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Incidences of preterm birth <32 gestational weeks (adjusted odds ratio, 35.75; 95% confidence interval, 3.46-368.82) were higher in the poor prognosis group than that in the favorable group. Endometriosis and artificial reproductive techniques were both associated with 19% of all cases of SHiP.
SHiP was associated with maternal death and poor fetal prognosis. Prematurity and persistent uterine contractions which might be misdiagnosed as placental abruption seem to contribute to poor fetal prognosis.
SHiP was associated with maternal death and poor fetal prognosis. Prematurity and persistent uterine contractions which might be misdiagnosed as placental abruption seem to contribute to poor fetal prognosis.
This study aimed to investigate geographical differences in the clinical features of Guillain-Barré syndrome (GBS) between patients from our region in Eastern China and patients from other areas.
A total of 595 patients fulfilling the diagnostic criteria for GBS or its variants were included from two large hospitals located in Eastern China. Data collection included demographics, antecedent events, clinical presentation and signs, electrophysiological subtypes, treatment, complications during hospitalization, clinical severity at nadir, and outcome at 12months, and these data were compared to data from a study conducted in Southern China and the Europe/Americas section of the International GBS Outcome Study.
The median (interquartile range) age of patients was 50(36-61)years, the ratio of men to women was 1.2, and 49% of patients had antecedent events. Patients in our region of Eastern China had pure motor predominant GBS (158/340, 46%) and 30% (103/340) had complications during hospitalization. Patients aged over 60years had a lower frequency of antecedent infections and single, axonal subtypes, but higher disability scores at entry, nadir, and 12months. When compared with the Europe/Americas data, our patients had a lower frequency of antecedent infection (46% vs. 63%), cranial nerve involvement (43% vs. 49%), sensory deficits (45% vs. 69%), pain (19% vs. see more 57%) and mechanical ventilation (11% vs. 17%), but a higher frequency of axonal subtype (35% vs. 6%). There was a higher frequency of patients with antecedent gastroenteritis (16% vs. 8%), mechanical ventilation (11% vs. 8%) and axonal subtypes (35% vs. 19%) in our region in Eastern China than in Southern China.
Patients with GBS in Eastern China showed significant clinical heterogeneity and differences when compared to other geographic areas.
Patients with GBS in Eastern China showed significant clinical heterogeneity and differences when compared to other geographic areas.BCR-ABL1 gene fusion associated with additional DNA lesions involves the pathogenesis of chronic myelogenous leukemia (CML) from a chronic phase (CP) to a blast crisis of B lymphoid (CML-LBC) lineage and BCR-ABL1+ acute lymphoblastic leukemia (BCR-ABL1+ ALL). The recombination-activating gene RAG1 and RAG2 (collectively, RAG) proteins that assemble a diverse set of antigen receptor genes during lymphocyte development are abnormally expressed in CML-LBC and BCR-ABL1+ ALL. However, the direct involvement of dysregulated RAG in disease progression remains unclear. Here, we generate human wild-type (WT) RAG and catalytically inactive RAG-expressing BCR-ABL1+ and BCR-ABL1- cell lines, respectively, and demonstrate that BCR-ABL1 specifically collaborates with RAG recombinase to promote cell survival in vitro and in xenograft mice models. WT RAG-expressing BCR-ABL1+ cell lines and primary CD34+ bone marrow cells from CML-LBC samples maintain more double-strand breaks (DSB) compared to catalytically inactive RAG-expressing BCR-ABL1+ cell lines and RAG-deficient CML-CP samples, which are measured by γ-H2AX. WT RAG-expressing BCR-ABL1+ cells are biased to repair RAG-mediated DSB by the alternative non-homologous end joining pathway (a-NHEJ), which could contribute genomic instability through increasing the expression of a-NHEJ-related MRE11 and RAD50 proteins. As a result, RAG-expressing BCR-ABL1+ cells decrease sensitivity to tyrosine kinase inhibitors (TKI) by activating BCR-ABL1 signaling but independent of the levels of BCR-ABL1 expression and mutations in the BCR-ABL1 tyrosine kinase domain. These findings identify a surprising and novel role of RAG in the functional specialization of disease progression in BCR-ABL1+ leukemia through its endonuclease activity.Recent studies demonstrated reduced hippocampal volumes in elderly healthy individuals who are cognitively normal but poor sleepers. The association between sleep quality and the pattern of volume loss across hippocampal subfields (HSs) is not well known. Thus, it is the focus of the present study. Sleep quality was self-assessed using the Pittsburgh Sleep Quality Index (PSQI). The HS volumes were measured using sub-millimetre in-plane resolution T2-weighted magnetic resonance imaging data. A total of 67 cognitively normal elderly individuals aged 60-83 years were classified into 30 normal sleepers with a PSQI less then 5 and 37 poor sleepers with a PSQI ≥5. The two groups were equivalent in age, gender distribution, ethnicity, education attainment, handedness and cognitive performance. Compared to normal sleepers, poor sleepers exhibited significantly lower normalised volumes in the left cornu ammonis field 1 (CA1), dentate gyrus (DG) and subiculum. In contrast, there were no significant differences in normalised grey and white matter volumes between the two groups. The global PSQI was negatively associated with the normalised volumes of the left CA1, DG and subiculum. Sleep duration was associated with the normalised volumes of the bilateral CA1, DG, left CA2 and subiculum. Verbal memory scores were associated with the left CA1 volume. In conclusion, poor sleep quality, especially insufficient sleep duration, was associated with volume loss in several HSs that are involved in specific learning and memory tasks. As the hippocampus does not regulate sleep, it is more likely that poor sleep leads to small hippocampi. Thus, based on this assumption, improving sleep quality of poor sleeper elderly individuals could benefit hippocampal health.
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