Do soldiers seek more mental health care after deployment? Analysis of mental health consultations in the Netherlands Armed Forces following deployment to Afghanistan

Background: Military deployment to combat zones puts military personnel to a number of physical and mental challenges that may adversely affect mental health. Until now, few studies have been performed in Europe on mental health utilization after military deployment. Objective: We compared the incidence of mental health consultations with the Military Mental Health Service (MMHS) of military deployed to Afghanistan to that of non-deployed military personnel. Method: We assessed utilization of the MMHS by the full cohort of the Netherlands Armed Forces enlisted between 2008 and 2010 through linkage of mental health and human resource information systems. Results: The total population consisted of 50,508 military (18,233 deployed, 32,275 non-deployed), who accounted for 1,906 new consultations with the MMHS. The follow-up was limited to the first 2 years following deployment. We observed higher mental health care utilization in deployed vs. non-deployed military personnel; hazard ratio (HR), adjusted for sex, military branch and time in service, 1.84 [95% CI 1.61–2.11] in the first and 1.28 [1.09–1.49] in the second year after deployment. An increased risk of adjustment disorders (HR 2.59 [2.02–3.32] and 1.74 [1.30–2.32]) and of anxiety disorders (2.22 [1.52–3.25] and 2.28 [1.50–3.45]) including posttraumatic stress disorder (5.15 [2.55–10.40] and 5.28 [2.42–11.50]), but not of mood disorders (1.33 [0.90–1.97] and 1.11 [0.68–1.82]), was observed in deployed personnel in the first- and second-year post-deployment, respectively. Military personnel deployed in a unit with a higher risk of confrontation with potentially traumatic events had a higher HR (2.13 [1.84–2.47] and 1.40 [1.18–1.67]). Conclusions: Though absolute risk was low, in the first and second year following deployment to Afghanistan there was an 80 and 30% higher risk for mental health problems resulting in a consultation with the Dutch MMHS compared to military never deployed to Afghanistan. These observations underscore the need for an adequate mental health infrastructure for those returning from deployment

Las instituciones científico-medicas en la Murcia del XVIII : un intento fracasado de renovación de la formación médica

Presentamos un estudio sobre dos intentos que, en la Murcia del siglo XVIII, pretendieron mejorar y actualizar la formación que recibían los profesionales sanitarios. Ambos fracasaron, aparentemente por falta de acuerdo entre sus promotores, si bien pensamos que las causas fueron más profundas y habría que buscarlas en la escasa actividad científica que se desarrolló en la ciudad, lo que hacía innecesaria la existencia de instituciones docentes o de otras como las Academias de Medicina

Preserved functional autonomic phenotype in adult mice overexpressing moderate levels of human alpha-synuclein in oligodendrocytes

Mice overexpressing human alpha-synuclein in oligodendrocytes (MBP1-alpha-syn) recapitulate some key functional and neuropathological features of multiple system atrophy (MSA). Whether or not these mice develop severe autonomic failure, which is a key feature of human MSA, remains unknown. We explored cardiovascular autonomic regulation using long-term blood pressure (BP) radiotelemetry and pharmacological testing. We instrumented 12 MBP1-alpha-syn mice and 11 wild-type mice aged 9 months for radiotelemetry. Animals were tested with atropine, metoprolol, clonidine, and trimethaphan at 9 and 12 months age. We applied spectral and cross-spectral analysis to assess heart rate (HR) and BP variability. At 9 months of age daytime BP (transgenic: 101 +/- 2 vs. wild type: 99 +/- 2 mmHg) and HR (497 +/- 11 vs. 505 +/- 16 beats/min) were similar. Circadian BP and HR rhythms were maintained. Nighttime BP (109 +/- 2 vs. 108 +/- 2 mmHg) and HR (575 +/- 15 vs. 569 +/- 14 beats/min), mean arterial BP responses to trimethaphan (-21 +/- 8 vs. -10 +/- 5 mmHg, P = 0.240) and to clonidine (-8 +/- 3 vs. -5 +/- 2 mmHg, P = 0.314) were similar. HR responses to atropine (+159 +/- 24 vs. +146 +/- 22 beats/min), and to clonidine (-188 +/- 21 vs. -163 +/- 33 beats/min) did not differ between strains. Baroreflex sensitivity (4 +/- 1 vs. 4 +/- 1 msec/mmHg) and HR variability (total power, 84 +/- 17 vs. 65 +/- 21 msec(2)) were similar under resting conditions and during pharmacological testing. Repeated measurements at 12 months of age provided similar results. In mice, moderate overexpression of human alpha-synuclein in oligodendrocytes is not sufficient to induce overt autonomic failure. Additional mechanisms may be required to express the autonomic failure phenotype including higher levels of expression or more advanced age

Electronic and bite angle effects in catalytic C-O bond cleavage of a lignin model compound using ruthenium xantphos complexes

The authors would like to thank the EPSRC (Global Engagement grant EP/K00445X/1 and critical mass grant EP/J018139/1) and the European Union (Marie Curie ITN ‘SuBiCat’ PITN-GA-2013-607044) for financial support. NMSF-Swansea and Mr. Stephen Boyer are kindly acknowledged for mass spectrometry and elemental analysis, respectively.Bite angle and electronic effects on the ruthenium-diphosphine catalysed ether bond cleavage of the lignin β-O-4 model compound 2-phenoxy-1-phenethanol were tested. Enhanced conversion of the substrate was observed with increasing σ-donor capacity of the ligands. Kinetic and thermodynamic data suggest oxidative addition of the dehydrogenated model compound to the diphosphine Ru(0) complex to be rate-limiting.PostprintPeer reviewe

Advanced model compounds for understanding acid-catalyzed lignin depolymerization : identification of renewable aromatics and a lignin-derived solvent

This work was funded by the EP/J018139/1, EP/K00445X/1 grants (NJW and PCJK), an EPSRC Doctoral Prize Fellowship (CSL), and the European Union (Marie Curie ITN ‘SuBiCat’ PITN-GA-2013-607044, CWL, NJW, PCJK, PJD, KB, JdeV).The development of fundamentally new approaches for lignin depolymerization is challenged by the complexity of this aromatic biopolymer. While overly simplified model compounds often lack relevance to the chemistry of lignin, the direct use of lignin streams poses significant analytical challenges to methodology development. Ideally, new methods should be tested on model compounds that are complex enough to mirror the structural diversity in lignin but still of sufficiently low molecular weight to enable facile analysis. In this contribution, we present a new class of advanced (β-O-4)-(β-5) dilinkage models that are highly realistic representations of a lignin fragment. Together with selected β-O-4, β-5, and β–β structures, these compounds provide a detailed understanding of the reactivity of various types of lignin linkages in acid catalysis in conjunction with stabilization of reactive intermediates using ethylene glycol. The use of these new models has allowed for identification of novel reaction pathways and intermediates and led to the characterization of new dimeric products in subsequent lignin depolymerization studies. The excellent correlation between model and lignin experiments highlights the relevance of this new class of model compounds for broader use in catalysis studies. Only by understanding the reactivity of the linkages in lignin at this level of detail can fully optimized lignin depolymerization strategies be developed.PostprintPeer reviewe

MICU1 Controls Both the Threshold and Cooperative Activation of the Mitochondrial Ca(2+) Uniporter.

Mitochondrial Ca(2+) uptake via the uniporter is central to cell metabolism, signaling, and survival. Recent studies identified MCU as the uniporter\u27s likely pore and MICU1, an EF-hand protein, as its critical regulator. How this complex decodes dynamic cytoplasmic [Ca(2+)] ([Ca(2+)]c) signals, to tune out small [Ca(2+)]c increases yet permit pulse transmission, remains unknown. We report that loss of MICU1 in mouse liver and cultured cells causes mitochondrial Ca(2+) accumulation during small [Ca(2+)]c elevations but an attenuated response to agonist-induced [Ca(2+)]c pulses. The latter reflects loss of positive cooperativity, likely via the EF-hands. MICU1 faces the intermembrane space and responds to [Ca(2+)]c changes. Prolonged MICU1 loss leads to an adaptive increase in matrix Ca(2+) binding, yet cells show impaired oxidative metabolism and sensitization to Ca(2+) overload. Collectively, the data indicate that MICU1 senses the [Ca(2+)]c to establish the uniporter\u27s threshold and gain, thereby allowing mitochondria to properly decode different inputs