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The aids for a transition down on the elementary level from the trot to the walk are ( 1 ) weight: stop posting and sit, (2) voice: \"w-a-l-k\" spoken in a drawn-out manner, (3) hand: check-release to loose rein, and (4) leg: alternating tapping/urging to walk forward united, following on a looped rein the gestures of the head and neck. The aids for a transition down on the intermediate level from the trot to the walk are ( I ) weight: stop posting and sit, (2) hands: give-and-take and (3) leg: squeeze-release action, alternating, urging the walk forward.

Show judges evaluated horses based on the new method: the quality of their movement over an outside course, their jumping ability and manners- their calmness and cooperation with their rider. [...] the Forward Riding System also owes much to the American hunter division.

In a survey of patients with advanced cancer, 69% of those with lung cancer and 81% of those with colorectal cancer had an inaccurate belief that chemotherapy was likely to cure them. Better methods of speaking realistically with patients about prognosis seem to be needed. Chemotherapy remains the primary treatment approach for patients with metastatic lung or colorectal cancer. Although efficacy has improved over time, chemotherapy is not curative, and the survival benefit that has been seen in clinical trials is usually measured in weeks or months. 1 – 3 Chemotherapy may provide some palliation, but it is also often associated with substantial treatment-related toxic effects. 2 – 5 To make informed decisions about whether to receive chemotherapy, patients with advanced lung or colorectal cancer need a realistic understanding of its likely benefits. Previous studies have shown that patients with advanced solid tumors overestimate their life expectancy. 6 – 9 Typically, . . .

Anti-inflammatory therapy with long-term colchicine prevented vascular recurrence in coronary disease. Unlike coronary disease, which is typically caused by atherosclerosis, ischaemic stroke is caused by diverse mechanisms including atherosclerosis and small vessel disease or is frequently due to an unknown cause. We aimed to investigate the hypothesis that long-term colchicine would reduce recurrent events after ischaemic stroke. We did a randomised, parallel-group, open-label, blinded endpoint assessed trial comparing long-term colchicine (0·5 mg orally per day) plus guideline-based usual care with usual care only. Hospital-based patients with non-severe, non-cardioembolic ischaemic stroke or high-risk transient ischaemic attack were eligible. The primary endpoint was a composite of first fatal or non-fatal recurrent ischaemic stroke, myocardial infarction, cardiac arrest, or hospitalisation (defined as an admission to an inpatient unit or a visit to an emergency department that resulted in at least a 24 h stay [or a change in calendar date if the hospital admission or discharge times were not available]) for unstable angina. The p value for significance was 0·048 to adjust for two prespecified interim analyses conducted by the data monitoring committee, for which the steering committee and trial investigators remained blinded. The trial was registered at ClinicalTrials.gov (NCT02898610) and is completed. 3154 patients were randomly assigned between Dec 19, 2016, and Nov 21, 2022, with the last follow-up on Jan 31, 2024. The trial finished before the anticipated number of outcomes was accrued (367 outcomes planned) due to budget constraints attributable to the COVID-19 pandemic. Ten patients withdrew consent for analysis of their data, leaving 3144 patients in the intention-to-treat analysis: 1569 (colchicine and usual care) and 1575 (usual care alone). A primary endpoint occurred in 338 patients, 153 (9·8%) of 1569 patients allocated to colchicine and usual care and 185 (11·7%) of 1575 patients allocated to usual care alone (incidence rates 3·32 vs 3·92 per 100 person-years, hazard ratio 0·84; 95% CI 0·68–1·05, p=0·12). Although no between-group difference in C-reactive protein (CRP) was observed at baseline, patients treated with colchicine had lower CRP at 28 days and at 1, 2, and 3 years (p<0·05 for all timepoints). The rates of serious adverse events were similar in both groups. Although no statistically significant benefit was observed on the primary intention-to-treat analysis, the findings provide new evidence supporting the rationale for anti-inflammatory therapy in further randomised trials. Health Research Board Ireland, Deutsche Forschungsgemeinschaft (German Research Foundation), and Fonds Wetenschappelijk Onderzoek Vlaanderen (Research Foundation Flanders), Belgium.

ObjectiveIt is evident that the gut microbiota and factors that influence its composition and activity effect human metabolic, immunological and developmental processes. We previously reported that extreme physical activity with associated dietary adaptations, such as that pursued by professional athletes, is associated with changes in faecal microbial diversity and composition relative to that of individuals with a more sedentary lifestyle. Here we address the impact of these factors on the functionality/metabolic activity of the microbiota which reveals even greater separation between exercise and a more sedentary state.DesignMetabolic phenotyping and functional metagenomic analysis of the gut microbiome of professional international rugby union players (n=40) and controls (n=46) was carried out and results were correlated with lifestyle parameters and clinical measurements (eg, dietary habit and serum creatine kinase, respectively).ResultsAthletes had relative increases in pathways (eg, amino acid and antibiotic biosynthesis and carbohydrate metabolism) and faecal metabolites (eg, microbial produced short-chain fatty acids (SCFAs) acetate, propionate and butyrate) associated with enhanced muscle turnover (fitness) and overall health when compared with control groups.ConclusionsDifferences in faecal microbiota between athletes and sedentary controls show even greater separation at the metagenomic and metabolomic than at compositional levels and provide added insight into the diet–exercise–gut microbiota paradigm.

Background Wearable resistance training (WRT) provides a means of activity- or movement-specific overloading, supposedly resulting in better transference to dynamic sporting performance. Objective The purpose of this review was to quantify the acute and longitudinal metabolic, kinematic and/or kinetic changes that occur with WRT during walking, running, sprint running or jumping movements. Data Sources PubMed, SPORTDiscus, Web of Science and MEDLINE (EBSCO) were searched using the Boolean phrases (limb OR vest OR trunk) AND (walk* OR run* OR sprint* OR jump* OR bound*) AND (metabolic OR kinetic OR kinematic) AND (load*). Study Selection A systematic approach was used to evaluate 1185 articles. Articles with injury-free subjects of any age, sex or activity level were included. Results Thirty-two studies met the inclusion criteria and were retained for analysis. Acute trunk loading reduced velocity during treadmill sprint running, but only significantly when loads of 11 % body mass (BM) or greater were used, while over-the-ground sprint running times were significantly reduced with all loads (8–20 %BM). Longitudinal trunk loading significantly increased jump performance with all loads (7–30 %BM), but did not significantly improve sprint running performance. Acute limb loading significantly increased maximum oxygen consumption and energy cost with all loads (0.3–8.5 %BM) in walking and running, while significantly reducing velocity during sprint running. Limitations The variation in load magnitude, load orientation, subjects, testing methods and study duration no doubt impact the changes in the variables examined and hence make definitive conclusions problematic. Conclusions WRT provides a novel training method with potential to improve sporting performance; however, research in this area is still clearly in its infancy, with future research required into the optimum load placement, orientation and magnitude required for adaptation.

Background Overweight and metabolic problems now add to the burden of illness in patients with Inflammatory Bowel Disease. We aimed to determine if a program of aerobic and resistance exercise could safely achieve body composition changes in patients with Inflammatory Bowel Disease. Methods A randomized, cross-over trial of eight weeks combined aerobic and resistance training on body composition assessed by Dual Energy X-ray Absorptiometry was performed. Patients in clinical remission and physically inactive with a mean age of 25 ± 6.5 years and Body Mass Index of 28.9 ± 3.8 were recruited from a dedicated Inflammatory Bowel Disease clinic. Serum cytokines were quantified, and microbiota assessed using metagenomic sequencing. Results Improved physical fitness was demonstrated in the exercise group by increases in median estimated VO 2max (Baseline: 43.41mls/kg/min; post-intervention: 46.01mls/kg/min; p  = 0.03). Improvement in body composition was achieved by the intervention group ( n  = 13) with a median decrease of 2.1% body fat compared with a non-exercising group ( n  = 7) (0.1% increase; p  = 0.022). Lean tissue mass increased by a median of 1.59 kg and fat mass decreased by a median of 1.52 kg in the exercising group. No patients experienced a deterioration in disease activity scores during the exercise intervention. No clinically significant alterations in the α- and β-diversity of gut microbiota and associated metabolic pathways were evident. Conclusions Moderate-intensity combined aerobic and resistance training is safe in physically unfit patients with quiescent Inflammatory Bowel Disease and can quickly achieve favourable body compositional changes without adverse effects. Trial registration The study was registered at ClinicalTrials.gov; Trial number: NCT02463916 .

Genome-wide association studies have identified the chromosome 10q26 (Chr10) locus, which contains the age-related maculopathy susceptibility 2 (ARMS2) and high temperature requirement A serine peptidase 1 (HTRA1) genes, as the strongest genetic risk factor for age-related macular degeneration (AMD) [L.G. Fritsche et al., Annu. Rev. Genomics Hum. Genet. 15, 151–171, (2014)]. To date, it has been difficult to assign causality to any specific single nucleotide polymorphism (SNP), haplotype, or gene within this region because of high linkage disequilibrium among the disease-associated variants [J. Jakobsdottir et al. Am. J. Hum. Genet. 77, 389–407 (2005); A. Rivera et al. Hum. Mol. Genet. 14, 3227–3236 (2005)]. Here, we show that HTRA1 messenger RNA (mRNA) is reduced in retinal pigment epithelium (RPE) but not in neural retina or choroid tissues derived from human donors with homozygous risk at the 10q26 locus. This tissue-specific decrease is mediated by the presence of a noncoding, cis-regulatory element overlapping the ARMS2 intron, which contains a potential Lhx2 transcription factor binding site that is disrupted by risk variant rs36212733. HtrA1 protein increases with age in the RPE–Bruch’s membrane (BM) interface in Chr10 nonrisk donors but fails to increase in donors with homozygous risk at the 10q26 locus. We propose that HtrA1, an extracellular chaperone and serine protease, functions to maintain the optimal integrity of the RPE–BM interface during the aging process and that reduced expression of HTRA1 mRNA and protein in Chr10 risk donors impairs this protective function, leading to increased risk of AMD pathogenesis. HtrA1 augmentation, not inhibition, in high-risk patients should be considered as a potential therapy for AMD.