Analytic bond-order potentials for the bcc refractory metals Nb, Ta, Mo and W.

Bond-order potentials (BOPs) are based on the tight-binding approximation for determining the energy of a system of interacting atoms. The bond energy and forces are computed analytically within the formalism of the analytic BOPs. Here we present parametrizations of the analytic BOPs for the bcc refractory metals Nb, Ta, Mo and W. The parametrizations are optimized for the equilibrium bcc structure and tested for atomic environments far from equilibrium that had not been included in the fitting procedure. These tests include structural energy differences for competing crystal structures; tetragonal, trigonal, hexagonal and orthorhombic deformation paths; formation energies of point defects as well as phonon dispersion relations. Our tests show good agreement with available experimental and theoretical data. In practice, we obtain the energetic ordering of vacancy, [1 1 1], [1 1 0], and [1 0 0] self-interstitial atom in agreement with density functional theory calculations.

Analytic environment-dependent tight-binding bond integrals: application to MoSi2.

We present the first derivation of explicit analytic expressions for the environmental dependence of the sigma, pi, and delta bond integrals within the orthogonal two-center tight-binding approximation by using the recently developed bond-order potential theory to invert the nonorthogonality matrix. We illustrate the power of this new formalism by showing that it not only captures the transferability of the bond integrals between elemental bcc Mo and Si and binary C11(b) MoSi2 but also predicts the absence of any discontinuity between first and second nearest neighbors for the ddsigma bond integral even though large discontinuities exist for ppsigma, pppi, and ddpi.

Thyroid hormone alterations in patients with shock and injury.

Serum concentrations of total T3 and T4, free T4, rT3, TSH, TBG and cortisol were measured on arrival in hospital in 33 adult injured patients, 26 of whom were received directly from the accident. Serum cortisol levels and all thyroid indices, except TBG, were altered substantially by injury. Compared with values from 57 healthy volunteers, statistically significant (P less than 0.01) decreases were found in the mean serum free and total T4 concentrations and the rT3 level. Similarly significant (P less than 0.001) increases were seen in the mean serum T3, TSH and cortisol concentrations. Repeated assessment of thyroid function in six patients suggested a biphasic response to injury by TSH, T3 and rT3. The first phase was of short duration (1-2 h). Serum levels of TSH and T3 were above normal, and rT3 was decreased. These data suggest participation by the thyroid in the 'fight-or-flight' response to life-threatening stress. The second phase was fully established 6-18 h after injury and was characterized by reductions in serum TSH, T3 and total and free T4 and a rise in rT3. This pattern persisted throughout the 2-week period of measurement. Thus, as in other critical illnesses, the 'low T3' syndrome is common in severely injured patients. However, changes in thyroid hormone metabolism after injury are of greater intensity and longer duration.

Effect of sleep deprivation on cholesterol metabolism and triglyceridaemia in male volunteers.

The effect of 5-day sleep deprivation (SD) on cholesterol metabolism, together with triglyceridaemia, was studied in seven healthy male volunteers. A 3-day control period was followed by 5 days (120 h) complete SD and 4 days recovery. Blood was collected at 9 a.m. and at 9 p.m. Vastus lateralis muscle biopsy was performed during the control period, on the 5th day of SD, and on day 3 of recovery. The value of muscle cholesterol was related to the non-collagen protein content. The plasma triglycerides (TG) varied in a circadian biorhythm, the amplitude of which declined gradually during SD. The morning triglyceridaemia was significantly decreased on days 3-5 of SD (35%-79% of initial values). On days 4 and 5 of SD, plasma cholesterol fell significantly to 78% and 88% of control values, respectively. The ratio of its esterified to unesterified fractions remained unchanged throughout SD. Basal activity of lecithin cholesterol acyltransferase (LCAT) showed no diurnal biorhythm; on the last 2 days of SD, LCAT activity fell significantly to 71%-80%. In contrast, the decrease in fractional esterification rate (FER) was insignificant. In the vastus lateralis muscle, total cholesterol (TC) was decreased by 40% at the end of SD, the reduction being greater for cholesterol esters (CE) (by 63%) than for free cholesterol (FC) (by 36%). The relative proportion of CE significantly decreased from an initial 14.7% to 9.2% on the last day of SD. During recovery after SD, plasma cholesterol and TG slowly returned to normal. LCAT activity and FER recovered quickly, within 48 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Fractional cholesterol esterification rate and muscle cholesterol of healthy young men.

A group of fourteen healthy young male volunteers was examined to define more exactly the relations between lecithin cholesterol acyltransferase activity (LCAT), fractional cholesterol esterification rate (FER), total cholesterol (TC) and its free and esterified fractions (FC, CE) in skeletal muscles under physiological conditions. The mean values (+/- S.D.) of LCAT activity (95.4 +/- 16.3 mumol .1(-1) per hour), and FER (7.45 +/- 1.54% per hour) corresponded to published data on normolipidaemic healthy men of normal body weight. The mean value of TC in muscles was 332 +/- 83 micrograms per 100 mg of non-collagen protein, of which 14 +/- 7.4 per cent was formed by cholesterol esters. There was positive correlation between TC in muscles and age. Significant positive correlations between FER and the content of esterified cholesterol in muscles, and between FER and the proportion of esterified to total muscle cholesterol were found. These results suggest a close interrelation of cholesterol ester metabolism in the plasma and in slow pool tissues.

Relationship of thyroid hormone patterns to survival in canine hemorrhagic shock.

6 of 13 dogs subjected to 1 h of hemorrhagic shock (BP = 45-50 mm Hg) died during the first convalescent day. Nonsurvivors had lower baseline plasma concentrations of total and free T4 and T3, as well as rT3, and higher T3 uptake values. During shock, dogs that died had significantly lower plasma levels of total and free T4 and T3 and higher T3 uptake. In general, intergroup differences were accentuated during resuscitation. After volume replenishment, indices of thyroid function had stabilized or improved in survivors, but were still deteriorating in dogs that ultimately died. There were no consistent hemodynamic differences between the two groups. Thus, parameters of thyroid metabolism appear to be good prognostic indicators in canine hemorrhagic shock.

Bleomycin stimulates both membrane (Na+-K+) ATPase and electrogenic (Na+-K+) pump and partially removes the inhibition by vanadium ions.

Bleomycin 2 X 10(-6) and 6 X 10(-6) mol.1(-1) increased the activity of specific (Na+-K+) ATPase of the rat brain microsomes. It also stimulated the electrogenic (Na+-K+) pump in intact skeletal muscle cells. The blocking effect of vanadyl (+4V) on membrane (Na+-K+) ATPase was eliminated completely by the drug, but the action of vanadate (+5V) was counteracted only partially. Electron paramagnetic resonance spectra revealed the formation of a +4V - bleomycin complex which is still able to activate the (Na+-K+) ATPase.

Thyroid hormone responses in hemorrhagic shock: study in dogs and preliminary findings in humans.

One hour of hemorrhagic shock in the dog produces alterations in thyroid hormone metabolism far exceeding those seen after elective surgery or thermal injury. The changes in plasma thyroid hormone levels cannot be fully explained by carrier protein loss. Plasma concentrations of total thyroxine (T4) and triiodothyronine (T3) were significantly decreased after only 20 minutes of shock, continued to decrease throughout shock and resuscitation, and remained depressed for several days thereafter. Both hormones reached nadirs during volume replacement of 42% and 17% of baseline, respectively. The total T4 level normalized by the fifth postshock day, but the T3 concentration was still depressed on the ninth day. Plasma albumin, the principal canine thyroid hormone carrier, was significantly reduced 20 minutes after hemorrhage and remained low throughout convalescence. Concentrations of free T4 and T3 decreased during shock, but not as much as the total T4 and T3 concentrations. Reverse T3 levels, corrected for albumin loss, and T3 uptake values were increased during shock and resuscitation. Similar alterations in circulating thyroid hormone concentrations were seen in three patients with major traumatic injury and/or shock. The thyroid hormone changes in shock may represent another example of the "euthyroid sick syndrome."

The effect of five days' fasting on skeletal muscle enzymes in obese men.

The effect of 120 hours' (five days) fasting on the activity of some enzymes of energy metabolism in skeletal muscles was investigated in six obese young men. The results revealed a significant decline in the activity of the following enzymes: triosophosphate dehydrogenase (by 20%), glycerol-3-phosphate dehydrogenase (by 24%), lactate dehydrogenase (by 13%), citrate synthase (by 20%), hydroxyacyl-CoA dehydrogenase (by 40%), while the hexokinase and malate dehydrogenase activities were not significantly altered. Contrary to muscles of non-obese healthy men (Vondra, Bass, Brodan, Kuhn, Andel, Veselková and Vítek 1982), a smaller decline of activities of the investigated enzymes occurred together with a paradoxical change of the enzyme pattern, namely a predominance of carbohydrate catabolism and a decline of the role of fatty acids in muscle energy metabolism.

Aggravating effect of alcohol on admission serum insulin patterns of patients with trauma and in a state of shock.

The effect of alcohol upon admission serum insulin levels was studied in 114 injured patients with mean blood alcohol levels of 130 +/- 71 milligrams per deciliter, ranging from 10 to 350. These data were compared with those of 133 similar patients with no measurable blood alcohol levels and with those of 47 healthy volunteers. Whereas marked hyperglycemia caused by trauma or shock was unaffected by alcohol ingestion, insulin levels were more depressed in patients with blood alcohol levels 29.5 +/- 15.3 microunits per milliliter versus 37.8 +/- 36.7 microunits per milliliter, p less than 0.025. In fatally injured patients with measurable alcohol concentrations, insulin and glucose levels were markedly different from those for the corresponding surviving patients, p less than 0.001 and less than 0.01, respectively, with particularly large differences in the insulin-glucose ratio, p less than 0.001. The spontaneous reappearance of the insulin response to hyperglycemia was dependent upon the elapsed time and the severity of injury. Regardless of the blood alcohol concentrations, in patients admitted within two hours, there was no correlation between the levels of insulin and glucose. In patients admitted within two to eight hours, a significant correlation was found only in those with no detectable alcohol blood levels, p less than 0.001. In addition, a remarkable similarity of mean different admission times. These findings suggest that, in alcohol intoxication, recovery of insulin secretions suppressed by acute trauma is delayed; metabolism of alcohol in acute trauma is probably reduced.

Effect of etiroxate on LCAT activity and on certain energy metabolism enzymes in the rat.

Etiroxate (Skleronorm Grünenthal R) was administered 42 days to male Wistar rats and their serum and liver cholesterol and triglyceride levels, the rate of esterification of free cholesterol in their plasma by lecithin cholesterol acyltransferase (LCAT) (EC 2.3.1.43) and thriosephosphate dehydrogenase (TPDH) (EC 1.2.1.12), lactate dehydrogenase (LDH) (EC 1.1.1.27), hexokinase (HK) (EC 2.7.1.1), c-glycerol-3-phosphate dehydrogenase (GPDH) (EC 1.1.1.8), malate dehydrogenase (MDH) (EC 1.1.1.37) citrate synthase (CS) (EC 4.1.3.7) and hydroxyacylcoenzyme A dehydrogenase (HOADH) (EC 1.1.1.35) activity were determined in their liver. After 14 and 28 days, animals given etiroxate (600 micrograms/kg) had smaller weight increments than the controls and a significantly lower plasma free and esterified cholesterol level, but a significantly higher liver cholesterol concentration. Their final plasma and liver cholesterol concentrations did not differ significantly from the control values. Plasma triglyceride levels were significantly raised in treated animals at all the given intervals. LCAT activity was significantly higher throughout the whole time of treatment, with the maximum increase in the last phase. Glycolytic and oxidative enzyme activities were significantly raised, whereas GPDH activity was the same as in the controls. The results show that etiroxate accelerates cholesterol turnover in the endogenous pool by activating LCAT and stimulating energy metabolism.