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1.
Hemosplenoperfusion (HSP) through the donor porcine spleen was used in complex treatment of 75 patients aged from 16 to 75 with pyo-septic complications of diseases and traumas of the abdominal cavity. The influence of HSP on the state of humoral immunity was estimated by the level of antibacterial antibodies to the antigens of E. coli, Ps. aeruginosa, Pr. mirabilis, St. aureus, Bact. fragilis, Bact. bifidum and antiendotoxin antibodies to glycolipid S. Minnesota RE 595, general cortical part of the lipopolysaccharide of Gram-negative bacteria. The use of HPS promoted the resolving of endogenous intoxication, elevation of the strain of humoral antibacterial immunity and is characterized by a reliable increase of the level of antibacterial antibodies in the dynamics of treatment.  相似文献   
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Background

Aneurysmal subarachnoid hemorrhage (aSAH) is an often devastating form of stroke. Aside from the initial hemorrhage, cardiac complications can occur resulting in neurogenic stress cardiomyopathy (NCM), leading to impaired cardiac function. We investigated whether aSAH patients with NCM had poorer long term functional outcomes than patients without NCM. Mortality, vasospasm, and delayed ischemic complications were also evaluated.

Methods

A retrospective study of all patients admitted for aneurysmal subarachnoid hemorrhage (aSAH) from January 2006 to June 2011 (n = 299) was conducted. Those patients who underwent an echocardiogram were identified (n = 120) and were assigned to the NCM (n = 49) category based on echocardiographic findings defined by a depressed ejection fraction (EF%) along with a regional wall motion abnormality (RWMA) in a non-vascular pattern. Primary outcome measures included in-hospital mortality and functional outcomes as measured by the Modified Barthel Index (mBI) at 3 months and one year. Secondary analysis determined if there was an association between NCM, cerebral vasospasm and delayed cerebral ischemia.

Results

16% of aSAH patients developed NCM. Mortality was higher (p < .001) in the NCM group (n = 23[46.9%]) than in the non-CM group (n = 28[11.2%]). Patients with NCM had poorer functional outcomes as measured by the mBI at both 3 months (p = .002) and 12 months (p = .014). The Hunt–Hess score was predictive of functional outcome as measured by the mBI at both 3 months (p = .002) as well as at 1 year (p = .014). NCM was associated with both death (p = .047 CI, 1.012–7.288) and vasospasm (p = .008 CI, 1.34–6.66) after correction for Hunt–Hess grade. Tobacco use (p < .001) and a history of diabetes mellitus (p < .009) were also associated with vasospasm. NCM was associated with higher in-hospital mortality (p = .047) in multivariate analysis.

Conclusion

NCM is seen in a substantial number of aSAH patients and when present, it is associated with higher mortality and poorer long-term functional outcomes. This finding may guide further prospective studies in order to determine if early recognition of NCM as well as optimization of cardiac output would improve mortality.  相似文献   
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The Microreader™ 23SP ID System is a novel STR kit, but there are no Mongolian data related to this kit. In this study, allelic frequencies and forensic parameters were obtained from 505 unrelated healthy Mongolians. These samples were amplified using the kit. The dataset successfully passed quality control after being submitted to STRidER (STRidER dataset reference STR000198). A total of 264 alleles were observed, with corresponding allelic frequencies ranged from 0.001 to 0.378. The combined power of discrimination (CPD) and combined probability of exclusion (CPE) of the 22 autosomal STR loci were 0.999999999999999999999999999217318 and 0.999999999776042, respectively. Furthermore, population differentiation comparisons involving previously reported groups were conducted.

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De novo intracerebral arteriovenous malformations (AVMs) are exceedingly rare with only seven reported cases in the literature. Although generally considered congenital by nature, the lesions do not manifest themselves clinically until the third or fourth decades of life. However, with the advent of improved imaging modalities and more frequent surveillance, an increasing number of de novo cases are being found challenging the concept AVMs develop in the perinatal/antenatal period. Alternatively, this phenomenon could represent a distinct entity in which lesion development occurs after birth. A PubMed search of “de novo cerebral arteriovenous malformation” was performed in which seven reported cases were found. The mean age at diagnosis was 14.7 years with a mean follow-up imaging study of 5.8 years. Lesion location was supratentorial in all previously described cases. This case involves an 18-year-old male with congenital hydrocephalus and seizures diagnosed at 7 months of age. The patient underwent a ventriculoperitoneal shunt and was followed frequently by a neurologist. The last diagnostic imaging was an unremarkable MRI of the brain at age 12. Seven years later, the patient presented with an intracerebral hemorrhage. A CT angiogram demonstrated a large brainstem AVM with an intraparenchymal hemorrhage and intraventricular extension. This case is unique in that it is the first infratentorial de novo AVM. The congenital nature of AVMs is challenged with the increasingly described series of patients with previously documented normal radiographic imaging. This suggests there may be a subset of patients genetically predisposed to postnatal development of AVMs.  相似文献   
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International Journal of Legal Medicine - A total of 550 individuals (265 males and 285 females) from Sierra Leone, a west-African coastal country, were genotyped using the Microreader™ 19X...  相似文献   
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Deleterious variants in the same gene present in two or more families with overlapping clinical features provide convincing evidence of a disease–gene association; this can be a challenge in the study of ultrarare diseases. To facilitate the identification of additional families, several groups have created “matching” platforms. We describe four individuals from three unrelated families “matched” by GeneMatcher and MatchMakerExchange. Individuals had microcephaly, developmental delay, epilepsy, and recessive mutations in TRIT1. A single homozygous mutation in TRIT1 associated with similar features had previously been reported in one family. The identification of these individuals provides additional evidence to support TRIT1 as the disease‐causing gene and interprets the variants as “pathogenic.” TRIT1 functions to modify mitochondrial tRNAs and is necessary for protein translation. We show that dysfunctional TRIT1 results in decreased levels of select mitochondrial proteins. Our findings confirm the TRIT1 disease association and advance the phenotypic and molecular understanding of this disorder.  相似文献   
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