The efficacy of SPORT as a dietary supplement on performance and recovery in trained athletes.

This study investigated the efficacy of SPORT (a popular dietary supplement) in improving performance and assisting recovery in 9 trained athletes. In a double-blind, crossover experiment, subjects ran at workloads of 60 and 80% of peak oxygen uptake (Peak VO2) for 5 min each with 5 min recovery after each bout and at 100% Peak VO2 until exhaustion. Two capsules of either SPORT or a gelatin placebo were administered 1 hr prior to exercise and immediately after each workload. Heart rate (HR) and blood lactate (BLa) were measured at 1 hr prior to exercise, immediately after the 100% exercise bout and at 5, 10, 20, and 45 min during recovery. No significant differences between treatments on HR and BLa measures at any of the 6 time periods, or on subjects' time to exhaustion were found. Under the conditions of this experimental design, SPORT had no beneficial effects on performance or recovery in trained athletes.     

Comparative Effects of Chronic Ethanol Consumption on the Properties of Mitochondria from Rat Brain and Liver

The effects of chronic alcohol consumption on biochemical properties of mitochondria isolated from liver and brain were compared in rats. As has been found in previous studies (reviewed in Thayer WS: Ann NY Acad Sci 492:193–206, 1987) in liver, ethanol consumption M to a 41% decrease in active phosphorylating (state 3) respiration and a 25% decrease in resting (state 4) respiration. These changes resulted in a 23% decrease in the respiratory control ratio (ratio of respiration rate in state 3 to that in state 4). These effects were associated with a 40% decrease in functional cytochrome oxidase content, determined spectrophotometrically as heme aa₃. By contrast, in brain mitochondria isolated from the same rats, ethanol consumption did not result in any significant changes in respiration rates, respiratory control ratio, or cytochrome contents. The findings demonstrate a differential pathobiologic response of brain and liver mitochondria to chronic ethanol consumption. Since the liver is predominant in metabolism of ingested ethanol, the findings of this study suggest that the deleterious effects of chronic alcohol consumption on the structure and function of liver mitochondria may be related to ethanol metabolism.     

合欢皮中新皂甙的结构鉴定

从合欢皮(Albizziae cortex)的95%乙醇提取物的正丁醇萃取部分中分离得到3个新的三萜皂甙,用化学方法及¹H-和¹³C-NMR,DEPT,COSY,TOCSY,HMQC-COSY,HMQC-TOCSY,HMBC,NOESY等波谱方法鉴定其结构为:I(1个三萜,9个糖,2个单萜),命名为合欢皂甙(julibroside)J₁;II(1个三萜,8个糖,2个单萜),命名为合欢皂甙J_{2;II(1个三萜,9个糖,2个单萜),命名为合欢皂甙J3。}     

Widespread distribution of dihydropyridine-sensitive calcium channels in the central nervous system

We have used microspectrofluorimetry and the Ca2+-sensitive dye fura-2 to analyze the effects of dihydropyridine drugs on the voltage-sensitive influx of Ca2+ into central nervous system neurons grown in primary culture. Depolarization, induced by raising [K+]o, produced a rapid increase in [Ca2+]i measured in single neurons from the cortex, hippocampus, striatum, septum, and cerebellum. These increases were slightly attenuated when external Na+ was replaced by choline+ and were absent in Ca2+-free (1 mM EGTA) media. The depolarization-induced uptake of Ca2+ by neurons from all regions of the brain was enhanced by the dihydropyridine agonist BAY K8644 (1 microM). The dihydropryidine antagonist nitrendipine (1 microM) inhibited calcium influx into hippocampal and striatal neurons by 79% and 31%, respectively, indicating that different routes of voltage-dependent calcium influx predominate in neurons from different brain regions. The results establish the widespread distribution of functional dihydropyridine-sensitive Ca2+ channels in the central nervous system.     

Occult intracellular calcium pools: relevance to neutrophil oxidant production

Human neutrophils use divalent cations for the stimulus-response coupling leading to the respiratory burst. We have studied the relevance of the extracellular versus intracellular calcium stores necessary for superoxide generation in neutrophils and neutrophil cytoplasts stimulated by N-formyl-methionyl-leucyl-phenylalanine (FMLP) and phorbol ester and our findings are as follows. (1) FMLP triggered superoxide anion (O2-) generation only in the presence of extracellular calcium, but phorbol myristate acetate (PMA) activation was independent of extracellular calcium. (2) inhibition of calcium transport channels with verapamil produced a dose-related inhibition of FMLP- and PMA-stimulated O2- production. Verapamil inhibition of FMLP-stimulated but not PMA-stimulated O2- was reversed simply by increasing extracellular calcium concentration. Cytosolic calcium loading with substimulatory concentrations of A23187 (0.3 to 0.6 mumol/L) (only in calcium-replete medium) could reverse the verapamil inhibition of PMA-triggered O2- generation. An inhibitor of intracellular calcium availability, 3,4,5-trimethoxybenzoic acid (TMB-8), similarly inhibited FMLP-stimulated and PMA-stimulated O2- production; this inhibition was reversible with A23187 calcium loading. (3) Verapamil, although it inhibited the functional oxidant response, had no inhibitory effect on fura 2-monitored cytosolic calcium rise induced by FMLP stimulation. (4) No cytosolic calcium increment was observed with PMA. O2- generation from enucleated polymorphonuclear leukocyte (PMN) cytoplasts was sensitive to inhibition by verapamil but was less so than O2- generation from intact PMNs. Cytoplasts, nearly depleted of cytoplasmic organelles and cytoskeleton, the potential sites of intracellular calcium stores, were markedly insensitive to the inhibitory effects of TMB-8.(ABSTRACT TRUNCATED AT 250 WORDS)     

Elevation of serum cystathionine levels in patients with cobalamin and folate deficiency

Homocysteine can be methylated to form methionine by the cobalamin- (Cbl) and folate-dependent enzyme, methionine synthase; serum levels of total homocysteine are elevated in greater than 95% of patients with either Cbl or folate deficiency. Homocysteine can also condense with serine to form cystathionine in a pyridoxal phosphate-dependent reaction catalyzed by cystathionine beta-synthase. Cystathionine is subsequently cleaved to cysteine and alpha-ketobutyrate by the pyridoxal phosphate-dependent enzyme gamma-cystathionase. To assess levels of cystathionine in Cbl and folate deficiency, we developed a new capillary gas chromatographic-mass spectrometric assay and measured cystathionine in the serum of normal subjects and patients with clinically confirmed deficiencies of these vitamins. The normal range for serum cystathionine was 65 to 301 nmol/L (median = 126 nmol/L) for 50 normal blood donors. In 30 patients with clinically confirmed Cbl deficiency, values for cystathionine ranged from 208 nmol/L to 2,920 nmol/L (median = 816 nmol/L) and 26 (87%) had levels above the normal range. In 20 patients with clinically confirmed folate deficiency, cystathionine concentrations ranged from 138 nmol/L to 4,150 nmol/L (median = 1,560 nmol/L) and 19 (95%) had values above the normal range. Five homozygotes for cystathionine beta-synthase deficiency had high values for serum-total homocysteine and low or low-normal values for serum cystathionine that ranged from 30 nmol/L to 114 nmol/L even though they were on treatment with pyridoxine and had partially responded. One patient with a defect in the synthesis of 5-CH3- tetrahydrofolate and five patients with defects in the synthesis of CH3- Cbl had high values for serum-total homocysteine and high values for cystathionine that ranged from 311 nmol/L to 1,500 nmol/L even though they were on treatment with folic acid and Cbl, respectively, and had partially responded. We conclude that levels of cystathionine are evaluated in the serum of most patients with Cbl and folate deficiency and that they are useful in the differential diagnosis of an elevated serum-total homocysteine level.     

Acquired immunodeficiency syndrome-associated non-Hodgkin's lymphomas and other malignancies in patients with hemophilia

Non-Hodgkin's lymphoma (NHL) is the most common human immunodeficiency virus (HIV)-associated malignancy in hemophiliacs. We studied the incidence and clinicopathologic features of NHL in 3,041 hemophiliacs followed at 18 US Hemophilia Centers between 1978 and 1989. Of the 1,295 (56.6%) who were HIV(+), 253 (19.5%) developed acquired immunodeficiency syndrome (AIDS), of whom 14 (5.5%) developed NHL. Three NHL occurred in HIV(-) hemophiliacs, for a 36.5-fold greater risk in HIV(+) than HIV(-) hemophiliacs (P < .001). The NHL incidence rate was 29-fold greater than in the US population by Surveillance, Epidemiology, and End Results (SEER) estimates (P < .001). Between 0 and 4 lymphomas have been observed per year between 1978 and 1989. At presentation 13 (92.9%) of the HIV(+) NHL were extranodal. Ten were stage IV, 1 stage II, and 3 stage IE. Ten (71.4%) were high-grade, 3 (21.4%) intermediate-grade, and 1 (7.1%) was a low-grade B-cell lymphoma. Epstein-Barr virus (EBV) DNA was detected in 36% by in situ hybridization, including one central nervous system (CNS) lymphoma. The mean CD4 cell count at NHL diagnosis was 64/mm3, the mean latency from initial HIV infection was estimated to be 59 months, and the median survival was 7 months. The incidence of basal cell carcinoma in HIV(+) hemophiliacs was 18.3-fold greater than in HIV(-) hemophiliacs (P < .001) and 11.4-fold greater than in the US population (P < .001). In conclusion, incidence rates of NHL and basal cell carcinoma in HIV(+) hemophiliacs are significantly increased over rates in HIV(-) hemophiliacs and over rates in the US population. Clinicopathologic presentation of NHL in HIV(+) hemophiliacs is similar to that in HIV(+) homosexual men.