Child ; Humans ; Inflammatory Bowel Diseases ; etiology ; pathology

Objective To introduce the clinical apply of middle and small skin defect in finger injury with lateral arm free perforator flap.Methods (1) Ten cadavers were injected with a modified lead oxide-gelatin mixture.Later,CT scan,three-dimensional reconstruction of the cutaneous perforator vessels on the later arm.Then simulate the flap design.All cadavers were dissected before CT scanning.(2) Eighteen cases of middle and small skin defects in finger injury were treated with lateral arm free flap.The defect area were from 3 cm × 4 cm to 6 cm × 9 cm.Results Our research showed that the average caliber diameter of perforators of profunda brachial artery(PBA) was (0.71 ± 0.15) mm,and Posterior radial collateral artery(PRCA) was (0.94±0.22)mm.The results of pedicle length of perforator of PBA was (2.74 ±0.42) cm:(2.96 ±0.37) cm,and PRCA was (4.78 ±0.63) cm:(4.86 ±0.51) cm.3D reconstructive results showed that the perforators of PBA and PRCA dominated the lateral upper arm area.The flap of 18 cases survived after the operation.The wound of providing area was directly sutured or skin grafting and got healing.All cases were followed up for 6 months to 3 years,and the average follow-up time was 11 months.There was a little swelling on the outlooks of the flap,but the texture and sensation of the flap was good.Conclusion The lateral arm free perforator flap has a stable vessel pedicle,good texture and sensation,so it was a good method to repair middle and small skin defect in finger injury.

Biomarkers, Tumor ; metabolism ; Hemangioendothelioma, Epithelioid ; metabolism ; pathology ; Hemangiosarcoma ; metabolism ; pathology ; Humans ; Immunohistochemistry ; Leiomyosarcoma ; metabolism ; pathology ; Lung Neoplasms ; metabolism ; pathology ; Nerve Sheath Neoplasms ; metabolism ; pathology ; Pulmonary Blastoma ; metabolism ; pathology ; Sarcoma ; metabolism ; pathology ; Sarcoma, Synovial ; metabolism ; pathology ; Solitary Fibrous Tumors ; metabolism ; pathology

Objective: To study the expression of function-unknown PNMA5 gene in hepatocellular carcinoma (HCC) and its relationship with proliferation of HCC. Methods: PNMA5 was over-expressed in HCC analyzed by gene expression profiling. We investigated the expression of PNMA5 through RT-PCR and real-time fluorescent quantitative PCR (RFQ-PCR) in normal liver tissues, HCC, and adjacent non-cancerous liver tissues (non-HCC). PNMA5 gene was silenced in Focus and PLC liver cancer cells by using RNA interference technology. The changes in cell growth curve were quantitatively analyzed by performing CCK-8 experiment after silencing the endogenous PNMA5 gene expression. Results: PNMA5 was mainly expressed in testis, ovary, and brain tissues out of the 14 kinds of normal human tissues. PNMA5 mRNA was significantly up-regulated in 42% (5/12) HCC specimens, which was 2-fold higher than that in non-HCCs (P < 0.05). Interestingly, the growth of Focus and PLC cells was markedly inhibited after silencing PNMA5 gene expression (P < 0.01), and the number of tumor cells progressing through G1 and entering S phase was significantly decreased as compared with the control cells transfected with siRNA-NC (P < 0.01). Conclusion: PNMA5 plays an important role in maintaining the malignant phenotype of HCC. It may be a novel tumor-testis associated gene. Further investigation of its function may help to find the new mechanism for the HCC tumorigenesis. PNMA5 may become a new candidate target in HCC treatment.

To study the chemical constituents from the root of Berchemia lineata (L.) DC., nine compounds were isolated from the EtOAc extract by using silica gel, RP-C18 silica gel column chromatography and preparative HPLC. Based on the spectroscopic analysis, their structures were identified as 5-hydroxy-7-(2'-hydroxypropyl)-2-methyl-chromone (1), (-)-(1'R, 2'S)-erythro-5-hydroxy-7-(1', 2'-dihydroxypropyl)-2-methyl-chromone (2), naringenin (3), eriodictyol (4), (+)-aromadendrin (5), (+)-taxifolin (6), (+)-catechin (7), (+)-epigallocatechin (8) and quercetin (9). Among them, compound 2 is a new chromone derivative. Compound 1 is a known chromone derivative and isolated from this genus for the first time. Compounds 3-9 are known flavonoids and isolated from this plant for the first time.

Acupuncture Therapy ; Adult ; Female ; Hemangioma, Cavernous ; physiopathology ; therapy ; Humans ; Lingual Frenum ; physiopathology ; Tongue Diseases ; physiopathology ; therapy

Autoimmune Diseases ; diagnosis ; immunology ; pathology ; surgery ; Humans ; Immunoglobulin G ; blood ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Pancreatectomy ; Pancreatitis ; diagnosis ; immunology ; pathology ; surgery

Objective Inflammatory bowel disease is an important chronic gastrointestinal disease of childhood and adolescence.Intestinal mucosa barrier damage plays an important role in its pathogenesis.This study attempts to use IL-1β stimulating Caco-2 cell monolayer simulates inflammatory intestinal epithelial barrier in vitro,provides the basis for studying the pathogenesis and treatment of IBD.Methods Caco-2 cells were cultivated in vitro until the 21st day to simulate intestinal epithelial cell monolayer barrier.The cells of inflammation group one were disposed with IL-1β for 2 h since the 5th day and detected TEER every other day until the 21st day.The cells of inflammation group two were disposed with IL-1 β at the 18th day for 0,12,24,48,72h, and detected TEER respectively.Normal control group cells were cultured with common medium and detected TEER at the corresponding time point.Results The TEER of Caco-2 cells gradually increased from the 5th to 15th days,reached 600Ω·cm2 in the 15th day of a plateau until to the 21st day.Since the 5th day,the TEER of inflammation group one were all lower than normal group,and still to the 21st day ＜ 500Ω·cm2.Inflammation group two shows the time dependence TEER gradually reduce,peaked at 48 hours,then a slight increase in 72 hours.Conclusion The Caco-2 cells cultured for 2 ～ 3 weeks can form intestinal epithelial monolayer barrier with polarity,then treated with IL-1 β can manufacture inflammatory intestinal epithelial barrier model in vitro.

Objective To evaluate the efficacy and safety of bicyclol tablet on hepatic lesions caused by Epstein-Barr virus( EBV) infection in children.Methods A single-center controlled retrospective study was conducted in 121 children with hepatic lesions caused by EBV infection for evaluating safety,tolerability, and efficacy of treatment with bicyclol tablets or Glycyrrhizin capsules.Childer n in bicyclol group ( n=63 ) were treatedw ith bicyclol at blets and cotn rol group ( n =58 ) were treated with Glycyrrhizin capsules.The course of the treatment were both 8 weeeks for two groups.The level of the EBV load pretreatment and plas-ma aminotransferase,blood routine,urine routine pretreatment and 1 week,4 weeks and 8 weeks after treat-mentw ere analyzed er trospectively.Rse ults (1) The pal smaA LT level sigin ficantly decreased in theb icy-clol group compared with that in the contro l group(P<0.01), se pecai lly the levle after 8 weeks treatm ent. (2) Bicycol l was more effce tive in the bicyclol group than Glycyrrhizin capslu se in the control group( P<0.01).(3) Both grousp had no significantlya dvesr e events.Conclusion Bicyclol tablet can derc ease plas-ma aminotransferase level,espce ially ALT,inc hildren caused by EBV infection with better efficiency and safety.

Objective Intestinal epithelial barrier damage is closely related to a variety of gastrointestinal disease,how to maintain its function effectively is the key to treat all these diseases.This research attempts to explore the protective effect and its mechanism of toll-like receptor 2 (Toll-like receptor,TLR2)on permeability of intestinal epithelial barrier by experiments in vitro,to lay a foundation for new treatment methods.Methods We cultured non-transfected Caco-2 cells,TLR2-deficiency Caco-2 cells,TLR2-overexpressed Caco-2 cells in normal control group until the 21 st d,then tested transepithelial electrical resistance(TEER) which reacts the permeability of epithelial barrier.We cultured 3 types of cells in inflammation group until the 19th d treated with 10 ng/ml IL-1 beta for 48 h,then tested TEER values at the 21st d.We treated 3 types of cells in inhibition group with PI3K/Akt pathway inhibitor for 1h befor IL-1 beta,then tested TEER values at the 21st d.Results TEER value of TLR2-deficiency Caco-2 cell monolayer significantly reduced (P ＜ 0.01),whereas TEER value of TLR2-overexpressed Caco-2 monolayer raised,but without statistically significant.TLR2 can prevent IL-1 beta caused TEER decreasing (P ＜ 0.01),but the effect disappeared after given PI3K/Akt pathway inhibitor.Conclusion TLR2 can regulate the permeability of intestinal epithelial barrier.In addition,TLR2 can protect permeability increasing caused by inflammation,this effect mediated by PI3 K/Akt pathway.