Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0599766 (functional recovery)
 13,441 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the cases of two patients who developed cranial nerve palsies after drinking ethylene glycol. A 33-year-old man developed multiple cranial nerve deficits nine days after the ingestion of ethylene glycol in a suicide attempt. Clinical findings included profound bilateral cranial nerve VII palsies and severe dysfunction of cranial nerves IX and X. The neuropathy occurred despite treatment with hemodialysis. The dysphagia completely cleared within two weeks, but at six months a severe bilateral cranial nerve VII dysfunction persisted. A 22-year-old man undergoing hemodialysis for ethylene glycol-induced renal failure developed bilateral cranial nerve VII dysfunction 14 days after ingestion. At a three-month follow-up, the patient demonstrated only moderate functional recovery. The etiology of the cranial nerve deficits is unknown but may be related to oxalate crystal deposition of ethylene glycol-induced pyridoxine dysfunction.
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PMID:Multiple cranial nerve deficits after ethylene glycol poisoning. 199 9

Function-dependent changes of calcium distribution were studied in the nerve-electroplaque synapses of Torpedo marmorata before and after the transmission of a nerve impulse. For the cytochemical demonstration of calcium at the ultrastructural level the oxalate-pyroantimonate technique was combined with electron spectroscopic imaging. Cholinergic synapses of the electric organ were stimulated in the presence of 4-aminopyridine, a drug which powerfully potentiates transmitter release. A single stimulus evoked a giant electrical discharge, which was followed by a long refractory period. Calcium cytochemistry was performed by fixing the tissue at four well defined functional states: (i) before and (ii) immediately after the giant discharge, and (iii) at 1 min or (iv) at 30 min of subsequent rest, corresponding to partial and complete functional recovery, respectively. In the non-stimulated synapses about 20% of synaptic vesicles contained small electron-dense precipitates. The element specific mapping by electron spectroscopic imaging clearly showed that calcium was present in the vesicular granules. The volume density of synaptic vesicles did not change among the four experimental states, but we detected a significant increase in the proportion of calcium containing vesicles at 1 min after the giant discharge. The vesicular calcium accumulation was transient: it returned to the control value at the end of the recovery period. Our data suggest that the synaptic vesicles play a role in sequestering the excess calcium which enters the nerve terminal during stimulation.
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PMID:Transient increase of calcium in synaptic vesicles after stimulation. 838 25

Heat stress (HS) and the subsequent expression of heat shock proteins has been shown to enhance post-ischemic functional recovery and reduce infarct size. The purpose of these experiments was to determine if HS pre-treatment preserves sarcoplasmic reticulum (SR) function, a cellular organelle that plays an important role in myocardial contractility. Anesthetized rats were heat stressed for 15 min by raising temperature to 42 degrees C. Twenty-four hours later the hearts were perfused by Langendorff's method and subjected to either 20 or 35 min of global ischemia, with a subset of hearts then being subjected to 10 or 20 min of reperfusion, respectively. SR function was assessed by oxalate-supported Ca2+ uptake rate in cell free preparations in the presence and absence of ruthenium red, a selective SR calcium release channel blocker Ca2+ uptake decreased significantly from 25.6 +/- 3.4 to 13.4 +/- 1.9 and 11.3 +/- 2.3 nmol/min/mg protein (mean +/- S.E.), following 20 and 35 min of ischemia, respectively. A similar trend was observed following reperfusion as well. No significant difference in Ca2+ uptake was observed between HS v control hearts. Similarly, in samples where the Ca2+ release channel was blocked with ruthenium red, decreased Ca2+ uptake rates were noted after both ischemia and reperfusion, with no significant differences seen between HS and non-HS hearts. There was significant improvement it developed pressure. +dP/dt and -dP/dt, with reduced creatine kinase release in HS v non-HS hearts. Western blot analysis demonstrated increased synthesis of 27- and 70-kDa heat shock proteins in HS but not in control animals. It is concluded that HS improves functional recovery and induces expression of 27- and 70-kDa heat shock proteins without preservation of SR function in the globally ischemic rat heart.
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PMID:Heat stress improves functional recovery and induces synthesis of 27- and 70-kDa heat shock proteins without preserving sarcoplasmic reticulum function in the ischemic rat heart. 889 47

An OxlT homology model suggests R272 and K355 in transmembrane helices 8 and 11, respectively, are critical to OxlT-mediated transport. We offer positive evidence supporting this idea by studying OxlT function after cysteine residues were separately introduced at these positions. Without further treatment, both mutant proteins had a null phenotype when they were reconstituted into proteoliposomes. By contrast, significant recovery of function occurred when proteoliposomes were treated with MTSEA (methanethiosulfonate ethylamine), a thiol-specific reagent that implants a positively charged amino group. In each case, there was a 2-fold increase in the Michaelis constant (K(M)) for oxalate self-exchange (from 80 to 160 microM), along with a 5-fold (K355C) or 100-fold (R272C) reduction in V(max) compared to that of the cysteine-less parental protein. Analysis by MALDI-TOF confirmed that MTSEA introduced the desired modification. We also examined substrate selectivity for the treated derivatives. While oxalate remained the preferred substrate, there was a shift in preference among other substrates so that the normal rank order (oxalate > malonate > formate) was altered to favor smaller substrates (oxalate > formate > malonate). This shift is consistent with the idea that the substrate-binding site is reduced in size via introduction of the SCH(2)CH(2)NH(3)(+) adduct, which generates a side chain that is approximately 1.85 A longer than that of lysine or arginine. These findings lead us to conclude that R272 and K355 are essential components of the OxlT substrate-binding site.
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PMID:Analysis of substrate-binding elements in OxlT, the oxalate:formate antiporter of Oxalobacter formigenes. 1692 10