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The strength characteristics of lightweight aggregate concrete confined by steel tube were studied experimentally. Based on the superposition of two materials, a method was established to calculate the combined strength of lightweight aggregate concrete steel tube: the accuracy of this calculation was verified experimentally. The research indicated that the confining effect of steel tube on lightweight aggregate concrete increased as the steel area ratio is enlarged. The confining effect coefficient of lightweight aggregate concrete can be taken as 3·4, which reflected the stress-performance improvement of lightweight aggregate concrete under trip-direction compression. Comparison between calculation and test results showed that the calculations were precise. The calculated result could be regard as ultimate strength at a coefficient of lateral deformation of 0·5, and as its design strength at a coefficient of lateral deformation of 0·3. [ABSTRACT FROM AUTHOR]

According to the structure characteristic, comprehensive scoring method for corrosion evaluation is proposed for steel box girder. The effects of multiple factors of corrosion are considered comprehensively. Several existing indicators are selected for steel box girder. In addition, two new indicators are put forward to reflect the structure characteristic. An indicator system for corrosion evaluation of steel box girder is set up including corrosion density, size, depth, area ratio, depth ratio and location. Scores and amplification coefficient corresponding to indicators are given. Corrosion evaluation indicators and process are offered, and the corrosion grade corresponding to the final score range is also divided. Based on all of the above, corrosion evaluation of comprehensive scoring method of steel box girder is established and its application is also supported by examples. [ABSTRACT FROM AUTHOR]

Twenty-one previously untreated lepromatous patients were randomized into two groups and treated with either 800 mg pefloxacin (PEFLO) or 400 mg ofloxacin (OFLO) once daily. The trial consisted of two parts: monotherapy from day 0 to day 56; and combined with the World Health Organization multidrug therapy (WHO/MDT) regimen for multibacillary (MB) leprosy from day 57 to day 180. Four patients were removed from the trial because the organisms recovered from their pretreatment biopsies failed to infect mice. Among the remaining 17 cases, four (23.5%) had primary resistance to dapsone but all of them were susceptible to rifampin. The initial (day 0) proportion of viable organisms, as measured by mouse foot pad inoculation, varied tremendously from patient to patient despite randomization during admission. Definite clinical improvement was noticed in virtually all patients after 22 doses of treatment with either PEFLO or OFLO. A significant fall in the morphological index (MI) occurred as early as after 8 doses of PEFLO or after 22 doses of OFLO; the bacterial load also showed a moderate degree of reduction during the period of monotherapy. Although single-dose PEFLO or OFLO displayed only a modest degree of bactericidal effect against Mycobacterium leprae, about 99.9%, or 4 logs, of organisms viable on day 0 were killed by 22 doses of either PEFLO or OFLO. No significant difference in the therapeutic effect was detected between the two regimens. During PEFLO or OFLO monotherapy, except in one patient (case no. 10), the side effects were few and mild. Case no. 10 developed a psychic disorder after 27 days of PEFLO monotherapy, presumably due to the treatment with PEFLO. All of the patients tolerated the period of combined therapy extremely well, although some asymptomatic and transient laboratory abnormalities were observed. Because both PEFLO and OFLO displayed rapid bactericidal activities in human leprosy and were well tolerated by the patients, further clinical trials and field trials in evaluating the therapeutic effects of combined regimens containing both rifampin and PEFLO or OFLO are being organized. Since this is the first clinical trial in leprosy employing nude mice, in combination with normal mice, for monitoring the therapeutic effects of antimicrobials, the advantages, limitations and appropriate timing in using nude mice are discussed.

The degree of cardiac and vascular beta-adrenoceptor blockade of bisoprolol and atenolol was determined by the chronotropic dose 25 (CD25) of isoproterenol (the dose of an intravenous isoproterenol bolus required to increase resting heart rate by 25 beats/min) and by the increase in forearm blood flow (venous occlusion plethysmography) to intrabrachial artery infusions of increasing doses of isoproterenol (0.12, 1.2, 4, 12, and 20 ng/min/100 ml forearm tissue). Measurements were taken following placebo and after one week's treatment with atenolol or bisoprolol under double-blind conditions using a within-patient crossover design. Two patients received 10 mg bisoprolol and 50 mg atenolol daily, and three patients 20 and 100 mg daily, respectively. Both beta-blockers produced a similar fall in blood pressure, heart rate, and plasma renin activity. While CD25 of isoproterenol was comparable for both drugs, forearm blood flow to intra-arterial infusion of isoproterenol increased to a greater extent following bisoprolol (20 mg) than during atenolol (100 mg) treatment. Equieffective cardiac beta-blockade with bisoprolol and atenolol was associated with a lesser degree of vascular beta-adrenoceptor blockade during treatment with the more cardioselective beta-blocker bisoprolol.

The role of adrenaline-induced postjunctional alpha 2 adrenoceptor-mediated vasoconstriction was studied in seven patients with essential hypertension (EHT) and eight normotensive subjects (NT) using forearm venous occlusion plethysmography. Adrenaline (0.01 to 0.08 micrograms/min/100 ml of tissue) infused into the forearm circulation via the brachial artery during alpha l adrenoceptor blockade with prazosin (0.05 micrograms/min/100 ml of tissue) and beta adrenoceptor blockade with propranolol (2 micrograms/min/100 ml of tissue) decreased forearm blood flow (FAF) dose-dependently below basal FAF (P less than 0.001). The adrenaline-induced decrease in FAF was greater in EHT than in NT (P less than 0.01) and was blocked in both groups by alpha 2 adrenoceptor blockade with yohimbine (30 micrograms/min/100 ml of tissue). The increase in FAF following postjunctional alpha-2 blockade as well as following postjunctional alpha-1 blockade was greater in EHT than in NT (P less than 0.01) but was similar in both groups following 'non-specific' vasodilation with sodium nitroprusside. Postjunctional alpha 1 and alpha 2 adrenoceptor-mediated vasoconstriction is enhanced in patients with essential hypertension. Adrenaline induced postjunctional alpha 2 adrenoceptor-mediated vasoconstriction could contribute to elevated vascular resistance in patients with EHT and elevated plasma adrenaline concentrations particularly in the presence of blunted beta adrenoceptor-mediated functions.

More than 20 years ago calcium antagonists were shown to lower elevated blood pressure. Today's worldwide recognition, at least in part, is due to rising research interest in cellular ion regulation abnormalities in essential hypertension. Using the human platelet as a model for the vascular smooth muscle cell, a direct relationship was observed between intracellular free calcium concentration and the height of blood pressure before as well as during different antihypertensive treatments. Calcium influx is an important determinant of vasoconstriction, and excess calcium influx-dependent vasoconstriction was shown with plethysmographical studies in patients with essential hypertension. Calcium antagonists acutely lower blood pressure by reducing intracellular calcium and peripheral vascular resistance. The degree of the attendant sympathetic nerve reflex activation and counterregulatory mechanisms codetermine the antihypertensive result of the individual. Chronic monotherapy with calcium antagonists results in an antihypertensive response that is related directly to the patient's age and pretreatment blood pressure and indirectly to renin. These studies led to a new treatment concept: calcium antagonists can be used as alternatives to diuretic drugs primarily in the older and low-renin patients and beta-blockers or converting enzyme inhibitors can be used in the younger or high-renin patients with greater efficacy. With the appropriate choice, calcium antagonists alone or combined with any other antihypertensive drug provide good blood pressure control with little subjective and objective adverse effects.

In essential hypertension, calcium-influx-dependent vasoconstriction is enhanced, and free calcium concentration in platelets is elevated. To investigate calcium-influx-dependent vasoconstriction as related to platelet calcium concentration blood pressure, forearm blood flow (FAF) and free calcium concentration in platelets were measured in five patients with essential hypertension before and after a 6-week treatment with nitrendipine or acebutolol. Starting from comparable basal values, the increase in FAF (ml/min/100 ml tissue) to intraarterially infused nitrendipine (20 micrograms/100 ml tissue) was 40.7 +/- 6.1 before and 30.7 +/- 12.3 after chronic nitrendipine treatment (p less than 0.05) and 41.6 +/- 6.2 before and 34.6 +/- 14.9 after chronic acebutolol treatment. The "nonspecific" vasodilator response to intraarterial sodium nitroprusside or to postischaemic reperfusion were similar before and during treatment. Platelet-free calcium concentration fell on nitrendipine (p less than 0.05) and on acebutolol (p less than 0.01) treatment. Antihypertensive treatment with calcium entry as well as beta-adrenoceptor blockade resulted in a reduction of calcium-influx-dependent vasoconstriction and a fall in free calcium concentration in platelets. Thus, increased calcium platelets may reflect increased calcium in vascular smooth muscle cells and arteriolar tone.

The antimycobacterial activities of two newer ansamycins, isobutylpiperazinylrifamycin SV (R-76-1) and cyclopentylrifamycin SV (DL 473), were compared with those of rifampin (RMP) both in vitro and in vivo. In terms of minimal inhibitory concentrations against a number of cultivable mycobacteria, R-76-1 was about eight times more active in vitro than RMP; whereas DL 473 was only slightly more active than RMP. Therapeutic activities of R-76-1 versus RMP and DL 473 versus RMP were compared, respectively, in the experimental infection of mice with Mycobacterium lepraemurium by different treatment schedules (immediate and delayed) and dosage regimens. R-76-1 appeared to have been three times more effective than RMP; DL 473 was also more effective than RMP in that an equivalent therapeutic effect could be obtained by fewer doses of DL 473 than of RMP, and in that DL 473 exerted a more prolonged activity than RMP. With the kinetic method and a dosage of 0.001% in the diet, R-76-1 demonstrated a bactericidal-type effect against M. leprae whereas RMP did not; with the proportional bactericidal method, R-76-1 possessed about three times the bactericidal activity of RMP against M. leprae. When drugs were administered once in 4 weeks, the RMP dose required to prevent multiplication of M. leprae in the foot pads of half of the mice was in the range of 1.25 to 2.5 mg/kg; whereas that of DL 473 was less than 0.625 mg/kg. With the proportional bactericidal method, even a single dose of 1.25 mg DL 473 per kg was active against M. leprae; whereas the smallest single active dose of RMP was 10 mg/kg. DL 473 in single doses of 5 mg/kg and 10 mg/kg was significantly more effective than RMP in equal doses and, among the intermittent regimens administered four times, once every 4 weeks, no significant differences of bactericidal activity were observed between RMP at 20 mg/kg and DL 473 at 0.625 mg/kg. A preliminary clinical trial of R-76-1 in 20 patients with lepromatous leprosy showed that the compound, administered in a dosage of 150 mg daily, was very effective.

The sympathetic nervous activity contributes to the pathophysiology of essential hypertension in an early phase and in younger patients mainly through increased beta-adrenoceptor-mediated functions and in a later phase and in older patients in whom beta-adrenoceptor-mediated functions are blunted, through increased alpha-adrenoceptor-mediated and calcium-influx-dependent vasoconstriction. Intracellular free calcium concentration is elevated in platelets of hypertensive patients and relates directly to the degree of their blood pressure, likely reflecting increased intracellular calcium concentration in vascular smooth muscle cells. A sympathetic factor is suggested further by the enhanced alpha 1-and alpha 2-adrenoceptor-mediated and calcium influx-dependent, vasoconstriction both of which are normalized by antihypertensive treatment in parallel with a normalization of intracellular free calcium and of the increased adrenaline sensitivity of platelets. The higher sensitivity to adrenaline for thrombin-induced calcium increases in platelets of hypertensive patients indicates potentiation of calcium influx (and mobilization from intracellular stores) by adrenaline, a mechanism that is mediated by alpha 2-adrenoceptors. As this effect is more pronounced in younger patients, increased adenylate cyclase sensitivity may prevail in the early and alterations in calcium influx-dependent mechanisms in the later phase of essential hypertension. The transition into a hypertensive state with reduced-reflex cardiovascular counterregulation codetermines the antihypertensive effectiveness of calcium antagonists in these patients.