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Respiratory competent

Griac, P., and Henry, S.A., 1996, Phosphatidylcholine biosynthesis in Saccharomyces cerevisiae Effects on regulation of phospholipid synthesis and respiratory competence. In Op den Kamp, J.A.F. (ed.), NATO ASI Series Molecular Dynamics of Biological Membranes. Springer, Verlag, pp. 339-346. [Pg.151]

In the presence of [PS7+], nam9-l strains are respiratory-deficient, but in a psi background, nam9-l strains are respiratory-competent (Chacinska et al., 2000). While the molecular target of the read-through event(s) leading to this phenotype is not yet characterized, this observation provides an extremely useful tool for further [P.S7+] studies a positive selection for the [psi ] state. [Pg.407]

The kinetic and equilibrium parameters of L-malate, succinate, citrate, and a-oxoglutarate uptake have been determined in mitochondria isolated from respiratory-competent cells grown under conditions of aerobic derepression, aerobic and anaerobic catabolite repression, and inhibition of mitochondrial protein synthesis, and also in mitochondria prepared from a respiratory-deficient cytoplasmic petite strain. The activity and kinetic characteristics of the systems were similar in all cases. It may be concluded that the protein components of these transport systems are coded entirely by nuclear DNA and are synthesized on the cytoplasmic ribosomes. [Pg.106]

Although mitochondria possess a protein-synthesizing system active both in vivo and in vitro, it is clear that the vast majority of mitochondrial proteins are synthesized on cytoplasmic ribosomes and are coded for by nuclear DNA. This conclusion is based, in part, on the observations that 85-95% of mitochondrial protein can be labeled with radioactive amino acids in the presence of chloramphenicol, but not cyclohexmide, and that only small qualitative differences can be detected in mitochondrial proteins between respiratory-competent yeast cells and cytoplasmic petites. ... [Pg.170]

In contrast to macrolides, the targets of (3-lactams, the penicillin binding proteins (PBPs) require several mutations in order to become resistant while simultaneously maintaining their viable function as cell wall transpeptidases/transglycosidases. Thus, in order to achieve clinically relevant resistance Streptococcus pneumoniae uses a unique strategy to rapidly accumulate several point mutations. Due to its natural competence for transformation during respiratory tract... [Pg.105]

Flumazenil Romazicon) is a benzodiazepine antagonist that specifically reverses the respiratory depression and hypnosis produced by the benzodiazepine receptor agonists. Its block of the amnesic effect of the agonists is less reliable. Flumazenil is particularly useful when an overdose of benzodiazepines has occurred. It is also employed when a benzodiazepine has been used to produce conscious sedation and rapid recovery of psychomotor competency is desirable. To avoid resedation, flumazenil may require administration by intravenous infusion. [Pg.296]

Mechanism of Action An antihistamine that competes with histamine for histamine receptor sites on cells in the blood vessels, G1 tract, and respiratory tract. Therapeutic Effect Relieves symptoms associated with seasonal allergic rhinitis, such as increased mucus production and sneezing and symptoms associated with allergic conjunctivitis, such as redness, itching, and excessive tearing. [Pg.109]

Mechanism of Action A second-generation piperazine that competes with histamine for Hj-receptor sites on effector cells in the GI tract, blood vessels, and respiratory tract. Therapeutic Effect Prevents allergic response, produces mild bronchodilation, blocks histamine-induced bronchitis. [Pg.238]

Since organophosphate toxicosis results in respiratory failure, the treatment approach for must include the maintenance of a patent airway. Artificial respiration may also need to be employed. The first pharmacological approach is the administration of atropine. Atropine competes with acetylcholine for its receptor site, thus reducing the effects of the neurotransmitter. N-methylpyridinium 2-aldoxime (2-PAM) is used in with atropine therapy as an effective means to restore the covalently bound enzyme to a normal state. It reacts with the phosphorylated cholinesterase enzyme removing the phosphate group. As previously mentioned, carbamates interact with cholinesterase by weak, ionic bonding thus 2-PAM is of no use to combat toxicosis caused by these compounds. However, atropine is effective to prevent the effects on respiration. [Pg.408]

Naloxone is a drug structurally related to the opioid class of analgesics such as morphine. Naloxone has virtually no intrinsic activity but can compete for opioid receptors. By reversibly competing for the p and K opioid receptors in the brain and spinal cord, it can reverse the sedation and respiratory depression associated with an overdose of morphine-like drugs. [Pg.142]

The toxicological implications in the effect of the respiratory poisons on the enzyme systems of mammals are not fully comprehended, even at this stage of knowledge. For instance, Dixon and Webb (44) point out that the respiration of most animal tissues is insensitive to carbon monoxide which, in the blood, competes with oxygen for the reduced hemoproteins whereas cyanide has a broad inhibitory spectrum which includes various oxidative systems at cellular level and, most importantly, the oxidized forms of the hemoproteins, especially methemoglobin. In this latter connection, phenazine methosulfate has recently been found effective as an experimental therapeutic in cyanide poisoning of mice (13). The respiratory poisons have just been reviewed by Hewitt and Nicholas (72). [Pg.65]


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