The effects of bright light treatment on subjective and objective sleepiness during three consecutive night shifts among hospital nurses – a counter-balanced placebo-controlled crossover study

Objectives:The objective was to investigate effects of timed bright light treatment on subjective and objective measures of sleepiness during three consecutive night shifts among hospital nurses.Methods:Thirty-five nurses were exposed to bright light (10,000 lux) and red dim light (100 lux) during three consecutive night shifts in a counter-balanced crossover trial lasting nine days, which included three days before and three days after the three night shifts. Light exposure for 30 minutes was scheduled between 02:00–03:00 hours on night 1, and thereafter delayed by one hour per night in order to delay the circadian rhythm. Subjective sleepiness was measured daily (heavy eyelids, reduced performance) and every second hour while awake (Karolinska Sleepiness Scale, KSS). Objective sleepiness (Psychomotor Vigilance Task, PVT) was measured at 05:00 hours during each night shift. Beyond nocturnal light exposure on the night shifts, no behavioral restrictions or recommendations were given at or off work.Results:Bright light treatment significantly reduced heavy eyelids during night shifts. However, results on KSS and PVT were unaffected by bright light. There were no differences in subjective sleepiness during the three days following the night shifts.Conclusions:This bright light treatment protocol did not convincingly reduce sleepiness among nurses during three consecutive night shifts. Nor did bright light impede the readaptation back to a day-oriented rhythm following the night shift period. Too few consecutive night shifts, inappropriate timing of light, and possible use of other countermeasures are among the explanations for the limited effects of bright light in the present study.     

P-R interval in relation to heart rate during exercise and the influence of posture and autonomic tone

P-R interval (PR) in relation to heart rate (HR) during exercise was studied in healthy men. When subjects were in a recumbent position, mean PR between HR 90–140 beats/min (bpm) decreased linearly from 167±8 ms to 136±5 ms. (Regression line: PR=0.287 HR +182.9, r=0.40). PR did not decrease further at HR up to 180 bpm. When subjects were in a sitting position, a further decrease occurred after HR 150–160 bpm. The shortest PR observed during exercise was 100 ms. The decrease of PR between HR 90–140 bpm was affected by atropine but not by propranolol. Higher HR was not achieved after propranolol, and after atropine there was no difference in PR in either exercise position compared to the two exercises without any drug. Thus, exercise induces a decrease in PR which is for the most part completed at HR 140–150 bpm and is mainly achieved by a withdrawal of the parasympathetic tone. PR at HR 90 bpm was correlated to body surface area, indicating that the PR duration is related to the body and heart dimensions.     

Alterations of fast axoplasmic transport in experimental methyl n-butyl ketone neuropathy.

Methyl n-butyl ketone (MBK) is known to produce a giant axonal neuropathy in man and experimental animals characterized pathologically by a gradual increase in the number of neurofilaments which become associated with focal areas of axonal swelling and thinning of the myelin sheath. Fast axoplasmic transport was studied in rats exposed to MBK. In 10 severely paralyzed rats exposed to MBK there was a significant impediment of fast axoplasmic transport following dorsal root ganglion injections (x +/- S.D. = 283.2 +/- 20.34 mm/day) compared to normal controls (417.6 +/- 23.78 mm/day). In rats undergoing injections into the ventral horn of the spinal cord there was a gradual impairment of the mean down flow rate for transport of [3H]leucine which correlated with the severity of the MBK induced neuropathy. Quantitative morphological determinations showed that the total number of neurotubules per unit cross-sectional myelin area and the number of neurotubules associated with mitochondria in swollen axons was unchanged from normal. The total number of mitochondria in randomly sampled axons varied significantly from controls but the absolute number of mitochondria associated with neurotubules was unchanged from normal. The results of these studies suggest that the impediment of fast axoplasmic transport may be related to the increased neurofilaments producing focal areas of axonal blockage.     

Primary tumors of the small intestine

In our department of surgery 28 patients with malignant and 10 with benign tumors of the small intestine were treated from 1940 to 1974. Fifteen patients with malignant and 7 with benign tumors underwent surgery with the intention to cure. Palliative operations or explorations were carried out on 13 patients with malignant tumors. Three patients with benign tumors were not operated on. The initial symptoms were vague: abdominal pain, nausea, anemia or bleeding in 75 and 80 percent of patients with malignant and benign tumors, respectively. The indication for operation in the malignant cases was, however, stenosis of the intestine or biliary tract or a palpable mass in 60 percent of the cases. At operation the tumors were thus in an advanced stage. Because the initial symptoms are vague, early diagnosis is difficult.The overall 5 year survival rate was 21 percent after surgery for malignant tumors. Among the patients considered by the surgeons to have had radical operations excluding cancer patients, 40 percent survived 5 years. The surgeon's opinion regarding “radical” operation as well as the presence or absence of metastases at microscopy were of limited prognostic value.     

IgM and IgG responses during chronic relapsing experimental allergic encephalomyelitis (r-EAE)

During chronic relapsing experimental allergic encephalomyelitis (r-EAE) in guinea pigs, serum IgM and IgG concentrations increased markedly early in disease. Serum IgM and IgG increased similarly in control animals immunized with Freund's incomplete adjuvant (FIA) and Mycobacterium tuberculosis (MT). In the chronic phase of r-EAE but not in control animals, elevated IgM was also found in central nervous system (CNS) extracts, suggesting intrathecal IgM synthesis. IgG antibodies against myelin and myelin basic protein (MBP) were regularly detected in r-EAE sera from day 21 post inoculation (p.i.), reaching maximum levels in the early chronic phase. IgG antibodies against galactocerebroside (GC) and galactose appeared in some r-EAE sera. Oligoclonal IgG bands were demonstrated in all r-EAE guinea pig sera 21-26 days p.i. The bands in serum decreased in number and strength in the chronic phase. They could be traced to antibodies against MT in 4 of 10 animals, but not to antibodies against myelin, MBP, GC or galactose. Oligoclonal IgG bands were also regularly visualized in r-EAE CNS 124 days p.i., suggesting persistent intrathecal IgG synthesis. They varied in number and migration between different regions of individual CNS. Oligoclonal CNS IgG was related to antibodies against MT in only one of 7 animals, and in no case to antibodies against myelin.     

Selective effect of some somatostatin analogs on glucagon as opposed to insulin release in rats in vivo

Cyclic somatostatin, at a dose of 700 but not 70 ng/kg/min, inhibited arginine-induced insulin and glucagon release as well as glucose stimulated insulin release in rats in vivo. Three somatostatin (S-S) analogs (D-Cys14-S-S, D-Trp8-D-Cys14-S-S and Ala2-D-Trp8-D-Cys14-S-S), at a dose of 70 ng/kg/min, suppressed arginine-induced glucagon but not insulin release. At the same dose, the first two of these analogs had no effect on glucose-induced insulin release, while the third one. Ala2-D-Trp8-D-Cys14-somatostatin, enhanced insulin release induced by glucose. A fourth analog, D-Trp8-somatostatin, was more potent than somatostatin with regard to arginine stimulated insulin and glucagon release, and equipotent with somatostatin with respect to glucose stimulated insulin release. These studies show, firstly, that the inhibitory effect of somatostatin analogs on arginine induced insulin release may be different from that when glucose is used as a stimulant and, secondly, that Ala2-D-Trp8-D-Cys14-somatostatin inhibits arginine-induced glucagon release while enhancing insulin release on glucose stimulation.