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Objective To investigate the dynamic changes of soluble fms-like tyrosine kinase 1 (sFlt-1),Amylase (AMY) and high sensitvie C reactive protein (hs-CRP) in the early diagnosis of acute pancreatitis (AP) and its clinical significance.Methods 72 patients with AP were selected and divided into mild group (n =45) and severe group (n =27).Another 30 healthy subjects in the same period were selected as control group (n =30).Serum sFlt-1 levels were measured by enzyme-linked immunosorbent assay (ELISA) on the 1st,3rd and 7th day after admission.Acute Physiology and Chronic Health Evaluation Ⅱ (APACHE Ⅱ) score was used to assess acute physiology and chronic health status,and AMY and hsCRP levels were measured.Results Serum levels of sFlt-1,AMY and hs-CRP in the severe group were significandy higher than those in the mild group on the 1 st,3rd and 7th day after admission (all P ＜ 0.01).The levels of sFlt-1,AMY and hs-CRP in the mild group were significantly higher than those in the control group (all P ＜ 0.01).The scores of APACHE Ⅱ in the severe group were significantly higher than those in the mild group on the 1st,3rd and 7th day after admission (all P ＜ 0.01).There was a positive correlation between serum sFlt-1 level and AMY,hs-CRP,APACHE Ⅱ scores on the first day of admission (respectively r =0.738,P =0.00;r =0.563,P =0.000;r =0.233,P =0.028),on the third day of admission (respectively r =0.622,P =0.000;r =0.584,P =0.000;r =0.218,P =0.032),on the seventh day of admission (respectively r =0.593,P =0.000;r =0.547,P =0.000;r =0.227,P =0.030).Receiver operating characteristic (ROC) curve analysis showed that the area under the curve (AUC) of serum sFlt-1,AMY and hs-CRP were 0.918 (95％ CI:0.865-0.971,P =0.000),0.948 (95％ CI:0.908-0.989,P=0.000) and 0.789 (95％ CI:0.696-0.882,P=0.000),respectively.Conclusions The level of sFlt-1 in peripheral blood is significantly increased in patients with AP,which is closely related to the severity of AP.Dynamic monitoring of serum sFlt-1,AMY and hs-CRP has important clinical value in the diagnosis,treatment,severity and prognosis of AP.
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[Objective] To analyze the frequency,type of chromosome 1 clonal abnormalities in hematologic malignancies,and to understand the clinical and biological significance of its occurrence.[Methods] Retrospectively analyzed of 256 cases of patients with hematologic malignancies cytogenetic R banding karyotype analysis [Results].Summarized the abnormal chromosomel karyotype and clinical data summary and combined with literature review.Results There were 25 samples with clonal disorder of chromosome 1 in 256 cases of patients with malignant hematologic disease,accounting for 9.8 percent of the total samples,including ALL-L2,ANLL-M2,MDS,MM,lymphoma with bone marrow involvement,CML with accelerated phase and blast crisis,plasma cell leukemia and chronic myelogenous monocytic leukemia.The types of the clonal disorder included chromosome 1 translocation with other chromosomes[including 3cases with t(1;19),and 2 cases with t(1;4)],there were 7 cases with chromosome 1 the increase or missing partly, and 7cases with increasing a full or partial deletion of chromosome 1,and also 3 cases with isochromosome of 1q.t(1 ; 19) can be found in B lymphocyte proliferative diseases,while t(1;14) was found in T-ALL.The clinical efficacy and short survival were found in 20 patients with chromosome 1 clonal abnormalities. [Conclusion] Chromosome I clonal abnormalities in hematologic malignancies is common in acute leukemia,MDS,MM,and atypical abnormality is more than typical abnormality.It is common in chromosome 1 translocation with other chromosomes,lq-trisomy.The recurrent chromosome abnormalities is t (1;19) and t (1;14),which is related with the leukemia immune phenotype.lq-trisoiny and amplification of 1q21 is effective in the therapy and guide the prognosis of MDS and MM.
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In order to supply some reference about the construction of network course of physiology, we summed up the establishing experience from the course design, construction and application.
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Researches have shown that melatonin is neuroprotectant in ischemia/reperfusion-mediated injury. Although melatonin is known as an effective antioxidant, the mechanism of the protection cannot be explained merely by antioxidation. This study was devoted to explore other existing mechanisms by investigating whether melatonin protects ischemia/reperfusion-injured neurons through elevating autophagy, since autophagy has been frequently suggested to play a crucial role in neuron survival. To find it out, an ischemia/reperfusion model in N2a cells was established for examinations. The results showed that autophagy was significantly enhanced in N2a cells treated with melatonin at reperfusion onset following ischemia and greatly promoted cell survival, while autophagy blockage by 3-MA led to the shortened N2a cell survival as assessed by MTT, transmission electron microscopy, and laser confocal scanning microscopy. Besides, the protein levels of LC3II and Beclin1 were remarkably increased in ischemia/reperfusion-injured N2a in the presence of melatonin, whereas the expression of p-PKB, key kinase in PI3K/PKB signaling pathway, showed a decrease when compared with untreated subjects as accessed by immunoblotting. Taken together these data suggest that autophagy is possibly one of the mechanisms underlying neuroprotection of melatonin.
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Objective To observe the alteration of coagulation function in the patients with stage Ⅲ～Ⅳ non-Hodgkin lymphoma and evaluate its clinical significance. Methods 62 patients with NHL and 20 healthy examiners were studied. The parameters of PT, APTT, TT and FIB in blood plasma were detected.Results The levels of APTT and FIB in NHL group were significantly higher than that in control group (P 0.05).Conclusion The NHL patients especially ⅢB～ⅣB patients usually accompany with abnormal coagulation function and hypercoagnlable states, and it' s necessary to monitor their coagulation function.
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Objective To compare the efficacy and adverse effects of 5 days' and 7 days' course of combination chemotherapy regimen HA in the treatment of chronic phase of chronic myelogenous leukemia (CML-CP). Methods 18 cases of CML-CP had received 5 days' course of combination chemotherapy regimen HA including homoharringtonine 4 mg/d and cytarabine 200 mg/d for 5 days. At the same time,another 18 patients diagnosed as CML-CP who were given 7 days' course of HA regimen including homoharringtonine 4 mg/d and cytarabine 200 mg/d for 7 days were compared on the efficacy including peripheral white blood cells, spleen size and cytogenetic responses and adverse effects. Results The complete remission(CR) rate was 50.0 % and 61.1 % in 5 days' and 7 days' treated groups, respectively (P >0.05). The incidence of severe bone marrow suppression in 7 days' group(16.7 %) was higher than that in 5 days' group(0)(P <0.05). Conclusion The 5 days' course of combination chemotherapy HA regimen is same as 7 days' course of HA regimen about their curative effects in CML-CP. But the incidence of severe bone marrow suppression in 7 days' group(16.7 %) was higher than that in 5 days' group (0).
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To investigate the role of mitochondria in neuronal apoptosis, ischemia-reperfusion mediated neuronal cell injury model was established by depriving of glucose, serum and oxygen in media. DNA fragmentation, cell viability, cytochrome C releasing, caspase3 activity and mitochondrial transmembrane potential were observed after N2a cells suffered the insults. The results showed that N2a cells in ischemic territory exhibited survival damage, classical cell apoptosis change, DNA ladder and activation of caspase3. Apoptosis-related alterations in mitochondrial functions, including release of cytochrome C and depression of mitochondrial transmembrane potential (deltapsim) were testified in N2a cells after mimic ischemia-reperfusion. Moreover, activation of caspase3 occurred following the release of cytochrome C. However, the inhibitor of caspase3, Ac-DEVD-CHO, couldn't completely rescue N2a cells from apoptosis. Administration of cyclosporine A, an inhibitor of mitochondria permeability transition pore only partly inhibited caspase3 activity and reduced DNA damage. Interestingly, treatment of Z-IETD-FMK, an inhibitor of caspase8 could completely reverse DNA fragmentation, but can't completely inhibit caspase3 activity. It was concluded that there were caspase3 dependent and independent cellular apoptosis pathways in N2a cells suffering ischemia-reperfusion insults. Mitochondria dysfunction may early trigger apoptosis and amplify apoptosis signal.