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Moges S. Ido Michael R. Frankel Ike S. Okosun Richard B. Rothenberg 《The American journal of emergency medicine》2018,36(2):262-265
Introduction
Intravenous alteplase reduces disability and improves functionality among acute ischemic stroke patients. Two decades after its approval, only a small fraction of patients get the treatment, and demonstrating its impact on mortality may make a strong case for its wider use. This study assessed the impact of thrombolytic treatment by alteplase on 1-year mortality and readmission among acute ischemic stroke patients.Method
The 2008–2013 Georgia Coverdell Acute Stroke Registry data were linked with the 2008–2013 hospital discharge and the 2008–2014 death data in Georgia. Multiple imputation was applied; a propensity score measuring the probability of receiving intravenous alteplase was calculated and used for matching. A conditional logistic regression was applied to compare 1-year mortality and readmission among propensity score matched pairs.Results
Overall, 20.3% of 9620 acute ischemic stroke patients died and 22.4% were readmitted in one year. The multivariable regression result showed that patients who did not receive IV alteplase had a 1.49 (95%CI: 1.09–2.04; p-value = 0.01) times higher odds of dying at one year than those who were treated with the thrombolytic agent. Among patients discharged home, no statistically significant difference was documented in the odds of being readmitted at least once within 365 days post-stroke discharge.Discussion and conclusion
After accounting for patient differences and missing value, intravenous alteplase is associated with reduction in long-term mortality. The results of this study suggest that patients who are identified as eligible for intravenous alteplase need to be offered the treatment. 相似文献94.
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Xu Zhang Chen Zhang Zhiguo Wu Zuowei Wang Daihui Peng Jun Chen Wu Hong Chengmei Yuan Zezhi Li Shunying Yu Yiru Fang 《Journal of affective disorders》2013
Background
A growing body of evidence highlights the existence of shared genetic susceptibility to both major depressive disorder (MDD) and bipolar disorder (BD), suggesting some potential genetic overlap between the disorders. Genome-wide association studies have identified consistent association of single nucleotide polymorphisms of the α-1 C subunit of the L-type voltage-gated calcium channel gene (CACNA1C) with MDD and BD, suggesting CACNA1C as a promising candidate gene for susceptibility to mood disorders. In the present study, we tested the association of CACNA1C with MDD and BD in Han Chinese.Methods
We genotyped three potentially functional polymorphisms in 635 MDD patients, 286 BD patients and 730 normal, control patients.Results
The genotype frequencies of SNP rs1051375 showed statistically significant differences between the BD and control groups (P=0.005). At the allele level, the difference of G allele frequency of rs1051375 between BD patients and control subjects was also significant (P=0.011; OR=1.30, 95% CI: 1.06–1.58). We found that GG genotype of rs1051375 carriers had a lower age at onset than those with the AG or AA genotype, and the mean±standard deviation ages at onset of GG, AG and AA carriers were 24.04±4.22, 25.76±4.75 and 25.78±4.33 years, respectively. Neither genotype nor allele frequencies of the three polymorphisms were found to be significantly different between the MDD patients and control subjects.Limitations
The relative small sample size in BD group should be considered a limitation of this study.Conclusions
Our initial findings support a potential association of CACNA1C as a genetic risk factor for BD susceptibility. 相似文献97.
Background
Although evidence suggests that there are neurobiological differences between unipolar depression in younger versus older adults, conflicting evidence exists about whether these manifest as clinically identifiable differences.Method
We conducted a systematic review of aetiological, phenomenological and outcome studies to examine the evidence for a distinction between early onset (EOD) and late onset (LOD) depression. A literature search was completed using the computer databases MEDLINE, EMBASE, PSYCHINFO and PUBMED for papers published between January 1982 and December 2012 which compared groups with EOD and LOD. Studies were included if they were of older people and compared symptoms, aetiological factors or outcomes. We conducted a quality assessment of included articles.Results
We identified 23 articles which met entry criteria. The only clinical feature which was different between the groups was a higher frequency of a family history of mood disorders in EOD.Limitations
The number of studies identified was low and their quality was generally poor.Conclusions
Although neurobiological studies have reported differences between EOD and LOD, generally these do not appear to translate into identifiable distinguishing clinical features. 相似文献98.
99.
We compared the growth of 183 children with short stature (≤ 2SD) and 73 children of
normal height at age six who were visiting the Tanaka Growth Clinic. We classified these
short children as suffering from either idiopathic short stature (ISS, n = 119), GH
deficiency (GHD, n = 33) or small-for-gestational-age short stature (SGASS, n = 31) on the
basis of subsequent test results and other factors. We also conducted a retrospective
study of changes in their height, wt and nutritional intake over time. The mean changes in
height SD score from birth to 6 yr were –0.24 SD in normal height children with a normal
birth length and +2.27 SD in normal height children with a low birth length. In short
children, these changes were –1.93 SD for children with ISS, –2.41 SD for those with GHD
and +0.58 for those with SGASS. The mean changes from birth to 6 mo were –0.84 SD, −1.03
SD and +0.38 SD in children with ISS, GHD and SGASS, respectively. The mean change in
height SD score from birth to age 1 yr was –1.07 SD, –1.44 SD and +0.35 SD, respectively.
The decrease in height SD score from birth to 6 mo accounted for 43.5% of the decrease in
height SD score from birth to 6 yr in children with ISS and it accounted for 42.6% of the
decrease in children with GHD. Only 19% of short children bottle-fed well, and 53% fed
poorly, as opposed to 56% and 16% of normal height children who fed well and poorly,
respectively. Post weaning, only 22% of short children ate well, and 56% fed poorly, as
opposed to 53% and 17% of normal height children who fed well and poorly, respectively.
These findings demonstrated that growth failure started from early infancy in ISS and GHD
children. It was suggested that poor nutritional intake in infancy and early childhood was
a partial cause of short stature at age 6. 相似文献
100.