glycogen and Pneumonia

Fasting is an important risk factor for hypoglycemia in children with malaria or pneumonia. Young children are more at risk because of impaired endogenous glucose production presumably due to smaller liver glycogen stores. The aim of this study was to measure the effect of a bolus of glucagon on glucose kinetics, as an indicator of glycogen content, in fasted children with malaria and pneumonia.. After a 16-h controlled fast, plasma glucose concentration and endogenous glucose production were measured using [6,6-2H2]glucose in six children with severe malaria and 12 children with severe pneumonia who were 1-5 years of age before and after a bolus glucagon.. Basal glucose concentration and endogenous glucose production were higher in children with malaria, p=0.034 and p=0.010, respectively. After glucagon, the increase in the plasma glucose concentration was higher in children with malaria (52±26% vs. 31±23%, p=0.029). Also, the increase in glucose production was higher in children with malaria (106±42% vs. 70±52%, p=0.023). There were no differences in the fasting duration or duration of illness.. This is the first study to show infectious disease-related differences in the adaptation of glucose metabolism to fasting in young children. It was found that basal glucose concentration and endogenous glucose production were higher in children with malaria. The increase in plasma glucose concentration and endogenous glucose production in response to glucagon was higher in children with malaria, indicating smaller glycogen stores in children with pneumonia.

Topics: Adaptation, Physiological; Blood Glucose; Child, Preschool; Fasting; Female; Gastrointestinal Agents; Glucagon; Glycogen; Humans; Hypoglycemia; Infant; Insulin; Liver; Malaria; Male; Models, Biological; Pilot Projects; Pneumonia; Risk Factors; Suriname

Two murine monoclonal antibodies (CL-3 and CL-37, both F(ab')2) to human endothelial-leukocyte adhesion molecule-1 (ELAM-1) were found to react immunohistochemically with rat pulmonary artery endothelial cells that had been pretreated with tumor necrosis factor (TNF alpha). CL-3, but not CL-37, blocked in vitro adherence of neutrophils to TNF alpha-treated endothelial cells and the killing of TNF alpha-treated rat endothelial cells by phorbol ester activated neutrophils. In rats treated systemically with CL-3, there was a 70% reduction in accumulation of neutrophils in glycogen-induced peritoneal exudates. Treatment of animals with CL-37 anti-ELAM-1 did not reduce neutrophil accumulation under the same conditions. When IgG immune complex deposition was induced in dermis and in lungs of rats, treatment with CL-3 anti-ELAM-1 markedly reduced vascular injury as measured by changes in vascular permeability (leakage of 125I-albumin) and hemorrhage (extravasation of 51Cr-red blood cells). The protective effects of CL-3 anti-ELAM-1 were related to greatly diminished recruitment of neutrophils (as assessed morphologically, by tissue extraction of myeloperoxidase, and by retrieval, via bronchoalveolar lavage, of neutrophils from lung). CL-37 had no protective effects in vivo after deposition of immune complexes in lung. Using either CL-3 or CL-37 anti-ELAM-1, immunohistochemical analysis of lungs undergoing IgG immune complex-induced injury revealed a striking upregulation of ELAM-1 in the lung vasculature (venules and interstitial capillaries), with a peak intensity developing between 3 and 4 h after deposition of immune complexes in lung. Vascular beds of spleen, liver, and kidney failed to show upregulation of ELAM-1 under these same conditions. The immunohistochemical reactivity of rat lung was abolished if the anti-ELAM-1 preparation was first absorbed with monolayers of human umbilical vein endothelial cells that had been pretreated with TNF alpha. Untreated human endothelial cells failed to cause loss of lung reactivity of the anti-ELAM-1 preparation. These data indicate that ELAM-1 is upregulated in the pulmonary vasculature of rats during deposition of immune complexes and that ELAM-1 appears to play an obligate role in the recruitment of neutrophils.

Topics: Animals; Antibodies, Monoclonal; Antigen-Antibody Complex; Cell Adhesion Molecules; E-Selectin; Endothelium, Vascular; Exudates and Transudates; Glycogen; Humans; Immunohistochemistry; Lung; Mice; Mice, Inbred BALB C; N-Formylmethionine Leucyl-Phenylalanine; Neutrophils; Pneumonia; Pulmonary Artery; Rats; Tumor Necrosis Factor-alpha

The assessment of lymphocytic functional activity and immunological reactivity in 114 cases of acute pneumonia provided additional information on the disease severity, potential complications, effectiveness of the treatment conducted, completeness of recovery. The study of immunological reactivity in acute pneumonia is beneficial in poor clinico-roentgenological manifestations. Combined treatment with levamisole promoted improvement of immunological reactivity and reduced the duration of disability.

Topics: Acute Disease; Adolescent; Adult; Alkaline Phosphatase; Bronchitis; Chronic Disease; Clinical Enzyme Tests; Female; Glycogen; Humans; Lymphocyte Activation; Male; Middle Aged; Peroxidase; Phytohemagglutinins; Pneumonia

Topics: Acid Phosphatase; Adolescent; Adult; Alkaline Phosphatase; Chronic Disease; Female; Glycogen; Humans; Male; Middle Aged; Neutrophils; Peroxidases; Pneumonia

Topics: Adolescent; Carbohydrates; Child; Child, Preschool; Glycogen; Humans; Lipids; Metabolic Diseases; Neutrophils; Pneumonia

Topics: Acid Phosphatase; Adolescent; Adult; Alkaline Phosphatase; Anti-Bacterial Agents; Chronic Disease; Glycogen; Humans; Leukocytes; Lymphocyte Activation; Lymphocytes; Middle Aged; Peroxidases; Pneumonia; Sulfanilamides

Myocardium of the children dying suddenly of respiratory infection complicated by pneumonia was studied histologically and histochemically. The observed morphological changes consisted in hemodynamic disorders and degenerative lesions of various intensities associated mostly with the disturbed protein metabolism in the cytoplasm of myocardial cells, especially in microfibrillae.

Topics: Cell Nucleus; Child, Preschool; Death, Sudden; Glycogen; Histocytochemistry; Humans; Infant; Infant, Newborn; Myocardium; Myofibrils; Necrosis; Pneumonia; Respiratory Tract Infections

Examination of macrophages, polymorphonuclear leukocytes (PMNL) and lymphocytes of the trachea, PMNL and blood lymphocytes, of the condition of pulmonary tissue in the time course of the process (1st day--l months) revealed an association between the developing cellular and tissue changes. The development of alterations in the lungs with predominant anabolic changes and moderate exudation are characterized by a decrease in the content of nucleoproteins (deoxyribonucleoproteins, ribonucleoproteins), and activity of NAD-diaphorase and alkaline phosphatase, an increase in the activity of acid phosphatase in the above-mentioned cells of the trachea and blood as well as by increased permeability of lysosomal membranes and degeneration of macrophages, PMNL and lymphocytes of the trachea. The above cellular changes in combination with increased permeability of PMNL and blood lymphocyte lysosomal membranes correspond to the development in the lungs of catabolic alterative lesions, marked exudation, and suppurative-necrotic processes. The increase in the content of nucleoproteins and NAD-diaphorase and alkaline phosphatase activity and the decrease in the acid phosphatase activity are accompanied by activation of proliferation in the lungs.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Glycogen; Glycoproteins; Glycosaminoglycans; Lung; Lymphocytes; Macrophages; Nucleoproteins; Oxidoreductases; Pneumonia; Rabbits; Trachea

Topics: Acid Phosphatase; Acute Disease; Adult; Aged; Alkaline Phosphatase; Chronic Disease; Glycogen; Humans; Leukocytes; Lipids; Middle Aged; Peroxidases; Pneumonia

The state of pulmonary surfactant in rabbits at different periods (3 to 60 days) of experimental pneumonia was compared with the changes of the redox enzymes in the alveolar epithelium and the cells of the inflammatory infiltrate. At the initial stage (3 to 7 days) of the cellular metabolism activation there occurred a transitory intensification of the synthesis of surfactant lipids with a relative suppression of phospholipid synthesis. Later the progress of dystrophic processes and parenchymal sclerosis was accompanied by reduction of the synthesis of all the surfactant components. Surfactant surface activity became stable at a low level. This is possibly connected with the specific regulation of the surfactant synthesis determined by functional peculiarities of the organ.

Topics: Animals; Cholesterol; DNA; Glycogen; Histocytochemistry; Lipids; Lung; Oxidoreductases; Phospholipids; Pneumonia; Proteins; Pulmonary Surfactants; Rabbits; RNA

Topics: Child, Preschool; DNA; Female; Glycogen; Histocytochemistry; Humans; Infant; Leukocytes; Male; Pneumonia; RNA

Topics: Alkaline Phosphatase; Child, Preschool; Glycogen; Histocytochemistry; Humans; Neutrophils; Pneumonia

Topics: Acid Phosphatase; Adolescent; Adult; Aged; Alkaline Phosphatase; Female; Glycogen; Humans; Leukocytes; Male; Middle Aged; Peroxidases; Pneumonia