Load-induced proteoglycan orientation in bone tissuein vivo andin vitro

Summary Previous studies of Alcian blue-induced birefringence in adult avian cortical bone showed that a short period of intermittent loading rapidly produces an increased level of orientation of proteoglycans within the bone tissue. In the absence of further loading, this persists for over 24 hours. We have proposed that this phenomenon could provide a means for “capturing” the effects of transient strains, and so provide a persistent, constantly updated strain-related influence on osteocyte populations related to the bones' averaged recent strain history, in effect, a “strain memory” in bone tissue. In our present study, we use the Alcian blue-induced birefringence technique to demonstrate that proteoglycan orientation also occurs after intermittent loading of both cortical and cancellous mammalian bonein vivo andin vitro. We also show that the change in birefringence is proportional to the magnitude of the applied strain, and that the reorientation occurs rapidly, reaching a maximal value after only 50 loading cycles. Examination of electron micrographs of bone tissue after staining with cupromeronic blue allows direct visualization and quantification of the change in proteoglycan orientation produced by loading. This shows that intermittent loading is associated with a realignment of the proteoglycan protein cores, bringing them some 5 degrees closer to the direction of collagen fibrils in the bone matrix.     

The development of a surveillance system to monitor emergency food relief in New York State.

A representative sample of emergency food relief (EFR) programs was selected on the basis of a census of 1,488 EFR programs in New York State. The census was a two-stage telephone survey. EFR was provided in every county although there was considerable variation in the amount of EFR per county. The soup kitchen and food pantry components of EFR had to be differentiated. The surveillance system was operational one year after the census began.     

Histidine, histamine, and the neuroregulation of food intake: a review and hypothesis

Feeding, a behavior regulated by the central nervous system (CNS), includes the acquisition of specific essential nutrients and the maintenance of energy balance. Modulation of feeding behavior is a normal part of survival, but certain pathological conditions interrupt or modify regulatory aspects of feeding, thereby leading to inappropriate intake. This review examines aspects of metabolism associated with the anorexia seen in animals suffering from protein-energy malnutrition (PEM). The main focus is the indispensable amino acid histidine (His), the biosynthetic precursor of the neurotransmitter histamine (HA). In kwashiorkor-like PEM, His is elevated in plasma and brain, whereas all other indispensable amino acids are decreased. The elevation of His in the brain is to concentrations five times normal. Because the rate of HA synthesis in the brain is a function of the His concentration, His elevation raises the possibility of a profound direct effect of CNS function. In children, PEM consistently produces the symptoms of depressed food intake, edema, growth failure, and psychomotor changes. One known central effect of HA is the stimulation of ACTH and corticosteroid release. Based on these observations, the hypothesis being examined is as follows: one component of the pathophysiological neuroregulation of food intake involved the His-induced variation of HA concentration in the hypothalamus and the subsequently altered neurochemical activity at the corticotropin-releasing factor (CRF) neurons o the paraventricular nucleus (PVN).     

Tonsils, obesity and obstructive sleep apnoea.

In this article the normal effects of anaesthesia on breathing are defined. Specific threats to the airway are identified and illustrated by reference to common clinical conditions.     

Cardiovascular, metabolic and neurologic effects of carbon monoxide and cyanide in the rat.

Levine-prepared, female Sprague-Dawley rats were used to investigate the effects of carbon monoxide (CO) and cyanide (CN) on heart rate, blood pressure, hematocrit, body temperature, blood glucose, lactate, and neurologic function. Rats were exposed to either 2400 ppm CO, 1500 ppm CO, 4 mg/kg NaCN, or both 1500 ppm CO and 4 mg/kg NaCN for 90 min, followed by 4 h of room air recovery. Following exposure to 2400 ppm CO, rats exhibited a significant bradycardia which normalized by 2 h of recovery. All groups exhibited an initial hypotension which was either maintained or exaggerated during exposure in all but the rats exposed to CN, and which returned to pre-exposure values by 90 min. All groups experienced a significant hypothermia during the exposure period, with those in the 1500 ppm CO or the CN returning to initial values over the recovery period. The only significant change in hematocrit was due to 2400 ppm CO (4.1% increase). During exposure, all groups experienced an initial surge in glucose concentration which was maintained in all but rats exposed to 2400 ppm CO. The greatest hyperglycemic response resulted from the combination of CO and CN, whereas 2400 ppm CO produced the smallest. CN alone produced no significant rise in lactate concentration. However, lactate concentration in all other groups was significantly elevated during the exposure period, returning to initial values by 4 h of recovery. Lactate concentrations and neurologic deficit in rats exposed to 1500 ppm CO, when added to those rats treated with CN, closely approximated the lactate and neurologic deficit of the combination treatment. Neurologic deficit was greatest in rats exposed to 2400 ppm CO. While in most cases the responses of the rats to CO and CN differed whether the substances were administered alone or in combination, a synergistic relationship is not suggested. An additive or less than additive relationship is more likely.