Sleep disorders, such as difficulty falling asleep, problems maintaining sleep, poor sleep efficiency, early awakening, and excessive daytime sleepiness, are prevalent in patients with cancer. Such problems can become chronic in some patients, persisting for many months or years after completion of cancer therapy. For patients with cancer, sleep is potentially affected by a variety of factors, including the biochemical changes associated with the process of neoplastic growth and anticancer treatments, and symptoms that frequently accompany cancer, such as pain, fatigue, and depression.Fatigue is highly prevalent and persistent in patients with cancer and cancer survivors. Although cancerrelated fatigue and cancer-related sleep disorders are distinct, a strong interrelationship exists between these symptoms, and a strong possibility exists that they may be reciprocally related. The majority of studies that have assessed both sleep and fatigue in patients with cancer provide evidence supporting a strong correlation between cancer-related fatigue and various sleep parameters, including poor sleep quality, disrupted initiation and maintenance of sleep, nighttime awakening, restless sleep, and excessive daytime sleepiness. This paper reviews the data from these studies with a view toward suggesting further research that could advance our scientific understanding both of potential interrelationships between sleep disturbance and cancer-related fatigue and of clinical interventions to help with both fatigue and sleep disturbance. The Oncologist 2007;12(suppl 1): [35][36][37][38][39][40][41][42]

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Summaryand Jamieson (2), and used extensively by Gardner et al. (9, l o ) ,In order to characterize the secretory capacity of isolated acinar cells, the effects of various secretagogues on amylase release were studied in guinea pigs. The effect of carbachol on amylase secretion reached a maximal level after a 30-min incubation and was dose dependent. At M, carbachol induced a 33% increase in amylase secretion over control values (P < 0.001); at M, there was an 8% increase over control (P < 0.05); and, at M, there was no change in amylase secretion. Muscarinic blockade with equimolar concentrations of atropine completely blocked the expected carbachol-induced increase in amylase secretion after both 30-and 60-min incubations. The response to secretin was neither significantly diierent from that to carbachol nor dose dependent over the concentraprovides an ideal model system for -studies of isolated acinar cells, pancreatic secretion in such cells has not been fully characterized. Cells prepared by this technique maintain the structural features found in intact tissue and demonstrate little if any damage when studied biochemically. In addition, the acinar cell preparation eliminates the "wash-out" and ductular components of the secretory process and allows identification of acinar cell responses alone. In order to-investigate the secretory capacity of isolated pancreatic acinar cells, we have explored the effects of a variety of stimuli on amylase secretion in such cells. The results obtained in these studies are discussed with regard to the potential mechanisms involved in stimulus-secretion coupling in pancreatic acinar cells. tion range tested. After a 30-min incubation, secretin induced MATERIALS AND METHODS significant increases in amylase secretion of 23%, 19%, and 23% at concentrations of M, 10-7 M, and M, respectively. Male Hartley strain albino guinea pigs were maintained at 22' As with carbachol, the response to secretin was blocked by and fed standard chow. For the 48 hr preceding each experiatropine. SecreCion of amylase in response to cholecystokinin-ment, animals were allowed water a d libitum, and were otherpancreozymin octapeptide (CCK-PZ) was maximal after a 30-wise fasted. After the Zday fast, the animals were stunned and min incubation and was dose dependent. CCK-PZ, at concen-.the" exsanguinated by severing the The pancreas was tions of 10-7 M and 10-9 M, induced signficant increases in immediately removed, trimmed of excess fat and connective secretion of 18% (P < 0.001) and 17% (P < 0.001), re-tissue, and placed in a Krebs-Ringer bicarbonate solution equilspectively. ~t 10-11 M, CCK-PZ did not evoke a significant in-ibrated with 95% oxygen-5% COP (pH 7.4) and containing 14 crease amylase secretion. ~h~ C C K -P Z -~, ,~~~~~ increase in mM glucose, soybean trypsin inhibitor 0.1 mglml, bovine serum amylase secretion was significantly less t b n that observed with albumin 2.5 mg/ml, 0.1 mM calcium, and 1.2 mM magnesium mrbachol (P < 0,05), was not significantly daerent from that (solution 1). T...