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Background. Substantial healthcare resources are devoted to panic disorder (PD) and coronary heart disease (CHD); however, the association between these conditions remains controversial. Our objective was to conduct a systematic review of studies assessing the association between PD, related syndromes, and incident CHD. Method. Relevant studies were retrieved from Medline, EMBASE, SCOPUS and PsycINFO without restrictions from inception to January 2015 supplemented with hand-searching. We included studies that reported hazard ratios (HR) or sufficient data to calculate the risk ratio and 95% confidence interval (CI) which were pooled using a random-effects model. Studies utilizing self-reported CHD were ineligible. Twelve studies were included comprising 1 131 612 persons and 58 111 incident CHD cases. Results. PD was associated with the primary incident CHD endpoint [adjusted HR (aHR) 1.47, 95% CI 1.24-1.74, p < 0.00001] even after excluding angina (aHR 1.49, 95% CI 1.22-1.81, p < 0.00001). High to moderate quality evidence suggested an association with incident major adverse cardiac events (MACE; aHR 1.40, 95% CI 1.16-1.69, p = 0.0004) and myocardial infarction (aHR 1.36, 95% CI 1.12-1.66, p = 0.002). The risk for CHD was significant after excluding depression (aHR 1.64, 95% CI 1.45-1.85) and after depression adjustment (aHR 1.38, 95% CI 1.03-1.87). Age, sex, length of follow-up, socioeconomic status and diabetes were sources of heterogeneity in the primary endpoint. Conclusions. Meta-analysis showed that PD was independently associated with incident CHD, myocardial infarction and MACE; however, reverse causality cannot be ruled out and there was evidence of heterogeneity.

Individuals with cancer, particularly those who are receiving systemic anticancer treatments, have been postulated to be at increased risk of mortality from COVID-19. This conjecture has considerable effect on the treatment of patients with cancer and data from large, multicentre studies to support this assumption are scarce because of the contingencies of the pandemic. We aimed to describe the clinical and demographic characteristics and COVID-19 outcomes in patients with cancer. In this prospective observational study, all patients with active cancer and presenting to our network of cancer centres were eligible for enrolment into the UK Coronavirus Cancer Monitoring Project (UKCCMP). The UKCCMP is the first COVID-19 clinical registry that enables near real-time reports to frontline doctors about the effects of COVID-19 on patients with cancer. Eligible patients tested positive for severe acute respiratory syndrome coronavirus 2 on RT-PCR assay from a nose or throat swab. We excluded patients with a radiological or clinical diagnosis of COVID-19, without a positive RT-PCR test. The primary endpoint was all-cause mortality, or discharge from hospital, as assessed by the reporting sites during the patient hospital admission. From March 18, to April 26, 2020, we analysed 800 patients with a diagnosis of cancer and symptomatic COVID-19. 412 (52%) patients had a mild COVID-19 disease course. 226 (28%) patients died and risk of death was significantly associated with advancing patient age (odds ratio 9·42 [95% CI 6·56–10·02]; p<0·0001), being male (1·67 [1·19–2·34]; p=0·003), and the presence of other comorbidities such as hypertension (1·95 [1·36–2·80]; p<0·001) and cardiovascular disease (2·32 [1·47–3·64]). 281 (35%) patients had received cytotoxic chemotherapy within 4 weeks before testing positive for COVID-19. After adjusting for age, gender, and comorbidities, chemotherapy in the past 4 weeks had no significant effect on mortality from COVID-19 disease, when compared with patients with cancer who had not received recent chemotherapy (1·18 [0·81–1·72]; p=0·380). We found no significant effect on mortality for patients with immunotherapy, hormonal therapy, targeted therapy, radiotherapy use within the past 4 weeks. Mortality from COVID-19 in cancer patients appears to be principally driven by age, gender, and comorbidities. We are not able to identify evidence that cancer patients on cytotoxic chemotherapy or other anticancer treatment are at an increased risk of mortality from COVID-19 disease compared with those not on active treatment. University of Birmingham, University of Oxford.

Abstract Rationale Obstructive sleep apnea (OSA) is associated with systemic hypertension. Either overnight intermittent hypoxia, or the recurrent arousals that occur in OSA, could cause the daytime increases in blood pressure (BP). Objectives To establish the role of intermittent hypoxia in the increased morning BP in patients with OSA. Methods Randomized, double-blinded, crossover trial assessing the effects of overnight supplemental oxygen versus air (sham) on morning BP, after continuous positive airway pressure (CPAP) withdrawal in patients with moderate to severe OSA. The primary outcome was the change in home morning BP after CPAP withdrawal for 14 nights, oxygen versus air. Secondary outcomes included oxygen desaturation index (ODI), apnea–hypopnea index (AHI), subjective sleepiness (Epworth Sleepiness Scale score), and objective sleepiness (Oxford Sleep Resistance Test). Measurements and Main Results Supplemental oxygen virtually abolished the BP rise after CPAP withdrawal and, compared with air, significantly reduced the rise in mean systolic BP (−6.6 mm Hg; 95% confidence interval [CI], −11.3 to −1.9; P = 0.008), mean diastolic BP (−4.6 mm Hg; 95% CI, −7.8 to −1.5; P = 0.006), and median ODI (−23.8/h; interquartile range, −31.0 to −16.3; P < 0.001) after CPAP withdrawal. There was no significant difference, oxygen versus air, in AHI, subjective sleepiness, or objective sleepiness. Conclusions Supplemental oxygen virtually abolished the rise in morning BP during CPAP withdrawal. Supplemental oxygen substantially reduced intermittent hypoxia, but had a minimal effect on markers of arousal (including AHI), subjective sleepiness, or objective sleepiness. Therefore intermittent hypoxia, and not recurrent arousals, appears to be the dominant cause of daytime increases in BP in OSA.

In megabar shock waves, materials compress and undergo a phase transition to a dense charged-particle system that is dominated by strong correlations and quantum effects. This complex state, known as warm dense matter, exists in planetary interiors and many laboratory experiments (for example, during high-power laser interactions with solids or the compression phase of inertial confinement fusion implosions). Here, we apply record peak brightness X-rays at the Linac Coherent Light Source to resolve ionic interactions at atomic (ångström) scale lengths and to determine their physical properties. Our in situ measurements characterize the compressed lattice and resolve the transition to warm dense matter, demonstrating that short-range repulsion between ions must be accounted for to obtain accurate structure factor and equation of state data. In addition, the unique properties of the X-ray laser provide plasmon spectra that yield the temperature and density with unprecedented precision at micrometre-scale resolution in dynamic compression experiments. Warm dense matter (WDM), which falls in the category between plasmas and condensed matter, is expected to exist in planetary interiors. Now, researchers use an X-ray laser to observe the transition to WDM.

Leber hereditary optic neuropathy (LHON) is a mitochondrial genetic disease that preferentially causes blindness in young adult males, affecting about 1 in 25 000 of the British population. It is characterised by bilateral subacute loss of central vision owing to focal degeneration of the retinal ganglion cell layer and optic nerve. Over 95% of LHON cases are primarily the result of one of three mitochondrial DNA (mtDNA) point mutations, G3460A, G11778A, and T14484C, which all involve genes encoding complex I subunits of the respiratory chain. An intriguing feature of LHON is that only ∼50% of males and ∼10% of females who harbour a pathogenic mtDNA mutation actually develop the optic neuropathy. This marked incomplete penetrance and gender bias imply that additional mitochondrial and/or nuclear genetic factors must be modulating the phenotypic expression of LHON. It is also likely that environmental factors contribute to the onset of visual failure. However, these secondary precipitating factors remain poorly defined at present. In this review, we describe the natural history of this optic nerve disorder and highlight issues relating to clinical diagnosis, management, and genetic counselling. We also discuss the findings of recently published studies and the light they shed on the complex aetiology and pathophysiology of LHON.

The health of several East Antarctic moss-beds is declining as liquid water availability is reduced due to recent environmental changes. Consequently, a noninvasive and spatially explicit method is needed to assess the vigour of mosses spread throughout rocky Antarctic landscapes. Here, we explore the possibility of using near-distance imaging spectroscopy for spatial assessment of moss-bed health. Turf chlorophyll a and b, water content and leaf density were selected as quantitative stress indicators. Reflectance of three dominant Antarctic mosses Bryum pseudotriquetrum, Ceratodon purpureus and Schistidium antarctici was measured during a drought-stress and recovery laboratory experiment and also with an imaging spectrometer outdoors on water-deficient (stressed) and well-watered (unstressed) moss test sites. The stress-indicating moss traits were derived from visible and near infrared turf reflectance using a nonlinear support vector regression. Laboratory estimates of chlorophyll content and leaf density were achieved with the lowest systematic/unsystematic root mean square errors of 38.0/235.2 nmol g−1 DW and 0.8/1.6 leaves mm−1, respectively. Subsequent combination of these indicators retrieved from field hyperspectral images produced small-scale maps indicating relative moss vigour. Once applied and validated on remotely sensed airborne spectral images, this methodology could provide quantitative maps suitable for long-term monitoring of Antarctic moss-bed health.

Overweight and obesity during pregnancy is associated with risk of a range of adverse health outcomes. While intervention studies aim to promote behavioral change, little is known about the underlying psychological mechanisms facilitating and hindering change. The aim of this study was to evaluate overweight and obese women’s perceptions of making behavior change during pregnancy. We explored beliefs through self-administrated questionnaires (n = 464) and semi-structured face-to-face interviews (n = 26). Questions were designed according to the Health Belief Model. A triangulation protocol was followed to combine quantitative and qualitative data. A total of 269 women (58 %) indicated that high gestational weight gain is a concern, with 348 (75 %) indicating excessive weight gain is associated with complications during pregnancy or child birth. Women were aware of maternal complications associated with high gestational weight gain, but had more limited awareness of neonatal complications. While most women indicated in questionnaires that healthy eating and physical activity were associated with improved health during pregnancy, they were unable to identify specific benefits at interview. Barriers to making healthy behavior changes were highly individualized, the main barrier being lack of time. While the majority (91 %) of women indicated that they would make behavior changes if the change made them feel better, only half felt confident in their ability to do so. Interventions for overweight and obese pregnant women should incorporate education about neonatal health consequences and benefits of healthy behavior change in addition to incorporating strategies to enhance self-efficacy.

The terrestrial flora of Antarctica's frozen continent is restricted to sparse ice-free areas and dominated by lichens and bryophytes. These plants frequently battle sub-zero temperatures, extreme winds and reduced water availability; all influencing their ability to survive and grow. Antarctic mosses, however, can have canopy temperatures well above air temperature. At midday, canopy temperatures can exceed 15°C, depending on moss turf water content. In this study, the optimum temperature of photosynthesis was determined for six Antarctic moss species: , , , , , and collected from King George Island (maritime Antarctica) and/or the Windmill Islands, East Antarctica. Both chlorophyll fluorescence and gas exchange showed maximum values of electron transport rate occurred at canopy temperatures higher than 20°C. The optimum temperature for both net assimilation of CO and photoprotective heat dissipation of three East Antarctic species was 20-30°C and at temperatures below 10°C, mesophyll conductance did not significantly differ from 0. Maximum mitochondrial respiration rates occurred at temperatures higher than 35°C and were lower by around 80% at 5°C. Despite the extreme cold conditions that Antarctic mosses face over winter, the photosynthetic apparatus appears optimised to warm temperatures. Our estimation of the total carbon balance suggests that survival in this cold environment may rely on a capacity to maximize photosynthesis for brief periods during summer and minimize respiratory carbon losses in cold conditions.

Key points Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is one of many clinical presentations associated with mutations in mitochondrial DNA (mtDNA) and a biochemical deficiency of respiratory chain complex I. While the 'common' 3243A->G mutation in the mitochondrial tRNALeu(UUR) (MTTL1) gene is detected in approximately 80% of patients with MELAS, the aetiology of the remaining 20% is heterogeneous, with different causative mutations occurring in MTTL1, other mitochondrial tRNA (mt-tRNA) genes, and the MTND genes encoding subunits of complex I. We report three unrelated patients with MELAS in whom the 3243A->G mutation could not be detected, but who expressed a specific deficiency of complex I activity in both skeletal muscle and cultured fibroblasts. By contrast, our experience with five patients with complex I deficiency caused by mutations in MTTL1 (two with 3243A->G and one each with 3250T->C, 3303C->T, and 3242G>A) 2 is that all but the 3242G>A patient had low mutant loads and normal complex I activity in fibroblasts (results not shown). [...]patients with mutations in MTND subunit genes express a complex I defect in fibroblasts more often than those with MTTL1 mutations.

α -Synuclein becomes misfolded and aggregated upon damage by various factors, for example, by reactive oxygen species. These aggregated forms have been proposed to have differential toxicities and their interaction with mitochondria may cause dysfunction within this organelle that contributes to the pathogenesis of Parkinson’s disease (PD). In particular, the association of α -synuclein with mitochondria occurs through interaction with mitochondrial complex I and importantly defects of this protein have been linked to the pathogenesis of PD. Therefore, we investigated the relationship between aggregated α -synuclein and mitochondrial dysfunction, and the consequences of this interaction on cell survival. To do this, we studied the effects of α -synuclein on cybrid cell lines harbouring mutations in either mitochondrial complex I or IV. We found that aggregated α -synuclein inhibited mitochondrial complex I in control and complex IV-deficient cells. However, when aggregated α -synuclein was applied to complex I-deficient cells, there was no additional inhibition of mitochondrial function or increase in cell death. This would suggest that as complex I-deficient cells have already adapted to their mitochondrial defect, the subsequent toxic effects of α -synuclein are reduced.