OBJECTIVE:To provide reference for clinical rational use of anti-epileptic drugs. METHODS:In this retrospective review,serum concentrations of anti-epileptic drugs in a total of 499 patients who were treated with anti-epileptic drugs (such as sodium phenytoin,phenobarbital,carbamazepine and valproate sodium) in our hospital during 2007 were analyzed statistically. RESULTS:Among the patients receiving one kind of anti-epileptic drugs,206 cases (61.49%) were within normal range in blood concentration versus only 45 cases (44.12%) for patients receiving combined drugs. In addition,the above four drugs (sodium phenytoin,phenobarbital,carbamazepine and valproate sodium) were detected in 59.68% of the patients who took Chinese medicines,and among them,3.23% were within normal range in blood concentration. CONCLUSION:Monitoring on serum concentrations of anti-epileptic drugs is conducive to a better control of therapeutic concentration. It is advisable to refrain from using anti-epileptic drugs in combination but to adopt individualized administration. In addition,great importance should be attached to whether there are chemo-synthetic drug components contained in Chinese medicine.

Objective We aimed to explore the experience of posttraumatic growth in patients with cervical cancer who had a hysterectomy at the childbearing age.Methods The phenomenological methodology was used in the study.An in-depth interview was conducted among 12 patients chosen by purposive sampling method.Results Through careful analysis and collation,three themes were identified:smashing the original assumption,searching the meaning of existence and rebuilding the new cognitive schemata.The experience of patients' was conformed to the model which was put forward by Tedeschi,and the theme changes in personal relationships,personal strength,altruism born from sufferings and new philosophy of life were conformed to theoretical connotation of PTG.Conclusions Clinical medical staff should update psychological nursing concept timely and taking advantages of PTG to help patients pass through their difficult period.

Objective To assss the clinical significance of Cystatin C(Cys C)as a marker of renal function in kidney transplant patients especially when infection or acute rejection occured.Methods Among 65 renal transplant recipients the concentrations of serum Cys C and serum creatinine(Scr)were determined before and one month after the transplantation,and also in the day and next day of occurrence of infection or rejection.Meanwhile,30 healthy persons and 30 infected patients without kidney transplantations were served as control.Results The concentrations of Cys C were nearly equal between healthy persons and the infected patients without kidney transplantations(P = 0.32).The level of serum Cys C and Scr dropped quickly in the first 3 days after transplantation(decreased by 69.2%,74.7%,75.8% for Cys C and 38.4%,74.5%,81.4% for Scr)(P

OBJECTIVETo observe the effect of sodium tanshinone II (A) sulfonate (STS) on Ang II -induced atrial fibroblast collagen synthesis and TGF-beta1 activation.

METHODAtrial fibroblasts of neonatal rats were cultured to determine the content of collagen protein. The original synthesis rate determined by the [3H]-proline incorporation method was taken as the index for myocardial fibrosis. The content of active TGF-beta1 and total TGF-beta1 in cell culture supernatants were tested and cultured by ELISA. The expression of thrombospondin-1 (TSP-1) was assessed by using Western blot.

RESULTAng II could significantly increase the content of atrial fibroblast collagen and the collagen synthesis rate, the TSP-1 expression and the concentration of active TGF-beta1, without any obvious change in total TGF-beta1. After the STS treatment, all of the indexes, apart from total TGF-beta1, were obviously down-regulated.

CONCLUSIONSTS could decrease the secretion of Ang II -induced atrial fibroblast collagen and the synthesis rate. Its mechanism is related to the inhibition of TSP-1/TGF-beta1 pathway.

Angiotensin II ; pharmacology ; Animals ; Collagen ; biosynthesis ; Fibroblasts ; cytology ; drug effects ; metabolism ; Gene Expression Regulation ; drug effects ; Heart Atria ; cytology ; Phenanthrenes ; pharmacology ; Rats ; Rats, Wistar ; Signal Transduction ; drug effects ; Thrombospondin 1 ; metabolism ; Transforming Growth Factor beta1 ; metabolism

This study investigated the correlation between and compared the effects of reactive oxygen species (ROS) and p38 mitogen-activated protein kinase α (p38MAPKα) in the ex vivo expanded umbilical cord blood (hUCB) CD133(+) cells. hUCB CD133(+) cells were cultured in the hematopoietic stem cells (HSCs) culture medium with N-acetylcysteine (NAC, an anti-oxidant), p38MAPKα-specific inhibitor (SB203580) or their combination. The levels of ROS and expression of phosphorylated p38MAPKα (p-p38) in CD133(+) cells were flow cytometrically detected. The efficacy of ex vivo expansion was evaluated by the density of CD133(+) cell sub-group colony-forming cells (CFC) and cobblestone area-forming cells (CAFC) assay. Our results showed decreased ROS levels in NAC, SB203580, and their combination treatment groups were almost 37%, 48%, and 85%, respectively. Furthermore, SB203580 abrogated the activation of p38MAPKα more obviously than NAC. Moreover, the CD133(+) cells in SB203580 treatment group had a 21.93±1.36-fold increase, and 14.50±1.19-fold increase in NAC treatment group, but only 10.13±0.57-fold increase in control group. In addition, SB203580 treatment led a higher level increase in the number of CFU and CAFC than NAC did. These findings suggested that, in expanded CD133(+) cells, ROS activates p38MAPKα, which, in turn, induces ROS production, and p38MAPKα might be the most suitable regulator in ROS-p38MAPKα pathway for the promotion of HSCs ex vivo expansion.

Leukemia seems to depend on a small population of "leukemia stem cells (LSCs)" for its growth and metastasis. However, the precise surviving mechanisms of LSCs remain obscure. Cellular senescence is an important obstacle for production and surviving of tumor cells. In this study we investigated the activated state of a pathway, in which reactive oxygen species (ROS) induces cellular senescence through DNA damage and phophorylation of p38 MAPK (p38), in myeloid leukemic CD34(+)CD38(-) cells. Bone marrow samples were obtained from patients with acute myeloid leukemia (AML, n=11) and chronic myeloid leukemia (CML, n=9). CD34(+)CD38(-) cells were isolated from mononuclear cells from these bone marrow samples, and K562 and KG1a cells (two kinds of myeloid leukemia cell lines) by mini-magnetic activated cell sorting. Hematopoietic stem cells (HSCs) from human cord blood served as controls. Intracellular ROS level was detected by flow cytometry. DNA damage defined as the γH2AX level was measured by immunofluorescence staining. Real-time RT-PCR was used to detect the expression of p21, a senescence-associated gene. Western blotting and immunofluorescence staining were employed to determine the p38 expression and activation. The proliferation and apoptosis of CD34(+)CD38(-) cells were detected by MTT assay and flow cytometry. Our results showed that ROS and DNA damage were substantially accumulated and p38 was less phosphorated in myeloid leukemic CD34(+)CD38(-) cells as compared with HSCs and H(2)O(2)-induced senescent HSCs. Furthermore, over-phosphorylation of p38 by anisomycin, a selective activator of p38, induced both the senescence-like growth arrest and apoptosis of CD34(+)CD38(-) cells from K562 and KG1a cell lines. These findings suggested that, although excessive accumulation of oxidative DNA damage was present in LSCs, the relatively decreased phosphorylation of p38 might help leukemic cells escape senescence and apoptosis.

Adult ; Brain Neoplasms ; complications ; Death, Sudden ; etiology ; Female ; Humans ; Nose Neoplasms ; complications

Objective To investigate the metabolism and function of the intestinal microbiota from liver cirrhosis patients.Methods Sixteen cases of liver cirrhosis and twenty normal individuals were selected , whose intestinal microbiota metagenomic DNA was extracted , followed by high-throughput Solexa sequencing and the bioinformatics analysis of metabo-lism and function annotation to compare the differences between the patients and normal subjects and find out about the cir -rhosis-related functions .Results The functional diversity was significantly reduced in the intestinal microbiota of cirrhotic patients.At the module or pathway level , the intestinal microbiota of patients showed an enrichment in metabolisms of drugs, essential amino acid , propanoate metabolism and inflammatory reaction , whereas an opposite tendency was observed in the metabolic ability of butyrate , bile acid and cell cycle .Conclusion Under the influence of liver cirrhosis , the growth environment in the intestine is destroyed , causing, the intestinal microbiota the exhibit some compensation to adapt to the changed intestinal micro-environment .

To investigate the morphogenetic process of human adenovirus type 41 (HAdV-41), 293TE cells were infected with purified wild-type HAdV-41, and ultrathin sections of infected cells were prepared and observed under a transmission electron microscope. Results showed that HAdV-41 entered host cells mainly through three ways: non-clathrin-coated pit, clathrin-coated pit, and direct penetration of plasma membrane. In addition, cell microvilli might help HAdV-41 enter cells. After entering into cells, HAdV-41 virus particles could be found in vacuoles or lysosomes or be in a free state in cytoplasm. Only free virus particles could be found near nuclear pores (NP), suggesting that the virus needed to escape from lysosomes for effective infection and viral nucleoprotein entered the nucleus through NP. Progeny viruses were as-sembled in the nucleus. Three types of inclusion bodies, which were termed as fibrillous inclusion body, condense inclusion body, and stripped condense inclusion body, were involved in HAdV-41 morphogenesis. In the late phase of viral replication, the membrane integrity of the infected cells was lost and viral particles were released extracellularly. This study reveals the partial process of HAdV-41 morphogenesis and provides more biological information on HAdV-41.
Adenovirus Infections, Human ; virology ; Adenoviruses, Human ; genetics ; growth & development ; physiology ; ultrastructure ; Cell Membrane ; virology ; Cell Nucleus ; virology ; Humans ; Virus Release ; Virus Replication

Cell Transformation, Neoplastic ; drug effects ; genetics ; Dimethyl Sulfoxide ; pharmacology ; Electroporation ; methods ; HL-60 Cells ; Humans ; Membrane Proteins ; genetics ; Neoplasm Proteins ; genetics ; RNA Interference ; RNA, Small Interfering ; genetics ; Stromal Interaction Molecule 1 ; Transfection