Child ; Choristoma ; pathology ; Diagnosis, Differential ; Follow-Up Studies ; Humans ; Male ; Neoplasms, Glandular and Epithelial ; pathology ; Thymus Gland ; pathology ; Thymus Neoplasms ; pathology ; Thyroid Neoplasms ; pathology

Objective To observe the ultrastructural change of intestinal mucosa in mice infected with Blastocystis hominis, and to study the pathogenic mechanism of B.hominis infection. Methods 20 Kunming mice were randomly divided into 4 groups: group A treated with immunosuppressant (dexamethasone), group B without immunosuppressant, group C as normal control and group D as immunosuppressant control. Groups A and B were then orally infected with 204 cysts of B. hominis. Groups C and D were treated as control by infusing same volume of Locke′s solution. Six days after inoculation, mice in each group were killed and mucosa of ileocecum was observed by transmission electron microscope (TEM) and scanning electron microscope (SEM). Results Under SEM, B. hominis located in enteric cavity and on the surface of ileocecum mucosa. Individual parasites also invaded into mucosa and its fold. Partial destruction of microvilli on the mucosa was observed. TEM observation indicated a reduction of microvilli on the surface of absorptive cells. Mitochondrial edema, rough endoplasmic reticulum dilatation and degranulation were found on absorptive cells and goblet cells. Lymphocyte infiltration and eosinophilia were found in intercellular stroma. Pathological changes in group A were more serious than that of group B. No abnormal change on the mucosal ultrastructure was found in groups C and D. Conclusions B. hominis infection causes significant ultrastructural lesion on the ileocecal mucosa in mice. Immune status of the mice can affect the degree of the lesion due to infection.

Objective To explore the enhancement effects and mechanisms of IL-32β on human cervical carcinoma cells C33A to hypoxic/hypoglycemic condition.Methods After cultured in hypoxia/hypoglycemic circumstance and normal circumstance for 20 hours respectively, the mRNA and protein expression of IL-32β in C33A cells were detected by real time-polymerase chain reaction (RT-PCR) and Western blotting respectively.Trypan blue stain was used to detect C33A cells viability in hypoxia/hypoglycemic circumstance and adding 10, 100,500 ng/ml IL-32β circumstance.The xenografted tumor of nude mice was established by intraperitoneal injection, and their volumes were tested for a given time after injecting 0, 1.0 mg/kg IL-32β.siRNA was used to construct IL-32β knockdown cells and detect the expression of VEGF.Results Under the hypoxia/hypoglycemic circumstance, the expressions of IL-32β mRNA were (6.12 ± 0.03) times of the normal circumstance (F =43.16, P ＜ 0.05), the expressions of IL-32β protein were (2.23 ± 0.04) times of the normal circumstance (F =22.32, P ＜ 0.05).The C33A cells viability in hypoxia/hypoglycemic circumstance was (51.92 ± 3.41) ％, whereas, viability in 10 ng/ml IL-32β group was (55.23 ± 3.92) ％ (F =14.25, P ＜ 0.05), viability in 100 ng/ml IL-32β group was (62.52 ± 4.14) ％ (F =35.53, P ＜ 0.01), viability in 500 ng/ml IL-32β group was (69.14 ± 2.45) ％ (F =56.28, P ＜ 0.01).After 28 days, the volume of xenografted tumor of 0 mg/kg IL-32β group was (578 ± 64)mm3, and 1.0 mg/kg IL-32β group up to (1 402 ± 142) mm3 (F =27.84, P ＜ 0.01).In addition, compared with control group, the expression of VEGF in IL-32β knockdown C33A cells was significantly decreased (F =36.85, P ＜ 0.05).Conclusion IL-32β can enhance the resistance to hypoxic/hypoglycemic condition of C33A cells, which is associated with the increase of VEGF.

Objective To investigate the protective effect of physcione on acute liver injury in rats.Methods Acute liver injury rat model was constructed with 2ml/kg CCl_4((?)3 d)via intragastric administration.The serum concentrations of alanine aminotransferase(ALT),aspartate aminotransferase(AST)and tumor necrosis factor (TNF)in different groups were detected.Hepatic histopathology of different groups was also observed to reflect the effect of physcione.Results The serum concentrations of ALT,AST and TNF in physcione group were significantly lower than those of model group(P

Objective To explore the role and clinical significance of interleukin-6(IL-6) in children with bronchial asthma.Methods Sera were collected from 29 cases with asthmatic attacks,32 asthmatic children who in stable conditions,and 20 health children.Serum IL-6 concentrations were measured by radioimmunoassay(RIA).Results 1.Asthmatic children appeared significantly higher levels of serum IL-6 during asthmatic attacks as compared to those in stable conditions and healthy ones respectively(P3 years old had significantly higher serum IL6 concentrations than ≤3 years old children in remission.Conclusion IL-6 may participate pathogenesis of asthma,and it may play different biological roles during asthmatic attacksas or stable conditions.

This paper is to report the exploration of the activation of Rho/ROCK signal pathway in 5-HT-induced proliferation of rat pulmonary artery smooth muscle cells (PASMCs) and the inhibitory effect of m-Nis on this pathway. PASMCs were cultured with the explant technique. MTT assay was used to explore the proliferation of PASMCs after 5-HT treated for different time and the intervening effect of m-Nis. RT-PCR and Western blot were used respectively to explore the mRNA expression of RhoA, ROCK1 and the protein expression of p-MYPT1 in 5-HT-treated PASMCs and intervening effect of m-Nis. The results of MTT assay suggested that 5-HT (1 µmol · L(-1)) treatment for 12-72 h significantly induced the proliferation of rat PASMCs (P<0.05 or P < 0.01), which were inhibited by m-Nis (1 x 10(-5), 1 x 10(-6), l x 10(-7), 1 x10(-8) mol · L(-1)) in dose-dependent manners (P < 0.05 or P < 0.01). Similarly, the mRNA expression of RhoA, ROCK1 and the protein expression of p-MYPT1 were also inhibited by m-Nis in different degrees (P < 0.05 or P < 0.01). Thus, the results of this study suggested that Rho/ROCK pathway played an important role in 5-HT-induced proliferation of rat PASMCs, m-Nis inhibited 5-HT-induced proliferation obviously, which may be related to the blockage of Rho/ROCK signal pathway.
Animals ; Cell Proliferation ; drug effects ; Myocytes, Smooth Muscle ; cytology ; drug effects ; Nisoldipine ; pharmacology ; Protein Phosphatase 1 ; metabolism ; Pulmonary Artery ; cytology ; Rats ; Serotonin ; pharmacology ; Signal Transduction ; rho-Associated Kinases ; metabolism ; rhoA GTP-Binding Protein ; metabolism

Objective To analyze the reasons of non-planned decannulation (NPD) of peripheraly inserted central catheter (PICC) and explore the applicable prevention strategies.Methods We retrospectively analyzed the clinical data of 432 patients who underwent PICC cannulations maintenance between July 2005 and June 2008.The reasons of 26 cases of NPD were analyzed.Results The main reasons of NPD included cannulation occlusion,cannulation ectopia or translocation,cannulation exfoliation,cannulation-related infections,mechanical phlebitis,and thrombus formation.The complications usually were caused by the poor cannulation material,incorrect fixation,top of canuulation not reaching superior vena cava,lack of management measures for outpatients,accidents,and others.Effective measures for preventing NPD included:use silica gel cannulation;ensure the top of canuulation reach the superior vena cava;and improve the communications between outpatients and nurses.Conclusion NPD of PICC may be caused by various reasons and effective prevention measures should be taken.

Antigens, CD34 ; metabolism ; Female ; Humans ; Hypoglycemia ; etiology ; Immunohistochemistry ; Middle Aged ; Pleura ; metabolism ; pathology ; surgery ; Solitary Fibrous Tumor, Pleural ; complications ; metabolism ; surgery ; Treatment Outcome ; Vimentin ; metabolism

OBJECTIVETo study the anti-inflammatory effect and the therapeutic efficacy of Qishen Huoxue Granule (QHG) in treating severe sepsis.

METHODSOne hundred and sixty-seven patients with severe sepsis were enrolled and randomly assigned to two groups, the 85 patients in the control group treated with conventional Western medicine and the 82 in the QHG group treated with conventional Western medicine plus QHG. Changes of tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), interleukin-10 (IL-10), procalcitonin (PCT), Marshall score, APACHE II score, ICU stay time and 28-day mortality were monitored and compared.

RESULTSCompared with the control group, IL-6 and TNF-alpha levels, the ICU stay time and 28-day mortality were significantly lower in the QHG group (all P < 0.05). During the QHG treatment, no severe adverse event was observed.

CONCLUSIONThe integrative treatment could reduce the blood levels of IL-6 and TNF-alpha, shorten the ICU stay time and decrease the 28-day mortality of patients with sepsis, showing a favor therapeutic prospect.

Aged ; Aged, 80 and over ; Drug Therapy, Combination ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Interleukin-6 ; blood ; Male ; Middle Aged ; Phytotherapy ; Sepsis ; blood ; drug therapy ; pathology ; Treatment Outcome ; Tumor Necrosis Factor-alpha ; blood

Induced pluripotent stem cells (iPSCs) can be propagated indefinitely, while maintaining the capacity to differentiate into all cell types in the body except for the extra-embryonic tissues. This iPSC technology not only represents a new way to use individual-specific stem cells for regenerative medicine but also constitutes a novel method to obtain large numbers of disease-specific cells for biomedical research. However, the low efficiency of reprogramming and genomic integration of oncogenes and viral vectors limit the potential application of iPSCs. Chemical-induced reprogramming offers a novel approach to generating iPSCs. In this study, a new combination of small-molecule compounds (SMs) (sodium butyrate, A-83-01, CHIR99021, Y-27632) under conditions of transient folate deprivation was used to generate iPSC. It was found that transient folate deprivation combined with SMs was sufficient to permit reprogramming from mouse embryonic fibroblasts (MEFs) in the presence of transcription factors, Oct4 and Klf4, within 25 days, replacing Sox2 and c-Myc, and accelerated the generation of mouse iPSCs. The resulting cell lines resembled mouse embryonic stem (ES) cells with respect to proliferation rate, morphology, pluripotency-associated markers and gene expressions. Deprivation of folic acid, combined with treating MEFs with SMs, can improve the inducing efficiency of iPSCs and reduce their carcinogenicity and the use of exogenous reprogramming factors.