NH emerges as a clear-cut clinical picture. It is a noninfrequent primary headache. The particular topography suggests the pain has a probable epicranial source conveyed by, or originated in, one/a few terminal branch(es) of the cutaneous nerves of the scalp.
Little information exists about caregivers of persons with multiple sclerosis (MS). Our aims were to describe the characteristics of a sample of caregivers of persons with MS, assess their perceived burden, health-related quality of life, and investigate factors influencing this burden. We studied 278 caregivers of persons with MS, recruited from a Spanish cross-sectional survey, measuring health-related quality of life by the 36-Item Short-Form Health Survey (SF-36) and burden by the Zarit Caregiver Burden Interview. Of the caregivers, 56.8% were female and their mean age was 50.1 +/- 12.6 years. Their main relationship with the person with MS was spouse/partner (52.9%) and son or daughter (25.9%). Caregiver General Health, Mental Health, Bodily Pain, and Role-emotional Functioning were the most affected dimensions on the SF-36. Multiple regression analysis showed that independent and significant predictors of burden were Role-emotional Functioning and Vitality dimensions SF-36 scores of caregivers, and the Expanded Disability Status Scale scores. The total adjusted variance explained by these variables (adjusted R(2)) was 0.512. Emotional factors and the disability of the person with MS were major predictors of burden. Psychological and social support should be considered to reduce caregiver burden.
Professional road cycling is an extreme endurance sport. Approximately 30,000-35,000 km are cycled each year and the racing season of professional riders includes ϳ90 competition days. In addition, despite the long duration of cycling events such as 3-week stage races, the relative contribution of intense exercise is surprisingly high during the more physically taxing events (mountain passes, time trials, sprints, "breakaways" etc.) [1].Several investigators have analyzed a number of physiological variables in professional cyclists, both in laboratory [2][3][4][5][6][7] and field settings [1,[8][9][10]. However, no prospective, long-term investigation has established the specific physiological adaptations which occur in professional cyclists as a response to training and competition during a typical sports season (generally including different periods in terms of training volume and/or intensity; i.e., precompetition or training, competition, and postcompetition or "active" rest periods). In a recent study (unpublished data), we found no overall training-effect on the ventilatory response (i.e., pulmonary ventilation, tidal volume, ventilatory equivalents, "timing" of respiration, etc.) in the same 13 subjects who formed the present study population. It was therefore considered of interest to extend this investigation to determine whether meta- ]. Finally, rms-EMG tended to increase during the season, with significant differences (pϽ0.05) observed mainly between the competition and rest periods at most workloads. In contrast, precompetition MPF values increased (pϽ0.05) with respect to resting values at most submaximal workloads but fell (pϽ0.05) during the competition period. Our findings suggest that endurance conditioning induces the following general adaptations in elite athletes: (1) lower circulating lactate and increased reliance on aerobic metabolism at a given submaximal intensity, and possibly (2) an enhanced recruitment of motor units in active muscles, as suggested by rms-EMG data.
Increased apoptosis has been reported in the heart of rats with spontaneous hypertension and cardiac hypertrophy. This study was designed to investigate the relationship between apoptosis and hypertrophy in cardiomyocytes from the left ventricle of spontaneously hypertensive rats (SHR). In addition, we evaluated whether the development of cardiomyocyte apoptosis is related to blood pressure or to the activity of the local angiotensin-converting enzyme (ACE) in SHR. The study was performed in 16-week-old SHR, 30-week-old untreated SHR, and 30-week-old SHR treated with quinapril (10 mg x kg[-1] x d[-1]) during 14 weeks before they were killed. Cardiomyocyte apoptosis was assessed by direct immunoperoxidase detection of digoxigenin-labeled 3'-hydroxyl ends of DNA. Nuclear polyploidization measured by DNA flow cytometry was used to assess cardiomyocyte hypertrophy. Compared with 16-week-old normotensive Wistar-Kyoto rats, 16-week-old SHR exhibited increased blood pressure (P<.001), increased rate of tetraploidy (P<.05), and similar levels of ACE activity and apoptosis. Compared with 30-week-old Wistar-Kyoto rats, 30-week-old SHR showed increased blood pressure (P<.001), increased ACE activity (P<.05), increased rate of tetraploidy (P<.01), and increased apoptosis (P<.01). Untreated 30-week-old SHR exhibited similar values of blood pressure and tetraploidy and higher ACE activity (P<.05) and apoptosis (P<.001) than 16-week-old SHR. A direct correlation (P<.01) was found between ACE activity and the apoptotic index in untreated 30-week-old SHR. The long-term administration of quinapril was associated with the normalization of ACE activity and apoptosis in treated SHR. These results suggest that the timing and mechanisms responsible for apoptosis and hypertrophy of cardiomyocytes are different in SHR. Whereas hypertrophy seems to be an earlier alteration that develops in parallel with hypertension, apoptosis develops later in association with overactivity of the local ACE. Our data suggest that cell death dysregulation may be a novel target for antihypertensive agents that interfere with the renin-angiotensin system in hypertension.
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