartan

Background and Objectives: Long-term pathological myocardial hypertrophy (MH) seriously affects the normal function of the heart. Dronedarone was reported to attenuate left ventricular hypertrophy of mice. However, the molecular regulatory mechanism of dronedarone in MH is unclear. Methods: Angiotensin II (Ang II) was used to induce cell hypertrophy of H9C2 cells.Transverse aortic constriction (TAC) surgery was performed to establish a rat model of MH.Cell size was evaluated using crystal violet staining and rhodamine phalloidin staining.Reverse transcription quantitative polymerase chain reaction and western blot were performed to detect the mRNA and protein expressions of genes. JASPAR and luciferase activity were conducted to predict and validate interaction between forkhead box O3 (FOXO3) and protein kinase inhibitor alpha (PKIA) promoter. Results: Ang II treatment induced cell hypertrophy and inhibited sirtuin 1 (SIRT1) expression, which were reversed by dronedarone. SIRT1 overexpression or PKIA overexpression enhanced dronedarone-mediated suppression of cell hypertrophy in Ang II-induced H9C2 cells. Mechanistically, SIRT1 elevated FOXO3 expression through SIRT1-mediated deacetylation of FOXO3 and FOXO3 upregulated PKIA expression through interacting with PKIA promoter. Moreover, SIRT1 silencing compromised dronedaronemediated suppression of cell hypertrophy, while PKIA upregulation abolished the influences of SIRT1 silencing. More importantly, dronedarone improved TAC surgery-induced MH and impairment of cardiac function of rats via affecting SIRT1/FOXO3/PKIA axis. Conclusions Dronedarone alleviated MH through mediating SIRT1/FOXO3/PKIA axis, which provide more evidences for dronedarone against MH.

Background and Objectives: Long-term pathological myocardial hypertrophy (MH) seriously affects the normal function of the heart. Dronedarone was reported to attenuate left ventricular hypertrophy of mice. However, the molecular regulatory mechanism of dronedarone in MH is unclear. Methods: Angiotensin II (Ang II) was used to induce cell hypertrophy of H9C2 cells.Transverse aortic constriction (TAC) surgery was performed to establish a rat model of MH.Cell size was evaluated using crystal violet staining and rhodamine phalloidin staining.Reverse transcription quantitative polymerase chain reaction and western blot were performed to detect the mRNA and protein expressions of genes. JASPAR and luciferase activity were conducted to predict and validate interaction between forkhead box O3 (FOXO3) and protein kinase inhibitor alpha (PKIA) promoter. Results: Ang II treatment induced cell hypertrophy and inhibited sirtuin 1 (SIRT1) expression, which were reversed by dronedarone. SIRT1 overexpression or PKIA overexpression enhanced dronedarone-mediated suppression of cell hypertrophy in Ang II-induced H9C2 cells. Mechanistically, SIRT1 elevated FOXO3 expression through SIRT1-mediated deacetylation of FOXO3 and FOXO3 upregulated PKIA expression through interacting with PKIA promoter. Moreover, SIRT1 silencing compromised dronedaronemediated suppression of cell hypertrophy, while PKIA upregulation abolished the influences of SIRT1 silencing. More importantly, dronedarone improved TAC surgery-induced MH and impairment of cardiac function of rats via affecting SIRT1/FOXO3/PKIA axis. Conclusions Dronedarone alleviated MH through mediating SIRT1/FOXO3/PKIA axis, which provide more evidences for dronedarone against MH.

Background and Objectives: Long-term pathological myocardial hypertrophy (MH) seriously affects the normal function of the heart. Dronedarone was reported to attenuate left ventricular hypertrophy of mice. However, the molecular regulatory mechanism of dronedarone in MH is unclear. Methods: Angiotensin II (Ang II) was used to induce cell hypertrophy of H9C2 cells.Transverse aortic constriction (TAC) surgery was performed to establish a rat model of MH.Cell size was evaluated using crystal violet staining and rhodamine phalloidin staining.Reverse transcription quantitative polymerase chain reaction and western blot were performed to detect the mRNA and protein expressions of genes. JASPAR and luciferase activity were conducted to predict and validate interaction between forkhead box O3 (FOXO3) and protein kinase inhibitor alpha (PKIA) promoter. Results: Ang II treatment induced cell hypertrophy and inhibited sirtuin 1 (SIRT1) expression, which were reversed by dronedarone. SIRT1 overexpression or PKIA overexpression enhanced dronedarone-mediated suppression of cell hypertrophy in Ang II-induced H9C2 cells. Mechanistically, SIRT1 elevated FOXO3 expression through SIRT1-mediated deacetylation of FOXO3 and FOXO3 upregulated PKIA expression through interacting with PKIA promoter. Moreover, SIRT1 silencing compromised dronedaronemediated suppression of cell hypertrophy, while PKIA upregulation abolished the influences of SIRT1 silencing. More importantly, dronedarone improved TAC surgery-induced MH and impairment of cardiac function of rats via affecting SIRT1/FOXO3/PKIA axis. Conclusions Dronedarone alleviated MH through mediating SIRT1/FOXO3/PKIA axis, which provide more evidences for dronedarone against MH.

BACKGROUNDDiabetic lower limb ischemia is a serious complication of diabetes mellitus. This study was conducted to investigate the effectiveness of distal arterial bypass treatment in diabetic patients with lower limb ischemia.

METHODSFrom July 2000 to July 2004, 96 lower limbs of 82 diabetic patients (type 2) with severe lower limb ischemia were treated in Xuan Wu Hospital. Arterial bypass with femoro-popliteal polytetrafluoroethylene (PTFE) and graft-tibial autologous grafts was performed on 31 limbs (32.3%). Popliteal-tibial artery bypass alone was performed on 22 limbs (22.9%). Combined iliac artery stenting, femoro-popliteal artery PTFE graft bypass, and graft-tibial artery autologous graft bypass was performed on 12 limbs (12.5%), and femoro-tibial artery graft bypass was performed on 10 limbs (10.4%). Popliteal-tibial-pedal artery graft bypass was performed on 7 limbs (7.3%).

RESULTSArterial grafts in 92 limbs of 79 patients were patent on discharge. Three patients with 4 ischemic limbs (3.7%) died of respiratory failure 12 hours, 3 days and 7 days after operation respectively. Early operation success rate was 96.3% (79/82). Graft patency rate of patients on discharge was 95.8% (92/96). The short-term total effectiveness rate was 83.3% (80/96). Foot ulcer healing rate was 35.7% (10/28). 97.4% (75/77) patients were followed up for a mean of 13.5 months. The long-term total effective rate was 80.7% (71/88). The total amputation rate was 4.5% (4/88). Mortality was 4.5%. The total graft patency rate was 90.9% (80/88).

CONCLUSIONIn the treatment of diabetic foot, distal lower limb arterial bypass can help to avoid amputation or lower the amputation level, and may promote foot ulcer healing and improve patient's quality of life.

Aged ; Aged, 80 and over ; Arteriovenous Shunt, Surgical ; Diabetic Angiopathies ; surgery ; Female ; Femoral Artery ; surgery ; Humans ; Ischemia ; surgery ; Lower Extremity ; blood supply ; Male ; Middle Aged ; Polytetrafluoroethylene ; Popliteal Artery ; surgery