Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

LDHk is a cancer-associated lactate dehydrogenase which is also found at high levels in normal mammalian retina. Such retinas share with most cancer tissues a dependence on aerobic glycolysis, leading to high production of lactate. However, retinas of lower vertebrate species are significantly less dependent on aerobic glycolysis. We find that retinas of species less dependent on aerobic glycolysis express significantly lower levels of an LDHk-like activity, less than or equal to the low levels seen in brains. The enzymes from lower species differ from the mammalian retinal enzyme in their pH optima and responsiveness to oxygen; but share a similar degree of inhibition by 5'-5'-dinucleoside tetraphosphates. Therefore, the expression pattern of LDHk in brain and retina of diverse vertebrate species suggests a link with the Warburg effect.
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PMID:LDHk in the retina of diverse vertebrate species: a possible link to the Warburg effect. 387 42

We have evaluated the reliability of the transcutaneous (t.c.) method of measurement of arterial PO2 and PCO2 in adult man. In 33 simultaneous measurements of 9 normals and 12 patients with a wide range of hypoxemia, we found: t.c. PCO2 = 3.62 + 1.29 PaCO2 +/- 7.3 (r = 0.96) and t.c. PO2 = 11.14 + 0.86 PaO2 +/- 9.89 (r = 0.92). Recalculating t.c. PCO2 to 37 degrees C we can obtain: t.c. PCO2 = 2.7 + 0.97 X PaCO2, stating that there is no significant difference between t.c. PCO2 and PaCO2. The t.c. apparatus detects 10 and 90% O2 pressure changes with a delay of time of about 15 s and 1 min, respectively; the t.c. method is therefore not suitable for detecting changes in PaO2 caused by sleep apnea of short duration. On the contrary the t.c. method provided a useful monitoring of arterial PO2 and PCO2 changes during the night in chronic obstructive pulmonary disease (COPD) and non-COPD patients. A nocturnal monitoring of t.c. PO2 and PCO2 seems: (a) absolutely necessary in non-COPD hypoxemics, especially if total lung capacity (TLC) and/or residual volume (RV) are significantly reduced; (b) not absolutely necessary in COPD hypoxemics, provided they have an enlarged TLC and/or a very expanded RV; (c) advisable in intermediate situations, e.g., in COPD hypoxemics with an associated restrictive disorder caused by heart failure, congestion of pulmonary bed, parenchymal or rib cage disease, in order to establish the optimal concentration of oxygen for each patient and to avoid severe nocturnal hypoxemia without producing a dangerous rise in PaCO2.
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PMID:Value of nocturnal monitoring of transcutaneous O2 and CO2 pressures in adults with respiratory failure. 392 61

The experiments on dogs have demonstrated that lung contusion and injury of the rib cage cause the increase in overall oxygen consumption and lung oxygen consumption within the first hours after trauma. During the next week in dogs with contusion lung gradual recovery of the initial levels is observed. In convalescents with rib cage injury the indices in this period remain increased, reaching maximal level in animals with fatal outcome several hours before death. The authors believe that the early posttraumatic period in closed chest trauma is characterized by the increase in the lung oxygen consumption.
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PMID:[Oxygen consumption in the lungs of dogs with a closed thoracic injury]. 395 12

We have carried out a study of the reaction of 13-hydroperoxy-9-cis,11-trans-octadecadienoic acid (linoleic acid hydroperoxide) with hematin. The major products are erythro-11-hydroxy-12,13-epoxy-9-octadecenoic acid, threo-11-hydroxy-12,13-epoxy-9-octadecenoic acid, 9,12,13-trihydroxy-10-octadecenoic acid, 13-keto-9,11-octadecadienoic acid, and 13-hydroxy-9,11-octadecadienoic acid. Several minor products have also been identified, including 9-hydroxy-12,13-epoxyoctadecenoic acid, 11-hydroxy-9,10-epoxy-12-octadecenoic acid, 9-hydroxy-10,12-octadecadienoic acid, and 9-keto-10,12-octadecadienoic acid. Oxygen labeling studies indicate that the observed products arise by at least two pathways. In the major pathway, hematin reduces 13-hydroperoxy-9,11-octadecadienoic acid by one electron to an alkoxyl radical that cyclizes to an adjacent double bond to form an epoxy allylic radical. The allylic radical either couples to the hydroxyl radical coordinated to hematin or diffuses from the solvent cage and couples to O2, forming a peroxyl radical. In the minor pathway, the hydroperoxide is oxidized by one electron to a 13-peroxyl radical that undergoes beta-scission to a pentadienyl radical and O2. Exchange of hydroperoxide-derived O2 for dissolved O2 occurs at this stage followed by coupling of O2 to either terminus of the pentadienyl radical. Both pathways of hydroperoxide metabolism generate significant quantities of peroxyl radicals that epoxidize the isolated double bonds of dihydroaromatic molecules. The products of hydroperoxide reaction with hematin and the oxygen labeling patterns are very similar to the products of unsaturated fatty acid hydroperoxide metabolism by platelets, aorta, and lung. Our results not only provide a mechanism for the formation of a series of mammalian metabolites of linoleic and arachidonic acids but also offer an estimate of the yield of peroxyl radicals generated during the process.
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PMID:Conversion of linoleic acid hydroperoxide to hydroxy, keto, epoxyhydroxy, and trihydroxy fatty acids by hematin. 398 58

Two infants with clinical and radiologic features of metatropic dwarfism presented in the neonatal period with episodes of cyanosis. Diagnostic studies to determine the etiology of these spells, including electrocardiogram, electroencephalogram, arterial blood gases, and metabolic and sepsis studies, were unremarkable. Chest roentgenograms revealed the characteristic long, narrow thoracic cage with no evidence of parenchymal disease. Cervical spine stability evaluation, pulmonary function studies, and chest impedance monitoring with qualitative air flow thermistor studies and transcutaneous oxygen monitoring were carried out. Both patients demonstrated a significant increase in resistance of the respiratory system following passive maneuvering of the head from a neutral position, suggestive of hypopharyngeal air flow obstruction. Obstructive sleep apnea resulting in cyanosis was documented in both patients. All other studies failed to yield a cause for the episodes of cyanosis. Our investigation failed to alter the clinical course which resulted in respiratory arrest and death by 7 months of age. A table is presented for the differentiation of skeletal dysplasias presenting in the perinatal period.
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PMID:Respiratory complications of metatropic dwarfism. 401 1

Non-invasive measurements were made of ventilation, its derivatives, the contributions of abdomen and rib cage and arterial oxygen saturation in six healthy normal men whilst awake and during sleep. Minute ventilation fell significantly during slow wave (SW) sleep and rapid eye movement (REM) sleep (awake = 6.3 1 min-1, SW sleep = 5.7 1 min-1, REM sleep = 5.4 1 min-1; p less than 0.04). Mean inspiratory flow also fell significantly but timing was unchanged. The abdominal (diaphragmatic) contribution to ventilation fell very significantly during SW sleep but returned to awake levels during REM sleep (awake 54%, SW sleep 38%, REM sleep 56%; p less than 0.007). There were also significant falls in arterial oxygen saturation during SW and REM sleep (awake 97.3%, SW sleep 96.5%, REM sleep 96.2%; p less than 0.002). These falls represent reductions in arterial oxygen tension similar to those seen in patients with chronic airways obstruction and can be accounted for entirely by the associated reduction in ventilation.
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PMID:Changes in ventilation and its components in normal subjects during sleep. 402 90

To examine the mechanism of exercise limitation associated with chest wall restriction (CWR), we compared the ramp (1 W/3 s) exercise performance of six untrained subjects with ankylosing spondylitis (AS) and six healthy subjects matched for age and body size. Subjects with AS had CWR (maximum rib cage expansion : 1.4 +/- 0.2 cm; means +/- sem). The maximum oxygen uptake (VO2max) of AS subjects (2.15 +/- 0.2 1-stpd) was less than their predicted VO2max (2.68 +/- 0.13 1-stpd; p less than 0.03) and the measured VO2max of matched healthy subjects (2.78 +/- 0.22 1-stpd; p less than 0.03). Subjects with AS achieved 95 percent of predicted maximum heart rate, and their maximum voluntary ventilation exceeded their maximum exercise ventilation by at least 15 l X min-1 unless parenchymal pulmonary disease was present. We conclude that maximum ramp exercise performance of AS subjects with CWR is decreased. Deconditioning or cardiovascular impairment rather than ventilatory impairment appears responsible for the observed reduction of VO2max.
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PMID:Exercise performance of subjects with ankylosing spondylitis and limited chest expansion. 404 61

Pectus excavatum is generally regarded as a cosmetic deformity; however, some children with pectus excavatum complain of chest pain and exercise limitation. Physiologic studies sometimes show mild restrictive changes and suggest an increased oxygen cost of breathing. Limitation of rib cage mobility related to the deformity may explain these findings. If rib cage mobility is limited, the ability of the actively inspiring rib cage to lower abdominal pressure would be decreased. If this were so, increased swings in abdominal pressure would be seen during the respiratory cycle, especially at times of stress such as during exercise. To test the hypothesis that pectus excavatum is associated with decreased rib cage mobility, we studied 11 patients with pectus excavatum and 11 control subjects. Four control subjects were also studied with rib cage mobility restricted by chest wall strapping sufficient to decrease vital capacity by 5, 10, and 40%. Gastric pressure was measured using balloon catheters and was used as an index of abdominal pressure. Flow at the mouth was recorded and integrated to give volume. Measurements were made at rest, immediately after exercise, and during graded voluntary inspiration to total lung capacity. Gastric pressure was related to tidal volume, and pressure-volume loops were constructed. There were no differences in abdominal pressure swings during respiration between the patients with pectus excavatum and the control subjects. Both groups showed moderate increase in gastric pressure during inspiration at rest and smaller increases or even decreases in abdominal pressure at end inspiration after exercise and at total lung capacity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rib cage mobility in pectus excavatum. 407 62

The effects of spontaneous high-frequency breathing (HFB) on lung function were evaluated in three subjects highly trained in the practice of yoga. Transpulmonary pressure was measured by an esophageal balloon catheter and gas flow by pneumotachography. The abdominal and rib cage contributions to tidal breathing were measured separately by respiratory inductive plethysmography. Gas exchange was studied by the conventional technique and by multiple inert gas elimination. During HFB, respiratory rate increased to 232 cycles/min with a tidal volume of 0.35 liter. This resulted in a more than 10-fold increase in expired minute ventilation to approximately 90 1/min. The transpulmonary pressure varied by 20 cmH2O, with the calculated elastic, resistive, and accelerative components varying by 2, 20, and 8 cmH2O, respectively. Respiratory work increased more than 200-fold in comparison with resting ventilation. A phase shift between thoracic and abdominal breathing was observed and was interpreted as a volume displacement of approximately 30 1/min between the two parts of the respiratory system. Arterial oxygen and carbon dioxide tension remained normal. Bohr dead space increased, while acetone dead space remained unaltered. A bimodal distribution of ventilation-perfusion ratios (VA/Q) was observed, with one mode in normal and another in "high" VA/Q regions.
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PMID:Effects of high-frequency breathing on pulmonary ventilation and gas exchange. 666 76

Phenomena associated with a deformation of short-time occurrence and noticed on concentration curves of tidal O2 and CO2 were examined in adult hens sitting quietly in a cage or suspended in prone position. During the episode of deformation, a decrease in arterial oxygen-gas tension was apparent. It was associated with a slight increase in arterial carbon-dioxide-gas tension and a slight acidic shift of arterial blood pH. The episode was associated with increases in intrapressure of the interclavicular and bilateral abdominal air sacs. The tracheal expiratory-gas flow changed in pattern. Hypoventilation due to reduction in tidal volume or respiratory rate could not be detected during the episode. The episode was suddenly terminated at the hen's body movement induced spontaneously or by pinching the comb, at coughlike activity or at no obvious change in behavior in a quietly resting position. Deformation similar to the spontaneous one could be induced by 3 ml-water flushing into the trachea or 0.1% methacholine aerosol inhalation. The mechanism responsible for the genesis of deformation was discussed. It was presumed to be based upon some mechanism, such as mucous accumulation in the lung, rather than upon the pulmonary smooth-muscle contraction.
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PMID:An analysis on the mechanism responsible for genesis of deformation of expiratory-gas-concentration curves in chickens. 680 76


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