Daily associations with cannabis use and sleep quality in anxious cannabis users.

INTRODUCTION: Cannabis is increasingly used to self-treat anxiety and related sleep problems, without clear evidence of either supporting or refuting its anxiolytic or sleep aid effects. In addition, different forms of cannabis and primary cannabinoids ∆9-tetrahydrocannabinol (THC) and cannabidiol (CBD) have differing pharmacological effects. METHODS: Thirty days of daily data on sleep quality and cannabis use were collected in individuals who use cannabis for mild-to-moderate anxiety (n = 347; 36% male, 64% female; mean age = 33 years). Participants self-reported both the form (flower or edible) and the ratio of THC to CBD in the cannabis used during the observation period. RESULTS: Individuals who reported cannabis use on a particular day also reported better sleep quality the following night. Moderation analyses showed that better perceived sleep after cannabis use days was stronger for respondents with higher baseline affective symptoms. Further, respondents who used cannabis edibles with high CBD concentration reported the highest perceived quality of sleep. CONCLUSIONS: Among individuals with affective symptoms, naturalistic use of cannabis was associated with better sleep quality, particularly for those using edible and CBD dominant products.

Sick sinus syndrome in nine West Highland white terriers.

Sick sinus syndrome is a clinical term used to describe the clinical signs of sinus node dysfunction. This paper describes the clinical data from nine West Highland white terriers, eight females and one male, in which a diagnosis of sick sinus syndrome was made. The most common clinical signs were episodic weakness and presyncope. Electrocardiographic findings included sinus bradycardia, sinus arrest with or without escape complexes, disturbances of atrioventricular conduction, paroxysmal supraventricular tachycardia, or some combination of these dysrhythmias. The main radiographic changes were mild right-sided cardiomegaly in five cases, and a slight increase in bronchial and interstitial markings in four, but there was no evidence of congestive heart failure in any of the dogs. Echocardiography revealed mild to moderate mitral endocardiosis in three cases with no other significant abnormalities. The dogs' responses to parenteral atropine were variable and were not necessarily related to their response to oral anticholinergic agents. Five of the dogs were initially treated with propantheline bromide, but in only two of them were the clinical signs controlled in the long term. Six of the dogs were successfully treated by the implantation of a transvenous pacemaker.

Ventricular septal defect in a blue duiker (Cephalophus monticola).

A 9-mo-old female blue duiker (Cephalophus monticola) weighing 3.9 kg was diagnosed with a cardiac murmur during quarantine examination. Evaluation of the heart by auscultation, electrocardiography, two-dimensional echocardiography, and Doppler color-flow echocardiography revealed a restrictive outlet ventricular septal defect with left atrial and left ventricular dilation. Trivial mitral, tricuspid, and aortic regurgitation was also noted. Though the duiker was clinically asymptomatic at the time of cardiac evaluation, it was found dead 1 wk later. The cause of death was not determined.

Acetylcholine is a vasodilator of porcine skeletal muscle arteries.

The purpose of this study was to test the hypothesis that porcine skeletal muscle arteries exhibit concentration-dependent vasodilation in response to acetylcholine (ACH) as observed in other mammals. We conducted three experiments. First, vasorelaxation responses to ACH were examined in isolated segments of femoral and brachial arteries, mounted on myographs and studied in vitro. Second, we determined whether resistance arteries from porcine skeletal muscle exhibit vasodilation in response to ACH by isolating second order arterioles (2-A) from the medial (MHT), deep-long (LOH) and lateral (LAT) heads of the triceps brachii muscles of four pigs. The rationale for selection of arterioles from these muscles was that these muscles represent muscles composed primarily of slow-oxidative, fast-oxidative-glycolytic, and fast-glycolytic muscle fiber types, respectively. 2-As were isolated and cannulated with micropipettes and intraluminal pressure set at 60 cm H2O. In both sets of in vitro experiments, we determined responses to an endothelium-independent dilator, sodium nitroprusside (10(-10)-10(-4) M), and to endothelium-dependent agents ACH (10(-10)-10(-4) M), and bradykinin (BK; 10(-11)-10(-6) M). Third, we used transcutaneous ultrasound imaging to measure changes in artery diameters and Doppler-principle measurements of blood flow velocities to estimate changes in total blood flow in the femoral vascular bed. Results reveal that ACH and BK produced similar vasorelaxation responses in femoral and brachial arteries and vasodilation of skeletal muscle 2-As. Also, ACH produced increases in blood flow and decreases in vascular resistance in the femoral vascular bed. These results indicate that the arterial tree of porcine skeletal muscle exhibits ACH-induced, endothelium-dependent vasodilation.

The experience of chronic nonmalignant pain.

This article reports the results of a survey of 204 persons with chronic nonmalignant pain who were members of a national self-help organization. The survey evaluated the organization, explored the perceived effect of pain on quality of life, and assessed experiences with and perceptions of health-care providers. Response rate was 40%. Of survey respondents, 50% reported inadequate pain relief. Respondents identified depression as one of the worst problems caused by their chronic pain: 50% reported that they had considered suicide due to feelings of hopelessness associated with their pain, 51% reported taking only as much medication as prescribed, and 44% reported taking less medication than prescribed. Further investigation is needed to describe the personal impact of chronic nonmalignant pain.

Effects of the beta-adrenergic agonist cimaterol on chicken muscle atrophy induced by stretch-release.

Thirty-eight White Leghorn chickens, 5 weeks of age, were used to investigate the effect of cimaterol on patagialis muscle (PAT) atrophy due to release of passive-stretch. Cimaterol (CIM) was mixed in a standard commercial chicken diet at 0.5 ppm. Passive-stretch of PAT for 7 days significantly (P < 0.01) increased muscle weight (43%), fiber cross-sectional area (40%) and DNA unit size (34%) compared with unstretched control muscle. In birds fed the standard diet, stretch-release (SR) resulted in immediate and rapid atrophy and by 5 days the stretch-released muscle reached the size of control muscles. In the CIM-fed birds, the atrophy was delayed for 5 days after SR, at which time muscle atrophy at a rate similar to the birds fed the standard diet occurred. It was concluded that cimaterol retarded muscle atrophy induced by stretch-release but the effect was transient and limited to the first 5 days of treatment.

Passive stretch of adult chicken muscle produces a myopathy remarkably similar to hereditary muscular dystrophy.

The wings of 10 chickens between 1 and 5 years of age were passively extended. An increase in plasma creatine phosphokinase activity was observed in 30 min, continued to rise for 24 h, and then declined, suggesting mechanically induced damage to muscle fibers. Wing muscles were removed and examined histologically at various times after stretch. Patagialis muscles, but not biceps brachii, showed the development of muscle fiber pathology. The patagialis muscle is less active than the biceps brachii and is stretched to a greater degree by wing extension. Susceptibility of muscles to development of pathology appeared to be correlated with the age of the chickens. Pathology was remarkably similar to that observed in young chickens with hereditary muscular dystrophy. Necrotic fibers exhibiting segmental necrosis, abnormal shapes, enlargement, splitting, vacuolation, and phagocytosis were evident. Of particular interest was the appearance of abnormal clusters of acetylcholinesterase activity along the sarcolemma. These sites were shown to appear on fibers of 2-week-old dystrophic chicks prior to necrosis and increase in plasma creatine phosphokinase activity. It is suggested that aging of inactive muscles may promote adhesions between muscle fibers rendering them susceptible to damage when stretched and that necrosis of dystrophic fibers may be initiated by a similar mechanism. Such could occur if the genetic defect resulted in interfiber adhesions. Support for this hypothesis by other reports in the literature is discussed.

Effects of stretch and denervation on protease activities of normal and dystrophic chicken muscle.

Changes of protease activities that follow passive stretch, denervation, and denervation plus stretch were followed in the patagialis muscle of normal and dystrophic chicks between 6 and 7 weeks of age. The baseline activities of cathepsin C, cathepsin D, and leucine aminopeptidase in dystrophic muscle were 2 to 3.5 times higher than in normal muscle. Passive stretch and denervation induced increases in protease activities by 40 to 120% in normal muscle, whereas the same treatments did not significantly affect the activities of the enzymes in dystrophic muscle. We conclude that the level of protease activity in dystrophic chicken muscle at 6 weeks of age had already attained a maximum limit and could not be increased even by denervation. In spite of protease activities, which were not different from control dystrophic muscle, denervated dystrophic muscles lost muscle weight rapidly whether they were stretched or not. They weighed 60% less than the innervated control muscle after 7 days. Inherently high protease activities in dystrophic muscle do not vary at this age regardless of whether or not the muscle is gaining or losing weight.

Stretch-induced growth in chicken wing muscles: nerve-muscle interaction in muscular dystrophy.

Skeletal muscle growth following denervation and denervation plus passive stretch was characterized in the patagialis muscle of normal and dystrophic chicks until 8 wk of age. In both genotypes, muscles denervated at 1 wk of age grew at reduced rates compared with contralateral control muscles whether or not they were passively stretched. Histograms of fiber size distributions as well as morphological criteria showed that passive stretch of denervated dystropic muscles substantially delayed the development of pathology. Denervation alone provided less protection. There was no evidence of fiber necrosis in any denervated dystrophic muscle, although many fibers did exhibit extreme hypertrophy and abnormal morphology. When denervated dystrophic muscles were allowed to reinnervate, growth and development of pathology was rapid. Because denervation, denervation with passive stretch, or passive stretch alone retards, but does not prevent, the development of pathology, it is concluded that dystrophy in the chick is a myogenic defect that is exacerbated by neurally mediated contractile activity.

Fitts' principles still applicable: computer monitoring of fighter aircraft emergencies.

When examining the impact of automation in the cockpit, a careful distinction must be drawn between the role of a multi-crew civilian aircraft and a single-seat military aircraft. For the former, there are some concerns that automation can have a negative impact on the crew by reducing their proficiency. However, for a single-seat military aircraft on an attack mission, the role of automation is not only helpful to the pilot now but in the future may be necessary to achieve mission success. These distinctions must constantly be brought to mind in explaining the concepts of Fitts' principles. For a single-seat military aircraft, it is believed that these principles still apply, and that computer monitoring of system failures will further enhance their application. Three approaches to computer-augmented system monitoring are discussed.

The ultrastructure of feline infectious peritonitis virus in feline embryonic lung cells.

The ultrastructure of feline infectious peritonitis virus in cultured feline embryonic lung cells is reported. Feline embryonic lung cells were infected with feline infectious peritonitis virus and studied by transmission electron microscopy. The virus was not apparent in the cultured cells until 24 h after infection when it occurred in the endoplasmic reticulum, perinuclear space, Golgi apparatus, free in the cytoplasm, in large vacuoles in the cytoplasm and outside the cell membrane. The virus possessed typical coronavirus morphology and was produced by budding into the endoplasmic reticulum. There was no evidence to indicate that this virus budded through the cell membrane. Multinucleate giant cells were formed by infection of the cultured cells with the virus. The host cells were destroyed by the virus and phagocytosed by apparently healthy cells.