Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Using mouse everted whole small intestine 7 days after a single dose of Phenoclor DP6 (hexachlorobiphenyl) at 1.0 g kg-1 body wt, absorption of D-glucose decreased significantly, probably owing to toxic traces of pentodicholobenzofuran in the PCB preparation and not its high chlorine content. D-glucose tissue accumulation decreased. The serosal fluid transfer also fell but not the gut fluid uptake. D-glucose absorption and fluid transfer remained unchanged following doses of other Phenoclor and Pyralene (PCB) compounds. 2. Using DP6, malabsorption of D-glucose and impaired serosal fluid transfer were not evident 7 days after a single dose of 0.1, 0.25 and 0.50 g kg-1 body wt. One to 21 days after a single dose (1.0 g kg-1 body wt) of DP6, D-glucose absorption and serosal fluid transfer decreased from 3 to 14 days but thereafter became normal. 3. Although absorption of D-galactose, D-glucose following membrane hydrolysis of D-maltose, and L-arginine, L-histidine, L-ornithine and L-proline decreased slightly 7 days after a single dose of Phenoclor DP6,the results were not significant, nor were changes in fluid transfer. 4. Following Phenoclor DP6-treatment, D-glucose malabsorption was abolished by an exogenous energy supply (D-mannose). DP6 affected intracellular metabolism and not the glucose carrier at the membrane brush border. 5. The body-weights and fresh small intestinal weights of mice treated with different PCBs remained unchanged after seven days. The histology of the small intestine showed minimal changes.
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PMID:Polychlorinated biphenyls (phenoclor and pyralene) and intestinal transport of hexoses and amino acids in mice. 82 75

The report deals with the case of a 10-year-old girl with chronic cystic fibrosis. She has been repeatedly treated at the hospital. She has been hospitalized due to respiratory deterioration. Cystic fibrosis is a rare disease, inherited autosomaly recessively, but is very complex in terms of diagnostic and treatment (2). The diagnosis is confirmed based on a clinical picture of the child, measure of Chloride in the sweat, chest X-ray, CT thorax, laboratory findings--genetic confirmation CFTR ( cystic fibrosis transmembrane conductance regulator) genes (3), which result in the production of hyper-viscous mucus and chloride malabsorption in the sweat glands ducts (5,6). Bronchial thickening and plugging and ring shadows suggesting bronchiectasis, segmental or lobar atelectasis are often. Computer tomography of the chest can be used to detect and localize thickening of bronchial airways walls, mucus plugging, hyperinflation and early bronchieactasiae. Pulmonary therapy: the object is to clear secretions from airways and to control infection (7). The diagnosis is originally set when she was 4 years old. She is now admitted due to a deterioration of the main disease. Day before admission in the hospital had a higher bodily temperature, cough and difficult breathing. She already treated conservatively (Ceftazidim, Ceftriakson, Kloksacillin) Since the girl is a chronic patient with bronchiectasie chronic walls of bronchi changes full of the mucus, who is not responding to conservative treatment (antibiotics), therapeutic and diagnostic flexible bronchoscopy had to be performed, resulting in a gram-negative bacteria pseudomonas aeruginosa--a typical bacteria for chronically sick C. F. patient. A pseudomonas therapy was prescribed according to the sensitive antibiogram, during which bronchoscopy was given locally on changes mucous pulmozyme and garamycin. Flexible bronchoscopy was performed as therapeutic. Local bronchoscopy findings:by aspiration of tracheo-bronchal truncus it was found hyperemia and a lot of mucous sticky secretion inside of tracheobronchal tree, especially middle lobe right side, lingual and basals part of the lungs. It was performed broncho-alveolar lavage and given steroids on the place of changed inflamed mucous membrane of the bronchi. It was also given pulmozyme to destroid mucous and make better spontaneously expectorations. Control chest x ray was performed and it was better.
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PMID:Therapeutic flexible bronchoscopy in child with cystic fibrosis. 1605 60

Cystic fibrosis (CF) is a multisystemic autosomal recessive disease caused by a defect in the expression of CFTR protein, i.e. chloride channel present in the apical membrane of respiratory, digestive, reproductive and sweat glands epithelium. It primarily occurs in the Caucasians, while being considerably or excep tionally rare in persons of other races. Absence, deficit or structural and functional abnormalities of CFTR protein lead to mucosal hyperconcentration in the respiratory, digestive and reproductive systems and malabsorption of chloride and sodium in the sweat glands. Thus, the clinical features of patients' with CF are predominated by respiratory, digestive and reproductive disorders, as well as the tendency to dehydration in the condition of increased sweating. Beside genotype variations, the degree of disease manifestation is also essentially influenced by various exogenous factors, such as the frequency and severity of respiratory infections, the level of aero-pollution, quality of immunoprophylaxis, patients' nutritional condition and other. Chloride concentration of over 60 mmol/L in sweat, a high level of immunoreactive chymotrypsinogen in blood and the verification of homozygous mutation of CFTR gene are the basic methods in the diagnostics of the disease. CF belongs to the group of severe and complex chronic diseases, and therefore requires multidisciplinary therapeutic approach. Owing to the improvement of healthcare provision, most patients with CF now survive into adulthood. In addition, their quality of life is also considerably improved.
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PMID:Cystic fibrosis. 2265 Jan 16

To address carbohydrates that are commonly used in biomedical applications with low binding affinities for boronic acid based detection systems, two chemical modification methods were utilized to increase sensitivity. Modified carbohydrates were analyzed using a two component fluorescent probe based on boronic acid-appended viologen-HPTS (4,4'-o-BBV). Carbohydrates normally giving poor signals (fucose, l-rhamnose, xylose) were subjected to sodium borohydride (NaBH4) reduction in ambient conditions for 1 h yielding the corresponding sugar alcohols from fucose, l-rhamnose and xylose in essentially quantitative yields. Compared to original aldoses, apparent binding affinities were increased 4-25-fold. The chlorinated sweetener and colon permeability marker sucralose (Splenda), otherwise undetectable by boronic acids, was dechlorinated to a detectable derivative by reactive oxygen and hydroxide intermediates by the Fenton reaction or by H2O2 and UV light. This method is specific to sucralose as other common sugars, such as sucrose, do not contain any carbon-chlorine bonds. Significant fluorescence response was obtained for chemically modified sucralose with the 4,4'-o-BBV-HPTS probe system. This proof of principle can be applied to biomedical applications, such as gut permeability, malabsorption, etc.
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PMID:Boronic acid recognition of non-interacting carbohydrates for biomedical applications: increasing fluorescence signals of minimally interacting aldoses and sucralose. 2913 Apr 64