OBJECTIVE: To delineate laboratory and clinical characteristics of a case with chronic myelogenous leukemia (CML) and co-occurrence of t(9;22)(q34;q11) and t(8;21)(q22;q22). METHODS: The patient was subjected to cytogenetic, molecular, morphological and immunophenotypic analyses. RESULTS: Cytogenetic analysis revealed presence of t(8;21)(q22;q22) in addition to t(9;22)(q34;q11) in the patient. Chimeric BCR/ABL and AML1/ETO genes were detected by fluorescence in situ hybridization (FISH). Transcripts of BCR/ABL210 and AML1/ETO fusion genes were detected by relative quantity PCR. Morphological study suggested that the patient was at the chronic phase of CML. No significant immunophenotypic abnormality was detected by flow cytometry. CONCLUSION Co-occurrence of t(8;21)(q22;q22) and t(9;22)(q34;q11) is rare in CML. Only 5 similar cases have been described previously. This case suggested that chromosomal alterations may precede morphological, flow cytometric and clinical changes and accelerate progression of the disease.
Chromosome Aberrations ; Chromosomes, Human ; Fusion Proteins, bcr-abl ; Humans ; In Situ Hybridization, Fluorescence ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; genetics ; Translocation, Genetic

Objective To analyze and summarize the imaging features of hepatic epithelioid hemangioendothelioma (EHE).Methods The retrospective and descriptive study was conducted.The clinicopathological data of 9 patients with EHE who were admitted to the Cancer Hospital of Chinese Academy of Medical Sciences between June 2012 and June 2016 were collected.Patients underwent computed tomography (CT) and magnetic resonance imaging (MRI) examinations.Number,size,location,shape,density or signal and enhancement method of lesions,with or without lesions fusion and relationship between lesions and vessels were analyzed by 2 imaging doctors.Lesions in left lobe of liver,right lobe of liver and caudate lobe of liver were respectively counted.Real number was a standard as less than 5 lesions and more than or equal to 5 lesions was represented as ≥ 5.Observation indicators:(1) overall imaging features of EHE;(2) MRI findings of EHE;(3) CT findings of EHE;(4) treatment and pathological features of EHE and results of follow-up.Patients received the corresponding treatment after imaging examinations.Follow-up using outpatient imaging examinations was performed to detect tumor recurrence and stable condition of patients up to December 2016.Results (1) Overall imaging features of EHE:of 9 patients with EHE,6 received plain and enhanced scans of MRI,3 received plain and enhanced scans of CT (1 combined with MRI),1 received enhanced scan of CT.Lesions in right lobe of liver were more than that in left lobe of liver,and there were fewest lesions in caudate lobe of liver.Lesions were round or similar-round shape,with a maximum diameter of 2.5-6.1 cm and an average diameter of 3.6 cm.Four patients had total 2-5 lesions and less than 5 lesions in each lobe of liver,without lesions fusion,including 1 with halo sign and capsule retraction sign and 1 with halo sign.Of other 5 patients,2 had more than or equal to 5 lesions in each lobe of liver and 3 had more than or equal to 5 lesions in 2 lobes of liver;4 had halo sign,lollipop sign,capsule retraction sign and a tendency of lesions fusion,1 had halo sign and capsule retraction sign.The halo sign,lollipop sign,capsule retraction sign and a tendency of lesions fusion were 7/9,4/9,6/9 and 4/9 in 9 patients,respectively.(2) MRI findings of EHE:6 patients received plain and enhanced scans of MRI.① Four patients had clearhalo sign on T2 weighted imaging (T2WI),in portal vein phase and hepatobiliary phase.Three patients had slightly central hyperintensity and thick ring of slightly peripheral hyperintensity on T2WI.There were slightly central hyperintensity and thin ring of slightly peripheral hypointensity in 1 patient,and the halo sign was seen by enhanced scan.There were central hyperintensity and peripheral hypointensity in 2 patients,and the halo signs were clearly seen in hepatobiliary phase.Some patients were combined with multiple manifestations.② There were no obvious halo sign on T2WI,annular enhancement in arterial phase by enhanced scan,no obvious halo sign in portal vein phase and hepatobiliary phase in 2 patients.There were hypointensity on T1WI and isointensity-hyperintensity on DWI in 6 patients.(3) CT findings of EHE:plain scan of CT in 4 patients showed slightly hypodense shadow,without calcification.Enhanced scan of CT in 3 patients showed that obvious halo-like enhancement was seen in portal vein phase and halo rings were less obvious than that by MRI examination.(4) Treatment and pathological features of EHE and results of follow-up:of 9 patients with EHE,4 underwent surgical resection based on lesions ≤5 and surgical specimens were detected by pathological examination,5 underwent interventional treatment and pathologic examination with biopsy.Gross specimen examination showed that lesions were solid and stiff,with greyish white section plane and infiltrative margin.Tumor cells consisted of epithelioid cells under the microscopy,without atypia and with rare mitotic figures,and vacuoles were seen in cytoplasm.Immunohistochemistry showed CD31 and CD34 were positive.Nine patients were followed up for 6-54 months.During the follow-up,4 patients with surgery had no recurrence and 5 patients with interventional therapy remained stable condition.Conclusions Imaging manifestations of hepatic EHE are the more typical when lesions of EHE became more.Hepatic EHE has a tendency of lesion fusion,halo sign,capsule retraction sign and lollipop sign.Imaging manifestations on T2WI with fat suppression,in portal vein phase and hepatobiliary phase are helpful to improve the diagnosis of hepatic EHE.

AIM:To explore the roles of Akt ( also called protein kinase B ) and active caspase-3 in the leptin-mediated chronic morphine antinociceptive tolerance in rats .METHODS: A model of chronic morphine antinociceptive tolerance was established in the SD rats .The protein levels of spinal Akt and cleaved caspase-3 were tested by Western blotting.The technique of immunohistochemical staining was used to detect the immunoreactivity positive cells of phospho -rylated ( p)-Akt and cleaved caspase-3 in the spinal cord .Double staining of immunohistochemistry was used to examine the cellular location of the p-Akt and cleaved caspase-3 positive cells.RESULTS: The chronic intrathecal injection of morphine (15 μg) for 7 d markedly upregulated the spinal protein levels of p-Akt and cleaved caspase-3 in the rats.Thirty min before injection of morphine , intrathecal injection of leptin antagonist (3μg) for 7 d significantly attenuated the upreg-ulation of the protein levels of p-Akt and cleaved caspase-3 induced by chronic morphine treatment .The p-Akt was exclu-sively observed in the spinal neurons .The cleaved caspase-3 was only localized with the spinal astrocytes .Intrathecal injec-ting the inhibitors of leptin , Akt and caspase-3 ameliorated the chronic antinociceptive tolerance .CONCLUSION: The spinal Akt pathway and active caspase-3 are involved in the leptin-mediated chronic morphine antinociceptive tolerance in rats.

[ ABSTRACT] AIM:To investigate the role of ATP-sensitive potassium ( KATP ) channels in the inhibitory effect of hydrogen sulfide ( H2 S) on high glucose ( HG)-induced inflammation mediated by necroptosis in H 9c2 cardiac cells. METHODS:The expression levels of receptor-interacting protein 3 ( RIP3; an indicator of necroptosis ) and cyclooxyge-nase-2 (COX-2) were determined by Western blot.The levels of interleukin-1β(IL-1β) and tumor necrosis factor-α( TNF-α) were detected by ELISA .RESULTS:After H9c2 cardiac cells were treated with 35 mmol/L glucose ( HG) for 24 h, the expression of RIP3 was significantly increased .Pre-treatment of the cells with 100 μmol/L diazoxide ( DZ; a KATP channel opener) or 400 μmol/L NaHS (a donor of H2S) for 30 min considerably blocked the up-regulation of RIP3 induced by HG.Moreover, pre-treatment of the cells with 100 μmol/L 5-hydroxydecanoic acid (5-HD; a KATP channel
blocker) attenuated the inhibitory effect of NaHS on HG-induced up-regulation of RIP3.On the other hand, co-treatment of the cells with 100μmol/L necrostatin-1 ( a specific inhibitor of necroptosis ) or pre-treatment of the cells with 100 μmol/L DZ or 400 μmol/L NaHS attenuated HG-induced inflammatory responses , evidenced by decreases in the expression of COX-2 and secretion levels of IL-1βand TNF-α.However , pre-treatment of the cells with 100 μmol/L 5-HD significantly attenuated the above anti-inflammatory effects of NaHS.CONCLUSION:KATP channels play an important role in the inhib-itory effect of H2 S on HG-induced inflammation mediated by necroptosis in H 9c2 cardiac cells.

Aim To investigate the role of the interac-tion between necroptosis ( Nec ) and p38 mitogen-acti-vated protein kinase ( MAPK) pathway in the high glu-cose (HG)-induced H9c2 cardiac cells injury.Meth-ods The cell viability was measured by cell counter kit-8 assay .The intracellular level of reactive oxygen species ( ROS ) was tested by DCFH-DA stating fol-lowed by photofluorography .Mitochondrial membrane potential ( MMP) was detected by Rhodamine 123 stai-ning followed by photofluorography . The expression levels of receptor interaction protein 3 ( RIP3, an indi-cator of Nec ) and p38 MAPK protein were tested by Western blot assay .Results The treatment of H9c2 cardiac cells with 35 mmol? L-1 glucose ( high glu-cose, HG) for 24 h induced considerable injuries , in-cluding a decrease in cell viability , increases in ROS generation as well as MMP loss .The co-treatment of the cells with 100 μmol? L-1 necrostatin-1(Nec-1,a specific inhibitor of Nec ) and HG for 24 h or the pre-treatment of the cells with 3 μmol? L-1 SB 2 0 3 5 8 0 ( an inhibitor of p38MAPK) for 60 min before HG exposure attenuated the above injuries induced by HG .Moreo-ver, the treatment of the cells with HG for 1,3,6,9, 12 ,24 ,36 and 48 h significantly increased the expres-sion levels of RIP3, peaking at 24 h.The co-treatment of the cells with 100 μmol? L-1 Nec-1 or the pre-treatment of the cells with 3 μmol? L-1 SB203580 considerably blocked the up-regulation of RIP3 expres-sion induced by HG .On the other hand , the co-treat-ment of the cells with 100 μmol? L-1 Nec-1 alleviated the HG-induced up-regulation of the expression of p-p38MAPK.Conclusion The interaction between Nec and p38 MAPK pathway mediates the HG-induced inju-ry in H9c2 cardiac cells.

AIM:Tostudywhe ther theangiotens in-(1-7)[Ang-(1-7)]/Mas receptor axis protects cardio-myocytes against high glucose (HG)-induced injury by inhibiting nuclear factor-κB (NF-κB) pathway.METHODS:The cell viability was measured by CCK-8 assay.The intracellular levels of reactive oxygen species ( ROS) were detected by DCFH-DA staining .The number of apoptotic cells was tested by Hoechst 33258 nuclear staining .Mitochondrial membrane potential ( MMP) was examined by JC-1 staining.The levels of NF-κB p65 subunit and cleaved caspase-3 protein were de-termined by Western blotting.RESULTS: Treatment of H9c2 cardiac cells with 35 mmol/L glucose (HG) for 30, 60, 90, 120 and 150 min significantly enhanced the levels of phosphorated ( p) NF-κB p65, peaking at 60 min.Co-treatment of the cells with 1 μmol/L Ang-(1-7) and HG for 60 min attenuated the up-regulation of p-NF-κB p65 induced by HG. Co-treatment of the cells with Ang-(1-7) at concentrations of 0.1~30μmol/L and HG for 24 h inhibited HG-induced cy-totoxicity, evidenced by an increase in cell viability .On the other hand, 1 μmol/L Ang-(1-7) ameliorated HG-induced apoptosis, oxidative stress and mitochondrial damage , indicated by decreases in the number of apoptotic cells , cleaved caspase-3 level, ROS generation and MMP loss .However, the above cardioprotective effects of Ang-(1-7) were markedly blocked by A-779, an antagonist of Ang-(1-7) receptor (Mas receptor).Similarly, co-treatment of H9c2 cardiac cells with 100 μmol/L PDTC ( an inhibitor of NF-κB) and HG for 24 h also obviously reduced the above injuries induced by HG.CONCLUSION:Ang-(1-7)/Mas receptor axis prevents the cardiomyocytes from the HG-induced injury by inhibiting NF-κB pathway .

Objective:To analyze the effect of endoscopic submucosal tunnel dissection on patients with large esophageal superficial neoplasms.Methods: Chosen patients with large esophageal superficial neoplasms in our hospital as research object, randomly divided into control group treated by endoscopic mucosal dissection (ESD) and observation group treated by endoscopic submucosal tunnel dissection(ESTD), compared surgery related indicators, complications and treatment outcomes.Results: 1)Observation group patients’ tumor stripping rate (23.17±4.73)/min was significantly higher than control group patients’ (12.65±2.19)/min; Intraoperative blood loss(9.14±0.67)ml, total length of hospital stay (7.34±1.89) d, were significantly less than control group patients with intraoperative blood loss(21.38±3.14)ml, total length of hospital stay (13.21±3.05)d, t value was 4.965, 5.395, 4.932, respectively(t=4.965,t=5.395,t=4.932;P<0.05); 2)Observation group patients esophageal bleeding ESTD rate(5.26%), esophageal stricture rate(31.58%), mediastinal emphysema rate(5.26%), esophageal perforation rate of 0, were significantly less than control group patients with esophageal bleeding rate(31.58%), esophageal stricture rate(5.26%), mediastinal emphysema rate(21.05%), esophageal perforation rate (26.32%), t value were 4.378, 4.378, 4.471, 5.758, (t=4.378,t=4.378,t=4.471,t=5.758;P<0.05); 3)Observation group patients with no recurrence during the follow-up period, control group patients with local recurrence rate of 21.05%, t value 8.623,P<0.05(t=8.623, P<0.05).Conclusion: Endoscopic tunnel mucosal stripping technique can effectively improve the complete tumor removal rate, during the process of optimization operation at the same time reduce the occurrence of complications, to the improvement of the prognosis of patients with positive clinical significance.

AIM:To investigate the roles of ATP-sensitive potassium ( KATP ) channels in high glucose-induced cardiac injury and the inhibitory effect of hydrogen sulfide ( H2 S) on the cardiomyocyte injury.METHODS:The expres-sion level of KATP channel protein was tested by Western blot.The cell viability was measured by CCK-8 assay.The number of apoptotic cells was observed by Hoechst 33258 nuclear staining.Mitochondrial membrane potential ( MMP) was exam-ined by JC-1 staining.RESULTS:After the H9c2 cells were treated with 35 mmol/L glucose ( high glucose, HG) for 1~24 h, the protein level of KATP channel was significantly reduced at 6 h, 9 h, 12 h and 24 h, reaching the minimum level at 12 h and 24 h.Pretreatment of the cells with 400μmol/L NaHS ( a donor of H2 S) prior to exposure to HG for 12 h con-siderably blocked the down-regulation of KATP channels induced by HG.Pretreatment of the cells with 100 μmol/L mito-chondrial KATP channel opener diazoxide, 50μmol/L non-selective KATP channel opener pinacidil or NaHS obviously inhibi-ted HG-induced injuries, leading to an increase in the cell viability, and decreases in the number of apoptotic cells and the MMP loss.Pretreatment with 100μmol/L mitochondrial KATP channel antagonist 5-hydroxydecanoic acid or 1 mmol/L non-selective KATP channel antagonist glibenclamide attenuated the above cardioprotective effects of NaHS.CONCLUSION:KATP channels mediate the inhibitory effect of H2 S on HG-induced cardiac injury.

Objectives To investigate the risk factors of cardiorenal syndrome type 1 (CRS1) in patients with acute myocardial infarction (AMI).Methods The medical date of hospitalized patients with AMI from January,2013 to February,2014 in Hunan Provincial People~ Hospital were reviewed.A total of 265 patients with AMI was divided into CRS1 and non-CRS1 groups.The univariate comparison and multivariate Logistic regression analysis were performed to obtain the CRS1 risk factors.Results In the 265 AMI patients,CRS1 was found in 59 patients (22.3％).Age,history of diabetes,Killip classification,left ventricular ejection fraction (LVFF),baseline serum creatinine,blood urea nitrogen,uric acid,baseline evaluated glomerular filtration rate (eGFR),serum sodium,the left anterior descending artery lesion,emergency percutaneous coronary intervention (PCI),β-blocker,and angiotensin converting enzyme inhibitor/angiotensin receptor antagonist (ACEI/ARB) were statistically different between CRS1 and non-CRS1 groups (all P ＜ 0.05).Multivariate logistic regression showed that age,history of diabetes,Killip classification,reduced LVEF,reduced eGFR,hyponatremia,the left anterior descending artery lesionn,emergency PCI non-undergo,and β-blocker non-use were independent risk factors for CRS1 after AMI.Conclusions CRS1 is a common complication in AMI patients,which is associated with many factors.Our data suggest that patients with AMI should be more comprehensively assessed and monitored,thereby preventing the occurrence of CRS1.

Objective To analyse clinical application of hepatitis B virus core antibody(HBcAb)detected by using the chemilu-minescence microparticle immunoassay.Methods A total of 1 6 830 specimen with positive HBcAb detected by using the two pairs of semi-hepatitis test from January 2012 to November 2014 were collected,and divided into three groups according to the cut off in-dex(COI)of detection results of HBcAb,including group 1.0-<9.0,group 9.0-<1 1.0 and group COI≥1 1.0,and detection re-sults were statistically analysed.The hepatitis B virus(HBV)DNA test was carried out in specimen with negative hepatitis B surface antigen(HBsAg)and hepatitis B surface antibody (HBsAb)and COI≥1 1.0.Results The detection rate of HBsAg(+)HBsAb(-) (13.84%)was significantly higher than other expression patterns in group ≥1 1.0(P <0.05).There was no statistically significant differences in positive rate among all expression patterns of HBsAg and HBsAb in the group 9.0-<1 1.0(P >0.05).The detec-tion rate of HBsAg(+)HBsAb(-)of group 9.0-<1 1.0 was significantly lower than that of the other two groups(P <0.05).A total of 304 specimen were HBsAg(-)HBsAb(-)and COI≥1 1,among them 64 specimen were HBV DNA postive and the posi-tive rate was 21.0%.Conclusion In the detection of HBcAb,COI≥1 1 and 1.0-<9.0 could be reference indicators for diagnosiing current and past HBV infection respectively,which should be combined with other laboratory indicators of HBV clinical data for comprehensive analysis.