Sex differences in social behavior: comparing social role theory and evolutionary psychology

In rats, copper deficiency leads to low copper metalloenzyme activity, high serum cholesterol, and cardiovascular lesions. In humans, moderately low copper intake may be common, but the consequences remain largely uncertain. The present study examined the effects of copper supplementation (2 mg/d for 4 weeks in a copper/placebo crossover design) in 20 adult men with moderately high plasma cholesterol. End-point measurements were three copper enzyme activities, erythrocyte superoxide dismutase (SOD), plasma ceruloplasmin (Cp), and plasma diamine oxidase (DAO), and three parameters related to the risk of cardiovascular disease (CVD), plasma cholesterol, plasma lipoprotein (a) [Lp(a)], and lag times for very-low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) oxidation in vitro. Although copper had no significant effects on any parameter for the entire study group, it did significantly increase two enzyme activities (SOD and DAO), as well as lipoprotein oxidation lag times, in 10 subjects in the lower half of a median split for precopper values. Thus, copper supplementation appeared to influence some types of measurements in subjects beginning with less than median values.     

Chronic carvedilol reduces mortality and renal damage in hypertensive stroke-prone rats

The effects of carvedilol, a novel vasodilating beta-blocker and antioxidant, and propranolol on survival, neurobehavioral deficits, cardiovascular parameters, plasma renin, plasma aldosterone levels and renal pathology were determined in stroke-prone spontaneously hypertensive rats. Stroke-prone spontaneously hypertensive rats were allowed access to 1% NaCl as the drinking solution and a high fat diet supplemented with carvedilol (1200 or 2400 ppm) or propranolol (2400 ppm). The control group consisted of stroke-prone spontaneously hypertensive rats placed on the same diet with no drug supplement. Animals fed propranolol had a blood level of 864 +/- 68 ng/ml, whereas carvedilol-fed animals had blood levels of 24 +/- 4 ng/ml at 1200 ppm and 471 +/- 145 ng/ml at 2400 ppm. Carvedilol and propranolol treatment resulted in significant beta adrenoceptor blockade. Both compounds reduced heart rate, but had no significant effects on systolic arterial blood pressure. Carvedilol- and propranolol-treated animals also exhibited significant, prolonged protection from neurobehavioral deficits and mortality (P < .01). Elevated plasma renin activity and aldosterone levels seen in untreated controls were significantly decreased by propranolol (P < .05), and to a considerably greater extent by the same dose of carvedilol (P < .01). Carvedilol decreased renal histopathological damage and cardiac hypertrophy to a greater extent (P < .01) than propranolol (at equal doses). Both carvedilol (P < .01)- and propranolol (P < .01)-treated animals had considerably reduced renal damage at 18 weeks of treatment. Carvedilol reduced renal damage more than propranolol (P < .05). In addition, the lower (1200 ppm) dose of carvedilol, which decreased neurobehavioral deficits and mortality, had no significant effects on organ mass or renal function, but significantly (P < .01) reduced renal damage. These data indicate that both beta adrenoceptor blockers, especially carvedilol to a considerably greater degree, convey significant protection in a genetic model of severe hypertension that results in renal and cardiovascular organ pathology, neurobehavioral deficits and premature death.     

One hundred years of orthopedics in the Netherlands. III. Bone tumors

In the fifties, patients with a malignant bone tumour were treated with radiotherapy, sometimes supplemented by resection, as recommended by the Bone Tumour Committee established in 1953. In the seventies, improvement of imaging techniques and chemotherapy made limb-saving surgery possible. Currently, 70% of patients with a malignant tumour of the locomotor apparatus are treated by limb saving, oncologically justified surgery. The surgical defects can be repaired with the aid of an endoprosthesis, or bone homografting or autografting. Children are often treated with an operation involving 180% rotation of the ankle to function as the knee, combined with a prosthesis. Adults are sometimes treated with this technique, but also with internal ('standard') prostheses and donor bone. The future will have to make clear which technique is to be preferred in which situation. Probably, typing and prognosis of various tumours may improve, leading to better insight into the treatment. Centralization of the treatment of rare tumours may also contribute to improvement of the treatment and its scientific research.     

Surfactant protein metabolism in vivo

The surfactant components saturated phosphatidylcholine, SP-B and SP-C, are secreted together in lamellar bodies, and at least a part of the de novo synthesized SP-A is secreted independently. The surface film forms from tubular myelin and loose lipid arrays, and it generates unilamellar vesicles that lack surfactant proteins and are thought to represent catabolic forms. The half-life values for the clearance of surfactant proteins from lungs range from 6.5 to 28 h and vary with species. There is minimal information about the associations of the surfactant proteins with lipids or with each other after film formation, although all surfactant components seem to be recycled back into lamellar bodies in type II cells. The relative importance of type II cells or macrophages to the catabolism of the protein components of surfactant remains to be characterized, as do regulators of surfactant homeostasis.     

Compensatory enlargement in coronary and femoral arteries is related to neither the extent of plaque-free vessel wall nor lesion eccentricity. A postmortem study

Arteries may demonstrate compensatory enlargement in response to plaque accumulation. It has been proposed that enlargement is achieved by the expansion of the nondiseased (plaque-free) vessel wall. In this study, we assessed this hypothesis. Post mortem, 32 atherosclerotic coronary arteries (left anterior descending, n = 10; left circumflex, n = 11; and right coronary, n = 11) and 54 atherosclerotic femoral arteries were pressure fixed. Cross sections (coronary arteries, n = 537; femoral arteries, n = 1602) were obtained for analysis every 2.5 mm for the coronary arteries and every 5.0 mm for the femoral arteries. From these cross sections, we determined the degree of remodeling and an eccentricity index. Finally, we measured the extent of plaque-free vessel wall. The plaque-free vessel wall was defined as (1) no plaque present or (2) plaque thickness < 0.5 mm. A very weak, negative correlation was observed between the degree of remodeling and the extent of the plaque-free vessel wall (coronary arteries: no plaque r2 = .13, P < .01; < 0.5 mm plaque r2 = .15, P < .05; femoral arteries: no plaque r2 = .02, P < .01; < 0.5 mm plaque r2 = 0.04, P < .01). The degree of remodeling did not correlate with the eccentricity index (coronary arteries r2 = .002, P > .05 and femoral arteries r2 = .001, P > .05). Thus, compensatory enlarged segments did not reveal a larger circumference of plaque-free vessel wall compared with segments that failed to enlarge. This study provides no support for the hypothesis that nondiseased vessel-wall expansion is responsible for compensatory enlargement in atherosclerotic arteries.     

Case study: worsening Tourette's disorder or withdrawal dystonia?

This case report focuses on withdrawal dystonia, a movement disorder associated with neuroleptics. Its occurrence in a patient with Tourette's disorder complicated the clinical picture. A misinterpretation of the symptoms led to ineffective management of the movement disorder. The presence of increased blinking with facial pain, dystonic movements, and other facial movements at each neuroleptic dose reduction pointed toward withdrawal dystonia rather than toward a worsening of Tourette's disorder. Implications for diagnosis and treatment are discussed.     

Reactivity of small intramyocardial arteries from atherosclerotic and non-atherosclerotic human hearts

Little is known about how the vascular reactivity of the coronary microcirculation is affected by upstream atherosclerotic disease. We have examined, with a wire myograph, the responses of intramyocardial arteries from hearts in which the epicardial vessels were either free of atherosclerotic lesions (non-diseased group) or were affected by atherosclerosis (diseased group). Vasodilator responses of preconstricted vessels to substance P (84.1 +/- 12.6 compared to 42.0 +/- 19.7%) were less in vessels from the diseased group (p < 0.05). In contrast, the relaxation to bradykinin (70.2 +/- 21.2 compared to 100.6 +/- 7.9%) was increased in vessels from the diseased group (p < 0.05). The dilator responses to acetylcholine, adenosine diphosphate, histamine and sodium nitroprusside showed no significant differences between arteries from each group. 5-Hydroxytryptamine was without any significant vasodilator effect in arteries from either group. Assessment of contractile function revealed that the responses to 5-hydroxytryptamine, acetylcholine, U46619, endothelin-1 and L-N(G)-monomethylarginine in each group were not significantly different. Histamine, noradrenaline and dopamine were without any significant contractile response. These results demonstrate that upstream atherosclerosis does not confer any global impairment of endothelium-dependent vasorelaxant responses or smooth muscle hyperreactivity to vasoconstrictors in the arteries that penetrate the myocardium.     

Improved GC/MS analysis of opiates with use of oxime-TMS derivatives

An improved gas chromatographic/mass spectrometric (GC/MS) assay is described for the quantitation of codeine and morphine as trimethylsyl (TMS) derivatives. The TMS derivatization of ketone-containing opiates results in the formation of multiple derivatives. Some of these products have retention times close to those of codeine-TMS and morphine-TMS. When the keto-opiates are present in samples assayed for codeine and morphine in urine, they can interfere with the quantitation of these commonly targeted opiates. The assay was improved with the addition of a pre-BSTFA derivatization step, whereby hydroxylamine was used to convert the keto-opiates into the corresponding oxime derivative. These derivatives were then reacted with BSTFA to form the TMS ethers and TMS oxime derivatives. The oxime step enabled production of single derivatives for hydrocodone and hydromorphone. In addition, the retention times for the oxime-TMS derivatives were increased so that they no longer elute near the targeted drugs of codeine and morphine. The addition of the oxime step does not affect the sylation of codeine and morphine, and the accuracy and precision of this assay were unaffected.