-
Kumar Jernigan posted an update 6 months, 3 weeks ago
5%, 8.3% and 4.2% of patients. Comparison between COPD patients and non-COPD patients showed that comorbidities, respiratory symptoms, chest x-ray abnormalities, life-threatening lesions, three vessel disease, pulmonary hypertension and right ventricle dysfunction were significantly more frequent in COPD patients.
There was a high prevalence of COPD among smoking patients with IHD, and most were undiagnosed despite being symptomatic. Smokers with IHD, especially if having respiratory symptoms, radiological or ultrasound abnormalities or life-threatening coronary lesions should be evaluated for airflow limitation.
There was a high prevalence of COPD among smoking patients with IHD, and most were undiagnosed despite being symptomatic. Smokers with IHD, especially if having respiratory symptoms, radiological or ultrasound abnormalities or life-threatening coronary lesions should be evaluated for airflow limitation.
Smoking represents a major issue for global public health. Owing to methodologic challenges, findings of an association between smoking and risk of knee osteoarthritis (OA) are inconsistent. We sought to assess the relation of onset of smoking cessation to the risk of OA sequelae, i.e., knee replacement, and to perform sub-cohort analysis according to weight change after smoking cessation.
Using The Health Improvement Network, we conducted a cohort study to examine the association between smoking cessation and risk of knee replacement among patients with knee OA. Participants who stopped smoking were further grouped into three sub-cohorts weight gain (body mass index increased>1.14kg/m
), no substantial weight change (absolute value of BMI change<1.14kg/m
), and weight loss (BMI loss>1.14kg/m
) after smoking cessation.
We identified 108 cases of knee replacement among 1,054 recent quitters (26.7/1,000 person-years) and 1,108 cases among 15,765 current smokers (17.4/1,000 person-years). The rate difference of knee replacement in recent quitter cohort vs current smoker cohort was 10.4 (95% confidence interval 5.3-15.6)/1,000 person-years and the adjusted hazard ratio (HR) was 1.30 (95%CI1.05-1.59). Compared with current smokers, risk of knee replacement was higher among quitters with weight gain (HR=1.42,95%CI1.01-1.98), but not among those with no substantial weight change (HR=1.29,95%CI0.90-1.83) or those with weight loss (HR=1.11,95%CI0.71-1.75).
Our large population-based cohort study provides the first evidence that smoking cessation was associated with a higher risk of knee replacement among individuals with knee OA, and such an association was due to weight gain after smoking cessation.
Our large population-based cohort study provides the first evidence that smoking cessation was associated with a higher risk of knee replacement among individuals with knee OA, and such an association was due to weight gain after smoking cessation.
Pain is the prevailing symptom of knee osteoarthritis. Central sensitisation creates discordance between pain and joint pathology. We previously reported a Central Pain Mechanisms trait derived from eight discrete characteristics Neuropathic-like pain, Fatigue, Cognitive-impact, Catastrophising, Anxiety, Sleep disturbance, Depression, and Pain distribution. We here validate and show that an 8-item questionnaire, Central Aspects of Pain in the Knee (CAP-Knee) is associated both with sensory- and affective- components of knee pain severity.
Participants with knee pain were recruited from the Investigating Musculoskeletal Health and Wellbeing study in the East Midlands, UK. CAP-Knee items were refined following cognitive interviews. Psychometric properties were assessed in 250 participants using Rasch-, and factor-analysis, and Cronbach’s alpha. Intra-class correlation coefficients tested repeatability. Associations between CAP-Knee and McGill Pain questionnaire pain severity scores were assessed using lineang treatments aiming to reduce the burden of knee pain.Corona virus disease 2019 (COVID-19) is a global emergency able to overwhelm the healthcare capacities worldwide and to affect the older generation especially. When addressing the pathophysiological mechanisms and clinical manifestations of COVID-19, it becomes evident that the disease targets pathways and domains affected by the main aging- and frailty-related pathophysiological changes. A closer analysis of the existing data supports a possible role of biological age rather than chronological age in the prognosis of COVID-19. There is a need for systematic, consequent action of identifying frail (not only older, not only multimorbid, not only symptomatic) persons at risk of poor outcomes.The entorhinal-hippocampal system contains distinct networks subserving declarative memory. This system is selectively vulnerable to changes of ageing and pathological processes. The entorhinal cortex (EC) is a pivotal component of this memory system since it serves as the interface between the neocortex and the hippocampus. KAND567 EC is heavily affected by the proteinopathies of Alzheimer’s disease (AD). These appear in a stereotypical spatiotemporal manner and include increased levels of intracellular amyloid-beta Aβ (iAβ), parenchymal deposition of Aβ plaques, and neurofibrillary tangles (NFTs) containing abnormally processed Tau. Increased levels of iAβ and the formation of NFTs are seen very early on in a population of neurons belonging to EC layer II (EC LII), and recent evidence leads us to believe that this population is made up of highly energy-demanding reelin-positive (RE+) projection neurons. Mitochondria are fundamental to the energy supply, metabolism, and plasticity of neurons. Evidence from AD postmortem brain tissues supports the notion that mitochondrial dysfunction is one of the initial pathological events in AD, and this is likely to take place in the vulnerable RE + EC LII neurons. Here we review and discuss these notions, anchored to the anatomy of AD, and formulate a hypothesis attempting to explain the vulnerability of RE + EC LII neurons to the formation of NFTs. We attempt to link impaired mitochondrial clearance to iAβ and signaling involving both apolipoprotein 4 and reelin, and argue for their relevance to the formation of NFTs specifically in RE + EC LII neurons during the prodromal stages of AD. We believe future studies on these interactions holds promise to advance our understanding of AD etiology and provide new ideas for drug development.