Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.9.3.1 (cytochrome oxidase)
 8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Experiments were carried out in chloralose-anesthetized cats to study the responses of neurons in the lateral thalamus to excitation of afferent fibres from the knee joint. 2. Single- and multi-unit recordings were made with tungsten electrodes in dorsoventral penetrations through the ventral posterior lateral nucleus (VPL) during electrical stimulation of the medial articular nerve (MAN) of the cat's knee joint at an intensity sufficient to excite slowly conducting unmyelinated fibers. The locations of the recording sites were verified by recovering electrolytic lesion sites in histological sections (Nissl and cytochrome oxidase staining). 3. The average earliest latency for excitation of thalamic responses was 19.1 +/- 8.5 (SD) ms (n = 50). The threshold for excitation of most thalamic units was found to correspond to peripheral joint afferent fibers of the A-delta group. 4. The majority of neurons responding to MAN stimulation were found to be dorsal or ventral to the low-threshold cutaneous hindlimb region of the lateral division of the VPL (stereotaxic coordinates: AP 9.0-11.5; ML 7.0-9.5). In the ventral periphery of the VPL, most neurons responding to MAN stimulation (11/14) were wide dynamic range (WDR) with a discrete cutaneous receptive field on the hindpaw digits. Six WDR neurons were found dorsal to the hindlimb VPL with a convergent receptive field on the hindlimb (but not hindpaw digits). No nociceptive-specific knee joint units were found. 5. Other neurons were found dorsal to the hindlimb VPL with large receptive fields often encompassing the whole contralateral leg, including skin and deep hindlimb structures, possibly in a region described as the dorsal portion of the posterior complex (POd). Some neurons were found with no receptive field. 6. This study provides the first observations on the responses of lateral thalamic neurons to stimulation of the MAN of the cat knee joint. These results demonstrate a central pathway conveying impulses from specific deep joint afferents of the MAN to the peripheral region of the VPL and overlying region known as the POd, regions implicated in the transmission of nociceptive information.
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PMID:Knee joint input into the peripheral region of the ventral posterior lateral nucleus of cat thalamus. 159 99

Using cyano-complexes of iron, tungsten, and molybdenum and a platinum working electrode, we have been able to attain and hold voltages in the range of 400 to 900 mV (vs. standard hydrogen electrode) in an aqueous medium. With this system we have obtained additional information in support of an earlier conclusion that cytochrome a3 has a high Em transition (i.e. greater than 460 mV) in addition to its Em in the 180-200 mV range (Hendler, R. W., K. V. S. Reddy, R. I. Shrager, and W. S. Caughey. 1986. Biophys. J. 49:717-729; Reddy, K. V. S., and R. W. Hendler. 1986. Biophys. J. 49:693-703). The proposed new transition has an Em near 770 mV and an n value greater than 1. The reduced form of the high-potential species of cytochrome a3 does not bind CO, in contrast to the reduced form of the low-potential species which does. A possible reaction scheme for cytochrome aa3 which incorporates the new information is presented.
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PMID:A new high potential redox transition for cytochrome aa3. 284 43

The Raman and infrared (IR) spectra of four tungsten metal carbyne complexes I, II, IV and V [Cl(CO)2(L)W[triple bond]CC6H4[triple bond](C[triple bond]CC6H4)n[triple bond]N[triple bond]C[triple bond]]2M (L = TMEDA, n = 0, M = PdI2 or ReCl(CO)3; L = DPPE, n = 1, M = PdI2 or ReCl(CO)3) were studied at high external pressure. Their pressure-induced phase transitions were observed near 20kbar (complexes I), 15 kbar (complexes II), 25 kbar (complex IV) and 30 kbar (complex V). The pressure-induced phase transition likely is first order in complex I and the pressure-induced phase transitions of complexes II, IV and V are mostly second order. The pressure sensitivities d nu/dp of nu(W[triple bond]C) are high in the low-pressure phase area and very low in the high-pressure phase area due to the pressure strengthening pi back-bonding from metal W to pi* orbital of C[triple bond]O in fragment Cl(CO)2(L)W[triple bond]C. The pressure strengthening metal pi back-bonding from metal Re or Pd to pi* orbital of C[triple bond]O or C[triple bond]N also happened to both of central metal centers of NCPd(I2)CN in complex I and NCReCl(CO)3CN in complex II.
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PMID:The pressure tunning Raman and IR spectral studies on the multinuclear metal carbyne complexes. 1568 8

Patients affected by sulfite oxidase (SO) deficiency present severe seizures early in infancy and progressive neurological damage, as well as tissue accumulation of sulfite, thiosulfate and S-sulfocysteine. Since the pathomechanisms involved in the neuropathology of SO deficiency are still poorly established, we evaluated the effects of sulfite on redox homeostasis and bioenergetics in cerebral cortex, striatum, cerebellum and hippocampus of rats with chemically induced SO deficiency. The deficiency was induced in 21-day-old rats by adding 200ppm of tungsten, a molybdenum competitor, in their drinking water for 9weeks. Sulfite (70mg/kg/day) was also administered through the drinking water from the third week of tungsten supplementation until the end of the treatment. Sulfite decreased reduced glutathione concentrations and the activities of glutathione reductase and glutathione S-transferase (GST) in cerebral cortex and of GST in cerebellum of SO-deficient rats. Moreover, sulfite increased the activities of complexes II and II-III in striatum and of complex II in hippocampus, but reduced the activity of complex IV in striatum of SO-deficient rats. Sulfite also decreased the mitochondrial membrane potential in cerebral cortex and striatum, whereas it had no effect on mitochondrial mass in any encephalic tissue evaluated. Finally, sulfite inhibited the activities of malate and glutamate dehydrogenase in cerebral cortex of SO-deficient rats. Taken together, our findings indicate that cerebral cortex and striatum are more vulnerable to sulfite-induced toxicity than cerebellum and hippocampus. It is presumed that these pathomechanisms may contribute to the pathophysiology of neurological damage found in patients affected by SO deficiency.
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PMID:Higher susceptibility of cerebral cortex and striatum to sulfite neurotoxicity in sulfite oxidase-deficient rats. 2752 30