12-O-tetradecanoylphorbol-13-acetate (TPA) is an activator of protein kinase C (PKC)extracted from the croton oil, it is one of the most powerful inducers of differentiation as well as a powerful tumor promoter. It is used by the study of induction and differentiation generally, because of it can induce the differentiation of tumor cell and promote the lymphocyte transformation and secrete of lymphokine, meanwhile,it is able to induce many kinds of cell of leukemic cell strain like HL-60, HEL and so on, Some literature reported that TPA had the function of differentiation of primary leukemic cell. The article mainly explains the induction and differentiation of leukemic cell by phorbol ester as well as its mechanisms, which to provide the theory evidence for prevention and cure of leukemia.

Objective To understand the epidemiological characteristic of bacterial food-poisoning in Zhuhai City to provide a scientific basis for the judgment ,control and prevention of bacterial food-poisoning .Methods The samples of bacterial food-poison-ing in the Zhuhai Municipal Bacterial Food-Poisoning Laboratory during 2011-2015 were detected according to two version of Mi-crobiological Examination of Food (implementation on 2004-01-01 and 2016-06-01 respectively ) ,and the detection results were sta-tistically analyzed .Results Thirty-seven cases of bacterial food-poisoning(430 samples) occurred in Zhuhai City in the recent five years ,among which 22 cases(124 strains of pathogenic bacteria) were detected ,the cause detection rate of bacterial food-poisoning events was 59 .46% .The pathogenic bacteria causing bacterial food-poisoning were mainly vibrio parahaemolyticus (97 strains , 78 .23% ) and Staphyloccocus aureus (12 strains ,9 .68% ) .The sample detection rate of anal swabs was highest (77 strains ,62 . 10% ) ,followed by feces samples(17 strains ,13 .71% ) .The seasonality distribution was obviously concentrated in the third quarter (99 strains of pathogenic bacteria ,79 .84% ) and second quarter o (16 strains ,12 .90% ) .Conclusion Vibrio parahaemolyticus and Staphyloccocus aureus were the main pathogenic bacteria causing bacterial food-poisoning in Zhuhai City during these recent five years ,and the seasonality distribution was mainly concentrated in the second and third quarter .It is important to improve health awareness of the whole people and strengthen the surveillance and supervision and management work of food-borne pathogenic bac-teria during the food production ,processing and storage process in order to reduce the occurrence of food-poisoning .

Objective To evaluate the safety of new-generation of antidepressants and amitriptyline in the treatment of depression in patients with coronary heart disease (CHD). Methods A total of 194 patients with first-episode depression with CHD were divided into amitriptyline group(n=40), venlafaxine group(n=40), mirtazapine group(n=48)and escitalo?pram group(n=66). The blood routine test, liver function, blood lipids and blood glucose (GLU) were monitored after treat?ment for six weeks, and which were compared before and after treatment. Results The levels of white blood cells (WBC) and neutrophil count (NE) were significantly lower in amitriptyline group after 6-week treatment (P<0.05), but the levels of acid alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (T-CHO) and GLU were significant?ly increased after treatment than those before treatment (P<0.05). The levels of WBC, NE and GLU were significantly de?creased in venlafaxine group after 6-week treatment (P<0.05). The levels of ALT, AST, low density lipoprotein (LDL) were significantly increased in mirtazapine group after six-week treatment (P<0.05). In escitalopram group, the level of three ac?yl glycerin (TG) was significantly increased after six-week treatment than before treatment ( P<0.05). There was a signifi?cant difference in AST change after treatment between venlafaxine group and mirtazapine group (P<0.05). There was a sig?nificant decrease in WBC in amitriptyline group than that of mirtazapine group after six-week treatment ( P<0.05). There was a significant decrease in NE in amitriptyline group than that of mirtazapine group and escitalopram group ( P<0.05). The increase level of AST was significant higher in amitriptyline group than that of venlafaxine group (P < 0.05). Conclusion Three different kinds of new-generation of antidepressants have fewer influence in routine blood test, liver function, blood lipids and blood glucose than those of amitriptyline in the treatment of depression in patients with CHD.

Objective:To analyze the level diversifies of plasma CCL19 and CCL21 in the male drug users infected HCV.Methods: The plasma CCL19 and CCL21,anti-HCV and HCV RNA were detected by ELISA quantitation,ELISA qualitation and Real-time RT-PCR respectively.Compared with 60 healthy man,the level diversifies of plasma CCL19 and CCL21 in 391 male drug users conducted as part of HCV Surveillance Programme in Zhuhai were analyzed.Results: 180 of 391 male drug users were infected HCV and the infection rate was 46.04%.The level of plasma CCL19 and CCL21 in the male drug users[anti-HCV(-)/HCV RNA(-)] were higher than that in the healthy man (P≤0.001).The level of plasma CCL19 and CCL21 in anti-HCV(-)/HCV RNA(+) group was lower than that in the others(P≤0.05) .Compared with that in the healthy man,the level of plasma CCL19 and CCL21 in the drug abuse anti-HCV(+)/HCV RNA(-) group had significant deviation(P<0.05).Conclusion: Drug abuse can heighten the level of plasma CCL19 and CCL21 in man.Increasing the level of plasma CCL19 and CCL21 may conduce to spontaneous HCV clearance.It may prognosticate that HCV infection will be persistent and have a bad consequence when the level of plasma CCL19 and CCL21 were degraded.

Objective] To amplify,clone and express of a gene encoding hexose transporter of Plasmodium falcipuram(PfHT1) from Southern China isolate FCC1/HN for studing the immune of recombinant which protective from malaria parasite infection. [Methods] Cultivation of P.falciparum isolate FCC1/HN in vitro; extraction of genomic DNA from FCC1/HN using the alkali specific cleavage method; PCR amplification of PfHT1 and cloning into eukaryotic expression vector, pEGFPN3. The recombinant was introduced into mammalian cells, HEPG2 by using liposome\|mediated transfection. [Results] The gene encoding PfHT1 was specifically amplified from the genomic DNA of P.falciparum isolate FCC1/HN. The size of amplified fragment was 1 516 base pair. The eukaryotic expression recombinant, pN3\|HT1 , was constructed and expressed steadily in the hepatocarcinoma cell lines, HEPG2. [Conclusion] The gene encoding PfHT1 was successfully amplified and cloned. The pN3\|HT1/HEPG2 cell line was built for expressing fusion protein of GFP\|HT1.

The present study retrospectively analyzed 2 patients suffering from refractory pure red cell aplasia after major ABO-incompatible hematopoietic stem cell transplantation who received treatment in the Henan Institute of Haematology between April 2004 and February 2006. Patient 1 was a 25-year-old female with acute lymphocytic leukemia in second remission, and patient 2 was a 16-year-old gid with acute myeloid leukaemia in second remission. The two patients received a transplant of human adipose tissue-dedved mesenchymal stem cells (1.0×106/kg). Both of them acquired rapid recovery from pure red cell aplasia without any side effects. These findings suggest that adipose tissue-dedved mesenchymal stem cells seem to be a promising therapeutic option in patients with refractory pure red cell aplasia after ABO-incompatible hematopoietic stem cell transplantation, in whom conventional treatment fails.

To assess the efficacy of cotransplantation of haploidentical mesenchymal stem calls (MSC) and hematopoietic stem cells (HSC) in the treatment of refractory severe aplastic anemia, Two child patients with refractory severe aplastic anemia admitted to Henan Institute of Haematology from August 2002 to December 2007 were selected. Adipose tissue-derived MSCs (AMSCs) were separately originated from haploidentical mother and peripheral blood stem calls (PBSCs) from HLA-identical sibling brother or sister of patients. The patient 1 received a cotransplantation of PBSCs and AMSCs (1 × 106/kg) at a dose of 4.5 × 108 mononuclear calls/kg (containing 4.41 × 106 CD34+ calls/kg and 0.11 ×105 CD3+ cells/kg); the patient 2 received a second PBSCT at a dose of 6.5 × 108mononuclear cells/kg (containing 4.62×106 CD34+ cells/kg and 0.12×105 CD3+ cells/kg) and AMSC (1 × 108/kg) from his haploidentical mother. The results show that the cotransplantation was successful. During the two years of follow up, the two patients exhibited good condition, with no other treatment or transfusion dependence.

BACKGROUND: There is no consistently effective therapy for patients with steroid-refractory acute graft-versus-host disease (GVHD). A variety of alternative approaches have been tested, including antithymocyte globulin, mycophenolate mofetil (MMF), pentostatin, and monoclonal antibodies; however, these treatments have been only modestly successful. OBJECTIVE: To further evaluate the efficacy of human adipose-derived stem cells (ASCs) as the salvage therapy for steroid-refractory acute GVHD. DESIGN: A clinical trial.SETTING: Department of Haematology, Henan Institute of Haematology, Henan Tumor Hospital.PARTICIPANTS: The clinical trial was performed at the Henan Institute of Haematology from September 2002 to August 2005. Eight patients were treated with ASCs for grades Ⅲ-Ⅳ steroid-resistant acute GVHD. The study was approved by the Ethics Committee at Henan Tumor Hospital and informed consent was obtained from patients and ASCs donors before they enrolled.METHODS: Eight patients with steroid-refractory grades Ⅲ-Ⅳ acute GVHD received intravenous infusions of ASCs. The ASCs dose was 1.0×106/kg. Seven patients were treated once and one patients twice. Four patients received ASCs from haplo-identical family donors and four from unrelated mismatched donors. MAIN OUTCOME MEASURES: The efficacy of human ASCs as the salvage therapy for steroid-refractory acute GVHD. RESULTS: No side effects were noted after the ASCs infusions. Acute GVHD disappeared completely in seven of eight patients and six of these seven patients are still alive after the median follow-up of 30 months (range 11-90 months) after the initiation of ASCs therapy. All four surviving patients were in good clinical condition and in remission of their hematological malignancy. Two patients died-one with no obvious response to ASCs died of multiorgan failure and one of relapse of leukemia. CONCLUSION: These results suggest that ASCs is a very promising treatment for severe steroid-resistant acute GVHD.

BACKGROUND: The treatment of chronic myelogenous leukemia (CML) is revolutionized by the tyrosine kinase inhibitor imatinib mesylate (imatinib). However, resistance to imatinib is increasingly recognized as a clinical problem, the prognosis of patients who develop imatinib resistance is poor, particularly in acute transformation phase of leukemia.OBJECTIVE: To characterize a novel CML cell line and to further elucidate the mechanisms of resistance to STI571.DESIGN: An observational comparative experiment.SETTING: Henan Institute of Haematology, Henan Tumor Hospital.MATERIALS: Thirty female BALB/c nu/nu mice with 5 weeks old were purchased from Animal Center, Chinese Academy of Medical Sciences. STI571 was kindly provided by Novartis (Nuremberg, Germany). VP-16 was purchased from Bristol-Myers Squibb (Munich, Germany); anti-P-gp from Santa Cruz Company, USA; anti-ab1 from BD Biosciences Company, USA. The disposal of experimental animal was coincidence with the ethical standard.METHODS: The experiment was performed in the Henan Institute of Haematology from September 2003 to November 2005. A novel K562 cell line (K562/VP16) was achieved after exposure of the K562 cells to VP16. A small subpopulation (SP K562/VP16) that was capable of excluding Hoechst 33342 in the K562/VP16 cell line was isolated by flowcytometry sorting. The rest of the K562/VP16 cells were classified as non-SP K562/VP16. In order to elucidate the mechanisms involved in K562/VP16 SP cells which became resistant to STI571, the expression of multidrug-resistant gene 1 (MDR1), Bcr-Abl and P-gp was detected in K562, non-SP K562/VP16, or K562/VP16 SP calls, respectively. Furthermore, one thousand cells of K562, K562/VP16 SP and non-SP cells were injected,respectively, intraperitoneally into the right flanks of ten 5-week-old female BALB/c nu/nu mice. The same experiment was repeated twice.MAIN OUTCOME MEASURES: Comparison of STI571 resistance and oncogenicity of non-SP K562/VP16 and K562/VP16 SP cells.RESULTS: The MDR-1 gene expression of the Mr 170 000 P-gp was detected in K562/VP16 non-SP and K562/VP16 SP cells but not in K562 cells. The expression levels of P-gp in the two K562/VP16 cell lines were similar (P ＞ 0.05).The levels of Bcr-Abl and Abl proteins were similar in the K562 cell line and in non-SP K562/VP16 and K562/VP16 SP cells (P ＞ 0.05). Compared with non-SP K562/VP16, the K562/VP16 SP cells were more resistant to STI571, and this resistance could hardly be reversed by many multidrug resistance inhibitors. In addition, in vivo study showed that the K562/VP16 SP cells induced oncogenicity in mice, while the K562/VP16 non-SP cells failed to do so.CONCLUSION: Bcr/abl gene amplification and MDR1 overexpression may not be an important clinical mechanism in the diversity of resistance development to imatinib treatment, and the development of drug resistance by leukemia cells may be at least partly due to a rare SP cells which drives leukemia occurrence and maintenance. So, these SP cells need to be targeted for effective cancer therapy.

Objective: To describe the molecular epidemiological characteristics of norovirus gastroenteritis outbreaks in Zhuhai from 2011 to 2016. Methods: Anal swab specimens were collected from 576 cases with 56 outbreaks of acute norovirus gastroenteritis from 2011 to 2016. Specimens were tested by real-time RT-PCR. Three to four of norovirus positive specimens were selected from every outbreak to amplify the VP1 gene by RT-PCR and one strain was chosen randomly from every outbreaks to determine the genotype by phylogenetic tree analysis. Results: Eight genotypes were identified from 56 outbreaks and all of them belonged to GⅡ genogroup. The genotype of norovirus strain changed with prevalence time. The GⅡ.4/2006b was dominant from 2011 to 2012, and replaced by GⅡ.4/Sydney _2012 during the 2012—2013 norovirus season, and both of them never appeared after Feb. 2013. GⅡ.17 was the only genotype during the 2014—2015 norovirus season. All the 7 outbreaks occurred from 2015 to 2016 were caused by GⅡ.3 norovirus. The GⅡ.17and GⅡ.3 were identified from Apr. to Sep. 2016; GⅡ.p16-GⅡ.2 were the only genotype in 12 outbreaks from Nov. to Dec. 2016. The GⅠ genogrope was never identified from 2011 to 2016 in Zhuhai. Conclusions The Norovirus GⅡ was the only pathogeny which caused the outbreaks of norovirus gastroenteritis. The recombinant norovirus strain GⅡ.p16-GⅡ.2 emerged and caused large outbreaks in the last two months of 2016 in Zhuhai; several recombinant strains of the GⅡ.p16 RdRp gene were found now, which suggests that attention should be focused on the prevalence and evolution of the recombinant norovirus.