Urge-to-cough: what can it teach us about cough?

The Urge-to-Cough is a component of the brain motivation system that mediates cognitive responses to cough stimuli. There are six stages to the cough motivation-to-action system: (1) stimulus, the trigger for the neural event; (2) urge, the physical need to respond to the stimulus; (3) desire, translation of urge into a central neural targeted goal; (4) action, physical response that satisfies the urge-desire; (5) evidence, feedback to the neural system on the action; (6) reward, sensory system that determines if the urge was satisfied. Urge-to-Cough is related to three fundamental types of cough: (1) reflex cough, (2) voluntary cough, and (3) behavioral cough. Urge-to-Cough with reflex cough can be studied by measuring the sensations elicited by a cough stimulus. Neural processes with voluntary cough can be studied using magnitude production cognitive psychometric methods. Results of these studies have shown if the subjects can reliably estimate their Urge-to-Cough, the urge increases with increasing cough stimulus, there is a correlation between the Urge-to-Cough and cough intensity, there is a threshold for eliciting the sensation of the urge that precedes the motor cough behavior, subjects can voluntarily produce coughs of varying magnitudes, the motor cough pattern is directly related to the perceived magnitude of a cough, volitional triggers of a cough are directly related to the reflex cough pattern, and neural triggers of cough initiate a stereotypic motor output. Understanding the Urge-to-Cough motivation-to-action system opens new strategies for research on central neural cough mechanisms.     

What can ancient mummies teach us about atherosclerosis?

Ancient mummies have captivated a wide variety of audiences for centuries. In order to better understand the evolution and causative features of atherosclerosis, the Horus group is applying modern scientific methods to study ancient mummies. We have used CT scanning to detect calcification in arteries as an indication of the presence of atherosclerosis, and are correlating these results with cultural and lifestyle features of various populations of ancient people as represented by their ancient mummified remains. We are also pursuing related studies of ancient DNA to define genotypes associated with atherosclerotic phenotypes.     

Aging,stress, and senescence in plants: what can biological diversity teach us?

Aging, stress, and senescence in plants are interconnected processes that determine longevity. We focus here on compiling and discussing our current knowledge on the mechanisms of development that long-lived perennial plants have evolved to prevent and delay senescence. Clonal and nonclonal perennial herbs of various life forms and longevities will be particularly considered to illustrate what biological diversity can teach us about aging as a universal phenomenon. Source–sink relations and redox signaling will also be discussed as examples of regulatory mechanisms of senescence at the organ level. Whether or not effective mechanisms that biological diversity has evolved to completely prevent the wear and tear of aging will be applicable to human aging in the near future ultimately depends on ethical aspects.

     

Cardiovascular education for people with rheumatoid arthritis: what can existing patient education programmes teach us?

Patient education is an integral component of the management of chronic diseases. Education programmes designed for people with RA have historically aimed to improve their arthritis symptoms and outcomes. Novel educational material is required to address significant comorbidities, particularly cardiovascular disease (CVD) associated with RA. We appraise the components of education programmes incorporated in disease management in people with RA and programmes used for CVD prevention in the general population, including their design and delivery, use of behaviour theory, evaluation and long-term efficacy. We then integrate the findings in order to inform the development of educational material specifically addressing CVD in RA. This approach may be useful for other major comorbidities of RA as well as other musculoskeletal conditions.     

Canine diabetes mellitus: can old dogs teach us new tricks?

Background Diabetes is common in dogs, with an estimated prevalence of 0.32% in the UK. Clinical signs, as in man, include polydipsia, polyuria and weight loss, associated with hyperglycaemia and glucosuria. Diabetes typically occurs in dogs between 5 and 12 years of age, and is uncommon under 3 years of age. Breeds predisposed to diabetes include the Samoyed, Tibetan Terrier and Cairn Terrier, while others such as the Boxer and German Shepherd Dog seem less susceptible. These breed differences suggest a genetic component, and at least one dog leucocyte antigen haplotype (DLA DRB1*009, DQA1*001, DQB1*008) appears to be associated with susceptibility to diabetes.Methods Canine diabetes can be classified into insulin deficiency diabetes (IDD), resulting from a congenital deficiency or acquired loss of pancreatic beta cells, or insulin resistance diabetes resulting mainly from hormonal antagonism of insulin function.Results There is no evidence for a canine equivalent of human type 2 diabetes. Adult-onset IDD, requiring insulin therapy, is the most common form, with pancreatitis and/or immune-mediated beta cell destruction considered to be the major underlying causes of the disease.Discussion Autoantibodies to insulin, recombinant canine GAD65 and/or canine islet antigen-2 have been identified in a proportion of newly diagnosed diabetic dogs, suggesting that autoimmunity is involved in the pathogenesis of disease in some patients.Conclusion The late onset and slow progression of beta cell dysfunction in canine diabetes resembles latent autoimmune diabetes of the adult in man.     

What can the national weight control registry teach us?

Given the high obesity rate and its economic burden, it is critical to better understand weight loss and maintenance. The National Weight Control Registry (NWCR) provides useful information about the strategies used by successful weight maintainers long term; recent data suggest that a diet with less food group variety will provide a lower calorie intake and that medical triggers have been associated with better initial weight loss and maintenance. The NWCR data suggest that long-term weight loss maintenance can be achieved and that health care practitioners may need to adjust weight control programs accordingly.     

Genetics of obesity: can an old dog teach us new tricks?

At one level, obesity is clearly a problem of simple physics, a result of eating too much and not expending enough energy. The more complex question, however, is why do some people eat more than others? Studies of human and mouse genetics over the past two decades have uncovered a number of pathways within the brain that play a key role in the control of food intake. A prime example is the leptin–melanocortin pathway, which we now know greatly contributes to mammalian appetitive behaviour. However, genetic disruption of this pathway remains rare and does not represent the major burden of the disease that is carried by those of us with ‘common obesity’. In recent years, genome-wide association studies have revealed more than 100 different candidate genes linked to BMI, with most (including many components of the melanocortin pathway) acting in the central nervous system and influencing food intake. So while severe disruption of the melanocortin pathway results in severe obesity, subtle variations in these genes influence where you might sit in the normal distribution of BMI. As we now enter this ‘post-genomics’ world, can this new information influence our treatment and management of obese patients?     

Chlamydia pneumoniae,and mycoplasma pneumoniae: Are they related to severe asthma in childhood?

Background: Mycoplasma pneumoniae and Chlamydia pneumoniae are frequent agents of acute respiratory diseases and they have been recognized as infectious triggers of asthma. Objective: To determine the frequency of these triggers and their relationship to severe asthma. Methods: 82 patients were enrolled in a prospective cross-sectional study from January 2007 to March 2013 and they were divided into three study groups: Group 1: 27 children with severe asthma, Group 2: 29 children with stable asthma and Group 3: 26 children which was the control group. Serological tests included IgG and IgM for both C. pneumoniae and M. pneumoniae. Results: Average age ± SD was 10.9 ± 2.5 for Group 1; 10.1 ± 2.9 for Group 2 and 9.9± 1.9 for Group 3 (p = 0.4). M. pneumoniae IgM was observed in 6/27 (22.2%) in Group 1, 2/29 (6.9%) in Group 2 and 0/26 in the Control Group (p = 0,01). C.pneumoniae IgM was present in 7/26 (26.9%) in Group 1, 2/29 (6.9%) in Group 2 and 0/26 in Group 3 (p = 0.005). No significant difference was observed between Group 2 and Group 3. M. pneumoniae IgG was observed in 7/27 (25.9%) in Group 1, 4/29 (13.7%) in Group 2 and 0/26 in the Control Group (p < 0,05). C.pneumoniae IgG was present in 8/26 (30.7%) in Group 1, 5/29 (17.2%) in Group 2 and 0/26 in Group 3 (p < 0,05). Conclusions: M. pneumoniae and C. pneumoniae may play a role in the development of severe asthma.     

Triggers of asthma and COPD: Are they different?

BackgroundAsthma symptoms can be triggered by a variety of factors commonly referred to as “triggers”. Some of these factors can also induce severe asthma exacerbations. Thus, it can be assumed that actions taken against such triggers may prevent the progression of the disease. However, limited data exist on the clinical importance of these triggers in patients with chronic obstructive pulmonary disease (COPD).ObjectiveTo compare the effect of triggers on symptoms and actions taken against certain modifiable triggers in patients with asthma and COPD.MethodsThe study was conducted in a university hospital between June 2009 and June 2010. Patients with asthma and COPD were asked to complete a questionnaire in which both the factors triggering symptoms and the actions taken against several triggers were assessed.ResultsThree hundred consecutive adult patients (150 asthma, 150 COPD) were enrolled to the study. The frequency of triggering factors was similar in both groups. Vaccination rates for influenza and pneumococcus were significantly higher in patients with COPD. However, such anti-allergic approaches as the use of strategies to decrease dust exposure, the use of anti-mite bed sheets, and the removal of pets from the home were more commonly employed by asthmatic patients.ConclusionThis study revealed that certain triggers affected COPD and asthma patients to the same degree. Therefore, triggers and strategies for controlling modifiable triggers should be more concentrated on during education in both groups. However, the preventive effect of these strategies on disease progression, particularly in patients with COPD, needs clarification.