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C Coker

Publications and source records attributed to C Coker.

At least 19 recordsLinked to original sources
PubMed2005

Antithrombin III pretreatment reduces neutrophil recruitment into the lung in a rat model of abdominal sepsis.

BACKGROUND: Antithrombin III (AT III) is a serine protease inhibitor and the mechanism of its anti-inflammatory action is still not understood. In the present study, we aimed to investigate the anti-inflammatory action of AT III on lung injury in a rat model of sepsis. METHODS: Three groups of animals were used in this controlled study: the sham-operated group (sham, n = 3) which only underwent a laparotomy; the control group (control, n = 7) which underwent cecal ligation and perforation (CLP); and the AT III-treated group (AT III, n = 6) which underwent CLP and received intravenous (i.v.) 250 U/kg AT III 30 min before induction of sepsis. Rats were killed 24 h after induction of sepsis by needle aspiration of the right ventricle after a sternotomy, and the lungs and trachea were removed en bloc under ether anesthesia. RESULTS: Pulmonary accumulation of polymorphonuclear leukocytes (PMN) was assessed by measuring lung tissue myeloperoxidase (MPO) activity. Lipid peroxidation in lung tissue was assessed by tissue thiobarbituric acid reactive substance (TBARS) levels. The plasma prostacyclin level was assessed by the plasma 6-keto prostaglandin F(1alpha)(6-keto-PGF(1alpha)) level, which is a stable derivative of prostacyclin. Histopathological changes in lung tissue were assessed by PMN count in the capillaries and alveolar spaces. The lung tissue TBARS level, MPO activity and PMN count in the control group were significantly higher than in the AT III group (P < 0.05). The change in plasma 6-keto-PGF(1alpha) level in the AT III group was insignificant compared with the control group (P = 0.15). CONCLUSIONS: AT III prevented pulmonary infiltration of PMN and subsequent injury by the endothelial release of prostacyclin in CLP-induced sepsis.

Abdominal Cavity↗
PubMed2002

MSG.

The Microgravity Science Glovebox (MSG) has been designed as a modular multi-user facility for performing a wide variety of materials, combustion, fluids and biotechnology investigations in the microgravity environment. Primarily it provides an enclosed and sealed Work Volume (WV) equipped with lighting, mechanical, electrical, data, gas and vacuum connections, and thermal control. The WV is provided with built-in glove ports for safe handling by the crew and isolates the item under investigation from the operator area and the general ISS environment. An attached Airlock (AL) allows specimens and tools to be inserted or removed during MSG operations with limited environmental exchange between the WV and the ISS cabin. The MSG facility will also accommodate minor repair/servicing of hardware requiring a clean and/or an encapsulated working environment (e.g. the Fluid Science Laboratory's investigation containers).

Equipment Design↗
PubMed2001

Proinflammatory cytokines, prostaglandins and zinc in febrile convulsions.

BACKGROUND: Some changes in the levels of proinflammatory cytokines, prostaglandins and zinc (Zn) in peripheral blood and cerebrospinal fluid (CSF) have been suggested to occur for the pathogenesis of febrile convulsions (FC). METHODS: In order to test this hypothesis, the levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 alpha, IL-1 beta and prostaglandins (PGE(2), PGF(2 alpha), PGD(2)) in the CSF and plasma and the levels of Zn in serum and CSF were investigated in children during the acute and late phases of FC. Results were compared with control subjects with meningismus. RESULTS: During the acute phase of FC, children had significantly elevated plasma levels of IL-1 beta, CSF levels of TNF-alpha, plasma levels of PGE(2), PGF(2 alpha) and PGD(2) and CSF levels of PGD(2) (P<0.05). A positive correlation between the degree of fever and plasma IL-1 beta levels was observed in both patients and controls. Three months after the acute phase of FC, plasma levels of IL-1 beta had returned to levels seen in controls. Children with FC also had significantly decreased serum Zn levels during the acute phase (P<0.05). However, there was no significant difference between the groups with respect to CSF Zn levels (P>0.05). CONCLUSIONS: During the acute phase of FC, patients had significantly increased plasma IL-1 beta and prostaglandin levels and decreased serum Zn levels. These changes may be responsible for FC pathogenesis.

Cytokines↗
PubMed2001

Identification of the domains of UreR, an AraC-like transcriptional regulator of the urease gene cluster in Proteus mirabilis.

Proteus mirabilis urease catalyzes the hydrolysis of urea to CO(2) and NH(3), resulting in urinary stone formation in individuals with complicated urinary tract infections. UreR, a member of the AraC family, activates transcription of the genes encoding urease enzyme subunits and accessory proteins, ureDABCEFG, as well as its own transcription in the presence of urea. Based on sequence homology with AraC, we hypothesized that UreR contains both a dimerization domain and a DNA-binding domain. A translational fusion of the leucine zipper dimerization domain (amino acids 302 to 350) of C/EBP and the C-terminal half of UreR (amino acids 164 to 293) activated transcription from the ureD promoter (p(ureD)) and bound to a 60-bp fragment containing p(ureD), as analyzed by gel shift. These results were consistent with the DNA-binding specificity residing in the C-terminal half of UreR and dimerization being required for activity. To localize the dimerization domain of UreR, a translational fusion of the DNA-binding domain of the LexA repressor (amino acids 1 to 87) and the N-terminal half of UreR (amino acids 1 to 182) was constructed and found to repress transcription from p(sulA)-lacZ (sulA is repressed by LexA) and bind to the sulA operator site, as analyzed by gel shift. Since LexA binds this site only as a dimer, the UreR(1-182)-LexA(1-87) fusion also must dimerize to bind p(sulA). Indeed, purified UreR-Myc-His eluted from a gel filtration column as a dimer. Therefore, we conclude that the dimerization domain of UreR is located within the N-terminal half of UreR. UreR contains three leucines that mimic the leucines that contribute to dimerization of AraC. Mutagenesis of Leu147, Leu148, or L158 alone did not significantly affect UreR function. In contrast, mutagenesis of both Leu147 and Leu148 or all three Leu residues resulted in a 85 or 94% decrease, respectively, in UreR function in the presence of urea (P < 0.001). On the contrary, His102 and His175 mutations of UreR resulted in constitutive induction in the absence of urea. We conclude that a dimerization domain resides in the N-terminal half of the polypeptide, that Leu residues may contribute to this function, and that sequences within the C-terminal half of UreR are responsible for DNA binding to the urease promoter regions. Selected His residues also contribute significantly to UreR function.

AraC Transcription Factor↗
PubMed2000

Pathogenesis of Proteus mirabilis urinary tract infection.

Proteus mirabilis is a causative agent of cystitis and pyelonephritis primarily in individuals with indwelling catheters or structural abnormalities of the urinary tract. The organism produces a variety of unique virulence factors that contribute to its pathogenicity and persistence in the human host.

Amidohydrolases↗
PubMed2000

H-NS is a repressor of the Proteus mirabilis urease transcriptional activator gene ureR.

Expression of Proteus mirabilis urease is governed by UreR, an AraC-like positive transcriptional activator. A poly(A) tract nucleotide sequence, consisting of A(6)TA(2)CA(2)TGGTA(5)GA(6)TGA(5), is located 16 bp upstream of the sigma(70)-like ureR promoter P2. Since poly(A) tracts of DNA serve as binding sites for the gene repressor histone-like nucleoid structuring protein (H-NS), we measured beta-galactosidase activity of wild-type Escherichia coli MC4100 (H-NS(+)) and its isogenic derivative ATM121 (hns::Tn10) (H-NS(-)) harboring a ureR-lacZ operon fusion plasmid (pLC9801). beta-Galactosidase activity in the H-NS(-) host strain was constitutive and sevenfold greater (P < 0.0001) than that in the H-NS(+) host. A recombinant plasmid containing cloned P. mirabilis hns was able to complement and restore repression of the ureR promoter in the H-NS(-) host when provided in trans. Deletion of the poly(A) tract nucleotide sequence from pLC9801 resulted in an increase in beta-galactosidase activity in the H-NS(+) host to nearly the same levels as that observed for wild-type pLC9801 harbored by the H-NS(-) host. Urease activity in strains harboring the recombinant plasmid pMID1010 (encoding the entire urease gene cluster of P. mirabilis) was equivalent in both the H-NS(-) background and the H-NS(+) background in the presence of urea but was eightfold greater (P = 0.0001) in the H-NS(-) background in the absence of urea. We conclude that H-NS represses ureR expression in the absence of urea induction.

Bacterial Proteins↗
PubMed1999

Functional characterization of alpha1-adrenoceptor subtypes in longitudinal and circular muscle of human vas deferens.

The alpha1-adrenoceptor subtype(s) mediating contraction to noradrenaline in longitudinal and circular muscle of human epididymal vas deferens was studied using competitive antagonists. The effects of the alkylating agents, phenoxybenzamine and chloroethylclonidine were also investigated. Noradrenaline evoked concentration-dependent contractions of longitudinal and circular muscle with comparable potencies (pD2; 5.6 and 5.5 respectively). The contractions in longitudinal and circular muscle respectively were inhibited by prazosin (pA2, 8.6 and pKB, 9.2), 5-methylurapidil (pKB, 8.7 and 9.1) and less potently by spiperone (pA2, 7.1) or BMY 7378 (pKB, 6.3 and 6.6). Contractions of the circular but not longitudinal muscle was comparatively insensitive to pretreatment with phenoxybenzamine. In contrast pretreatment with chloroethylclonidine reduced the contractions in both muscle types and also enhanced phenoxybenzamine-sensitivity in longitudinal but not circular muscle. The results suggest that contractions evoked by noradrenaline in both muscle types of human vas deferens is mediated via activation of alpha1-adrenoceptors with pharmacological profile of the alpha1A-subtype. However the involvement of alpha1A-adrenoceptor variants, such as the hypothesised alpha1L-subtype may underlie the differential effects of phenoxybenzamine in longitudinal and circular muscle. Factors contributing to chloroethylclonidine-sensitivity are discussed.

Adrenergic alpha-Agonists↗
PubMed1999

Urinary zinc excretion and zinc status of patients with beta-thalassemia major.

In this study, zinc status and urinary zinc excretion with and without desferrioxamine (DFO) infusion and the relationship between urinary zinc excretion and renal tubular dysfunction in thalassemia major (TM) patients were investigated. Forty TM patients were given four DFO infusions on alternate days over a 1-wk period prior to the transfusion. On each day that DFO was given, a 24-h urine collection initiated. DFO was omitted for 1-wk before the following transfusion and during the period four 24-h urine collections were performed. Twenty healthy children provided 24-h urine collection as controls. Blood samples were taken on each of two consecutive transfusion days of the patients and from the controls. Urinary zinc excretion was measured and plasma and red blood cell (RBC) zinc analysis were performed by inductively coupled plasma-atomic emission spectrophotometry. Urinary N-acetyl-beta-D-glucosaminidase (NAG) activity and creatinine were determined in morning urine specimens. The mean plasma zinc concentration was significantly lower in the patients not given DFO compared to the values of the patients given DFO and the control group. The mean RBC zinc concentration (micromol/g Hb) in the patients (with and without DFO) and the control group were similar. Urinary zinc excretion was significantly higher in the patients receiving DFO compared to the control group, whereas urinary zinc excretion in the patients not given DFO was not different from the controls. Urinary NAG indices (U/g Cr) were significantly higher in the patients compared to controls. Urinary zinc excretion was correlated with the urinary NAG indices.

Adolescent↗
PubMed1999

Infantile spasm: the effect of corticotropin (ACTH) on the free amino acid profile in cerebrospinal fluid.

Increased excitatory amino acid neurotransmission has been implicated in the pathogenesis of infantile spasm. In this study we studied the profile of free amino acids in cerebrospinal fluid (CSF) from 16 patients with infantile spasm before corticotropin (ACTH) treatment. After 10 weeks ACTH therapy the profile of amino acids in CSF was studied once more in eight of the patients. Eleven patients were in the symptomatic group, and five in the cryptogenic group. Increased aspartate levels were measured in CSF following ACTH therapy (P<0.05). It was concluded that aspartate might have an important role in hypothalamic-hypophyseal axis in patients with infantile spasm.

Adrenocorticotropic Hormone↗
PubMed1999

Sequential use of deferiprone and desferrioxamine in primary school children with thalassaemia major in Turkey.

The effectiveness of the sequential use of deferiprone and desferrioxamine (DFO) in children with thalassaemia major was examined. Seven thalassaemic children in whom urinary iron induced by deferiprone was sufficient to maintain a negative iron balance were enrolled in the long-term trial. Deferiprone at a dose of 75 mg/kd/day in 3 divided doses was given for 4 school days a week. The group was given DFO at a dose of 40-50 mg/kg/day s.c. over 8-12 h with a battery-operated pump for 2 days at the weekend. In addition to the safety variables, they were monitored for serum ferritin levels at 2-month intervals and hepatic iron concentrations in liver tissues were determined at the beginning and the 6th month of therapy. The severity of hepatic damage was graded according to the Knodell hepatic activity index and the fibrosis was quantified. None of the patients suffered adverse effects of the therapy but a transient increase in serum ALT levels was noted. A nonsignificant decline in serum ferritin was observed (p = 0.08), a significant reduction in hepatic iron concentration was also determined (p = 0. 03). The hepatic activity index in liver tissues of the patients at the 6th month of the sequential therapy significantly decreased (p = 0.03) whereas fibrosis scores did not differ significantly (p = 0. 25).

Adolescent↗
PubMed1999

Influence of investigative and operative procedures on serum prostate-specific antigen concentration.

We determined the effect of cystoscopy (flexible and rigid), transrectal ultrasonography (with and without needle biopsy of the prostate) and transurethral resection of the prostate or bladder tumour on the serum prostate-specific antigen (PSA) concentration. Samples were taken from 60 men before and up to 14 days following these procedures. Flexible cystoscopy did not result in a significant increase in serum PSA concentration, with a median increase of 0.1 microgram/L (P > 0.05). Small but statistically significant increases in serum PSA levels 1 day post-procedure were observed following rigid cystoscopy and transrectal ultrasound without biopsy. The median increase in serum PSA concentration following rigid cystoscopy was 0.15 microgram/L (P = 0.04) and following transrectal ultrasound was 0.3 microgram/L (P = 0.01). In both cases the serum PSA level had normalized by 2 days post-procedure. Transurethral resection of bladder tumours resulted in a variable rise in serum PSA, with a median increase of 2.6 micrograms/L after 1 day, which returned to normal over 7-14 days. Ultrasound-guided needle biopsy of the prostate and transurethral resection of the prostate produced significant increases in serum PSA levels, which took up to fourteen days to return to normal. The median increase in serum PSA following needle biopsy was 6.0 micrograms/L and following transurethral resection of the prostate (TURP) was 13 micrograms/L. Samples for PSA measurement may safely be taken within 24-48 h of flexible cystoscopy and transrectal ultrasonography (TRUS) providing prostatic biopsy is not carried out. For other procedures it is necessary to wait for at least 14 days to ensure that false positive PSA results are not obtained.

Aged↗
PubMed1998

Effect of vitamin E on vascular responses of thoracic aorta in rat experimental arthritis.

1. Vascular contractile and relaxant responses were evaluated in isolated aortic rings of adjuvant-induced arthritic rats in comparison with control rats, and the effect of an antioxidant treatment on the development of the arthritis was investigated by vitamin E administration (100 mg/kg/day, i.m., for 26 days). 2. Arthritis was induced by an intradermal injection of Freund's complete adjuvant into rat paw. Vascular responses, arthritic lesions and serum copper levels were evaluated after 26 days from adjuvant inoculation. 3. Serum copper levels were significantly lower in arthritic rats than in the control. 4. The contractile response of aortic rings to phenylephrine (PE), but not to KCl, was increased in preparations from arthritic rats, which could be explained by an enhancement of intracellular calcium contents. 5. Acetylcholine (Ach)-mediated endothelium-dependent and sodium nitroprusside (SNP)-mediated endothelium-independent relaxations were not changed significantly in vascular preparations from arthritic rats. 6. In arthritic rats, vitamin E treatment improved arthritic lesions with an increase in copper levels. Despite this ameliorating effect, vitamin E treatment caused an increase in contractile response to PE and a decrease in the relaxant response to Ach and SNP in arthritic rats. 7. These data show that vitamin E provides ameliorating effects in improving systemic signs of experimental arthritis, but it fails to restore abnormalities in vascular function, indicating that adjuvant-induced alterations in vascular function may include mechanisms other than oxygen-free radical formation.

Analysis of Variance↗
PubMed1998

Aluminum in total parenteral nutrition solutions produces portal inflammation in rats.

BACKGROUND: Aluminum contaminates parenteral nutrition solutions and accumulates in bone and liver of patients receiving total parenteral nutrition therapy. Although previous reports have shown that parenteral administration of aluminum in pharmacologic doses to rats results in the production of elevated total serum bile acid concentrations alone or in combination with decreased bile flow, they have failed to demonstrate any abnormalities in the histologic appearance of liver tissue. The effects of aluminum in total parenteral nutrition and of aluminum chloride on total serum bile acid concentrations, aluminum contents of the liver, and histopathologic changes in the liver were studied in rats. METHODS: The aluminum concentrations in the aluminum chloride solution and total parenteral nutrition formula were equal (300 microg/l). They were given intraperitoneally as follows: control group, 0.9% saline for 14 days; T7 group, total parenteral nutrition for 7 days; A7 group, aluminum chloride for 7 days; A14 group, aluminum chloride for 14 days; T7A7 group, total parenteral nutrition for 7 days and aluminum chloride for the next 7 days; and T7O7 group, total parenteral nutrition for 7 days and 0.9% saline for the next 7 days. Volumes of 0.9% saline, aluminum chloride, and total parenteral nutrition given to rats were equal. During the experiment, rats were maintained on rat chow and water ad libitum. Serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, alkaline phosphatase, and bile acid concentrations and aluminum content of the liver were measured. The liver was evaluated histopathologically by light microscope, and a morphologic portal inflammation index was calculated. RESULTS: Portal inflammation was present in all groups except the control group. The morphologic portal inflammation correlated with hepatic aluminum accumulation in all groups and was the highest in the T7A7 group. Levels of serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, and alkaline phosphatase did not correlate with the histopathologic findings, but serum bile acid concentrations correlated with morphologic portal inflammation and hepatic aluminum accumulation in all groups. Hepatic aluminum accumulation also correlated with the duration of exposure to total parenteral nutrition and aluminum chloride concentration. CONCLUSION: Aluminum in contaminating doses, not in pharmacologic doses, accumulates in the liver and can produce hepatobiliary dysfunction characterized by portal inflammation detectable in histologic examination of liver tissue.

Alanine Transaminase↗
PubMed1997

Ischemic damage to the prostate during cardiac surgery: a clinical model.

BACKGROUND: To determine if altered tissue perfusion during cardiac surgery results in ischemic tissue damage to the prostate, as suggested by a rise in prostatic-specific antigen (PSA). METHODS: Twenty-nine male patients undergoing elective coronary artery bypass grafting were studied. Ten male patients undergoing elective gastrointestinal surgery served as controls. PSA levels were determined preoperatively and six hourly intervals postoperatively for 48 hr. All patients underwent urethral catheterization at induction of anesthesia. RESULTS: All patients (100%) who had undergone cardiac bypass surgery showed rises in serum PSA during 48 hr of postoperative follow-up. At the 6-hr postoperative interval, the mean PSA was significantly different from the mean baseline value (paired two tailed Student's t test, P < 0.001) in 27 of the 29 (93%) patients. In contrast, the PSA values in the 10 gastroenterological controls did not change at 6 hr (P > 0.2) or during the next 48 hr. One patient in the cardiac group showed a very marked elevation in serum PSA of greater than 50 times normal preoperative levels. CONCLUSIONS: Statistically significant rises in PSA levels are seen following coronary bypass surgery. This rise may be caused by ischemic nontrauma related damage to the prostate and suggests a possible pathophysiological mechanism for the clinically episodic symptoms of prostatism seen in elderly men.

Coronary Artery Bypass↗
PubMed1996

Hypozincaemia in febrile convulsion.

UNLABELLED: To understand further the role role of trace elements in pathogenesis of febrile convulsions, serum zinc (Zn), copper (Cu), magnesium (Mg) and CSF An, Cu, Mg and protein levels were measured by spectrometry in patients with febrile convulsion (n = 19), bacterial meningitis (n = 9), viral CNS infection (n = 16) and in the control group (n = 10) which consisted of children with signs of meningeal irritation due to upper respiratory tract infection but normal CSF findings. Samples were obtained within 6 h after admission to hospital. Mean serum and CSF Zn levels in the febrile convulsion group were significantly lower than in the other groups (for serum Zn: 0.66 +/- 0.03 mg/1 vs 0.98 +/- 0.07 mg/1, 1.06 +/- 0.08 mg/1, 1.05 +/- 0.09 mg/1 P < 0.05; for CSF Zn: 22.96 +/- 1.62 micrograms/1 vs 75.47 +/- 6.9 micrograms/1, 50.32 +/- 5.235 micrograms/1, 39.85 +/- 2.81 micrograms/1 P < 0.05). A linear relationship was established between serum Zn and CSF Zn levels (P < 0.001). Mean CSF Zn, Cu and protein levels in the bacterial meningitis group were significantly higher than in the other groups (for CSF Cu 63.94 +/- 6.33 micrograms/1 vs 38.77 +/- 2.70 micrograms/1, 35.84 +/- 3.48 micrograms/1, 33.86 +/- 2.88 micrograms/1 P < 0.05; for CSF protein 0.80 +/- 0.12 g/1 vs 0.22 +/- 0.02 g/1, 0.53 +/- 0.08 g/1, 0.19 +/- 0.01 g/1 P < 0.05). In children with meningitis, the elevation of the mean CSF Zn and Cu levels may result from the breakdown of the blood-brain barrier and subsequent leakage of trace elements and protein from serum to CSF. There was no significant difference between the four groups in terms of mean serum Mg and mean CSF Mg levels. CONCLUSION: Serum and CSF Zn levels are decreased in children with febrile seizures. Zinc deprivation may play a role in the pathogenesis of febrile seizures.

Adolescent↗
PubMed1996

Glucose metabolism and catecholamine responses during physical exercise in non-insulin-dependent diabetes.

Blood glucose, lactate, insulin, C-peptide, norepinephrine and epinephrine concentrations were determined in non-insulin-dependent diabetic patients and in healthy controls before, during and after moderate exercise, to evaluate the effects of physical exercise on glucoregulation. Ten diabetic and ten healthy control females bicycled 14 minutes at 60% of their maximal heart rates. In the diabetic patients, there were no significant changes in blood glucose levels post-exercise, while in controls the 60 minute post-exercise levels were higher than those measured in mid-exercise (p < 0.05). Lactate concentrations increased with exercise in both groups in a similar manner, with highest values at the end of exercise. No significant changes in insulin and C-peptide levels were induced with exercise in either group. Norepinephrine and epinephrine concentrations increased 2.5-3 fold with exercise in both groups (p < 0.05 for all values) but in the diabetics an earlier and prolonged catecholamine response was observed. We propose that catecholamines prevent hypoglycaemia during exercise when changes in insulin and C-peptide do not occur. In diabetic patients with good metabolic control, the glucoregulatory response to exercise is not worse than in anthropometrically similar controls with similar levels of fitness.

Blood Glucose↗