Human hip impingement morphology: an evolutionary explanation.

We examined the morphology of mammalian hips asking whether evolution can explain the morphology of impingement in human hips. We describe two stereotypical mammalian hips, coxa recta and coxa rotunda. Coxa recta is characterised by a straight or aspherical section on the femoral head or head-neck junction. It is a sturdy hip seen mostly in runners and jumpers. Coxa rotunda has a round femoral head with ample head-neck offset, and is seen mostly in climbers and swimmers. Hominid evolution offers an explanation for the variants in hip morphology associated with impingement. The evolutionary conflict between upright gait and the birth of a large-brained fetus is expressed in the female pelvis and hip, and can explain pincer impingement in a coxa profunda. In the male hip, evolution can explain cam impingement in coxa recta as an adaptation for running.

Patterns of violent aggression-induced brain c-fos expression in male mice selected for aggressiveness.

Mice selected for aggressiveness (long and short attack latency mice; LALs and SALs, respectively) constitute a useful tool in studying the neural background of aggressive behavior, especially so as the SAL strain shows violent forms of aggressiveness that appear abnormal in many respects. By using c-Fos staining as a marker of neuronal activation, we show here that agonistic encounters result in different activation patterns in LAL and SAL mice. In LALs, agonistic encounters activated the lateral septum, bed nucleus of stria terminalis, medial amygdala, paraventricular nucleus of the hypothalamus, anterior hypothalamic nucleus and tuber cinereum area (both being analogous with the rat hypothalamic attack area), dorsolateral periaqueductal gray, and locus coeruleus. This pattern is similar with that seen in the territorial aggression of male mice, rats and hamsters, and non-lactating female mice. SALs showed strong fight-induced activations in the central amygdala and lateral/ventrolateral periaqueductal gray. In this strain, no activation was seen in the lateral septum and the dorsolateral periaqueductal gray. This pattern is similar with that seen in other models of violent aggression, e.g., in attacks induced by hypothalamic stimulation in rats, quiet biting in cats, lactating female mice, and hypoarousal-driven abnormal aggression in rats. We suggest here that the excessive activation of the central amygdala and lateral/ventrolateral periaqueductal gray--accompanied by a smaller activation of the septum and dorsolateral periaqueductal gray--underlay the expression of violent attacks under various circumstances.

Endocrine stress response in rats subjected to singular orbital puncture while under diethyl-ether anaesthesia.

In an attempt to assess possible discomfort in rats subjected to orbital puncture while under diethyl-ether anaesthesia, their endocrine stress response was determined. Concentrations of corticosterone, adrenaline and noradrenaline were measured in plasma obtained via a jugular catheter from rats subjected to diethyl-ether anaesthesia with or without orbital puncture. No statistically significant differences were found between the punctured and non-punctured rats as to peak levels of plasma corticosterone and adrenaline as well as for the times required by the increased concentrations to return to baseline values. The rate by which the plasma noradrenaline level returned to baseline values was somewhat decreased by orbital puncture. Diethyl-ether anaesthesia alone produced a marked endocrine response when compared with handling and novelty stress associated with the induction of anaesthesia. It is concluded that diethyl-ether anaesthesia causes pronounced increases in the plasma levels of the selected stress hormones and that orbital puncture does not amplify this response. It is suggested that diethyl-ether anaesthesia masks any effects of orbital puncture.

Amylin-induced in vivo insulin resistance in conscious rats: the liver is more sensitive to amylin than peripheral tissues.

UNLABELLED: Amylin is a polypeptide of 37 amino acids, predominantly synthesized in pancreatic Beta cells. The peptide was suggested to be dysregulated in Type 2 (non-insulin-dependent) diabetes mellitus and it antagonized certain actions of insulin in vitro in rat muscle. This led to speculation that amylin is involved in the pathogenesis of Type 2 diabetes. We have examined the in vivo effects of rat amylin, amidated at the carboxy-terminus, on insulin-mediated carbohydrate metabolism in conscious rats, using the hyperinsulinaemic (+/- 1 nmol/l) euglycaemic (6 mmol/l) clamp technique combined with [3-3H]-glucose infusion. Basal plasma amylin levels were less than or equal to 75 pmol/l. Applied amylin levels of 220 +/- 75 pmol/l (infusion rate of 12.5 pmol/min) antagonized only the insulin action on liver, resulting in a 100% increase of hepatic glucose output. Amylin levels of 4750 +/- 750 pmol/l (infusion rate of 125 pmol/min) induced a 250% increase of insulin-inhibited hepatic glucose output and, in addition, a 30% decrease of insulin-stimulated peripheral glucose up-take. Amylin did not affect: 1) the metabolic clearance rate of insulin, 2) the levels of plasma glucagon, epinephrine, norepinephrine, and corticosterone, 3) in vitro insulin binding and insulin-stimulated receptor autophosphorylation. This suggests that amylin antagonizes insulin action via binding to a yet unknown receptor. IN CONCLUSION: amylin causes in vivo insulin resistance and the liver seems the predominant organ regulated by this hormone. The in vivo effects of amylin mimic the pathophysiological abnormalities of insulin action in Type 2 diabetes.