OBJECTIVE: To explore the keypoints and methods of pharmaceutical care provided by clinical pharmacists in nutritional support for patients with severe burn. METHODS: Through summarizing the pharmaceutical care process in nutrition support therapy in large area burn patients, the contents of pharmaceutical care including the requirements for thermal energy and nutrients, choice of drugs, nutrition support pathway, complication prevention, application of other special nutrients and so on were described. RESULTS: Through pharmaceutical care, the nutritional support regimen was adjusted, which improved the safety and effectiveness of drug treatment and laid the foundation for related treatments for patients with severe burn. CONCLUSION: Nutritional support is one of the important measures in the treatment of severe burn patients. Pharmaceutical care can improve the standardization and effectiveness of nutritional support treatment. At the same time, the value of clinical pharmacists can be reflected through collaborative service with doctors and nurses.

Air Pollutants, Occupational ; adverse effects ; analysis ; Dust ; analysis ; Environmental Monitoring ; instrumentation ; methods ; Humans ; Industry ; Inhalation Exposure ; statistics & numerical data ; Maximum Allowable Concentration ; Occupational Exposure ; statistics & numerical data ; Quartz

Objective To establish a specific fluorescence quantitative method for determining the mRNA expression of Toll-like receptor3(TLR3)in peripheral blood mononuclear cells(PBMCs).Methods Using the Beacon Designer 2.1 software,specific primers and Taqman-MGB probe were designed.The plasmid pMD18-T-TLR3 was constructed as calibrator and the amplified fragment was obtained by reverse- transcript-PCR(RT-PCR).RNA quantification based on cycle threshold values(Ct)was used to establish the standard curve.According to which,the TLR3 mRNA levels in 30 normal individuals,20 patients with primary biliary cirrhosis(PBC)and 20 ones with chronic liver cirrhosis induced by HBV were calculated automatically by software after the fluorescence of PCR product was detected continuously during amplification.Results The linear detection range of the assay for TLR3 gene and ?-actin was 10~2-10~8(r= -0.9974)and 10~3～10~8(r=-0.9984),respectively.The coefficient of variation of both intra-and inter- assay reproducibility for high concentration sample were 6.7% and 8.7%,respectively,and those for low concentration sample were 12.3% and 14.0%.The TLR3 mRNA expression level ranges from 3.46?10~2- 4.51?10~3 copies/?g RNA,4.92?10~2-1.42?10~4 copies/?g RNA and 2.58?10~2-7.17?10~3 copies/?g RNA for 30 healthy individuals,20 PBC patients and 20 ones with chronic liver cirrhosis induced by HBV, respectively.Conclusion We have successfully set up a FQ-RT-PCR method for detecting TLR3 mRNA, which may be used as an excellent tool for the clinic and basic study on the expression of TLR3 gene.

Adult ; Blood Platelets ; chemistry ; CD40 Antigens ; blood ; CD40 Ligand ; blood ; Cholesterol ; blood ; Female ; Humans ; Hypercholesterolemia ; blood ; drug therapy ; Male ; Middle Aged ; Simvastatin ; therapeutic use

OBJECTIVETo investigate the roles of p38 MAPK in apoptosis of the normal liver cell, the paratumor cirrhosis hepatocellular cell and the hepatocellular carcinoma cell.

METHODSThree cell lines were adopted (the normal liver cell line HL-7702, the paratumor cirrhosis hepatocellular cell line QSG-7701 and the hepatocellular carcinoma cell line QGY-7703) and treated with Diamminedichloroplatin (DDP, cisplatin) and p38MAPK inhibitor SB203580. The apoptosis and cell cycles were detected by flow cytometry and electromicroscopy. The expressions of p38MAPK, CDC25B, p34cdc2 and cyclinB1 were detected by immunocytochemical staining , confocal microscopy and western blot.

RESULTSThe apoptotic rates in all three cell lines pretreated with DDP increased obviously and the rates in normal liver cells and HCC cells increased continuously even after SB203580 treatment, whereas in paratumor cirrhosis cells the rate decreased and the cell cycle stopped at S phase.

CONCLUSIONCisplatin induces apoptosis in the paratumor cirrhosis hepatocellular cell line QSG-7701 via activation of p38MAPK pathway and it differs in the normal liver cells from the hepatocellular carcinoma cells.

Apoptosis ; drug effects ; Carcinoma, Hepatocellular ; metabolism ; pathology ; Cell Line, Tumor ; Cisplatin ; pharmacology ; Humans ; Imidazoles ; pharmacology ; Liver Neoplasms ; metabolism ; pathology ; Pyridines ; pharmacology ; p38 Mitogen-Activated Protein Kinases ; metabolism

OBJECTIVETo investigate the effects of host-derived p38 mitogen-activated protein kinase subunit 38 (p38MAPK) and the hepatitis B virus X antigen (HbxAg) on cell proliferation and apoptosis in human hepatocellular carcinoma (HCC), and to study the mechanism underlying hepatocarcinogenesis.

METHODSLiver tissues were biopsied from healthy individuals and patients with chronic hepatitis B (CHB), liver cirrhosis, paratumor cirrhosis, and HCC. Immunohistochemical staining was used to detect expressions of HBxAg, p38MAPK, cell cycle G2/M phase-related factors (cdc25B, p34cdc2, cyclin B1), and cell proliferation factor ki-67.The terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling method (known as TUNEL) was used to detect apoptosis.

RESULTSThe highest rates of HBxAg were detected in CHB (65.0%) and HCC (44.4%) liver samples, and the antigen was mainly expressed in nuclei. Increasingly higher rates of p38MAPK, cdc25B, cyclin B1, and p34cdc2 expression were detected with increases in disease severity: normal liver (40.0%, 20.0%, 20.0%, and 30.0%, respectively), chronic hepatitis B (60.0%, 65.0%, 40.0%, and 50.0%, respectively), liver cirrhosis (65.0%, 75.0%, 70.0%, and 55.0%, respectively), paratumor cirrhosis (66.7%, 75.0%, 75.0%, and 63.9%, respectively), and HCC (77.8%, 80.6%, 80.6%, and 72.2%, respectively). In addition, the intracellular location of p38MAPK expression was different under different disease conditions, showing nuclear expression in CHB and liver cirrhosis samples and cytoplasmic expression in paratumor cirrhosis and HCC samples (x2 = 1.11, P more than 0.05). The proliferation index (PI) and the apoptosis index (AI) were both increased along with disease severity (normal more than CHB more than paratumor cirrhosis more than HCC) (PI: 0.0000+/-0.000, 0.0502+/-0.011, 0.0411+/-0.009, 0.0762+/-0.017; AI: 0.0351+/-0.024, 0.0607+/-0.022, 0.0562+/-0.013, 0.0716+/-0.011), with the notable exception for liver cirrhosis (PI: 0.1810+/-0.036 and AI: 0.1200+/-0.018). PI in poorly-differentiated HCC (0.2285+/-0.062) was significantly higher than in well-differentiated HCC (0.1216+/-0.032, t = 2.082, P = 0.044). AI in well-differentiated HCC (0.152+/-0.026) was significantly higher than in poorly-differentiated HCC (0.081+/-0.022, t = 2.129, P = 0.041).

CONCLUSIONSIn the process of hepatocarcinogenesis, HBxAg may cause a series of abnormal changes in cell cycle, proliferation and apoptosis by affecting the expression of p38MAPK.

Apoptosis ; Carcinoma, Hepatocellular ; metabolism ; pathology ; Cell Cycle ; Cell Division ; Cell Proliferation ; Hepatitis B, Chronic ; pathology ; Humans ; Liver Cirrhosis ; pathology ; Liver Neoplasms ; metabolism ; pathology ; Trans-Activators ; metabolism ; p38 Mitogen-Activated Protein Kinases ; metabolism

OBJECTIVESTo establish a primary biliary cirrhosis (PBC) model by AMAM2 autoantigen injection into C57BL/6 mice.

METHODSMice of the model group were immunized intraperitonealy with 200 microl of purified recombinant AMAM2 autoantigen in complete Freund's adjuvant (CFA). Mice immunized with bovine serum albumin and CFA in the same way were used as negative controls. Sixty-six weeks later, mice were sacrificed and their sera were collected. Sera samples were assayed for AMAM2 autoantibody, alkaline phosphatase (ALP), ALT and total bilirubin (TBil). Their liver, stomach, muscle and kidney tissues were sectioned and stained using HE to observe the pathological changes.

RESULTSAntibodies to AMAM2 autoantigen were readily induced in the model group. The mice in the model group had no significant changes in the level of serum ALT and TBil but had an obvious increase of ALP (P<0.05). The stomach, muscle and kidney tissues showed no evident damage while the livers had obvious pathological changes, including bile duct degeneration or proliferation, and mononuclear cell infiltration.

CONCLUSIONThe AMAM2 autoantigen-induced PBC animal model was successfully established in C57BL/6 mice in our experiment and its characteristic biochemical and pathology are quite similar to that in the early stage of human PBC. This model may provide a useful experimental approach for further study of the pathogenesis and clinical treatment of human PBC.

Animals ; Autoantigens ; immunology ; Disease Models, Animal ; Liver Cirrhosis, Biliary ; etiology ; Mice ; Mice, Inbred C57BL ; Mitochondria ; immunology

HUANG Zong-xu, who studied from Mr. Cheng Dan-an, the founder of Chengjiang acupuncture school, is a famous acupuncturist of Fujian Province. Through collecting and sorting of Mr. Huang's theses and medical records, his academic characteristics of acupuncture and moxibustion were summarized as follows. Paying attention to meridians and collaterals and treatment based on syndrome differentiation; valuing the needling sensation as well as being good at reinforcing and reducing methods; thinking highly of taking care of spleen and stomach, ombination of needles and herbal medicine to treat difficult miscellaneous diseases; being adept in externd therapy and penetration needling and diet prescriptions, as well as attaching importance on health preserving.
Acupuncture ; education ; history ; Acupuncture Therapy ; history ; methods ; China ; History, 20th Century ; History, 21st Century ; Humans ; Meridians ; Moxibustion ; history

Biomarkers, Tumor ; metabolism ; Carcinoma, Hepatocellular ; genetics ; metabolism ; CpG Islands ; Cyclin-Dependent Kinase Inhibitor p57 ; genetics ; metabolism ; DNA Methylation ; Gene Expression Regulation, Neoplastic ; Humans ; In Situ Hybridization ; Liver ; metabolism ; Liver Neoplasms ; genetics ; metabolism ; Polymerase Chain Reaction ; methods ; Promoter Regions, Genetic ; RNA, Messenger ; genetics ; metabolism

Animals ; Heparin ; pharmacology ; Hepatocytes ; cytology ; metabolism ; Mice ; Promoter Regions, Genetic ; genetics ; Transforming Growth Factor beta ; genetics