BackgroundFasting during the month of Ramadan for Muslims is a unique metabolic model that includes abstinence from food and fluid intake during the period from dawn to sunset as well as a reduction in meal frequency and alterations in the sleep-wakefulness cycle. Leptin, neuropeptide-Y and insulin are thought to play an important role in long-term regulation of caloric intake and energy expenditure. However, the long-term changes and interactions between these factors during this pattern of fasting are not known.Subjects and MethodsThe study was conducted on 46 healthy female volunteers (age, 22±2 years; BMI, 25.3±0.7 kg/m2). Anthropometrical measurements, estimation of body fat and fasting serum levels of neuropeptide Y, leptin, insulin and glucose were estimated at baseline (day 1), days 14 and 28 of the month of Ramadan and 2 weeks after Ramadan.ResultsBaseline serum levels of leptin correlated positively with body fat (r=0.87, P=0.0002). Serum leptin levels exhibited a significant increase by approximately 41 % and neuropeptide-Y levels were decreased by 30.4% throughout the month of Ramadan. In addition, a significant correlation (r=0.63, P=0.0001) was found between changes in serum leptin and serum insulin. However, changes in serum neuropeptide-Y levels did not correlate with those of leptin or insulinConclusionsLong-term fasting with interrupted nocturnal eating is associated with significant elevations in serum leptin and insulin and reduction in serum neuropeptide-Y. The changes in serum leptin are likely mediated through insulin. However, changes in neuropeptide-Y appears to be mediated independently of leptin or insulin during this type of fasting

A problem-based learning (PBL) curriculum was introduced at McMaster University more than three decades ago. Not many schools have adopted the system despite its distinct advantages. The present paper examines the challenges of teaching physiology in a PBL curriculum and gleans through the literature supporting PBL. It appears that one of the reasons why PBL is not becoming readily acceptable is the lack of concrete reports evaluating the curricular outcomes. The suggestion (R.E. Thomas. Med Educ. 31:320-329, 1997) to standardize and internationalize all components of validated PBL curricula is quite valid. A database needs to be generated that can be easily accessed by traditional institutions to see the rationality and easy implementation of the PBL curriculum.

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Recent studies indicated an enhanced expression of Endothelin (ET) in the kidney contralateral to the vascular clip in two-kidney, one-clip (2K-1C) Goldblatt hypertension. We proposed that the enhanced intrarenal ET production might be responsible for altered haemodynamic and excretory capability of the unclipped kidney (UK) of 2K-1C renovascular hypertensive rats. Therefore, we examined the changes in arterial pressure and split renal function in the clipped (CK) and UK simultaneously, in response to chronic administration of the selective ETA receptor blocker (A-127722), given orally at a dose of 30 mg/kg/day for 3 weeks starting from the beginning of the 4th week of clipping. Systolic pressure averaged 177 +/- 7 mmHg in control rats (n=15) and 164 +/- 9 mmHg in treated rats (n=16) and the difference was not statistically different. Glomerular filtration rate (GFR), renal plasma flow (RPF) and renal vascular resistance (RVR) in the UK were not different between control and treated groups. Data were then analyzed by classifying rats as moderate hypertensives (MAP < 180 mmHg), and severe hypertensives (MAP > 180 mmHg). In the moderately hypertensive group, average MAP was 143 +/- 5 mmHg and 138 +/- 4 mmHg in control (n=9) and treated (n=10) groups, respectively. In the severely hypertensive group, average MAP was 192 +/- 5 mmHg and 188 +/- 5 mmHg in control (n=6) and treated (n=6) groups, respectively. GFR and RPF were significantly improved in the UK of only the severely hypertensives who received the antagonist. However, the ET(A) antagonist blunted the sodium loss in both CK and UK of severely hypertensive rats. We conclude that ET(A) receptors do not play a role in the progression of hypertension in 2K-1C renovascular hypertensive rats. Yet, ET(A) receptors play an important role in altering renal hemodynamics of the unclipped kidneys in severe degrees of renovascular hypertension.

The transport of ĤO−3 (Jsm) from a ĤO−3‐buffered serosal to an unbuffered mucosal saline solution has been studied in rat caecum in vitro. Carbachol, bethanechol and acetylcholine (ACh) caused a concentration‐dependent fall in Jsm with similar maximum effects. 1,1‐Dimethyl‐4‐phenyl‐piperazinium iodide (DMPP) also inhibited Jsm but the effect was less than with the other drugs. Maximum cholinoceptor inhibition was less than that obtained with anoxia. Responses were blocked by atropine (10−5 m) but hexamethonium (2 × 10−4 m) significantly altered the response only to DMPP. Physostigmine (10−5 m) shifted the ACh response curve to the left but physostigmine itself caused inhibition of Jsm which was blocked by atropine. Substitution of mucosal Cl− by NO−3 reduced Jsm to a similar extent to maximum cholinoceptor effect and abolished responses to bethanecol. Anoxia further reduced Jsm in the presence of NO−3. Mucosal SITS and DIDS (1 mm) reduced Jsm but this was less than the maximum inhibition seen with drugs acting on cholinoceptors or mucosal Cl− removal. Serosal DIDS caused a similar inhibition. We conclude that cholinoceptor agonists inhibit but do not abolish luminal bicarbonate transport by an action on muscarinic receptors.