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Objective:To investigate the risk factors for hemorrhagic transformation (HT) in patients with acute posterior circulation ischemic stroke (PCIS) and its impact on outcomes.Methods:From July 2016 to October 2019, patients admitted to the Department of Neurology, the People's Hospital of Zhengzhou and diagnosed as PCIS were enrolled retrospectively. Their demography, clinical data, laboratory and imaging findings were collected. HT was defined as no intracranial hemorrhage detected by the first head CT/MRI after onset, and intracranial hemorrhage was found during head CT/MRI reexamination within 10 d after onset. Symptomatic HT was defined as intracranial hemorrhage indicated by imaging reexamination and the National Institutes of Health Stroke Scale (NIHSS) score was higher than the baseline. The outcome was evaluated by the modified Rankin Scale at 3 months after onset, and >2 were defined as poor outcome. Multivariate logistic regression analysis was used to identify the independent risk factors for HT, symptomatic HT, and poor outcomes. Results:A total of 242 patients with PCIS were enrolled. Their age was 68.02±12.0 years, and 111 were females (45.9%). The baseline median NIHSS score was 5.9 (interquartile range: 3.1-8.8). HT occurred in 19 patients (7.9%), and 14 of them (73.7%) were symptomatic HT. Follow-up at 3 months showed that 74 patients (30.58%) had poor outcomes, of which 12 died. Multivariate logistic regression analysis showed that higher baseline systolic blood pressure (odds ratio [ OR] 1.076, 95% confidence interval [ CI] 1.021-1.135, P=0.006; OR 1.161, 95% CI 1.087-1.240, P<0.001) and larger infarct volume ( OR 31.293, 95% CI 4.542-215.592, P<0.001; OR 2.084, 95% CI 1.414-3.073, P<0.001) were the independent risk factors for HT and symptomatic HT. The higher NIHSS score ( OR 1.511, 95% CI 1.307-1.746; P<0.001), diabetes mellitus ( OR 2.041, 95% CI 1.054-3.952; P=0.034) and symptomatic HT ( OR 4.514, 95% CI 1.458-13.979; P=0.009) were the independent risk factors for poor outcomes. Conclusions:HT is rare in patients with PCIS. Higher baseline systolic blood pressure and larger infarct volume are the independent risk factors for HT in patients with PCIS. Higher baseline NIHSS scores, diabetes mellitus, and symptomatic HT are the independent risk factors for poor outcomes in patients with PCIS.
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Objective To investigate the occurrence law of autophagy in trophoblast cells from preeclampsia and its underlying mechanisms.Methods Twenty cases of placenta tissues were collected from women suffered from preeclampsia and normal pregnant women respectively.Autophagosome of trophoblast cells were observed by transmission electron microscope.The expressions of LC3-Ⅱ/Ⅰ and Atg4B in placenta tissues were detected by western blot and real-time PCR.Results Compared with the control group,typical autophagosomes of trophoblast cells were observed by transmission electron microscope.The ratio of LC3-Ⅱ / Ⅰ in placenta of PE patients was increased (1.43 ± 0.23) compared with control group (0.59 ±0.12),and the expression of Atg4B was up-regulated in both mRNA [(1.73 ±0.16) folds] and protein levels (0.71 ± 0.13) compared with control group (P ＜ 0.05).Conclusions Autophagy was significantly up-regulated in trophoblast cells from patients suffered from preeclampsia.Thus,all the data suggest that autophagy might be involved in the generation of preeclampsia.
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Myelodysplastic/myeloproliferative uclassifiable (MDS/MPN-U) is a rare myeloid neoplasm characterized by myelodysplasia and myeloproliferation at the time of initial presentation, which is usually a diagnosis of exclusion. The molecular pathogenesis of MDS/MPN-U patients remains to be elucidated. Among five patients diagnosed with MDS/MPN-U, three patients harboured RUNX1 (AML1) mutations; one carried somatic mosaicism of RUNX1 mutation with JAK2(V617F) mutation and one had dual RUNX1 and FLT3-internal tandem duplication mutations with progression to acute myeloid leukaemia (AML). Germline mutation of TP53 was detected as a sole genetic lesion in one patient. JAK2(V617F) and somatic mosaicism of KRAS and TET2 mutations co-existed in one patient. Otherwise, no alterations were detected in PTPN11, NRAS, CBL and ASXL1 genes. ETV6-PDGFRB fusion transcript was not detected in all patients. Four patients recieved haematopoietic stem cell transplantation (HSCT); three patients relapsed and one achieved complete remission after three donor lymphocyte infusions. Our findings suggest that the mutational spectrum observed in childhood MDS/MPN-U is quite different from that seen in juvenile myelomonocytic leukaemia and, to some extent, resemble chronic myelomonocytic leukaemia. Moreover, two patients had constitutional alterations of genes frequently found in AML. Further investigations are required to define the roles of these genetic alterations in the pathogenesis of childhood MDS/MPN-U.
