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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The effects of varying PCO2 on lactate uptake and intracellular pH (pHi) were studied in the isolated rat liver perfused with differing concentration of lactate. 2. In general, pHi and lactate uptake are inversely related to PCO2, and pHi and lactate uptake are directly related to each other, but the quantitative aspects and significance of these relationships vary with the availability of lactate. A model of hepatic lactate metabolism is proposed which may account for the quantitative variation. 3. The metabolism of lactate within the hepatocyte exerts a destabilizing effect on hepatocyte cell pH, in contrast to the buffering effect seen in predominantly glycolytic tissues. 4. An attempt is made to relate the findings to the disturbances of lactate metabolism in clinical respiratory failure.
Clin Sci Mol Med 1978 Aug
PMID:Effect of varying PCO2 on intracellular pH and lactate consumption in the isolated perfused rat liver. 2 97

1. The question whether respiratory muscle fatigue ever causes respiratory failure is over 40 years old, but we still have no definitive answer to this question. Skeletal muscle fatigue occurs when the rate of energy consumption of the muscle is greater than the energy supplied, so that energy stores are utilized and eventually become depleted. 2. Five factors which are important in the development of muscle fatigue (a, the tension developed by the muscle; b, the maximum tension the muscle can develop; c, the energy stored within the muscle; d, the energy supplied to the muscle; e, the efficiency of the muscle). These can be affected in many diseases, so disposing to fatigue, thus respiratory muscle fatigue is likely to be a common occurrence. 3. Respiratory muscle fatigue can in principle easily be diagnosed at the bedside by application of a simple electromyographic technique used to detect fatigue in other skeletal muscles.
Clin Sci Mol Med 1977 Nov
PMID:Respiratory muscle fatigue: a cause of respiratory failure? 58 26

1. The concentration of metabolites in intercostal and quadriceps muscle, and pulmonary function, were studied in twelve patients with chronic obstructive lung disease and acute respiratory failure before, during and after standardized treatment at an intensive care unit. The findings were compared with those obtained in hospitalized patients of comparable age with non-pulmonary diseases. 2. On admission, when the patients had marked hypoxaemia, hypercapnia and acidosis, the concentrations of ATP and creatine phosphate were low in both intercostal and quadriceps muscle, particularly the latter. The lactate concentration was increased in relation to control values but glycogen did not differ significantly. 3. In response to therapy, the Pa,CO2 and the patient's acidosis decreased, the vital capacity increased and lung mechanics improved along with the clinical condition. At the same time there were significant increases in the concentrations of ATP, creatine phosphate and glycogen in intercostal and quadriceps muscles, to values similar to, and for glycogen in excess of, those found in control subjects. Lactate concentration fell significantly during treatment. 4. In view of the low initial muscle concentrations of ATP and creatine phosphate in the patients, it is suggested that dysfunction of the respiratory muscles may be an important component of respiratory failure. Moreover, the concentration of energy-rich compounds in muscle rose significantly as the patients responded to treatment, which emphasizes the importance of adequate nutritional therapy in this disorder.
Clin Sci Mol Med 1977 Apr
PMID:Muscle metabolism in patients with chronic obstructive lung disease and acute respiratory failure. 86 35

Because granulocyte colony-stimulating factor (G-CSF) is known to induce granulopoiesis and activate mature neutrophils, this factor could be important in determining the number and functional activity of neutrophils at sites of lung disease. The purpose of this study was to evaluate the ability of lung immune and inflammatory cells to produce G-CSF, and to seek evidence for the spontaneous production of this factor by cells recovered by lavage from controls and patients with lung diseases in which neutrophils may play a pathogenetic role. Lavage cells from controls produced little G-CSF spontaneously. Alveolar macrophages (AM), but not lymphocytes, produced large amounts following endotoxin stimulation. Lavage cells from patients with respiratory failure associated with bacterial pneumonia, but not those with respiratory failure from noninfectious causes, spontaneously released G-CSF (32 +/- 24 and less than 1 U/10(6) AM, respectively). Lavage cells from five of 15 patients with sarcoidosis and one of five patients with diffuse pulmonary fibrosis also spontaneously released G-CSF, which could not be explained by endotoxin exposure. The release of G-CSF by endotoxin-dependent and -independent mechanisms could play a role in the recruitment and activation of neutrophils in bacterial pneumonia and participate in the pathogenesis of some interstitial lung diseases.
Am J Respir Cell Mol Biol 1991 Feb
PMID:Spontaneous release of granulocyte colony-stimulating factor (G-CSF) by alveolar macrophages in the course of bacterial pneumonia and sarcoidosis: endotoxin-dependent and endotoxin-independent G-CSF release by cells recovered by bronchoalveolar lavage. 170 67

Male lung cancer patients with poor performance status [Eastern Cooperative Oncology Group (ECOG) index 3-4] have an endocrinological dysfunction as assessed by serum testosterone and sex hormone-binding globulin (SHBG) levels. Patients who respond to therapy regain normal free testosterone levels within 12 weeks post chemotherapy, whereas non-responders continue to exhibit subnormal levels. The perturbations of endocrinological variables in patients with lung cancer is not due to development of hypoxia, as patients with respiratory failure maintain a significantly lower testosterone level compared to cancer patients. The development of a deficiency in total testosterone concentrations in lung cancer patients is correlated to their performance status, and not to the presence of metastatic disease. The mechanisms responsible for the endocrinological dysfunction in patients with lung cancer remain unknown.
J Steroid Biochem Mol Biol 1991 Sep
PMID:Gonadal endocrine dysfunction in patients with lung cancer: relation to responsiveness to chemotherapy, respiratory function and performance status. 191 28

This report describes the development of hyperplasia of both the thymus and the peripheral T-cell system with advancing age in the Buffalo rat. Buffalo/Mna rats do not show age-related thymic involution, but rather develop thymic hyperplasia with advancing age. This thymic growth is expansile and there is no infiltration of the surrounding tissues. Because the enlarging thymus occupies the thoracic cavity, most of the rats die of respiratory failure by the age of 24 months. Thymic enlargement is due to primary hyperplasia of cortical epithelial cells and the large number of proliferating lymphocytes. The hyperplastic epithelial cells are bizarre in shape and strongly positive when stained with Th-3 monoclonal antibody (MoAb), anti-thymosin antibody and anti-EGF antibody, but negative with Th-4 MoAb. The patterns of distribution of CD-5+, CD-4+ and CD-8+ lymphocytes within the hyperplastic thymus are similar to those seen in young rats of other species. The high level of T-cell emigration from the thymus to the periphery appears to persist throughout life, since the percentage of normal splenic T-cells also increase with advancing age and exceed 70% of the total by 24 months of age. This thymic enlargement with abnormal hyperplasia of cortical epithelial cells can be prevented by hypophysectomy.
Virchows Arch B Cell Pathol Incl Mol Pathol 1990
PMID:Age-related hyperplasia of the thymus and T-cell system in the Buffalo rat. Immunological and immunohistological studies. 197 97

Alterations in pulmonary surfactant are partly responsible for the respiratory insufficiency seen under septic shock process. We have used an experimental model of LPS-induced shock in rats to examine the cells responsible for the pulmonary surfactant synthesis and its relationship to lung injury. (14C)Choline incorporation into phosphatidylcholine was significantly reduced in lung homogenates or type II cells obtained from LPS-treated animals. Addition of LPS in vitro fails to increase (14C)choline incorporation in type II cells obtained from LPS-treated animals. We suggest that this depression of pulmonary phosphatidylcholine synthesis may partly explain the occurrence of respiratory failure with septic shock.
Mol Cell Biochem 1990 Mar 27
PMID:Effect of Escherichia coli lipopolysaccharide on phosphatidylcholine biosynthesis by rat lung and alveolar type II cells. 218 66

Congenital alveolar proteinosis (CAP), a cause of respiratory failure in fill-term newborns, often leads to death in infancy despite medical therapy. We recently described an inherited deficiency of surfactant protein B (SP-B) (N. Engl. J. Med. 1993; 328:406-410) in two siblings with CAP. The SP-B deficiency was accompanied by marked abnormalities, both quantitative (increase) and qualitative (distribution), of SP-A and SP-C in the lungs of the affected infants. Ultrastructural studies of the lung of one of these infants and of a third affected sibling born in the index family showed abundant alveolar concentric multilamellated structures and membranous vesicles but no typical tubular myelin. In addition, membranous vesicles from type II cells and immunogold labeled SP-A and SP-C were found between type II cells and their basement membrane despite intact interepithelial cell junctions. These findings suggest an important role for SP-B in the directionality of surfactant secretion and in the formation of tubular myelin.
Am J Respir Cell Mol Biol 1994 Aug
PMID:Ultrastructure of lung in surfactant protein B deficiency. 804 84

Human surfactant protein B (SP-B) is a 79-amino acid, phospholipid-associated polypeptide expressed by respiratory epithelial cells of the lung. SP-B is essential for lung function, enhancing the spreading and stability of surfactant phospholipids that serve to reduce surface tension at the alveolar air-liquid interface. Congenital absence of SP-B results in neonatal respiratory failure and death. In the present work, we constructed a replication-deficient adenoviral vector, Av1SP-B1, in which the human SP-B cDNA is expressed under control of the Rous sarcoma virus (RSV) promoter in an E1-E3-deleted adenovirus type 5 (Ad5)-based vector system. Av1SP-B1 was produced in 293 kidney cells, directing the synthesis of the SP-B protein and SP-B peptides. Av1SP-B1 directed the synthesis of SP-B mRNA, precursor and active 8-9 kD polypeptide in immortalized mouse lung epithelial cells (MLE-12 cells), demonstrating complete processing to the human SP-B protein by these cells. Synthesis of human SP-B mRNA was detected as early as 12 h after infection and was maximal 48 h after infection in vitro. Northern blot analysis demonstrated that human SP-B mRNA was expressed in the lungs of cotton rats infected with Av1SP-B1 but not in those of uninfected animals or in animals infected with a reporter adenoviral vector, Av1LacZ4. In situ hybridization demonstrated the abundance and localization of the transferred human SP-B mRNA.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Respir Cell Mol Biol 1994 Sep
PMID:Adenoviral-mediated gene transfer of human surfactant protein B to respiratory epithelial cells. 808 69

Erectile impotence is commonly encountered in male patients with respiratory failure and hypoxia. In this study, 42% of the patients experienced reversal of sexual impotence during long-term oxygen therapy (LTOT). We examine the association between sexual impotence, gonadal axis hormones, hypoxia, and oxygen therapy. Nineteen sexually impotent male patients eligible for LTOT (pO2 < 7.3 kPa during stable disease) and with sexual impotence received oxygen therapy for 1 month (n = 12) or 24 h (n = 7). pO2, LH, FSH, testosterone, and SHBG (sex hormone binding globulin) were monitored. Five of 12 patients receiving oxygen for 1 month regained sexual potency. The responders showed a significant increase in arterial pO2 and serum testosterone, and a decline in SHBG compared to non-responders. None of the patients receiving oxygen for 24 h experienced reversal of sexual impotence, despite a significant increase in pO2. In these patients, serum testosterone did not increase significantly. Reversal of sexual impotence may be achieved in some patients with respiratory failure. The oxygen therapy must, however be administered for an adequate length of time.
J Steroid Biochem Mol Biol 1993 Dec
PMID:Reversal of sexual impotence in male patients with chronic obstructive pulmonary disease and hypoxemia with long-term oxygen therapy. 827 14


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