Gene/Protein Disease Symptom Drug Enzyme Compound
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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lung surfactant protein-A (SP-A) is a major phospholipid-associated glycoprotein in surfactant, and is a useful immunohistochemical marker for lung adenocarcinoma. Carcinoembryonic antigen (CEA) has not been immunohistochemically detected in mesothelioma. In pleural effusions due to malignant mesothelioma, very low concentrations of SP-A and CEA can be expected. We studied the value of combined determinations of CEA and SP-A in pleural fluid to distinguish between lung adenocarcinoma and mesothelioma. SP-A and CEA concentrations were measured in pleural effusions from 78 patients with lung adenocarcinoma and 10 with malignant mesothelioma. SP-A concentrations in pleural effusions due to lung adenocarcinoma and mesothelioma were 516 +/- 140 and 16.9 +/- 3.6 ng.ml-1 (mean +/- SEM), respectively. CEA concentrations in pleural effusions due to lung adenocarcinoma and mesothelioma were 239 +/- 92.4 and 1.7 +/- 0.3 ng.ml-1, respectively. SP-A values did not exceed 100 ng.ml-1 in any of 10 mesotheliomas, whilst in 37 of 78 lung adenocarcinomas they did. CEA values did not exceed 10 ng.ml-1 in any of 10 mesotheliomas, whilst in 53 of 78 lung adenocarcinomas they did. Increased values of SP-A and/or CEA were found in pleural effusions from 67 of 78 lung adenocarcinomas. It is concluded that a combination of CEA and SP-A assays in pleural effusions will be helpful for discriminating lung adenocarcinoma from mesothelioma.
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PMID:Lung surfactant protein-A and carcinoembryonic antigen in pleural effusions due to lung adenocarcinoma and malignant mesothelioma. 778 85

Recent data indicate that epidermal growth factor (EGF) is a potent mitogen to normal pituitary cells. Its receptor (EGFR or c-erbB-1), a cellular homologue of a viral oncoprotein erbB, is knonw to be overexpressed in many tumors, but little is known about the expression of EGF and EGFR in pituitary tumors. Immunocytochemical analyses of EGF, EGFR, and c-erbB-2 (an EGFR-related oncoprotein) were carried out on paraffin-embedded sections of 54 pituitary tumors. In sections from normal pituitary, EGF was localized mainly in the gonadotrophs and thyrotrophs. EGFR was detected in only 5-10% of the cells in all of the normal pituitary sections and was almost undetectable in all (34/34) of the hormone-secreting tumors (19 GH-, 9 ACTH-, 4 PRL- and 2 TSH-secreting tumors). However, in 16/20 of the samples from clinically nonfunctioning tumors, EGFR was markedly overexpressed. The EGFR found in these tumors and in the normal tissue was not the truncated form of the EGFR because all sections stained positively with monoclonal antisera to both the intra- and extracellular domains of the EGFR. EGF was coexpressed in the same NFT samples that stained positively for EGFR and was also found in 2/19 GH-, 2/4 PRL-, and 1/2 of TSH-secreting tumors. The expression of c-erbB-2 was detected in all normal tissue, all NFT, and about half of GH-secreting tumors. No correlation was found with clinical parameters other than tumor categories. Because the overexpression of structurally intact EGFR was confined to NFT, the response of the tumor cells to EGF in vitro was examined. The addition of 1 nM EGF to NFT-derived cells resulted in an increase in [3H]thymidine uptake to 237.5 +/- 19.8% (mean +/- SEM, n = 3) of the control value. EGF also stimulated EGFR messenger RNA levels, shown by Northern blot analysis. In contrast, the expression of glycoprotein hormone common alpha-subunit gene in the tumor cells was reduced by EGF, T3, and 17 beta-estradiol. The novel findings of overexpression of EGFR in most NFT combined with the in vitro response to EGF resulting in an increase in tumor cell growth, up-regulation of EGFR gene and suppression of hormone gene expression implicate a role for EGF and its receptor in the development and/or progression of NFT.
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PMID:Expression of epidermal growth factor (EGF), its receptor, and related oncoprotein (erbB-2) in human pituitary tumors and response to EGF in vitro. 795 24

To determine whether induced sputum samples might provide a useful means for evaluating the effects of therapy on airway mucosal inflammation, we examined induced sputum samples obtained before and after 6 days of treatment with prednisone (0.5 mg/kg/day) or placebo in a randomized, double-blind study of 24 asthmatic subjects. Induced sputum was analyzed for total and differential cell counts and for concentrations of eosinophil cationic protein, albumin, and mucin-like glycoprotein. We found that the mean (+/- SEM) percentage of eosinophils in sputum samples from the prednisone-treated group fell from 14.1% +/- 5.0% at baseline to 1.8% +/- 0.8% after treatment, a decrease significantly greater than in the placebo-treated group (from 10.3% +/- 4.9% to 11.1% +/- 4.0%; p = 0.002). The absolute number of eosinophils also decreased significantly more in the prednisone-treated group than in the placebo-treated group (p = 0.04). In addition, eosinophil cationic protein levels in induced sputum fell more in the prednisone-treated group than in the placebo-treated group (from 324 +/- 131 ng/ml to 144 +/- 84 ng/ml vs 173 +/- 50 ng/ml to 188 +/- 47 ng/ml; p = 0.002). Furthermore, prednisone treatment was associated with a significant increase in peak expiratory flow, an effect that was significantly correlated with the decrease in eosinophil percentage in induced sputum (rs = 0.64, p = 0.04). Prednisone treatment was not associated with any significant change in the concentrations of albumin or mucin-like glycoprotein. We conclude that analysis of induced sputum is a useful noninvasive method for studying the effects of asthma therapy on airway eosinophilic inflammation.
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PMID:Analysis of induced sputum to examine the effects of prednisone on airway inflammation in asthmatic subjects. 796 55

A computer-based technique for the quantification of abnormal bowel uptake in Crohn's disease has been developed and compared with pre-existing clinical, laboratory and scintigraphic methods of assessment. The standard technique for labelling leucocytes with 99mTc-HMPAO is applied. Images were obtained at 40, 120 and 240 min after the injection of radiolabelled leucocytes. The count in the bowel area after subtracting background activity corrected to the injected dose and image acquisition times is the 'scan score', an objective measure of disease activity. The scan score is significantly higher in patients with clinically active disease (mean 82.1 +/- SEM 13.6) than in those with quiescent disease (24.7 +/- 7.0) (p < or = 0.005). Optimum separation between active and quiescent disease is achieved with a threshold scan score of 20. The scan score was comparable in small bowel disease (73.3 +/- 16.2), large bowel (94.4 +/- 33) and disease at both locations (94.1 +/- 19.2). The scan score correlated favourably with Crohn's Disease Activity Index (rs = 52, p < or = 0.0001), Harvey & Bradshow Simple Index (rs = 0.4, p < or = 0.001), serum C-reactive protein (rs = 0.72, p < or = 0.001), serum alpha acid glycoprotein (rs 0.67, p < or = 0.001), haemoglobin (rs = 0.66, p < or = 0.001), platelet count (rs = 0.47, p < or = 0.006), albumin (rs = 0.61, p < or = 0.0001) and faecal 111Indium excretion (rs = 0.78, p < or = 0.001), but not with the ESR (rs = 0.22, p < or = 0.4).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Background subtraction: a new approach to the assessment of disease activity in Crohn's disease using 99mTc-HMPAO-labelled leucocytes. 797 51

Protein S is a vitamin K-dependent glycoprotein acting as a cofactor for activated protein C and thereby exerting an antithrombotic effect. When compared to values recorded in the 10 healthy normal weight normolipidemic control subjects (80.1% +/- 5.16; mean +/- SEM), plasma protein S-antigen (PS:Ag) level was found to be significantly (p < 0.01) decreased in the 11 patients with decompensated cirrhosis of the liver (54.72% +/- 4.89) and in the 12 surgical patients in critical condition (59.2 +/- 4.96), while obviously (p < 0.001) increased plasma levels were noted in the group including 20 overweight and hyperlipidemic subjects (113% +/- 3.1). Since the low PS:Ag level was associated with a decreased serum cholinesterase (CHE) activity, while both plasma PS:Ag and serum CHE activity were increased in overweight and hyperlipidemic subjects it is considered that impaired or respectively enhanced hepatic protein synthesis is at least partially responsible for changes affecting this antithrombotic plasma protein.
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PMID:Plasma protein S-antigen (PS:Ag) in selected disease states. 808 8

Mullerian inhibiting substance (MIS) is a glycoprotein hormone produced in Sertoli cells of the fetal and postnatal testis, and granulosa cells of the pubertal ovary. We examined MIS expression in a nonhuman primate, the cynomolgus macaque monkey (Macaca fascicularis), to define an animal model for studying MIS gene regulation. Changes in testicular MIS mRNA with age were assessed by in situ hybridization of prepubertal to adult testes, Northern analysis of pubertal and adult specimens, and determination of serum MIS concentrations from infancy to adulthood. We found that MIS expression was highest in the youngest animals and decreased progressively with increasing age. Serum MIS concentrations correlated inversely with increasing age (r = -0.74), body weight (r = -0.79), and testicular volume (r = -0.73), but not with testosterone levels (r = -0.35). The mean MIS concentrations +/- SEM for the four developmental age groups were 270.6 +/- 23.8 (infants), 195.5 +/- 18.5 (juveniles), 102.7 +/- 28.4 (peripubertals), and 51.6 +/- 7.1 (adults). This study confirms that nonhuman primate and human MIS are highly homologous and have similar developmental patterns. The normative data for serum MIS concentrations in cynomolgus monkeys at different ages and developmental stages will be invaluable for further work examining MIS regulation.
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PMID:Developmental changes in mullerian inhibiting substance in the cynomolgus monkey, Macaca fascicularis. 812 32

The release of platelet activating factor (PAF-ACETHER or PAF) and its precursors in the gastric lumen was assessed in 13 normal subjects in basal condition and after stimulation by gastrin. Acid, pepsin, and sialic acid outputs were determined under the same conditions. Gastric juice was collected using a nasogastric tube after overnight fast in basal condition for 60 minutes, then under pentagastrin infusion (6 micrograms/kg/hr for 60 minutes). Platelet activating factor was detected at low concentration in 4/13 subjects under basal condition (mean (SEM) 1.2 (0.6) pg/hr) while high concentrations of lyso platelet activating factor (6.1 (1.8) microgram/hr) and of alkyl-acyl-glycerophosphocholine (AAGPC) (11.5 (3) micrograms/hr) were found in 13 and 11 subjects, respectively. Platelet activating factor was not detected during pentagastrin infusion, while lyso platelet activating factor and alkyl-acyl-glycerophosphocholine were detected in 13 and in 12 subjects, respectively. Compared with the basal condition these platelet activating factor precursors increased significantly (p < 0.001) going up to fivefold baseline (31.8 (6.8) micrograms/hr and 53 (9.3) micrograms/hr respectively) in response to pentagastrin. There was a positive correlation between platelet activating factor precursors and acid or pepsin output but not between platelet activating factor precursors and sialic acid. As sialic acid may be considered an index of mucus glycoprotein degradation, it seems that gastrin stimulation of gastric epithelial cells results in a concomittant secretion of platelet activating factor precursors, acid, and pepsin irrespective of mucus glycoprotein degradation.
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PMID:Gastric secretion of platelet activating factor and precursors in healthy humans: effect of pentagastrin. 817 52

The high incidence of clinical remission after faecal diversion for Crohn's colitis suggests the faecal stream may play a part in the inflammatory mechanism. The effect of faecal diversion (n = 22) and restoration of intestinal continuity (n = 10) was assessed in patients with Crohn's colitis and compared with controls. Faecal diversion produced significant improvement in the disease activity index mean (SEM) (before 176 (9); after 114 (9), p < 0.01) and serum albumin concentrations (before 33 (3.0); after 38 (3.0), p < 0.05) in all patients with Crohn's colitis. The crypt cell production rate (CCPR) was maintained after faecal diversion for Crohn's colitis but fell in the control group (before = 3.6 (0.8)), at two (1.4 (0.4), p < 0.02), and six weeks (1.6 (0.4), p < 0.05). Mucosal glucosamine synthetase activity, reflecting glycoprotein synthesis, was significantly lower in patients with Crohn's colitis (analysis of variance p < 0.05) after diversion but was maintained in the control group. Restoration of intestinal continuity failed to produce reciprocal changes. The sustained cellular proliferation and fall in glycoprotein synthesis in Crohn's colitis after faecal diversion may represent the end of an exaggerated protective response and regenerative hyperplasia after exclusion of the faecal stream. This study suggests the faecal stream may participate in the inflammatory process in Crohn's colitis. The underlying mechanism is unknown.
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PMID:Faecal diversion for Crohn's colitis: a model to study the role of the faecal stream in the inflammatory process. 830 75

The reliability and clinical applications of computerised image analysis measurement of bowel uptake of Tc-99m HMPAO labelled leucocytes has been examined as a measure of disease activity in Crohn's disease. In 54 studies carried out on 33 patients with established Crohn's disease, the mean 'scan score', a quantitative assessment of image intensity, was 82.1 SEM (13.6), in patients with clinically active disease compared to 24.7 (7.0) in those with quiescent disease, p < or = 0.0005. A significant correlation was found between the scan score and Crohn's Disease Activity Index (rs = 0.52, p < 0.0001), and Harvey and Bradshaw Simple Index (rs = 0.4, p < 0.004). A low scan score correctly identified seven patients whose raised Crohn's Disease Activity Index incorrectly indicated active disease because symptoms used in calculation of the index were not caused by active inflammation. Of the laboratory measurements, the scan score correlated with the haemoglobin (rs = 0.66, p < 0.0001), albumin level (rs = -0.6, p < 0.0001), C-reactive protein (rs = 0.7, p < 0.0001), alpha-acid glycoprotein (rs = 0.57, p < 0.001), and platelet count (rs = 0.47, p < or = 0.006), but not with the erythrocyte sedimentation rate (rs = 0.2, p < or = 0.25). The scan score was raised in all patients who had clinically active disease but normal laboratory tests. The results of this study indicate that the scan score provides an objective indicator of disease activity in Crohn's disease which may be superior to clinical indices, and also to laboratory tests which although objective are often normal in the presence of active disease.
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PMID:Quantification of disease activity in Crohn's disease by computer analysis of Tc-99m hexamethyl propylene amine oxime (HMPAO) labelled leucocyte images. 843 55

We examined the plasma protein binding of an acidic drug (warfarin bound to albumin) and a basic drug [lidocaine (lignocaine) bound to alpha 1-acid glycoprotein] in 15 patients with insulin-dependent diabetes mellitus (IDDM) and 15 matched controls. We also examined protein binding of warfarin and lidocaine in 30 patients with non-insulin-dependent diabetes (NIDDM) and 25 controls. Compared with control, the binding of both warfarin (98.81 +/- 0.02 vs 98.57 +/- 0.03%, mean +/- SEM) and of lidocaine (69 +/- 2 vs 58 +/- 2%) was significantly reduced in IDDM. This group had lower concentrations of both albumin and alpha 1-acid glycoprotein (AAG), achieving statistical significance vs control for albumin only. In the patients with NIDDM, who had a similar level of glycosylated haemoglobin, while there was no significant difference in the binding of lidocaine there was a significant increase in warfarin binding compared with the control population (99.01 +/- 0.03 vs 98.82 +/- 0.04%). This study suggests that binding of both acidic and basic drugs is altered in both IDDM and NIDDM.
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PMID:Plasma protein binding of lidocaine and warfarin in insulin-dependent and non-insulin-dependent diabetes mellitus. 845 25


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