ObjectiveTo investigation the clinical features and immunophenotypes of mantle cell lymphoma (MCL).MethodsThe clinical data of 23 patients of MCL were reviewed prospectively.Age,sex,Ann-Arbor staging,symptoms and bone marrow biopsies were analyzed.Serum lactat dehydrogenates (LDH) level,CD5,CD20 and CyclinD1 were determined.ResultsThe median age was 62 years old (range 44-74),15 patients(65.2％)were more than 60 years old.Among 23 patients,the male-to-female ratio was 4.4∶1,Twenty-one patients (91％) presented with advanced stage (Ann Arbor stage Ⅲ 12 cases and Ⅳ 9 cases) at initial diagnosis.Twenty patients (87.0 ％) were lymph node involvement.The serum LDH level was high in 11 patients.CD5 was positively expressed in 14 (60.8 ％) of all patients.CD20 was positively expressed in 21 (91.3 ％) of all patients.Cyclin D1 was over-expression in 19 (82.6 ％) of all patients.ConclusionThe MCL shows a predilection for occurrence in older males.The majority of patients are advanced stage disease (Ann Arbor stage Ⅲ/Ⅳ ) are at initial diagnosis. Most of patients display lymph node involvement manifestations.Bone marrow infiltration is frequent.The immunophenotype of MCL resembles the mature B-lymphocyte (CD+20),with coexprssion of the T-cell antigen CD5.It has been demonstrated that CyclinD1 are over express in this histotype of MCL.CyclinDl over-expression could be considered as hallmark of MCL.

Aim: To determine whether the inhibition of K-80003-activated p-ERK could potentiate the anticancer effect of K-80003 in vitro and in vivo. Methods: The effects of K-80003 in combination with the MEK inhibitor cobimetinib on ERK activation and tumor cell apoptosis in breast cancer cells were detected by Western blot and immunohistochemical staining in MCF-7 breast cancer cells and MMTV-PyMT mammary transgenic mice. Results: K-80003 activation of ERK in MCF-7 breast cancer cells and in MMTV-PyMT mammary transgenic mice was strongly inhibited by co-treatment with cobimetinib. The co-treatment also resulted in a strong induction of apoptosis and inhibition of the growth of tumor cells in vitro and in animals, as compared with K-80003 alone. It was detected that K-80003 in combination with cobimetinib synergistically inhibited the growth of MMTV-PyMT tumor strongly, suggesting that K-80003 activation of ERK serves as an escape mechanism by which tumor cells develop resistance to K-80003 treatment. Conclusion: An attractive approach is identified to enhance the therapeutic effect of K-80003 and to overcome potential resistance associated with the K-80003 therapy.

Child ; Congresses as Topic ; Forecasting ; Humans ; Internationality ; Pediatrics

The aim was to investigate the effect of particle size on transfection efficiency of chitosan (CS)-based nanoparticles. Nanoparticles were synthesized through complex coacervation CS with plasmid DNA (pDNA). Three kinds of pDNA/CS nanoparticles with different sizes (250, 580 and 1300 nm) were prepared by altering the adding rate and the vortexing time. The particle size, zeta potential and the stability in cultural medium were evaluated by zetasizer. The association efficiency was determined by spectrofluorophotometer. The combination of chitosan with pDNA as well as the ability to protect pDNA from nuclease degradation was analyzed by gel electrophoresis. The transfection efficiency of pDNA/CS nanoparticles in HEK293 cells was investigated by flow cytometry. Using CS grafted fluorescein isothiocyanate as a fluorescent marker, the adsorption features of the nanoparticles were visualized by fluorescence microscopy and the cellular uptake percent was quantitated by flow cytometry. The internalization process of the nanoparticles was visualized by confocal laser scanning microscopy (CLSM) using nanoparticles of the size of 250 nm. Results showed that the three kinds of pDNA/CS nanoparticles had no differences in zeta potential, association efficiency, protection ability, stability and transfection efficiency in HEK293. The nanoparticles were all adsorbed on cell surface in the form of aggregates, and similar cellular uptake percent as well as quantities were observed 4 h post-incubation with HeLa cells. CLSM images showed that the aggregates below 2 microm could be internalized by endocytosis. These results suggest that the transfection efficiency of pDNA/CS nanoparticles does not depend on particle size in the range from 250 nm to 1300 nm.
Chitosan ; administration & dosage ; chemistry ; metabolism ; DNA ; administration & dosage ; Endocytosis ; Genetic Vectors ; HeLa Cells ; Humans ; Nanoparticles ; Particle Size ; Plasmids ; Transfection

OBJECTIVETo investigate the role of vascular endothelial growth factor (VEGF) in the pathogenesis of severe acute pancreatitis (SAP) in rats.

METHODSSixty-four male SD rats were randomly divided into control group and SAP group, and in the latter group, SAP was induced by retrograde injection of 5% sodium taurocholate in the pancreaticobiliary duct. The rats were sacrificed at 1, 3, 6 and 12 h after the operation, and the severity of pancreatitis was assessed according to histological scoring. The serum levels of VEGF were examined with enzyme-linked immunosorbent assay, and the expression of VEGF in the pancreatic tissues was measured by SP immunohistochemistry. Another 30 SD rats were randomized into the control group, SAP group and SAP+recombinant rat VEGF injection group, and the vascular permeability of the pancreatic microcirculation was determined by Evans Blue leakage test.

RESULTSAt each of the time points for measurement, both the serum VEGF level and scores of pancreatic tissue injury were significantly higher in SAP group than in the control group (P<0.05). Compared with the control group, the expressions of VEGF in the pancreatic tissues of SAP group were significantly up-regulated following the operation (P<0.05). The vascular permeability of the pancreatic microcirculation significantly increased after the onset of SAP, and injection of recombinant rat VEGF significantly increased the leakage rate of Evans Blue.

CONCLUSIONVEGF may play an important role in the pathogenesis of pancreatitis and in causing edema and hemorrhage in SAP, and the level of serum VEGF may reflect the severity of pancreatic injury.

Acute Disease ; Animals ; Biomarkers ; Capillary Permeability ; physiology ; Male ; Pancreatitis ; metabolism ; pathology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Vascular Endothelial Growth Factor A ; blood

OBJECTIVETo study the effects of methyl protodioscin on the [Ca2+]i and the ATPase activity in cardiomyocytes, as well as their mechanisms.

METHODThe cardiomyocytes were randomly divided into three groups, the control group treated with no serumal DMEM, the MPD group treated with MPD and the dilthiazem group treated with dilthiazem. Fluorospectrophotometer was used to determined the level of myocardial cell intracellular Ca2+ [Ca2+]i. In the experiment of ATPase activity on cellular membrane, the cardiomyocytes were randomly divided into two groups, the control group treated with no serumal DMEM, the MPD group treated with MPD. The activity of Na+-K+-ATPase,Ca2+-Mg2+-ATPase and Mg2+-ATP ATPase were determined. The quantitative analysis of SERCA2a mRNA expression was studied by RT-PCR that the groups and treatments in cardiomyocytes same as the experiment for ATPase activity assay.

RESULTUnder the quiescent condition, compared to the control group, the level of [Ca2+]i in cardiomyocytes of the MPD group and dilthiazem group was no different. After treatment with 40 mmol x L(-1) KCl, [Ca2+] was significantly lower in the MPD group and the dilthiazem group, and the intensity of peak value in time course of 60 s, the dilthiazem group and the MPD group also were lower than the control group (P < 0.001). Ca2+-Mg2+-ATPase and Na+-K+-ATPase in cultured rat were increased after treated with MPD compared to treatment with no serumal DMEM (P < 0.05, P < 0.01), but Mg2+-ATPase in these groups had no different. The expression of SERCA2a mRNA between the MPD group and the control group was no different. MPD could not up-regulated or down-regulated SERCA2a in endocytoplasmic reticulum.

CONCLUSIONMethyl protodioscin could block the volt dependent form calcium channel in cellular membrane, and up-regulate the function of sodium pump and calcium pump, so that it could remain low calcium in the internal environment in cardiomyocytes.

Animals ; Ca(2+) Mg(2+)-ATPase ; metabolism ; Calcium ; metabolism ; Calcium Channels ; drug effects ; Cell Membrane ; drug effects ; metabolism ; Cells, Cultured ; Diltiazem ; pharmacology ; Diosgenin ; analogs & derivatives ; pharmacology ; Enzyme Activation ; drug effects ; Female ; Male ; Myocytes, Cardiac ; drug effects ; metabolism ; Rats ; Rats, Sprague-Dawley ; Saponins ; pharmacology ; Sarcoplasmic Reticulum Calcium-Transporting ATPases ; metabolism ; Sodium-Potassium-Exchanging ATPase ; drug effects

OBJECTIVETo investigate the startup detail of circulation dysfunction and its role in the progress of delayed neuropsychologic sequelae (DNS) after carbon monoxide (CO) poisoning with comparison with the model of ischemia-reperfusion.

METHODSThe ischemia-reperfusion rat model was established by Pulsinelli-Brierley method, and the CO poisoning rats model by i.p. injected with CO repeatedly respectively, and the rats were identified with DNS following the experiment of pathology and the ethnology.

RESULTSThe whole blood viscosity, plasma viscosity, hematocrit and fibrinogen increased significantly immediately after reperfusion, and recovered gradually with the ischemia-reperfusion rat model. The whole blood viscosity decreased significantly immediately after CO treated i.p. Especially at low shear rate, the hematocrit also declined remarkably in the early stage after CO treatment. But 1day later, these parameters turned to the trend of the ischemia-reperfusion rats. There was a prominent elevation of both indexes until the 14th day following CO injection i.p.

CONCLUSIONThere are significantly sustained hyper-coagulation and hyper-viscosity with circulation in rats after CO poisoning compared with ischemia-reperfusion model during the period of DNS, which might contribute to increase cerebral circulation resistance, blocked blood flow, and deteriorate hypoxemia in progression of DNS.

Animals ; Blood Circulation ; Carbon Monoxide Poisoning ; physiopathology ; Disease Models, Animal ; Hemorheology ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; physiopathology

OBJECTIVETo investigate the protective effects of captopril against lung injury in a rat model of severe acute pancreatitis (SAP).

METHODSSeventy-two male SD rats were randomized into sham-operated group (SO group), SAP group and captopril intervention group (CAP group). Serum amylase and myeloperoxidase (MPO) activity in the lung tissue were examined at 1, 6 and 12 h after the operation. TNF-α and AngII in the lung tissue were detected by ELISA, and the histopathological changes of the pancreas and lung were observed microscopically.

RESULTSThe MPO activity , which was similar between SAP group and CAP group at 1 h, were significantly lowered in CAP group at 6 and 12 h (P<0.05). Serum amylase level and the levels of TNF-α and AngII in the lung tissue homogenate were all reduced significantly in CAP group as compared to those in SAP group (P<0.01). The pathological injury of the lung was obviously lessened in CAP group in comparison with that in SAP group.

CONCLUSIONCaptopril can ameliorate SAP-induced lung injury in rats.

Amylases ; blood ; Angiotensin II ; metabolism ; Animals ; Captopril ; pharmacology ; therapeutic use ; Disease Models, Animal ; Lung ; metabolism ; pathology ; Lung Injury ; etiology ; prevention & control ; Male ; Pancreatitis ; complications ; drug therapy ; Peroxidase ; metabolism ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; metabolism

Acute Lung Injury ; metabolism ; virology ; Adult ; Disease Outbreaks ; Extravascular Lung Water ; metabolism ; Humans ; Influenza A Virus, H1N1 Subtype ; pathogenicity ; Influenza, Human ; metabolism ; virology ; Male ; Respiratory Distress Syndrome, Adult ; metabolism ; virology