Adolescent ; Fetus ; parasitology ; pathology ; Humans ; Male ; Teratoma ; parasitology ; pathology

Objective:To analyze the clinical characteristics of primary acute myeloid leukemia (AML) (non-M3 type) in children suffering from different levels of platelet count(PLT).Methods:In the Tumor Hospital of Zhengzhou University from January 2014 to December 2018, laboratory and clinical data of 247 de novo primary AML pediatric patients were retrospectively reviewed.According to the PLT before treatment, patients were divided into very low platelet group (VLG), low platelet group (LG) and non-lowing platelet group (NLG), with<50×10 9/L, ≥50×10 9/L but <125×10 9/L and ≥125×10 9/L as the boundaries.All patients were followed up until June 30, 2019.Meanwhile, the follow-up data was obtained by consulting medical records or by telephone.SPSS 17.0 software was applied for data analysis. Results:In general clinical features, a different group of hemoglobin (Hb) content, fusion gene AML- ETO and clinical risk stratification were statistically significant in different PLT groups ( χ2=11.270, 12.115 and 12.848, respectively, all P<0.05). However, the differences of other indicators in different groups of PLT were not statistically significant (all P>0.05). There were no statistically significant differences in terms of 3-year disease-free survival(DFS) rate (59.3%, 36.3%, 50.4%) among the 3 groups (all P>0.05). The median total survival(OS)time(40.5 months)and 3-year OS rate(41.0%) of NLG patients were significantly higher than those of VLG(23.1 months, 30.1%)and LG(14.1 months, 18.2%)patients, with statistically significant differences( χ2=7.798 and 6.553, respectively, all P<0.05). The univariate analysis of gender, white blood cell(WBC), Hb, PLT, lactic dehydrogenase(LDH), FLT3-ITD, NPM1, DNMT3A, CEPBA, C-KIT, AML-ETO, molecular genetic prognosis, complete remission(CR), and hemopoietic stem cell transplantation(HSCT) displayed that DNMT3A mutation was an adverse factor that affects patients′ OS ( χ2 =5.834, P<0.05), and the positive factors that influences OS were non-reducing PLT before treatment, and obtaining CR and subsequent HSCT ( χ2=7.798, 79.168, and 31.337, respectively, all P<0.05). Multi-factor analysis revealed that the independent protective factors that affect patients′ OS were the non-reducing PLT before treatment, and obtaining CR and subsequent HSCT( Wald=42.760, 15.918, and 10.183, respectively, all P<0.05). Conclusions:Before treatment, non-reducing PLT is a protective factor for primary childhood AML patients, and the prognosis is satisfying.

AIM: To investigate the relationships between antiproliferative mechanisms of probucol and protein expressions of signaling molecules ERK1/2, MKP-1, HO-1 and Trx-1 in rat aortic smooth muscle cells (RASMCs) stimulated with ox-LDL. METHODS: The effects of probucol on cell cycle, cell proliferation and the expressions of ERK1/2, MKP-1, HO-1 and Trx-1 in the presence of ox-LDL were observed by means of MTT test, FCM and Western blotting. RESULTS: (1) Probucol significantly inhibited the proliferation of RASMCs stimulated with ox-LDL. A value in 100 μmol/L probucol+35 mg/L ox-LDL group was reduced by 34.9% as compared to ox-LDL group (P<0.01). (2) Probucol protected against ox-LDL-induced RASMCs proliferation through inducing cell growth arrest at G_0/G_1 phase and cell apoptosis. (3) ox-LDL increased the expression of p-ERK1/2 by 34.7% (P<0.01) and decreased MKP-1 by 60.0% (P<0.01), respectively, as compared to control. Probucol attenuated the increase in ox-LDL-stimulated p-ERK1/2 level by 15.7%, but increased MKP-1 expression by 2 times (P<0.01). (4)ox-LDL at concentration of 35 mg/L decreased the intracellular Trx-1 expression by 28.9% (P<0.05), and slightly increased the level of HO-1 expression as compared to control (P<0.05). Probucol enhanced the expression of Trx-1 by 91.6% (P<0.01) and HO-1 by 31.9% (P<0.01), respectively as compared to ox-LDL group. CONCLUSION: Probucol inhibits ox-LDL-stimulated the proliferation of RASMCs through increases in MKP-1/HO-1 expression, suppression of cell cycle progression and induction of cell apoptosis.

Epilepsy is a complications of brain injury or stroke,and is a common diseases in reha-bilitation or neurology department.Transcranial magnetic stimulation as a classical treatment means for stroke or brain injury,but also can promote the recovery of epilepsy.However,there is no clear clinical re-port for safety of epilepsy patients use both donepezil and transcranial magnetic stimulation .The article re-views the literature.Clinicians maybe provided some help.

OBJECTIVETo introduce a method by reversed ulnar fasciocutaneous flap incised form the ulnar side of the fifth metacarpal area for repairing the soft tissue defect of the fifth finger.

METHODSFrom May 2001 to September 2001, ten patients with the soft tissue defects of the thenar side, dorsal side or ulnar side of the fifth finger were treated with the reversed ulnar fasciocutaneous flap incised from the fifth metacarpal area. The axial line of the flap was the line from ulnar side of the head of the fifth metacarpal bone to the pisiform level. The revolving point of the flap pedicle was 0.5-1 cm near the proximal end of the metacarpal-phalangeal joint.The area of the flap was form 5.0 cm x 3.5 cm to 1.5 cm x 1.0 cm.

RESULTSAll flaps of the ten cases were alive. 5-7 months followed-up show that, after operation, the flap present sensation in 6-12 mm, with soft texture and good appearances.

CONCLUSIONSThe advantages of this operative method were as follows: the reversed ulnar fasciocutaneous flap of the fifth metacarpal area have reliable blood supply, it was easily dissected and with good texture. So far this kind of flap is a good choice in repairing the soft tissue of the fifth finger.

Adolescent ; Adult ; Fascia ; transplantation ; Female ; Finger Injuries ; surgery ; Humans ; Metacarpal Bones ; surgery ; Middle Aged ; Reconstructive Surgical Procedures ; Soft Tissue Injuries ; surgery ; Surgical Flaps ; Young Adult

Objective To investigate drug resistance genes and epidemic characteristics of β-lactamase carried by carbapenem-resistant Acinetobacter baumannii (CRAB) in the respiratory intensive care unit(RICU) in a hospital.Methods Clinically isolated CRAB from RICU patients in October-December 2015 were collected.Five drug resistance genes (KPC-2,IMP,VIM,NDM-1,OXA-23) were specifically amplified by polymerase chain reaction (PCR),amplified products were performed agarose gel electrophoresis and sequencing analysis,the homology was analyzed with pulsed-field gel electrophoresis (PFGE).Results A total of 22 CRAB strains were isolated in October-December 2015,19 (86.36％) of which were isolated from sputum.The resistance rate of 22 CRAB strains to compound sulfamethoxazole was 59.09 ％,resistance rate to minocycline was 9.09 ％,all were sensitive to polymyxin B,resistance rates to other antimicrobial agents were more than 80％.Three kinds of resistance genes KPC-2,IMP and NDM-1 were not found by PCR amplification,positive rates of VIM and OXA-23 were both 100％.PFGE homology analysis revealed that 22 strains were divided into 13 different types,each type contained 1-5 strains,9 types(69.23％) contained only 1 strain respectively,the other 4 types (30.77％) contained 2-5 strains.A5,A7,and A8;A9,A11,A14,A19 and A22;A4,A10 and A12;A16 and A18 were of the same type respectively.Conclusion The main types of β-lactamase-resistant genes of CRAB in RICU are VIM and OXA-23.Homology analysis shows a small parts are of the same clone strains,which reveals epidemic of a small scale.

Studies concerning the association between arsenic exposure and hepatitis B virus (HBV) infection have been lacking.The present study aimed to examine the association between total urinary arsenic (TUA) and infection of HBV.A total of 5186 participants from National Health and Nutrition Examination Survey (NHANES) 2003-2014 were included in the analysis.We used logistic regression to evaluate the association.We defined two measures of TUA.TUA1 was the sum of arsenous acid,arsenicacid,monomethylarsonic acid and dimethylarsenic acid.TUA2 was defined as TUA minus arsenobetaine and arsenocholine.The results showed that the weighted overall prevalence of HBV infection was 6.08％.For NHANES 2003-2014,the medians (interquartile range) of TUA1 and TUA2 were 5.60 μg/L (3.97-8.09 μg/L) and 4.91 μg/L (2.36-9.11 μg/L),respectively.Comparing the highest quartile to the lowest quartile after multivariable adjustment showed that the odds ratios (ORs) and 95％ confidence intervals (CIs) for TUA1 and TUA2 were 2.44 (1.40-4.27) and 2.84 (1.60-5.05),respectively.In conclusion,elevated urinary arsenic was associated with the risk of HBV infection.Further studies,especially prospective studies,are needed to confirm the causal relationship between arsenic exposure and HBV infection.

The purpose of this study was to determine the combined effect of transmyocardial laser revascularization (TMLR) and the implantation of endothelial progenitor cells (EPCs) on cardiac function of ischemic hearts in canines. The left anterior descending artery (LAD) was occluded to establish the canine model of acute myocardial infarct (AMI). Four weeks later, the animals were randomly divided into four groups: TMLR group, in which transmyocardial laser-induced channels were established at the ischemic region; EPCs+TMLR group, in which EPCs were locally transplanted into laser-induced channels at the ischemic region; EPCs group, in which the EPCs were injected into the ischemic region; control group, in which the AMI animals received neither TMLR nor EPCs. The peripheral blood (50 mL) was sampled in all groups. Mononuclear cells from the peripheral blood were separated and cultured to obtain spindle-shaped attaching (AT) cells in vitro. AT cells were labeled with 1, 1'-dioctadecyl-1 to 3,3, 3',3'-tetramethyl-indocarbocyanine perchlorate (DiI) before injecting into the laser-induced channels or ischemic region. Four weeks after the first operation, TMLR was performed in the TMLR group and EPCs+TMLR group, and at the same time, the EPCs originating from the AT cells were mixed with calcium alginate (CA). Then the EPCs-CA composites were implanted into myocardial channels induced by laser in the EPCs+TMLR group, and into the myocardial infarct area in the EPCs group. All dogs underwent echocardiography at second month after LAD occlusion. Finally the samples of myocardium around the LAD were subjected to histochemical and immunohistologic examinations. The results showed there was no significant difference in the diameter of left atrium and ventricle before treatment among all groups (P>0.05). Eight weeks after modeling, the regional contractility in the LAD territory in the EPCs+TMLR group was increased as compared with control group and TMLR group, but there was no significant difference between control group and TMLR group. Neoangiogenesis was observed in the EPCs+TMLR group, and the fibrosis was seen in the TMLR group. There was no significant difference in neoangiogenesis around the channels induced by laser among EPCs+TMLR, EPCs and TMLR groups. It was concluded that TMLR combined with EPCs could improve the regional and global cardiac function in AMI, and augment neovascularizaiton in channels of ischemic myocardium induced by laser.

OBJECTIVETo recognize the importance of analyzing the result of immunohistochemical staining correctly.

METHODReview of the three misdiagnosed cases lymphoma and exploring the causes of misdiagnosis through reviewing their clinics, histopathology and immunohistochemistry.

RESULTSCase 1 of lymphocyte rich classical Hodgkin's lymphoma (LRCHL) was misdiagnosed as follicular lymphoma (FL) initially, the RS cells were overlooked morphologically and wrongly determined BCL-2 and CD20-positive cells as tumor cells immunohistochemically; also once misdiagnosed as nodular lymphocyte predominant Hodgkin's lymphoma (NLPHL) because the CD20-negative RS misjudged cells as the positives. Case 2 of AML tumor cells expressed TdT, CD7 and CD43 unspecifically, which misdiagnosed as T-cell lymphoblastic lymphoma (T-LBL). Case 3 of type B1 thymoma was misdiagnosed as T-LBL, because CK wasn't expressed satisfactorily resulting in neglecting neoplastic epithelial cells, and lymphocytes in the background were TdT and CD99-positive.

CONCLUSIONThe diagnosis of lymphoma should be based on morphology, immunohistochemistry, clinics, and genetics. Moreover, the correct judgment of immunohistochemical staining is essential to make right diagnosis.

Adult ; Diagnostic Errors ; Female ; Humans ; Immunohistochemistry ; Lymphoma ; diagnosis ; Male ; Middle Aged

The present study was to determine the effect of c-SRC on the viability of human cervical cancer HeLa cells and the expression of phosphorylated signal transducer and activator of transcription-3 (p-STAT3) of the cell. Post-transfection of c-SRC RNA interference vector, RT-PCR and Western blot were utilized to observe the contents of c-SRC mRNA and protein, respectively, in HeLa cells. The MTT was used to observe the viability of the cells. Cell cycle was observed by flow cytometry. The content of p-STAT3 in the cells was also investigated after knockdown of c-SRC. Knockdown of c-SRC significantly decreased the contents of c-SRC mRNA and protein in the cells. The viability of the cells decreased by 23.1%, 29.3%, 38.6% and 45.0% (all P < 0.05), respectively, after the cells were transfected with c-SRC RNA interference vector for 24, 48, 72, and 96 h. The number of S-phase cells decreased by 5.6%, 10.0%, 15.2% and 19.9% (all P < 0.05), respectively, after transfection of c-SRC RNA interference vector for 24, 48, 72, and 96 h. The content of p-STAT3 also decreased when c-SRC was knockdowned. Compared with the control group, after treatment of HeLa cells with STAT3 inhibitor Piceatannol for 24, 48, 72, and 96 h, the cell viability decreased by 23.8%, 29.7%, 37.3% and 45.4% (all P < 0.05), respectively, while increase of c-SRC content could not reverse the inhibitory effect. These results suggest that the inhibited viability of HeLa cells caused by knockdown of c-SRC is associated with the decreased content of p-STAT3 protein.
Cell Survival ; Female ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Genes, src ; genetics ; HeLa Cells ; Humans ; Phosphorylation ; RNA, Messenger ; biosynthesis ; genetics ; STAT3 Transcription Factor ; genetics ; metabolism ; Transfection