Adolescent ; Aortic Valve ; abnormalities ; Aortic Valve Insufficiency ; complications ; pathology ; surgery ; Aortic Valve Stenosis ; complications ; pathology ; surgery ; Child ; Endocarditis ; complications ; pathology ; surgery ; Female ; Heart Defects, Congenital ; complications ; pathology ; surgery ; Heart Valve Prosthesis Implantation ; Humans ; Male ; Rheumatic Heart Disease ; complications ; pathology ; surgery

OBJECTIVETo investigate the effects of angelicanaphtha on proliferation, cell cycle, apoptosis, and collagen synthesis of human umbilical vein endothelial cells (HUVEC).

METHODSHUVEC was cultured and passaged in Dulbecco's modified Eagle's medium (DMEM) and treated with angelicanaphtha 1 mg/ L, 4 mg/L, and 16 mg/L at 1, 3, 5, and 7 day respectively. The proliferation was measured with MTT method. The cell cycle and apoptosis were analyzed with flow cytometry and collagen synthesis was determined with radioimmunoassay.

RESULTSThe proliferation of the HUVEC was accelerated by angelicanaphtha < or =4 mg/L and inhibited by angelicanaphtha at 16 mg/L (P < 0.05). Lower concentration (< or = 4 mg/L) of Angelicanaphtha decreased cells in G0/G1 phase and increased significantly cells in S phase and inhibited the apoptosis (P < 0.05). However, angelicanaphtha at 16 mg/L increased cells in G0/G1 phase and decreased cells in S phase and induced the apoptosis (P < 0.05). The collagen synthesis of HUVEC was inhibited by angelicanaphtha in concentration-dependent manner (P < 0.05 or 0.01).

CONCLUSIONThe proliferation effects of angelicanaphtha on HUVEC had dualistic regulation of increase by lower-concentration and inhibition by higher-concentration. Collagen synthesis of HUVEC was inhibited by angelicanaphtha in concentration-dependent manner.

Angelica sinensis ; Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; Collagen Type III ; biosynthesis ; Endothelial Cells ; cytology ; drug effects ; metabolism ; Humans ; Oils, Volatile ; pharmacology ; Umbilical Veins ; cytology

OBJECTIVETo study the signal roles of protein tyrosine kinase (PTK) on proliferation and collagen synthesis of fibroblasts derived from hypertrophic scar(HS-FB) and normal skin (NS-FB) by interferon-gamma (IFN-gamma) or transforming growth factor beta1 (TGF-beta1).

METHODSHS-FB and NS-FB were cultured and passaged in Dulbecco's modified Eagle's medium(DMEM). The PTK activity in unstimulated or IFN-gamma or TGF-beta1-stimulated HS-FB and NS-FB (10,30,60 and 120 min) were assayed by phosphorus (32P) incorporation. Cell proliferation was determined with MTT stain. The type III procollagen was measured by radioimmunoassay.

RESULTSTGF-beta1 did not change PTK activity but it increased predominately proliferation and collagen synthesis of HS-FB and NS-FB in time-dependent fashion. Genistein, an inhibitor of PTK, inhibited HS-FB and NS-FB to proliferate and synthesize collagen but it could not change the roles on proliferation and collagen synthesis by TGF-beta1. IFN-gamma activated transiently PTK (P < 0.05) and increased proliferation and collagen synthesis of both fibroblast (P < 0.05, at 30 min, 60 min). As the recovery of PTK activity, the proliferation and collagen synthesis were inhibited by IFN-gamma at 120 min. Furthermore, Genistein abrogated the transient increased roles and partly reversed the longterm inhibitory functions by IFN-gamma (P < 0.05) . There were no difference on PTK activity, proliferation and collagen synthesis between HS-FB and NS-FB.

CONCLUSIONSPTK did not mediate the signal of TGF-beta1 but transduced the signal of transient increased roles of IFN-gamma. Inhibited or activated PTK might mediate the signal of decreasing or increasing proliferation and collagen synthesis of fibroblast.

Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; Cicatrix, Hypertrophic ; metabolism ; pathology ; Collagen ; biosynthesis ; Dermis ; metabolism ; Fibroblasts ; cytology ; metabolism ; Humans ; Interferon-gamma ; pharmacology ; Protein-Tyrosine Kinases ; metabolism ; Signal Transduction ; Transforming Growth Factor beta1 ; pharmacology ; Wound Healing

OBJECTIVETo study emetic and anti-emetic effects of Rhizoma pinelliae in minks.

METHODThe emetic effect of raw pinellia 2 g kg(-1) (i.g.) was investigated. Three preparations of Rhizoma pinelliae (processed with ginger) were made by ethanol extraction, water extraction and water decoction respectively and their effects on emesis model induced by cisplatin (7.5 mg kg(-1), i.p.) or apomorphine (1.6 mg kg(-1), s.c.) were then studied; the effect of the decoction of ginger-processed Rhizoma pinelliae on rotation-induced emesis model in minks was also observed.

RESULTThe emesis was induced by raw pinellia in minks (P < 0.01); ginger-processed Rhizoma pinelliae, metoclopramide and ondansetron significantly inhibit the emesis induced by cisplatin and apomorphine (P < 0.05).

CONCLUSIONGinger-processed Rhizoma pinelliae exhibits a anti-emetic effect in minks, which may be mediated by inhibiting the function of the vomiting center in central nervous system.

Animals ; Antiemetics ; therapeutic use ; Drugs, Chinese Herbal ; isolation & purification ; therapeutic use ; Ginger ; Hot Temperature ; Male ; Mink ; Phytotherapy ; Pinellia ; chemistry ; Plants, Medicinal ; chemistry ; Rhizome ; chemistry ; Technology, Pharmaceutical ; methods ; Vomiting ; chemically induced ; drug therapy

OBJECTIVETo study the roles of protein kinase C (PKC) in effect of interferon-gamma (IFN-gamma) on wound healing and cicatrization.

METHODSIFN-gamma was applied on the wound and into the scar tissues of rabbit ear before or after wound healing. PKC activities in the tissues from 0, 3, 6 d, 11-16 d post-wounding and from 14, 30 and 45d post-epithelization were measured by phosphorus (32p) incorporation. The time of wound epithelization and scar changes were also observed.

RESULTSThe PKC activity in granulation tissue, wound margin tissue and scar tissue elevated obviously in comparing with that of normal skin (P < 0.01). IFN-gamma did not change PKC activity (P > 0.05). But it delayed the wound healing (P < 0.01) and inhibited scar hyperplasia (P <0.05).

CONCLUSIONSPKC might not mediate the signal of IFN-gamma inhibiting the wound healing and scar hyperplasia. But PKC might be related to the wound healing and scar hyperplasia.

Animals ; Cicatrix ; metabolism ; Female ; Interferon-gamma ; pharmacology ; Male ; Protein Kinase C ; drug effects ; metabolism ; Rabbits ; Signal Transduction ; Skin ; injuries ; Wound Healing ; drug effects

OBJECTIVETo analyze the effect of sorafenib as salvage therapy used before and/or after allogeneic hematopoietic stem cell transplantation (allo-HSCT) in refractory relapsed FLT3-positive acute myeloid leukemia (AML).

METHODSA total of 16 patients with refractory relapsed FLT3-positive AML, including 10 refractory relapsed pre-transplantation and 6 relapsed after allo-HSCT, were enrolled in this retrospective study. Sorafenib treatment protocols included sorafenib in combination with chemotherapy inducing remission, and sorafenib monotherapy as mauntenance treatment after complete remission (CR).

RESULTSThirteen of the 16 patients achieved CR after one or two courses of induction therapy, including 7 refractory relapsed pre-transplantation and 6 relapsed after allo-HSCT. With a median follow up of 472 (range, 59-1569) days post-transplantation, 12 patients survived and 4 died. Causes of death included leukemia relapse (n=3) and acute graft-versus-host disease (n=1). The 2-year overall and disease-free survival post-transplantation of the 16 patients were (75.0±10.8) % and (50.5±13.7) % respectively. The main side effect of sorafenib was the skin rash. The incidence of rash was lower in the patients used sorafenib pre-transplantation than those post-transplantation (30.0% vs 75.0%, P=0.043).

CONCLUSIONSorafenib used as salvage therapy befor and/or after transplantation for refractory relapsed FLT3-positive AML could reduce the relapse rate and improve the survival.

Antineoplastic Agents ; therapeutic use ; Disease-Free Survival ; Graft vs Host Disease ; Hematopoietic Stem Cell Transplantation ; Humans ; Induction Chemotherapy ; Leukemia, Myeloid, Acute ; genetics ; therapy ; Mutation ; Niacinamide ; analogs & derivatives ; therapeutic use ; Phenylurea Compounds ; therapeutic use ; Recurrence ; Remission Induction ; Retrospective Studies ; Salvage Therapy ; Treatment Outcome ; fms-Like Tyrosine Kinase 3 ; genetics

OBJECTIVETo compare the regulatory effects of electro-acupuncture (EA) at acupoints Zusanli (ST36) and Hegu (LI4) on the visceral hyper-sensitivity in the rat model of irritable bowel syndrome (IBS), and to explore the acting targets and specialty of acupoints.

METHODSExcept 8 rats of the normal control group, the rest 32 rats were prepared to set up the IBS models. IBS animal model was prepared by enema with acetic acid. Model rats were divided into three groups. Except for rats in the model group for control, those in the other two groups were treated 20 min by EA on ST36 (EA-ST36) and LI4 (EA-LI4) respectively for 2 weeks to observe the effect on behavior response of viscera sensitivity. The changes of neuropeptide (NPY), the somatostatin (SS) levels in blood and tissues of brain and intestine were monitored as well.

RESULTSThe volume thresholds for abdomen uplifting and back hunching were obviously increased after EA-ST36 (P<0.05), but showed insignificant change after EA-LI4. NPY contents lowered and SS contents increased in model rats; both EA-ST36 and EA-LI4 could raise the level of thalamic NPY (P<0.01 and P<0.05, respectively), but showed insignificant effects on NPY in colonic tissue. As for SS content, its colonic level could be reduced by EA-S36 and EA-LI4 (P<0.01 and P<0.05, respectively), however, its blood level was affected only by EA-ST36 (P<0.05).

CONCLUSIONSEA-ST36 or EA-LI4 could regulate the NPY in thalamus and SS in colonic tissue, the former could affect blood level of SS as well. It is deemed that NPY and SS may be the key substances for regulating the action of acupuncture in the brain-intestinal axis; their different levels could be regarded as an indicator for the functional difference between the acupoints.

Acupuncture Points ; Animals ; Brain ; metabolism ; Electroacupuncture ; methods ; Irritable Bowel Syndrome ; metabolism ; physiopathology ; Neuropeptide Y ; metabolism ; Rats ; Rats, Wistar ; Somatostatin ; metabolism ; Viscera ; physiopathology

To explore the efficacy of sorafenib combined with chemotherapy and donor lymphocyte infusion (DLI) in patients with FLT3-positive acute myeloid leukemia (AML) relapsed after allogeneic hematopoietic stem cell transplantation (allo-HSCT).Of the 14 patients relapsed after allo-HSCT,9 achieved complete remission after salvage therapy of sorafenib combined with chemotherapy and DLI,6 with complete molecular remission,2 with partial remission,and 3 with no response.With a median follow up of 220 (range,30-1 782) days after post-transplantation relapse,7 patients were still alive and 7 died.Salvage therapy of sorafenib combined with chemotherapy and DLI shows a decent therapeutic effect for FLT3-positive AML relapsed after allo-HSCT.

The aim of this study is to investigate the effects of the metformin on the formation of hepatic fibrosis in type 2 diabetic rats and discuss its mechanism of liver-protecting activity. After SD rats were fed with high-fat and high-sucrose diet for four weeks, low-dose streptozotocin (STZ) was injected intraperitoneally to make the animal mode of type 2 diabetes. Then, all diabetic rats was fed with the high-fat diet and metformin (ig, 100 mg x kg(-1)) was given orally to metformin group for four months. After the last administration, fasting blood glucose was determined. The livers were removed to calculate the hepatic coefficient and to make HE and Picro acid-Sirius red staining, immunohistochemistry (alpha-SMA and TGFbeta1) and TUNEL staining in order to evaluate the effect of metformin on the hepatic fibrosis. The animal model of type 2 diabetes with hepatic fibrosis was successfully made. Metformin can significantly alleviate the lesions of hepatic steatosis and fibrosis, markedly reduce the expressions of alpha-SMA and TGFbeta1 in liver tissue of type 2 diabetic rats. However, TUNEL staining result suggested that metformin could not reduce apoptosis of hepatocytes. The results suggest that metformin can inhibit the formation of hepatic fibrosis in type 2 diabetes.
Actins ; metabolism ; Animals ; Apoptosis ; drug effects ; Blood Glucose ; metabolism ; Body Weight ; drug effects ; Diabetes Mellitus, Experimental ; drug therapy ; etiology ; metabolism ; pathology ; Diabetes Mellitus, Type 2 ; drug therapy ; etiology ; metabolism ; pathology ; Diet, High-Fat ; Female ; Hepatocytes ; pathology ; Hypoglycemic Agents ; pharmacology ; therapeutic use ; Liver ; metabolism ; pathology ; Liver Cirrhosis, Experimental ; drug therapy ; metabolism ; pathology ; Male ; Metformin ; pharmacology ; therapeutic use ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Streptozocin ; Transforming Growth Factor beta1 ; metabolism

The study was aimed to investigate the different prognosis of acute myeloid leukemia (AML) with inv (16). A 13-year-old patient diagnosed as M4Eo presenting with bulky lymphadenopathy was reported, the curative process of patients was presented and the related issues were discussed. The karyotype and inv (16) were detected by conventional cytogeneties and fluorescence in situ hybridization (FISH), respectively, the immunophenotype was detected by flow cytometry. The results showed that conventional cytogenetics and FISH analysis revealed inv (16). Induction therapy included idarubicin and cytarabine. After complete remission, patient received consolidation theray containing high-dose cytarabine (HDAC). FISH analysis revealed poor response of patient to HDAC. It is concluded that bulky lymphadenopathy in AML with inv (16) may be a negative prognostic sign. FISH for inv (16) is specific and constitutes an reliable tool to be used for diagnosis and minimal residual disease (MRD).
Acute Disease ; Adolescent ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Chromosome Inversion ; Chromosomes, Human, Pair 16 ; genetics ; Cytarabine ; administration & dosage ; Humans ; Idarubicin ; administration & dosage ; Leukemia, Myeloid ; complications ; diagnosis ; genetics ; Lymphatic Diseases ; complications ; diagnosis ; genetics ; Male ; Neoplasm, Residual ; Prognosis