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OBJECTIVES: Introduction of the International Classification of Diseases, Tenth Revision (ICD-10) in 2015 was aimed for a more detailed classification of mortality statistics of diseases, such as classifying the anatomical locations for intracerebral hemorrhage (ICH). We aimed to describe the demographics and in-hospital mortality of specified ICH locations based on ICD-10 classification. MATERIALS AND METHODS: Patients with a principal diagnosis of spontaneous ICH in the United States, extracted from the Nationwide Inpatient Sample (NIS) from 2015 to 2018. Subgroups of ICH locations were analyzed individually for age, gender, ethnicity, in-hospital mortality, hospital length of stay (LOS), hospital cost, and EVD placement. RESULTS: During the study period, there were 408,285 ICH patients with a mean age of 66.28 (17.11) years, 52.09% male, mainly Intraventricular (21.87%) and cortical hemispheres (19.83%). Total ICH in-hospital mortality was 21.07%, while brainstem was associated with the highest in-hospital mortality (40.68%) followed by intraventricular (33.08%) and multiple localized locations (30.16%). The mean hospital length of stay was 9.56(14.10) days, and the mean hospital cost was $32,453.38(56,851.59). Intraventricular Hemorrhage had the highest hospital LOS 12.39(17.44) and the highest hospital cost $47,385.25(76,187.5). CONCLUSIONS: Our results characterized the demographics of ICH in the US with in-hospital mortality of one out of five patients. Detail breakdown of ICH locations can improve the mortality statistics and provide more information about the ICH locations with higher hospital expenses.

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It has been suggested that in environments where there is greater fear of litigation, resident autonomy and education is compromised. Our aim was to examine failure rates on American Board of Surgery (ABS) examinations in comparison with medical malpractice payments in 47 US states/territories that have general surgery residency programs. We hypothesized higher ABS examination failure rates for general surgery residents who graduate from residencies in states with higher malpractice risk. We conducted a retrospective review of five-year (2010-2014) pass rates of first-time examinees of the ABS examinations. States' malpractice data were adjusted based on population. ABS examinations failure rates for programs in states with above and below median malpractice payments per capita were 31 and 24 per cent (P < 0.01) respectively. This difference was seen in university and independent programs regardless of size. Pearson correlation confirmed a significant positive correlation between board failure rates and malpractice payments per capita for Qualifying Examination (P < 0.02), Certifying Examination (P < 0.02), and Qualifying and Certifying combined index (P < 0.01). Malpractice risk correlates positively with graduates' failure rates on ABS examinations regardless of program size or type. We encourage further examination of training environments and their relationship to surgical residency graduate performance.

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BACKGROUND: Our aim was to study pass rates of the American Board of Surgery (ABS) examinations for examinees from programs in the Southwestern Surgical Congress (SWSC) compared with the rest of the United States (Non-SWSC). METHODS: A retrospective review of pass rates of ABS Qualifying Examination (QE), Certifying Examination (CE), and QE/CE index from 2005 to 2015 was conducted. RESULTS: From 2005 to 2010, SWSC outperformed Non-SWSC in QE (88% vs 85%, P < .02), CE (86% vs 82%, P < .01), and QE/CE (77% vs 72%, P < .01). From 2010 to 2015, SWSC outperformed Non-SWSC in QE (91% vs 86%, P < .01) and QE/CE (77% vs 71%, P < .01) but did not achieve statistical significance in CE (83% vs 81%, P = .09). CONCLUSIONS: SWSC programs outperformed Non-SWSC across QE and CE in the early period, but only on QE in the late period. We encourage SWSC states and regional surgical societies to evaluate performance on ABS examinations and collaborate to improve surgical training.

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OBJECTIVE: A nondesignated preliminary surgery (NDPS) position encompasses 1 year of training provided by many general surgery residencies. Our aim was to assess factors predicting success and provide evidence for program directors to support career guidance to preliminary residents. METHODS: Retrospective cohort study of 221 NDPS residents who entered 5 university-based institutions were identified from 2009 to 2013. Records for trainees were reviewed. We defined primary success as obtaining a categorical position in the specialty of choice and secondary success as obtaining a categorical position in any specialty immediately after finishing their NDPS training. Statistical evaluation was performed using chi-square analysis, independent t-test and logistic regression using α <0.05. RESULTS: Of the 221 NDPS residents, 217 (98%) completed postgraduate year (PGY)-1 and 65 (29%) completed PGY-2. Totally, 90 (41%) obtained categorical general surgery positions, 89 (40%) obtained categorical positions in other specialties, and 42 (19%) failed to obtain a categorical position immediately after their NDPS years. Ultimately, 139 (63%) of residents achieved primary success and 40 (18%) additional residents obtained categorical positions in specialties other than their first choice, resulting in a total of 179 (81%) of residents obtaining categorical positions. Mean United States Medical Licensing Examination step 1 and step 2 scores for those who obtained secondary success were 227 and 234 vs. 214 and 219, respectively, for those who failed to secure a categorical position (p < 0.01). United States Medical Licensing Examination step 2 score was a significant predictor of primary (p < 0.03) and secondary success (p < 0.02). Of 65 PGY-2 NDPS residents, 32 (49%) achieved primary success, and 11 (17%) others achieved secondary success for a total of 43 (66%). For PGY-2 NDPS, American Board of Surgery In-Training Examination was the only significant predictor of primary and secondary success (p < 0.02 and p < 0.05). CONCLUSIONS: NDPS training provides a viable and successful opportunity for at least 81% of young physicians to pursue their career goals even after an unsuccessful first match.

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Ethanol exposure during pregnancy is an established cause of birth defects, including neurodevelopmental defects. Most adult neurons are produced during the second trimester-equivalent period. The fetal neural stem cells (NSCs) that generate these neurons are an important but poorly understood target for teratogenesis. A cohort of miRNAs, including miR-153, may serve as mediators of teratogenesis. We previously showed that ethanol decreased, while nicotine increased miR-153 expression in NSCs. To understand the role of miR-153 in the etiology of teratology, we first screened fetal cortical NSCs cultured ex vivo, by microarray and quantitative RT-PCR analyses, to identify cell-signaling mRNAs and gene networks as important miR-153 targets. Moreover, miR-153 over-expression prevented neuronal differentiation without altering neuroepithelial cell survival or proliferation. Analysis of 3'UTRs and in utero over-expression of pre-miR-153 in fetal mouse brain identified Nfia (nuclear factor-1A) and its paralog, Nfib, as direct targets of miR-153. In utero ethanol exposure resulted in a predicted expansion of Nfia and Nfib expression in the fetal telencephalon. In turn, miR-153 over-expression prevented, and partly reversed, the effects of ethanol exposure on miR-153 target transcripts. Varenicline, a partial nicotinic acetylcholine receptor agonist that, like nicotine, induces miR-153 expression, also prevented and reversed the effects of ethanol exposure. These data collectively provide evidence for a role for miR-153 in preventing premature NSC differentiation. Moreover, they provide the first evidence in a preclinical model that direct or pharmacological manipulation of miRNAs have the potential to prevent or even reverse effects of a teratogen like ethanol on fetal development.

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BACKGROUND: Ethanol is a potent teratogen. Its adverse neural effects are partly mediated by disrupting fetal neurogenesis. The teratogenic process is poorly understood, and vulnerable neurogenic stages have not been identified. Identifying these is a prerequisite for therapeutic interventions to mitigate effects of teratogen exposures. METHODS: We used flow cytometry and qRT-PCR to screen fetal mouse-derived neurosphere cultures for ethanol-sensitive neural stem cell (NSC) subpopulations, to study NSC renewal and differentiation. The identity of vulnerable NSC populations was validated in vivo, using a maternal ethanol exposure model. Finally, the effect of ethanol exposure on the ability of vulnerable NSC subpopulations to integrate into the fetal neurogenic environment was assessed following ultrasound guided, adoptive transfer. RESULTS: Ethanol decreased NSC mRNAs for c-kit, Musashi-1and GFAP. The CD24(+) NSC population, specifically the CD24(+)CD15(+) double-positive subpopulation, was selectively decreased by ethanol. Maternal ethanol exposure also resulted in decreased fetal forebrain CD24 expression. Ethanol pre-exposed CD24(+) cells exhibited increased proliferation, and deficits in cell-autonomous and cue-directed neuronal differentiation, and following orthotopic transplantation into naïve fetuses, were unable to integrate into neurogenic niches. CD24(depleted) cells retained neurosphere regeneration capacity, but following ethanol exposure, generated increased numbers of CD24(+) cells relative to controls. CONCLUSIONS: Neuronal lineage committed CD24(+) cells exhibit specific vulnerability, and ethanol exposure persistently impairs this population's cell-autonomous differentiation capacity. CD24(+) cells may additionally serve as quorum sensors within neurogenic niches; their loss, leading to compensatory NSC activation, perhaps depleting renewal capacity. These data collectively advance a mechanistic hypothesis for teratogenesis leading to microencephaly.

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Upstream events that trigger initiation of cell division, at a point called START in yeast, determine the overall rates of cell proliferation. The identity and complete sequence of those events remain unknown. Previous studies relied mainly on cell size changes to identify systematically genes required for the timely completion of START. Here, we evaluated panels of non-essential single gene deletion strains for altered DNA content by flow cytometry. This analysis revealed that most gene deletions that altered cell cycle progression did not change cell size. Our results highlight a strong requirement for ribosomal biogenesis and protein synthesis for initiation of cell division. We also identified numerous factors that have not been previously implicated in cell cycle control mechanisms. We found that CBS, which catalyzes the synthesis of cystathionine from serine and homocysteine, advances START in two ways: by promoting cell growth, which requires CBS's catalytic activity, and by a separate function, which does not require CBS's catalytic activity. CBS defects cause disease in humans, and in animals CBS has vital, non-catalytic, unknown roles. Hence, our results may be relevant for human biology. Taken together, these findings significantly expand the range of factors required for the timely initiation of cell division. The systematic identification of non-essential regulators of cell division we describe will be a valuable resource for analysis of cell cycle progression in yeast and other organisms.

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