Non-steroidal anti-inflammatory drugs( NSAIDs)are widely used in clinical practice,and their gastrointestinal adverse effects have attracted more and more attentions. Although many investigations were focused on gastroduodenal mucosal injury induced by NSAIDs over times,small intestinal injury has become the new hot-spot because of its high morbidity rate in recent years. The mechanisms of NSAIDs-induced small intestinal injury have not been fully elucidated and no specific prevention and treatment modalities have been developed. In this article,the mechanisms of NSAIDs-induced small intestinal injury and the preventive and therapeutic effect of muscovite were reviewed.

Objective To discuss the relationship between c-reactive protein and prognosis of acute coronary syndrome.Methods C-reactive protein of 60 acute coronary syndrome aged patients was evaluated.The patients were divided into two groups:one group with higher CRP level and another group with normal CRP level.The following-up duration was 6 months.After correct therapy,the morbidity of re-angina,arrbythmia,heart failure,re-infarction and cardiac death was compared.Results The morbidity of re-angina,arrhythmia,heart failure,re-infarction,cardiac death was 46.3%(19/41),43.9%(18/41),9.8%(4/41),22.0%(9/41),7.3%(3/41)respectively in higher Clip levd group;The morbidity of re-angina,arrhythmia,heart failure,re-infarction was 15.8%(3/19),10.5%(2/19),5.3%(1/19),5.3%(1/19)respectively in normal CRP group and there was no cardiac death accident.There was significant difference between the two groups.Conclusion CRP plays an important role in the onset of acute coronary syndrome,and its level is related with the higher morbidity of re-angina,arrbythmia,heart failure,re-infarction and cardiac death.

OBJECTIVESTo investigate whether antisense Bmi-1 plasmid could inhibit the proliferation of Jurkat cells.

METHODSThe antisense plasmid was constructed by PCR amplification of a 171 bp segment spanning Bmi-1 start codon and zinc finger structure and the PCR product was subsequently inserted reversely to plasmid pLNCX2. The final construct was confirmed through restriction enzyme digestion. G418 was added into the medium after the plasmid was successfully introduced into Jurkat cells by using lipofectin-mediated DNA transfection. The proliferation of Jurkat cells were determined by MTT and colony formation assays. Cell cycle was determined by flow cytometry. The p16 expression of Jurkat cells was studied by immunofluorescent histochemistry.

RESULTSThe growth rate of antisense Bmi-1 transfected Jurkat cells was significantly lower than that of the controls, and the colony forming capacity of the transfected cells decreased significantly (P < 0.01), the colony numbers being (90.7 +/- 9.07)/10(3) cells, (83.3 +/- 6.11)/10(3) cells and (56.0 +/- 5.56)/10(3) cells for control cells, empty plasmid transfected Jurkat cells and antisense Bmi-1 transfected Jurkat cells, respectively. The percentage of G, phase cells was increased and the p16 expression of antisense Bmi-1 transfected cells was significantly upregulated than that of control cells.

CONCLUSIONAntisense Bmi-1 can inhibit the growth and upregulate the expression of p16 of Jurkat cells in vitro.

Cell Cycle ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; Genetic Vectors ; Humans ; Jurkat Cells ; Nuclear Proteins ; genetics ; Oligonucleotides, Antisense ; genetics ; Plasmids ; genetics ; Polycomb Repressive Complex 1 ; Proto-Oncogene Proteins ; genetics ; Repressor Proteins ; genetics ; Transfection

Structural modifications were performed with natural product of oleanolic acid to search for novel anticancer drugs. Ten oleanolic acid derivatives were designed and obtained by the reaction of oxidation, acylation or hydrolyzation, etc. The cytotoxic activity of derivatives was evaluated against HeLa, HepG2 and BGC-823 cells in vitro by MTT assay, gefitinib and etoposide used as a positive control. The results showed that compound 5a was particularly active to inhibit HepG2 cells growth, and anti-tumor activity of compound 7 on HeLa cells was significantly stronger than oleanolic acid. They are worthy to be studied further.

Objective To investigate the value of contrast-enhanced ultrasonography (CEUS) in the diagnosis of tuberculous mesenteric lymphadenitis by analyzing its enhancement pattern. Methods The conventional ultrasound and contrast-enhanced ultrasound images of 62 patients with tuberculous mesenteric lymphadenitis confirmed by needle core biopsy or surgery were retrospectively analyzed. The location, size, shape, internal echo and posterior enhancement of mesenteric lymph nodes were recorded. All cases were divided into two groups:the maximum diameter of the lymph node≤20 mm and the maximum diameter of the lymph node >20 mm, and the patterns of enhancement in two groups were analyzed. Results The conventional ultrasound of 62 cases with tuberculous mesenteric lymph nodes showed enlargement. And the echogenicity was hypoechoic or heterogeneity, containing punctate or clusters of calcification in 19 cases (30.6%). After CEUS, there were three forms of enhancements:rim enhancement in 29 cases (46.8%);inhomogeneous enhancement in 21cases (33.9%);non-enhancement in 12 cases (19.3%). Rim enhancement was more common in the≤20 mm group, while inhomogeneous enhancement was more common in the lymph nodes>20 mm. There was statistically significant difference of the enhancement type between the≤20 mm group and the>20 mm group (χ2=6.782, P=0.034). Conclusions Most of tuberculous mesenteric lymph nodes showed rim and inhomogeneous enhancement in CEUS, and the sizes of mesenteric lymph node tuberculosis influenced the CEUS enhancement patterns. CEUS may provide useful information for the diagnosis of the tuberculous mesenteric lymph node.

BACKGROUNDBmi-1 gene determines the proliferative capacity of normal and leukemia stem cells. Expression of Bmi-1 has been found in all types of myeloid leukemia cells in both humans and mice. This study aimed at assessing the effect of antisense Bmi-1 expression on K562 cells proliferation and p16 protein (p16) expression.

METHODSA transcriptional repressor, Bmi-1 cDNA was cloned by reverse transcriptase polymerase chain reaction (RT-PCR) of its mRNA from K562 cells. A plasmid expressing antisense Bmi-1 mRNA was then constructed by reverse design of PCR primers and cloned to the plasmid pLNCX2; G418 was added to the medium after the plasmid was successfully introduced in K562 cells by lipofectin-mediated DNA transfection. The effects of the antisense expression on the proliferation of K562 cells were analyzed by using microculture tetrazolium and colony forming. Cell cycle was analyzed by using flow cytometry. The p16 expression of K562 cells was observed by immunofluorescence histochemical stain.

RESULTSK562 cells transfected with antisense Bmi-1 plasmid grew significantly slower than that of controls (the parental K562 and cells transfected with empty plasmid). The colony forming ability of antisense Bmi-1 plasmid transfected cells decreased significantly (P < 0.01) compared with controls. The p16 expression of cells transfected with antisense Bmi-1 was upgraded more apparently than that of controls.

CONCLUSIONThe antisense Bmi-1 gene can inhibit the growth of K562 cell and upgrade expression of p16 in K562 cells.

Cell Cycle ; Cell Proliferation ; Cyclin-Dependent Kinase Inhibitor p16 ; analysis ; Humans ; K562 Cells ; Nuclear Proteins ; antagonists & inhibitors ; genetics ; Plasmids ; Polycomb Repressive Complex 1 ; Proto-Oncogene Proteins ; antagonists & inhibitors ; genetics ; RNA, Antisense ; physiology ; Repressor Proteins ; antagonists & inhibitors ; genetics

Objective To study changes of the autoimmune antibody level in patients after autologous hematopoietic stem cell transplantation(CD_(34)~+).Methods Twelve patients with SLE received autologous hematopoietic stem cell transplantation.All they survived and their immune system were recoverd after a period of time.The serum autoimmune antibody levels were measured before and after the transplantation,Results The antibody levels became normal 6 months after transplantation.Conclusion Autologous hematopoietic stem cell transplantation can effectively reduces the level of autoimmune antibody in patients with SLE.

Objective To investigate the diagnostic correlation and sensitivity of amplitude integrated electroencephalogram (aEEG),brainstem auditory evoked potential (BAEP) and cranial magnetic resonance imaging (MRI) for acute bilirubin encephalopathy (ABE) in the newborn.Method Term and near-term neonates (gestational age ≥ 35 weeks) with hyperbilirubinemia (the level of bilirubin over than 95th percentile) of high and intermediate risk group admitted in the neonatal ward of Guangxi Maternal and Child Health Care Hospital from Jan 2014 to Dec 2015 were recruited retrospectively.The infants were assigned to ABE group and non-ABE group according to the diagnostic criteria of ABE.The clinical data of the newborns were collected and the diagnostic correlation between clinical diagnosis and aEEG,BAEP and cranial MRI were analyzed.The receiver operating characteristic (ROC) curve was adopted to assess the diagnostic efficiency of the peak level of serum bilirubin,aEEG,BAEP and cranial MRI on the early diagnosis of ABE.Result A total of 152 newborns with hyperbilirubinemia were recruited,including 33 cases in the ABE group and 119 cases in non-ABE group.(1) The results of aEEG and MRI were marginally positively correlated with clinical diagnosis of ABE (aEEG:r =0.487,P ＜ 0.001;MRI:r =0.220,P=0.018),while the results of BAEP were closely related to the clinical diagnosis of ABE (r =0.593,P ＜ 0.001);(2) The results of BAEP and MRI on the diagnosis of ABE were positively correlated with those of aEEG (BAEP:r =0.424,P ＜ 0.001;MRI:r =0.307,P ＜ 0.001).(3) The area under the ROC curves for predicting the onset of ABE were 0.899 for the peak level of serum bilirubin,0.767 for BAEP,0.738 for aEEG and 0.590 for MRI.Conclusion There was the correlation on the diagnosis of ABE among the methods of aEEG,BAEP and MRI.The combined diagnosis of the three methods could play a complementary role.The aEEG contributed to the early diagnosis of ABE with high sensitivity.

Craniofacial Dysostosis ; Humans ; Receptors, Fibroblast Growth Factor