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Objective: It is unclear whether trauma center care is associated with improved outcomes in older adults with traumatic brain injury (TBI) compared to management at nontrauma centers. Our primary objectives were to describe the long-term outcomes of older adults with TBI and to evaluate the association of trauma center transport with long-term functional outcome., Methods: This was a prospective, observational study at five emergency medical services (EMS) agencies and 11 hospitals representing all 9-1-1 transfers within a county. Older adults (≥55 years) with TBI (defined as closed head injury associated with loss of consciousness and/or amnesia, abnormal Glasgow Coma Scale [GCS] score, or traumatic intracranial hemorrhage) and transported by EMS from August 2015 to September 2016 were eligible. EMS providers completed standardized data forms and emergency department (ED) and hospital data were abstracted. Functional outcomes were measured using the Extended Glasgow Outcome Scale (GOS-E) at 3- and 6-month intervals by telephone follow-up. Reasons for disabilities were coded as due to head injury, due to illness or injury to other part of body, or due to a mixture of both. To evaluate the association of trauma center transport and functional outcomes, we conducted multivariate ordinal logistic regression analyses on multiple imputed data for 1) all patients with TBI and 2) patients with traumatic intracranial hemorrhage., Results: We enrolled 350 patients with TBI; the median (Q1, Q3) age was 70 (61, 84) years, 187 (53%) were male, and 91 patients (26%) had traumatic intracranial hemorrhage on initial ED cranial computed tomography (CT) imaging. A total of 257 patients (73%) were transported by EMS to a Level I or II trauma center. Sixty-nine patients (20%) did not complete follow-up at 3 or 6 months. Of the patients with follow-up, 119 of 260 patients (46%) had moderate disability or worse at 6 months, including 55 of 260 patients (21%) who were dead at 6-month follow-up. Death or severe disabilities were more commonly attributed to non-TBI causes while moderate disabilities or better were more commonly due to TBI. On adjusted analysis, an abnormal GCS score, higher Charlson Comorbidity Index scores, and the presence of traumatic intracranial hemorrhage on initial ED cranial imaging were associated with worse GOS-E scores at 6 months. Trauma center transport was not associated with GOS-E scores at 6 months for TBI patients and in patients with traumatic intracranial hemorrhage on initial ED CT imaging., Conclusions: In older adults with TBI, moderate disability or worse is common 6 months after injury. Over one in five of older adults with TBI died by 6 months, usually due to nonhead causes. Patients with TBI or traumatic intracranial hemorrhage did not have improved functional outcomes with initial triage to a trauma center., (© 2020 by the Society for Academic Emergency Medicine.)

Mitochondrial diseases are a group of genetic disorders leading to the dysfunction of mitochondrial energy metabolism pathways. We aimed to assess the clinical phenotype and the biochemical cerebrospinal fluid (CSF) biogenic amine profiles of patients with different diagnoses of genetic mitochondrial diseases. We recruited 29 patients with genetically confirmed mitochondrial diseases harboring mutations in either nuclear or mitochondrial DNA (mtDNA) genes. Signs and symptoms of impaired neurotransmission and neuroradiological data were recorded. CSF monoamines, pterins, and 5-methyltetrahydrofolate (5MTHF) concentrations were analyzed using high-performance liquid chromatography with electrochemical and fluorescence detection procedures. The mtDNA mutations were studied by Sanger sequencing, Southern blot, and real-time PCR, and nuclear DNA was assessed either by Sanger or next-generation sequencing. Five out of 29 cases showed predominant dopaminergic signs not attributable to basal ganglia involvement, harboring mutations in different nuclear genes. A chi-square test showed a statistically significant association between high homovanillic acid (HVA) values and low CSF 5-MTHF values (chi-square = 10.916; p = 0.001). Seven out of the eight patients with high CSF HVA values showed cerebral folate deficiency. Five of them harbored mtDNA deletions associated with Kearns-Sayre syndrome (KSS), one had a mitochondrial point mutation at the mtDNA ATPase6 gene, and one had a POLG mutation. In conclusion, dopamine deficiency clinical signs were present in some patients with mitochondrial diseases with different genetic backgrounds. High CSF HVA values, together with a severe cerebral folate deficiency, were observed in KSS patients and in other mtDNA mutation syndromes.

Ectopic lipid accumulation in the liver is implicated in metabolic disease in an age- and sex-dependent manner. The role of hepatic lipids has been well established within the scope of metabolic insults in mice, but has been insufficiently characterized under standard housing conditions, where age-related metabolic alterations are known to occur. We studied a total of 10 male and 10 female mice longitudinally. At 3, 7 and 11 months of age, non-invasive 1 H-magnetic resonance spectroscopy ( 1 H-MRS) was used to monitor hepatic lipid content (HLC) and fatty acid composition in vivo, and glucose homeostasis was assessed with glucose and insulin challenges. At the end of the study, hepatic lipids were comprehensively characterized by nuclear magnetic resonance (NMR) and liquid chromatography-mass spectrometric analyses of liver tissue samples. In males, HLC increased from 1.4 ± 0.1% at 3 months to 2.9 ± 0.3% at 7 months (p < 0.01) and 2.7 ± 0.3% at 11 months (p < 0.05), in correlation with fasting insulin levels (p < 0.01, r = 0.51) and parameters from the insulin tolerance test (ITT; p < 0.001, r = -0.69 versus area under the curve; p < 0.01, r = -0.57 versus blood glucose drop at 1 h post-ITT; p < 0.01, r = 0.55 versus blood glucose at 3 h post-ITT). The metabolic performance of females remained the same throughout the study, and HLC was higher than that of males at 3 months (2.7 ± 0.2%, p < 0.01), but comparable at 7 months (2.2 ± 0.2%) and 11 months (2.2 ± 0.1%). Strong sexual dimorphism in bioactive lipid species, including diacylglycerols (higher in males, p < 0.0001), phosphatidylinositols (higher in females, p < 0.001) and omega-3 polyunsaturated fatty acids (higher in females, p < 0.01), was found to be in good correlation with metabolic scores at 11 months. Therefore, in mice housed under standard conditions, sex-specific composition of bioactive lipids is associated with metabolic protection in females, whose metabolic performance was independent of hepatic cytosolic lipid content., (Copyright © 2017 John Wiley & Sons, Ltd.)

Background: Lesbian, gay, bisexual, or questioning (LGBQ) high school students experience higher rates of homelessness than their heterosexual peers. Moreover, LGBQ high school students are more likely to stay in riskier locations (eg, with a stranger) and less likely to stay in a shelter. This study tested whether these trends also apply to middle school students., Methods: Using representative data, we examined sexual identity and homelessness among Los Angeles Unified School District middle school students., Results: Nearly 10% of middle school students identified as LGBQ and 23.5% experienced at least 1 night of homelessness during the previous year. Contrary to high school data, LGBQ students did not experience higher rates of homelessness overall. However, when limiting the sample to students who had experienced homelessness, LGBQ students were more than 5 times as likely as heterosexual students to have stayed in a public place and 63% as likely to have stayed in a shelter., Conclusions: Lesbian, gay, bisexual, or questioning students are more likely to experience public homelessness. Schools must implement homelessness surveillance systems to assist in identifying early episodes of homelessness, thereby reducing the likelihood of poor physical and mental health outcomes associated with chronic homelessness., (© 2015, American School Health Association.)

1. The role of the endothelium in the effects of cooling on the response to cholinoceptor stimulation of the rabbit central ear (cutaneous) and femoral (non-cutaneous) arteries was studied using 2 mm long cylindrical segments. 2. Concentration-response curves for acetylcholine (10(-9)-10(-5) M), methacholine (10(-9)-10(-5) M) and sodium nitroprusside (10(-9)-10(-4) M) were isometrically recorded in arteries under conditions, with and without endothelium or following pretreatment with the nitric oxide-synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 10(-6)-3 x 10(-4) M) at 37 degrees C and at 24 degrees C (cooling). 3. Ear and femoral arteries showed endothelium-dependent relaxation to acetylcholine and methacholine at 37 degrees C and 24 degrees C. The extent of relaxation of the control ear arteries, but not of the control femoral arteries, to acetylcholine and methacholine increased during cooling. 4. L-NAME (10(-6)-3 x 10(-4) M) reduced in a concentration-dependent way the response of ear arteries to acetylcholine at both 37 degrees C and 24 degrees C, this reduction being more potent at 37 degrees C. L-Arginine (10(-5)-10(-3) M) reversed in a concentration-dependent manner the inhibitor effects of 10(-5) M L-NAME at both temperatures. 5. Sodium nitroprusside caused a concentration-dependent relaxation in both arteries that was endothelium-independent. However, the extent of relaxation to this nitrovasodilator in ear and femoral arteries was lower at 24 degrees C. 6. These results suggest that cooling augments the reactivity of cutaneous (ear) arteries, but not that of non-cutaneous (femoral) arteries to cholinoceptor stimulation by endothelium-mediated mechanisms.Cooling could therefore facilitate the stimulated release of endothelial nitric oxide in cutaneous vessels.

1. The effects of cooling on the response of the rabbit central ear (cutaneous) and femoral (non-cutaneous) arteries to stimulation of adrenoceptors and the role of the endothelium in these effects, were studied in 2 mm long cylindrical segments. 2. Concentration-response curves for noradrenaline (10(-9)-3 x 10(-4) M), phenylephrine (alpha 1-adrenoceptor agonist, 10(-9)-3 x 10(-4) M) and B-HT 920 (alpha 2-adrenoceptor agonist, 10(-7)-10(-3) M) were recorded isometrically in arteries with and without endothelium at 37 degrees C and at 24 degrees C (cooling). To analyze further the endothelial mechanisms in the responses to adrenoceptor stimulation during cooling, the effects of the adrenoceptor agonists on ear arteries in the presence of NG-nitro-L-arginine methyl esther (L-NAME) (10(-5) M) were also determined. 3. In every condition tested, the three adrenoceptor agonists produced a concentration-dependent arterial contraction and the order of potency in ear and femoral arteries was noradrenaline greater than or equal to phenylephrine greater than B-HT 920. The response of ear and femoral arteries to phenylephrine or B-HT 920 was blocked by prazosin (10(-6) M). Yohimbine (10(-6) M) decreased slightly the response of ear arteries and increased that of femoral arteries to B-HT 920. 4. The sensitivity of both ear and femoral arteries to the three adrenoceptor agonists was significantly lower at 24 degrees C than at 37 degrees C. 5. In ear arteries, endothelium removal or treatment with L-NAME did not influence the response at 37 degrees C, but did increase it during cooling to adrenoceptor stimulation.In femoral arteries, endothelium removal increased the sensitivity to noradrenaline and, especially, to B-HT 920 at 37 degrees C, but did not affect the response at 24 degrees C.6. The results suggest that: (a) rabbit ear and femoral arteries are equipped mainly with alpha 1-adrenoceptors;(b) at 37 degrees C, the contraction of the ear artery to adrenoceptor agonists is mostly endothelium-independent, and in the femoral artery the contraction to alpha 2-adrenoceptor activation is endothelium-dependent; (c) cooling inhibits the contraction to adrenoceptor agonists in both ear and femoral arteries: in the ear artery probably by increasing the availability of endothelial nitric oxide, but in the femoral artery by depressing the sensitivity of alpha-adrenoceptors in the smooth musculature.7. The results suggest that the endothelium may modulate the adrenoceptor response of cutaneous arteries during changes in temperature.

1. The effects of cooling on the response of rabbit central ear artery to endothelin-1 and the role of the endothelium in these effects were studied in 2 mm long cylindrical arterial segments. 2. Concentration-response curves for endothelin-1 (10(-10)-3 x 10(-7) M) were recorded isometrically in arteries with and without endothelium at 37 degrees C and during cooling (24 degrees C). To analyze further the endothelial mechanisms of the response to endothelin-1 during cooling, the effects of this peptide in the presence of NG-nitro-L-arginine methyl ester (L-NAME) (10(-4) M) or meclofenamate (10(-5) M) were also determined. 3. In every condition tested, endothelin-1 produced a marked, concentration-dependent arterial contraction. Sensitivity of intact arteries to this peptide was consistently lower at 24 degrees C than at 37 degrees C. At 37 degrees C there were comparable responses of arteries with and without endothelium, but at 24 degrees C arteries without endothelium showed a higher sensitivity than intact arteries to endothelin-1. 4. L-NAME (10(-4) M) increased the maximal contraction at 37 degrees C, and both the sensitivity and maximal contraction at 24 degrees C of intact arteries to endothelin-1. Meclofenamate (10(-5) M) did not affect the arterial response to endothelin-1. 5. Sensitivity of arteries with and without endothelium to nitroprusside (10(-9)-10(-3) M) was significantly decreased during cooling, and endothelium removal did not affect the relaxation to this nitrovasodilator. 6. These results suggest that cooling decreases sensitivity of cutaneous arteries (ear artery) to endothelin-1 probably by increasing the availability of endothelial nitric oxide.