Inhibition of the delayed-type hypersensitivity response by staphylococcal enterotoxin B-induced suppressor T cells

Staphylococcal enterotoxin B (SEB) is a member of a family of gram-positive bacterial exotoxins which act as superantigens in both mouse and man. The administration of this toxin has been shown to inhibit antibody responses in vivo. We have previously shown that SEB is a potent inducer in vitro of multiple T suppressor cell populations. The present studies show that administration of microgram quantities of this toxin result in a reduced capacity to manifest a delayed-type hypersensitivity (DTH) response. In addition, we find that the failure to generate a normal DTH response appears to be due to the generation of a T suppressor cell population following SEB administration. Adoptive transfer studies show that the suppressor cells bear the CD5+ I-J+ CD4- CD8- Thy 1+ surface phenotype. The relationship of these cells to suppressor T cell populations generated following in vitro activation by SEB is discussed.     

Excitotoxic Brain Injury Suppresses Striatal High-Affinity Glutamate Uptake in Perinatal Rats

In immature rodent brain, the glutamate receptor agonist N-methyl-D-aspartate (NMDA) is a potent neurotoxin. In postnatal day (PND)-7 rats, intrastriatal injection of 25 nmol of NMDA results in extensive ipsilateral forebrain injury. In this study, we examined alterations in high-affinity [3H]glutamate uptake (HAGU) in NMDA-lesioned striatum. HAGU was assayed in synaptosomes, prepared from lesioned striatum, the corresponding contralateral striatum, or unlesioned controls. Twenty-four hours after NMDA injection (25 nmol), HAGU declined 44 +/- 8% in lesioned tissue, compared with the contralateral striatum (mean +/- SEM, n = 6 assays, p less than 0.006, paired t test). Doses of 5-25 nmol of NMDA resulted in increasing suppression of HAGU (5 nmol, n = 3; 12.5 nmol, n = 3; and 25 nmol, n = 5 assays; p less than 0.01, regression analysis). The temporal evolution of HAGU suppression was biphasic. There was an early transient suppression of HAGU (-28 +/- 4% at 1 h; p less than 0.03, analysis of variance, comparing changes at 0.5, 1, 2, and 3 h after lesioning); 1 or 5 days postinjury there was sustained loss of HAGU (at 5 days, -56 +/- 11%, n = 3, p less than 0.03, paired t test, lesioned versus contralateral striata).(ABSTRACT TRUNCATED AT 250 WORDS)     

尖吻蝮咬伤与心脏损害：附20例分析

本文报告尖吻蝮咬伤并心脏受累20例。经中西医结合治愈19例(95％),死亡1例(5％),并对其发病机理及治疗进行了讨论。     

Determination of buprenorphine by high-performance liquid chromatography with fluorescence detection: application to human and rabbit pharmacokinetic studies

A rapid, sensitive, precise and accurate high-performance liquid chromatographic assay with fluorescence detection was developed for the determination of buprenorphine in human, rabbit, pig and dog plasma. It is comprised of only a one-step extraction procedure with hexane—isoamyl alcohol at pH 9.25 and reversed-phase chromatography on a μPorasil column. The recoveries of buprenorphine and nalbuphine (internal standard) were greater than 90%. Calibration graphs were linear over the concentration range 3–300 ng/ml with a coefficient of variation, both within-day and between-day, of less than 9% at any level. The limit of detection was 1.0 ng/ml of plasma based on a signal-to-noise ratio of 3. Eight other clinically used narcotics were investigated to check for potential interferences and their analytical conditions. The possible decomposed compounds of buprenorphine were also checked for the specificity of this assay. The method has been succesfully applied to the stability and pharmacokinetic studies of buprenorphine. Buprenorphine in plasma did not decompose significantly at −20°C for four weeks. Pharmacokinetic application in six rabbits and a surgical patient revealed that buprenorphine followed a linear three-compartment model with two distribution phases. The two distribution and elimination half-lives and the clearance of buprenorphine were 1.32, 24.8 and 230 min and 224 ml/min in human plasma, and 0.94, 12.5 and 232 min and 30 ml/min in rabbit plasma.     

Interaction of nitrogen dioxide with human plasma. Antioxidant depletion and oxidative damage.

Nitrogen dioxide (NO2.) is often present in inhaled air and may be generated in vivo from nitric oxide. Exposure of human blood plasma to NO2. caused rapid losses of ascorbic acid, uric acid and protein thiol groups, as well as lipid peroxidation and depletions of alpha-tocopherol, bilirubin and ubiquinol-10. No increase in protein carbonyls was detected. Supplementation of plasma with ascorbate decreased the rates of lipid peroxidation, alpha-tocopherol depletion and loss of uric acid. Uric acid supplementation decreased rates of lipid peroxidation but not the loss of alpha-tocopherol. We conclude that ascorbic acid, protein -SH groups, uric acid and alpha-tocopherol may be important agents protecting against NO2. in vivo. If these antioxidants are depleted, peroxidation of lipids occurs and might contribute to the toxicity of NO2..     

Fentanyl and medetomidine anaesthesia in the rat and its reversal using atipamazole and either nalbuphine or butorphanol.

The intraperitoneal injection of anaesthetic agents is a simple and convenient method of anaesthetizing rats. However, all of the anaesthetic combinations in current use which are administered by intraperitoneal injection produce prolonged sedation, and full recovery of consciousness may take several hours. Fentanyl, a mu agonist opioid, and medetomidine, an alpha 2-adrenoceptor agonist were mixed and administered as a single intraperitoneal injection. Combinations of 300 micrograms/300 micrograms/kg and 300 micrograms/200 micrograms/kg of fentanyl/medetomidine were shown to produce surgical anaesthesia in the rat. This anaesthetic regimen produced significant respiratory depression (P less than 0.01) and animals did not regain their righting reflex until 193 +/- 21 min (mean +/- 1 SD) after injection. Administration by intraperitoneal injection of atipamezole, a specific alpha 2-adrenoceptor antagonist (1 mg/kg) mixed with a mu antagonist/k agonist opioid (nalbuphine, 2 mg/kg or butorphanol 0.4 mg/kg), resulted in a rapid (less than 8 min) reversal of anaesthesia and the associated respiratory depression, and apparent full recovery of consciousness.     

Root nodule development: origin, function and regulation of nodulin genes

The symbiotic root nodule, an organ formed on leguminous plants, is a product of successful interactions between the host plant and the soil bacteria, Rhizobium spp. Plant hormones play an important role in the genesis of this organ. The hormonal balance appears to be modulated by the signals produced by bacteria. Many host genes induced during nodule organogenesis and the symbiotic state have been identified and characterized from several legumes. These genes encode nodule-specific proteins (nodulins) which perform diverse functions in root nodule development and metabolism. Formation of a subcellular compartment housing the bacteria is essential to sustain the symbiotic state, and several nodulins are involved in maintaining the integrity and function of this compartment. The bacteroid enclosed in the perbacteroid membrane behaves as an 'organelle,'completely dependent on the host for all its requirements for carbon, nitrogen and other essential elements. Thus it seems likely that the nodulins in the peribacteroid membrane perform specific transport functions. While the function of a few other nodulins is known (e.g. nodulin-100, nodulin-35), a group of uncharacterized nodulins exists in soybean root nodules. These nodulins share structural similarities and seem to have been derived from a common ancestor. Induction of nodulin genes occurs prior to and independent of nitrogen fixation, and thus is a prelude to symbiosis. Although some of the early nodulin genes are induced prior to or during infection, induction of late nodulins requires endocytotic release of bacteria.     

Effect of gas atmosphere on the development of one-cell bovine embryos in two culture systems

The effect of two concentrations of oxygen on the development of bovine embryos was compared using two separate co-culture systems. In Experiment I, bovine oocytes were matured and fertilized in vitro and were then co-cultured for 7 days in 20 mul drops of M199 with 10% fetal calf serum containing oviduct cells. When cultures were performed in an atmosphere of 5% CO(2) in air (20% O(2)) or in a mixture of 5% CO(2), 5% O(2) and 90% N(2) (5% O(2)), 22 of 179 (12%) and 56 of 179 (31%) zygotes developed to or beyond the late morula stage (P<0.0001), respectively. After freezing, thawing and 48 hours of additional culture, 2 of 21 (10%) and 18 of 53 (34%) embryos were judged viable (P<0.001) within the respective treatment groups. In Experiment II, zygotes produced by the same means were co-cultured in 0.5 ml of M199 containing 10% fetal calf serum with monolayers of buffalo rat liver (BRL) cells. In 20% O(2), 51 of 177 (29%) zygotes developed into viable embryos, while in 5% O(2) only 9 of 177 (5%) were judged viable after 7 days of culture (P<0.0001). Post-freezing survival rates were 53% and 67% for embryos from the two respective oxygen concentration treatment groups. The transfer of 20 Grade 1 frozen/thawed embryos produced by co-culture with BRL cells produced six pregnancies (30%). These experiments show that the critical effect of oxygen concentration on embryo development in vitro and the ability of embryos produced by in vitro procedures to survive freezing can be influenced by the type of culture system employed.     

A model for mercuric ion reduction in recombinant Escherichia coli

Plasmid-encoded mercuric reduction involves transfer of Hg(2+) across the cellular envelope and reduction to Hg(0) by the cytoplasmic mercuric reductase using NADPH. A mathematical model was developed for the binding and transfer of Hg(2+) by transport proteins and the subsequent reduction of Hg(2+). The values of the model parameters were determined using experimental data. The derived rate expressions were similar to the previously experimentally determined ones. The model predicted that a differential amplification of the transport protein relative to mercuric reductase expression levels may enhance the Hg(2+) reduction rate in whole cells.