Brain collateral circulation is an essential compensatory mechanism in response to acute brain ischemia. To study the temporal evolution of brain macro and microcollateral recruitment and their reciprocal interactions in response to different ischemic conditions, we applied a combination of complementary techniques (T2 weighted magnetic resonance imaging [MRI], time of flight [TOF] angiography [MRA], cerebral blood flow [CBF] imaging and histology) in two different mouse models. Hypoperfusion was either induced by permanent bilateral common carotid artery stenosis (BCCAS) or 60 minute transient unilateral middle cerebral artery occlusion (MCAO). In both models, collateralization is a very dynamic phenomenon with a global effect affecting both hemispheres. Patency of ipsilateral posterior communicating artery (PcomA) represents the main variable survival mechanism and the main determinant of stroke lesion volume and recovery in MCAO whereas the promptness of external carotid artery retrograde flow recruitment together with PcomA patency, critically influence survival, brain ischemic lesion volume and retinopathy in BCCAS mice. Finally, different ischemic gradients shape microcollateral density and size.

Disturbances in the experience of time have been a commonly reported feature of depressive disorders since the beginning of modern psychiatry and psychological research. However, qualitative research approaches to investigate the phenomenon are rarely used. We employed content analysis to investigate disturbances of time experience in Major Depressive Disorder. Our analysis from 25 participants showed that individuals with Major Depressive Disorder subjectively seem to have lost the ability to influence or change the present, resulting in an impersonal and blocked future. The present is rendered meaningless, the past unchangeably negative, and the passage of time turned into a dragging, inexorable, and viscous continuance. The overall,—possibly intersubjective—concept of time experience, remains largely intact, causing or adding to depressive mood and suffering. We elaborate on how these findings reflect previous theories on the experience of time in depression. This study might encourage future inquiries into both the phenomenal and neuroscientific foundation of time experience under psychopathological conditions.

Background Enterococci are frequent pathogens causing nosocomial infections in Germany. Infections due to strains with vancomycin resistance are high when compared with other European states. Therefore, the study aimed to describe the recent progression of nosocomial infections due to vancomycin-resistant enterococci (VRE) in Germany. Methods We analyzed data from two components of the German national nosocomial infection surveillance system for the period 2007–2016. For primary bloodstream infections (BSIs) and urinary tract infections (UTIs) we used data from intensive care units and for surgical site infections (SSIs) data from surgical departments. In a sensitivity analysis, we considered only data from participants that participated continuously from 2007 to 2016 (“core group”). We calculated proportions of VRE among all nosocomial enterococcal infections with 95% confidence intervals (95% CIs) and trends over time. A multivariable logistic regression was used to compare occurrence of VRE proportions among German federal states. Results Enterococcal infections from 857 ICUs and 1119 surgical departments were analyzed. On ICUs, the proportion of vancomycin resistance in enterococci causing nosocomial infections significantly increased for BSIs from 5.9 to 16.7% and for UTIs from 2.9 to 9.9%; for surgical site infections, the proportion of VRE increased from 0.9 to 5.2% (P < 0.001 for all). In the core group, the increase of VRE was more pronounced in ICUs (BSIs: 5.5 to 21.6%; UTIs: 2 to 11.2%) but was not seen in surgical departments (SSIs: 1.5 to 2.8%). Compared with the most populous German federal state North Rhine Westphalia, enterococcal infections in Hesse (Odds Ratio (OR) 2.3, 95% CI 1.7–3.1), Saxony (OR 2.5, 95% CI 1.8–3.5) and Thuringia (OR 1.9, 95% CI 1.4–2.6) were more likely to be caused by vancomycin-resistant strains. Conclusion In Germany, the proportion of VRE in nosocomial infection due to enterococci is still increasing. It remains unclear, why a large variation in the proportion of VRE exists between German federal states.

Background This pilot trial aimed to study the feasibility and effects on quality of life (QOL) and well-being of short-term fasting (STF) during chemotherapy in patients with gynecological cancer. Methods In an individually-randomized cross-over trial patients with gynecological cancer, 4 to 6 planned chemotherapy cycles were included. Thirty-four patients were randomized to STF in the first half of chemotherapies followed by normocaloric diet (group A;n = 18) or vice versa (group B;n = 16). Fasting started 36 h before and ended 24 h after chemotherapy (60 h-fasting period). QOL was assessed by the FACIT-measurement system. Results The chemotherapy-induced reduction of QOL was less than the Minimally Important Difference (MID; FACT-G = 5) with STF but greater than the MID for non-fasted periods. The mean chemotherapy-induced deterioration of total FACIT-F was 10.4 ± 5.3 for fasted and 27.0 ± 6.3 for non-fasted cycles in group A and 14.1 ± 5.6 for non-fasted and 11.0 ± 5.6 for fasted cycles in group B. There were no serious adverse effects. Conclusion STF during chemotherapy is well tolerated and appears to improve QOL and fatigue during chemotherapy. Larger studies should prove the effect of STF as an adjunct to chemotherapy. Trial registration This trial was registered at clinicaltrials.gov: NCT01954836.

Objective Ayurveda is commonly used in South Asia to treat knee osteoarthritis (OA). We aimed to evaluate the effectiveness of Ayurvedic treatment compared to conventional conservative care in patients with knee OA. Method According to American College of Rheumatology (ACR) criteria knee OA patients were included in a multicenter randomized, controlled, open-label trial and treated in 2 hospital clinics and 2 private outpatient clinics in Germany. Participants received either a multi-modal Ayurvedic treatment or multi-modal conventional care with 15 treatments over 12 weeks respectively. Primary outcome was the change on the Western Ontario and McMaster University Osteoarthritis (WOMAC) Index after 12 weeks. Secondary outcomes included WOMAC subscales; the pain disability index and a pain experience scale, numeric rating scales for pain and sleep quality, quality-of-life and mood, rescue medication use, and safety issues. Results One hundred fifty-one participants (Ayurveda n = 77, conventional care n = 74) were included. Changes of the WOMAC Index from baseline to 12 weeks were more pronounced in the Ayurveda group (mean difference 61.0 [95%CI: 52.4;69.6]) than in the conventional group (32.0 [95%CI: 21.4;42.6]) resulting in a significant between-group difference (p < 0.001) and a clinically relevant effect size (Cohen's d 0.68 [95% CI:0.35;1.01]). Similar trends were observed for all secondary outcomes at week 12. Effects were sustained at follow-ups after 6 and 12 months. Conclusion Results suggest that Ayurvedic treatment is beneficial in reducing knee OA symptoms. Further studies should be conducted to confirm the magnitude of the effect and to clarify the role of different treatment components and non-specific effects. Registration at clinicaltrials.gov (NCT01225133; initial release 10/06/2010).

Omega-6 polyunsaturated fatty acid (n-6 PUFA) is the predominant polyunsaturated fatty acid (PUFA), especially in Western diet. A high omega-6/omega-3 ratio in Western diets is implicated in the development of cardiovascular diseases and inflammatory processes. Studies in animal models and in humans have demonstrated beneficial effects of omega-3 PUFA (n-3 PUFA) in a variety of diseases, including cardiac arrhythmias and inflammatory diseases, as well as breast and colon cancer. The molecular mechanisms underlying the effects of n-3 PUFA are still not well understood. Possible mechanisms include competition between n-3 and n-6 PUFAs at the cyclooxygenase (COX) and lipoxygenase (LOX) and cytochrome P450 levels, and subsequent formation of oxylipins with specific anti-inflammatory or anti-arrhythmic effects. In this study, we report the impact of routine long-term treatment with prescription-grade n-3 PUFA (either 840 mg or 1680 mg per day) on blood cell membrane fatty acid composition, as well as plasma oxylipin patterns, in a patient population with severe hyperlipidemia and cardiovascular disease who are on standard lipid-lowering and cardioprotective medications. Lipidomics analyses were performed by LC/ESI-MS/MS. Supplementation led to a dose- dependent increase in n-3 PUFA eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in the blood cell fraction. We also observed a dose-dependent increase in EPA- and DHA-derived epoxy metabolites, whereas the effect of n-3 PUFA supplementation on LOX-dependent EPA- and DHA-derived hydroxy metabolites was less pronounced, with a tendency towards lower metabolites in subjects with higher n-3 PUFA levels. These data thus generally confirm effects of n-3 PUFA supplementation observed previously in healthy individuals. Additionally, they indicate a suppressive effect of high n-3 PUFA supplementation on the formation of LOX metabolites in the context of concomitant aspirin medication.

Studies on human physical performance in extreme environments have effectively approached the investigation of adaptation mechanisms and their physiological limits. As scientific interest in the interplay between physiological and psychological aspects of performance is growing, we aimed to investigate cardiac autonomic control, by means of heart rate variability, and psychological correlates, in competitors of a subarctic ultramarathon, taking place over a 690 km course (temperatures between +5 and −47°C). At baseline (PRE), after 277 km (D1), 383 km (D2), and post-race (POST, 690 km), heart rate (HR) recordings (supine, 15 min), psychometric measurements (Profile of Mood States/POMS, Borg fatigue, and Karolinska Sleepiness Scale scores both upon arrival and departure) were obtained in 16 competitors (12 men, 4 women, 38.6 ± 9.5 years). As not all participants reached the finish line, comparison of finishers (FIN, n = 10) and non-finishers (NON, n = 6), allowed differential assessment of performance. Resting HR increased overall significantly at D1 (FIN +15.9; NON +14.0 bpm), due to a significant decrease in parasympathetic drive. This decrease was in FIN only partially recovered toward POST. In FIN only, baseline HR was negatively correlated with mean velocity [r −0.63 (P.04)] and parasympathetic drive [pNN50+: r −0.67 (P.03)], a lower HR and a higher vagal tone predicting a better performance. Moreover, in FIN, a persistent increase of the long-term self-similarity coefficient, assessed by detrended fluctuation analysis (DFAα2), was retrieved, possibly due to higher alertness. As for psychometrics, at D1, POMS Vigor decreased (FIN: −7.0; NON: −3.8), while Fatigue augmented (FIN: +6.9; NON: +5.0). Sleepiness increased only in NON, while Borg scales did not exhibit changes. Baseline comparison of mood states with normative data for athletes displayed significantly higher positive mood in our athletes. Results show that: the race conditions induced early decreases in parasympathetic drive; the extent of vagal withdrawal, associated to the timing of its recovery, is crucial for success; pre-competition lower resting HR predicts a better performance; psychological profile is reliably depicted by POMS, but not by Borg fatigue scales. Therefore, assessment of heart rate variability and psychological profile may monitor and partly predict performance in long-duration ultramarathon in extreme cold environment.

The dataset presented in this article complements the article entitled “Myeloid cells contribute indirectly to VEGF expression upon hypoxia via activation of Müller cells” (C. Nürnberg, N. Kociok, C. Brockmann, T. Lischke, S. Crespo-Garcia, N. Reichhart, S. Wolf, R. Baumgrass, S.A. Eming, S. Beer- Hammer, and A.M. Joussen). This complementary dataset provides further insight into the experimental validation of the VEGFfl/fl LysMCre (here named VEGFmcko) knockout model used in the main article through genomic and quantitative Real-Time PCR in various murine tissues as well as additional flow cytometry data and immunohistochemical stainings. By providing these data, we aim to enable researcher to reproduce and critically analyze our data.

Background: Nijmegen breakage syndrome is an autosomal recessive disorder characterized by microcephaly, immunodeficiency, hypersensitivity to X-irradiation, and a high predisposition to cancer. Nibrin, the product of the NBN gene, is part of the MRE11/RAD50 (MRN) complex that is involved in the repair of DNA double strand breaks (DSBs), and plays a critical role in the processing of DSBs in immune gene rearrangements, telomere maintenance, and meiotic recombination. NBS skin fibroblasts grow slowly in culture and enter early into senescence. Case presentation: Here we present an incidental finding. Skin fibroblasts, derived from a 9 year old NBS patient, showed a mosaic of normal diploid cells (46,XY) and those with a complex, unbalanced translocation. The aberrant karyotype was analysed by G-banding, comparative genomic hybridization, and whole chromosome painting. The exact breakpoints of the derivative chromosome were mapped by whole genome sequencing: 45,XY,der(6)(6pter → 6q11.1::13q11 → 13q21.33::20q11.22 → 20qter),-13. The deleted region of chromosomes 6 harbors almost 1.400 and that of chromosome 13 more than 500 genes, the duplicated region of chromosome 20 contains about 700 genes. Such unbalanced translocations are regularly incompatible with cellular survival, except in malignant cells. The aberrant cells, however, showed a high proliferation potential and could even be clonally expanded. Telomere length was significantly reduced, hTERT was not expressed. The cells underwent about 50 population doublings until they entered into senescence. The chromosomal preparation performed shortly before senescence showed telomere fusions, premature centromere divisions, endoreduplications and tetraploid cells, isochromatid breaks and a variety of marker chromosomes. Inspection of the site of skin biopsy 18 years later, presented no evidence for abnormal growth. Conclusions: The aberrant cells had a significant selective advantage in vitro. It is therefore tempting to speculate that this highly unbalanced translocation could be a primary driver of cancer cell growth.

Parametric mapping techniques provide a non-invasive tool for quantifying tissue alterations in myocardial disease in those eligible for cardiovascular magnetic resonance (CMR). Parametric mapping with CMR now permits the routine spatial visualization and quantification of changes in myocardial composition based on changes in T1, T2, and T2*(star) relaxation times and extracellular volume (ECV). These changes include specific disease pathways related to mainly intracellular disturbances of the cardiomyocyte (e.g., iron overload, or glycosphingolipid accumulation in Anderson-Fabry disease); extracellular disturbances in the myocardial interstitium (e.g., myocardial fibrosis or cardiac amyloidosis from accumulation of collagen or amyloid proteins, respectively); or both (myocardial edema with increased intracellular and/or extracellular water). Parametric mapping promises improvements in patient care through advances in quantitative diagnostics, inter- and intra-patient comparability, and relatedly improvements in treatment. There is a multitude of technical approaches and potential applications. This document provides a summary of the existing evidence for the clinical value of parametric mapping in the heart as of mid 2017, and gives recommendations for practical use in different clinical scenarios for scientists, clinicians, and CMR manufacturers.

The poor healing potential of tendons is still a clinical problem, and the use of Platelet Rich Plasma (PRP) was hypothesized to stimulate healing. As the efficacy of PRPs remains unproven, platelet lysate (PL) could be an alternative with its main advantages of storage and characterization before use. Five different blood products were prepared from 16 male donors: human serum, two PRPs (Arthrex, (PRP-ACP); RegenLab (PRP-BCT)), platelet concentrate (apheresis, PC), and PL (freezing-thawing destruction of PC). Additionally, ten commercial allogenic PLs (AlloPL) from pooled donors were tested. The highest concentration of most growth factors was found in AlloPL, whereas the release of growth factors lasted longer in the other products. PRP-ACP, PRP- BCT, and PC significantly increased cell viability of human tenocyte-like cells, whereas PC and AlloPL increased Col1A1 expression and PRP-BCT increased Col3A1 expression. MMP-1, IL-1β, and HGF expression was significantly increased and Scleraxis expression decreased by most blood products. COX1 expression significantly decreased by PC and AlloPL. No clear positive effects on tendon cell biology could be shown, which might partially explain the weak outcome results in clinical practice. Pooled PL seemed to have the most beneficial effects and might be the future in using blood products for tendon tissue regeneration.

The mammalian circadian clock coordinates physiology with environmental cycles through the regulation of daily oscillations of gene expression. Thousands of transcripts exhibit rhythmic accumulations across mouse tissues, as determined by the balance of their synthesis and degradation. While diurnally rhythmic transcription regulation is well studied and often thought to be the main factor generating rhythmic mRNA accumulation, the extent of rhythmic posttranscriptional regulation is debated, and the kinetic parameters (e.g., half-lives), as well as the underlying regulators (e.g., mRNA-binding proteins) are relatively unexplored. Here, we developed a quantitative model for cyclic accumulations of pre-mRNA and mRNA from total RNA-seq data, and applied it to mouse liver. This allowed us to identify that about 20% of mRNA rhythms were driven by rhythmic mRNA degradation, and another 15% of mRNAs regulated by both rhythmic transcription and mRNA degradation. The method could also estimate mRNA half-lives and processing times in intact mouse liver. We then showed that, depending on mRNA half-life, rhythmic mRNA degradation can either amplify or tune phases of mRNA rhythms. By comparing mRNA rhythms in wild-type and Bmal1−/− animals, we found that the rhythmic degradation of many transcripts did not depend on a functional BMAL1. Interestingly clock-dependent and -independent degradation rhythms peaked at distinct times of day. We further predicted mRNA-binding proteins (mRBPs) that were implicated in the posttranscriptional regulation of mRNAs, either through stabilizing or destabilizing activities. Together, our results demonstrate how posttranscriptional regulation temporally shapes rhythmic mRNA accumulation in mouse liver.

Alpha-Synuclein (α-Syn) accumulation is considered a major risk factor for the development of synucleinopathies such as Parkinson’s disease (PD) and dementia with Lewy bodies. We have generated mice overexpressing full-length human α-Syn fused to a membrane-targeting signal sequence under the control of the mouse Thy1-promotor. Three separate lines (L56, L58 and L62) with similar gene expression levels, but considerably heightened protein accumulation in L58 and L62, were established. In L62, there was widespread labelling of α-Syn immunoreactivity in brain including spinal cord, basal forebrain, cortex and striatum. Interestingly, there was no detectable α-Syn expression in dopaminergic neurones of the substantia nigra, but strong human α-Syn reactivity in glutamatergic synapses. The human α-Syn accumulated during aging and formed PK-resistant, thioflavin-binding aggregates. Mice displayed early onset bradykinesia and age progressive motor deficits. Functional alterations within the striatum were confirmed: L62 showed normal basal dopamine levels, but impaired dopamine release (upon amphetamine challenge) in the dorsal striatum measured by in vivo brain dialysis at 9 months of age. This impairment was coincident with a reduced response to amphetamine in the activity test. L62 further displayed greater sensitivity to low doses of the dopamine receptor 1 (D1) agonist SKF81297 but reacted normally to the D2 agonist quinpirole in the open field. Since accumulation of α-Syn aggregates in neurones and synapses and alterations in the dopaminergic tone are characteristics of PD, phenotypes reported for L62 present a good opportunity to further our understanding of motor dysfunction in PD and Lewy body dementia.

Objective: Restoring the circulation is the primary goal in emergency treatment of cerebral ischemia. However, better understanding of how the brain responds to energy depletion could help predict the time available for resuscitation until irreversible damage and advance development of interventions that prolong this span. Experimentally, injury to central neurons begins only with anoxic depolarization. This potentially reversible, spreading wave typically starts 2 to 5 minutes after the onset of severe ischemia, marking the onset of a toxic intraneuronal change that eventually results in irreversible injury. Methods: To investigate this in the human brain, we performed recordings with either subdural electrode strips (n = 4) or intraparenchymal electrode arrays (n = 5) in patients with devastating brain injury that resulted in activation of a Do Not Resuscitate–Comfort Care order followed by terminal extubation. Results: Withdrawal of life‐sustaining therapies produced a decline in brain tissue partial pressure of oxygen (ptiO2) and circulatory arrest. Silencing of spontaneous electrical activity developed simultaneously across regional electrode arrays in 8 patients. This silencing, termed “nonspreading depression,” developed during the steep falling phase of ptiO2 (intraparenchymal sensor, n = 6) at 11 (interquartile range [IQR] = 7–14) mmHg. Terminal spreading depolarizations started to propagate between electrodes 3.9 (IQR = 2.6–6.3) minutes after onset of the final drop in perfusion and 13 to 266 seconds after nonspreading depression. In 1 patient, terminal spreading depolarization induced the initial electrocerebral silence in a spreading depression pattern; circulatory arrest developed thereafter. Interpretation: These results provide fundamental insight into the neurobiology of dying and have important implications for survivable cerebral ischemic insults. Ann Neurol 2018;83:295–310

Background: The challenges of today’s society call for more knowledge about how to maintain all aspects of cognitive health, such as speed/attention, memory/learning, visuospatial ability, language, executive capacity and social cognition during the life course. Main text: Medical advances have improved treatments of numerous diseases, but the cognitive implications have not been sufficiently addressed. Disability induced by cognitive dysfunction is also a major issue in groups of patients not suffering from Alzheimer’s disease or related disorders. Recent studies indicate that several negative lifestyle factors can contribute to the development of cognitive impairment, but intervention and prevention strategies have not been implemented. Disability due to cognitive failure among the workforce has become a major challenge. Globally, the changing aging pyramid results in increased prevalence of cognitive disorders, and the diversity of cultures influences the expression, manifestation and consequences of cognitive dysfunction. Conclusions: Major tasks in the field of cognitive medicine are basic neuroscience research to uncover diverse disease mechanisms, determinations of the prevalence of cognitive dysfunction, health-economical evaluations, and intervention studies. Raising awareness for cognitive medicine as a clinical topic would also highlight the importance of specialized health care units for an integrative approach to the treatment of cognitive dysfunctions.

Background: Symptomatic intracranial hemorrhage (sICH) after intravenous thrombolysis with recombinant tissue-plasminogen activator (rt-PA) for acute ischemic stroke is associated with a poor functional outcome. We aimed to develop a score assessing risk of sICH including novel putative predictors—namely, pretreatment with statins and severe renal impairment. Methods: We analyzed our local cohort (Berlin) of patients receiving rt-PA for acute ischemic stroke between 2006 and 2016. Outcome was sICH according to ECASS-III criteria. A multiple regression model identified variables associated with sICH and receiver operating characteristics were calculated for the best discriminatory model for sICH. The model was validated in an independent thrombolysis cohort (Basel). Results: sICH occurred in 53 (4.0%) of 1,336 patients in the derivation cohort. Age, baseline National Institutes of Health Stroke Scale, systolic blood pressure on admission, blood glucose on admission, and prior medication with medium- or high-dose statins were associated with sICH and included into the risk of intracranial hemorrhage score. The validation cohort included 983 patients of whom 33 (3.4%) had a sICH. c-Statistics for sICH was 0.72 (95% CI 0.66–0.79) in the derivation cohort and 0.69 (95% CI 0.60–0.77) in the independent validation cohort. Inclusion of severe renal impairment did not improve the score. Conclusion: We developed a simple score with fair discriminating capability to predict rt-PA- related sICH by adding prior statin use to known prognostic factors of sICH. This score may help clinicians to identify patients with higher risk of sICH requiring intensive monitoring.

Background: Flavonoids exert anti-inflammatory properties and modulate oxidative stress in vitro, suggesting a protective effect on lung function, but epidemiological studies examining this association are scarce. Methods: A stratified random sample was drawn from the GA2LEN screening survey, in which 55,000 adults aged 15 to 75 answered a questionnaire on respiratory symptoms. Post-bronchodilator spirometry was obtained from 2850 subjects. Forced vital capacity (FVC), the ratio between the forced exhaled volume in 1 second (FEV1) and FVC (FEV1/FVC), FVC below lower limit of normal (FVC < LLN), and FEV1/FVC < LLN were calculated. Intake of the six main subclasses of flavonoids was estimated using the GA2LEN Food Frequency Questionnaire. Adjusted associations between outcomes and each subclass of flavonoids were examined with multivariate regressions. Simes’ procedure was used to test for multiple comparisons. Results: A total of 2599 subjects had valid lung function and dietary data. A lower prevalence of FVC < LLN (airway restriction) was observed in those with higher total flavonoid (adjusted odds ratio (aOR), higher vs. lowest quintile intake 0.58; 95% Confidence Interval (CI) 0.36, 0.94), and pro-anthocyanidin intakes (aOR 0.47; 95% CI 0.27, 0.81). A higher FEV1/FVC was associated with higher intakes of total flavonoids and pro- anthocyanidins (adjusted correlation coefficient (a β-coeff 0.33; 0.10, 0.57 and a β-coeff 0.44; 95% CI 0.19, 0.69, respectively). After Simes’ procedure, the statistical significance of each of these associations was attenuated but remained below 0.05, with the exception of total flavonoids and airway restriction. Conclusions: This population-based study in European adults provides cross-sectional evidence of a positive association of total flavonoid intake and pro-anthocyanidins and ventilatory function, and a negative association with spirometric restriction in European adults. View Full-Text

Background: Tungiasis (sand flea disease) is a neglected tropical skin disease caused by female sand fleas (Tunga spp.) embedded in the skin of the host. The disease is common in sub-Saharan Africa and predominantly affects children living in impoverished rural communities. In these settings tungiasis is associated with important morbidity. Whether tungiasis impairs life quality has never been studied. Methods: The study was performed in 50 children with tungiasis, living in resource-poor communities in coastal Kenya. Based on the Dermatology Life Quality Index (DLQI) a tool was developed to determine life quality impairment associated with tungiasis in children, the tungiasis- related Dermatology of Life Quality Index (tungiasis-related-DLQI). Pain and itching were assessed using visual scales ranging from 0–3 points. The intensity of infection and the acute and chronic severity of tungiasis were determined using standard methods. Results: Seventy eight percent of the patients reported a moderate to very large effect of tungiasis on life quality at the time of the diagnosis. The degree of impairment correlated with the number of viable sand fleas present in the skin (rho = 0.64, p < 0.001), the severity score of acute clinical pathology (rho = 0.74, p < 0.001), and the intensity of pain (rho = 0.82, p < 0.001). Disturbance of sleep and concentration difficulties were the most frequent restriction categories (86% and 84%, respectively). Four weeks after curative treatment, life quality had improved significantly. On the individual level the amelioration of life quality correlated closely with the regression of clinical pathology (rho = 0.61, p < 0.001). Conclusion: The parasitic skin disease tungiasis considerably impairs life quality in children in rural Kenya. After effective treatment, life quality improves rapidly.

This cross-sectional study is aimed at assessing sodium (Na) and potassium (K) content and the molar Na:K ratios of the most commonly available ready-to-eat street foods in Tajikistan and Kyrgyzstan. Four different samples of each of these foods were collected and 62 food categories were evaluated through bromatological analysis. Flame photometry was used to quantify sodium and potassium concentrations. The results show that home-made foods can be important sources of sodium. In particular, main dishes and sandwiches, respectively, contain more than 1400 and nearly 1000 mg Na in an average serving and provide approximately 70% and 50% of the maximum daily recommended values. Wide ranges of sodium content were found between individual samples of the same home-made food collected from different vending sites from both countries. In industrial foods, sodium contents ranged from 1 to 1511 mg/serving in Tajikistan, and from 19 to 658 mg/serving in Kyrgyzstan. Most Na:K ratios exceeded the recommended level of 1.0 and the highest ratios were found in home-made snacks (21.2) from Tajikistan and industrial beverages (16.4) from Kyrgyzstan. These findings not only improve data on the nutritional composition of foods in these countries, but may also serve as baseline information for future policies and interventions. View Full-Text

The Psychiatric Genomics Consortium-Posttraumatic Stress Disorder group (PGC- PTSD) combined genome-wide case–control molecular genetic data across 11 multiethnic studies to quantify PTSD heritability, to examine potential shared genetic risk with schizophrenia, bipolar disorder, and major depressive disorder and to identify risk loci for PTSD. Examining 20 730 individuals, we report a molecular genetics-based heritability estimate (h2SNP) for European- American females of 29% that is similar to h2SNP for schizophrenia and is substantially higher than h2SNP in European-American males (estimate not distinguishable from zero). We found strong evidence of overlapping genetic risk between PTSD and schizophrenia along with more modest evidence of overlap with bipolar and major depressive disorder. No single-nucleotide polymorphisms (SNPs) exceeded genome-wide significance in the transethnic (overall) meta- analysis and we do not replicate previously reported associations. Still, SNP- level summary statistics made available here afford the best-available molecular genetic index of PTSD—for both European- and African-American individuals—and can be used in polygenic risk prediction and genetic correlation studies of diverse phenotypes. Publication of summary statistics for ∼10 000 African Americans contributes to the broader goal of increased ancestral diversity in genomic data resources. In sum, the results demonstrate genetic influences on the development of PTSD, identify shared genetic risk between PTSD and other psychiatric disorders and highlight the importance of multiethnic/racial samples. As has been the case with schizophrenia and other complex genetic disorders, larger sample sizes are needed to identify specific risk loci.