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At least 973 records · Page 54Linked to original sources
PubMed1997

CCK-A- and CCK-B-like receptors in the gallbladder and stomach of the alligator (Alligator mississippiensis).

Autoradiographic analysis of radioligand binding was used to localize and characterize cholecystokinin (CCK) receptors expressed in the stomach and gallbladder of the American alligator (Alligator mississippiensis). Alligator gallbladder smooth muscle expresses a CCK-A receptor subtype, and stomach oxyntic mucosa expresses a distinct receptor subtype, termed CCK-B/X because of its similarities to both CCK-B and CCK-X receptors. Both the gallbladder and the stomach binding sites have very low affinities for a panel of nonpeptide receptor agonists and antagonists that are selective for mammalian CCK-A and CCK-B receptors. These results suggest that CCK receptor subtypes diverged from the ancestral CCK-X receptor in an early amniote, prior to the divergence of mammals and reptiles in vertebrate phylogeny, and that CCK-A receptors may have evolved before CCK-B receptors. Our findings support the hypothesis that the evolution of gastrin preceded the evolution of two separate CCK receptor subtypes.

Alligators and Crocodiles↗
PubMed1997

Purification, amino acid sequence, synthesis, and receptor selectivity of alligator gastrin.

Gastrin-like immunoreactive peptides were extracted from the gastric antrum of the American alligator (Alligator mississippiensis) and purified by fractionation using C18 Sep-Paks, Sephadex G-50, pH stable C8 reversed-phase HPLC, and C18 reversed-phase HPLC. Three major immunoreactive peaks were purified and found to correspond to 49, 45, and 34 residue peptides by microsequence analysis. The amino acid sequence of the largest peptide was DWLASLSQDQ KHLISKFLPH IYGELAN QEN YWQEDDALHD HDYPGWMDF-amide. The two smaller peptides corresponded to carboxyl-terminal 45 and 34 residue fragments of the 49 residue peptide. The putative proteolysis of the 49 residue peptide to the two shorter peptides occurs at cleavage sites that are unusual in biosynthetic processing. Mass spectral analysis confirmed the molecular weights that were predicted from the amino acid sequences, thus revealing the absence of any post-translational modifications, such as sulfation. Although the three alligator gastrins resemble mammalian cholecystokinin in having a tyrosine residue in the seventh position from the carboxyl terminus, this tyrosine is apparently nonsulfated as in turtle gastrin. When tested by radioreceptor assay, a synthetic replicate of alligator gastrin-49 exhibited a gastrin-like pattern of biological activity on mammalian CCK-A and CCK-B receptors. Comparison of the amino acid sequences of known peptides revealed that alligator gastrin is most similar to turtle gastrin (76% identical), followed by frog gastrin (51% identical), chicken gastrin (49% identical), and human gastrin (12% identical). These similarities closely reflect vertebrate phylogeny and support the hypothesis that functionally distinct gastrins evolved from CCK in early tetrapods. However, gastrin evolved via different mechanisms in the mammalian lineage (mechanism unknown) versus the amphibian and reptilian/avian lineages, in which two different single nucleotide base changes can account for the separate evolution of amphibian gastrin and reptilian/avian gastrin.

Alligators and Crocodiles↗
PubMed1993

Secretin receptors in a new preparation of plasma membranes from intrahepatic biliary epithelium.

Secretin is thought to cause choleresis by acting on a receptor expressed by bile duct epithelial cells. In this study, the receptor was characterized using a new preparation of intrahepatic bile duct plasma membranes. Hyperplastic biliary trees were obtained from 3-week bile duct-ligated rats. The biliary trees were homogenized, filtered, and subjected to an aqueous two-phase partition technique to yield highly purified plasma membranes (confirmed by a 14-fold enrichment in gamma-glutamyl transpeptidase activity and a 10-fold enrichment in 125I-secretin binding). 125I-secretin bound saturably with high affinity and in a dose-dependent fashion (Kd = 1.3 +/- 0.1 nM, Bmax = 273 +/- 23 fmole/mg) to purified plasma membranes. The binding characteristics of secretin were most consistent with a single site receptor model. Competitive binding studies indicated that the secretin-related peptides glucagon, peptide histidine isoleucine, gastric inhibitory peptide, and growth hormone releasing factor did not inhibit binding. Vasoactive intestinal peptide (1 microM) reduced maximal binding by 19 +/- 1%. The GTP analogs guanylylimidodiphosphate and guanosine 5'-O-[3-thiotriphosphate] (1 microM) inhibited binding by 16 +/- 2 and 13 +/- 1%, respectively. In conclusion, secretin binds to a specific, high-affinity receptor in intrahepatic bile duct epithelium that is coupled to a G-protein-linked signal transduction system.

Animals↗
PubMed2002

Robust and efficient regulation of transgene expression in vivo by improved tetracycline-dependent lentiviral vectors.

We developed a panel of lentiviral vectors that displayed tetracycline-regulated transgene expression over two orders of magnitude in bulk, non-selected populations of transduced cells in vitro and in vivo. The robust expression and homogeneous response indicated that most transduced vector genomes were transcription competent and responsive to regulation, providing the lentiviral vector with a novel competitive advantage for gene transfer. After ex vivo transduction and transplantation of cord blood CD34+ cells into NOD/SCID mice, reporter gene expression could be switched "on" and "off" in human hematopoietic cells in vivo for prolonged times, proving integration of the regulated expression system into long-term repopulating cells. By vector injection into established tumor grafts, we achieved efficient delivery and quantitative regulation of transgene expression in vivo. By these approaches, gene function studies can now be performed in in vivo models of human hematopoiesis and cancer. In the future, regulated lentiviral vectors will improve the safety and efficacy of gene therapy.

Animals↗
PubMed1991

Alterations in receptors for sensory neuropeptides in human inflammatory bowel disease.

Glutamate and several neuropeptides are synthesized and released by subpopulations of primary afferent neurons. These sensory neurons play a role in regulating the inflammatory and immune responses in peripheral tissues. We have explored what changes occur in the location and concentration of receptor binding sites for sensory neurotransmitters in two human inflammatory diseases, ulcerative colitis and Crohn's disease, using quantitative receptor autoradiography. The sensory neurotransmitter receptors included bombesin, calcitonin gene-related peptide-alpha, cholecystokinin, galanin, glutamate, somatostatin, neurokinin A (substance K), substance P, and vasoactive intestinal polypeptide. Of the nine receptor binding sites examined only binding sites for substance P and vasoactive intestinal peptide were significantly altered in the inflamed tissue. These data suggest that substance P is involved in regulating the inflammatory and immune responses in human inflammatory diseases and indicate a specificity of efferent action for each sensory neurotransmitter in peripheral tissues.

Adolescent↗
PubMed1993

Linkage disequilibrium of three polymorphic RFLP markers in the apolipoprotein AI-CIII gene cluster on chromosome 11.

We analysed the allelic and genotypic frequencies of three restriction fragment length polymorphisms in the region of chromosome 11 encoding apolipoprotein AI and CIII genes in a free-living population from South Italy (Calabria). These markers are located at -2500 and -78 bp from the transcription start site of apolipoprotein AI gene (XmnI and MspI, respectively), and in the 3' untranslated region of apolipoprotein CIII gene (SstI). XmnI and SstI label rare alleles (X2 and S2 indicate the presence of the site), whereas the absence of the MspI site (because of a G to A transition) marks the rare allele, M2. Pairwise linkage disequilibrium analysis was determined. Two significant non-random associations were found: a positive disequilibrium between ApoA1/XmnI and ApoA1/MspI markers (P < 0.0001), and a negative disequilibrium between ApoA1/XmnI and ApoC3/SstI markers (P < 0.05). Statistical analysis showed a significant difference in the S2-M2 haplotype frequency between the group of subjects with serum cholesterol levels in the highest decile (P < 0.005) and the group with serum cholesterol levels below the highest decile. The allelic frequency for each locus showed no significant difference between the two groups for all other metabolic parameters, included total cholesterol serum levels. These haplotypes are a more precise measure of genetic variations in the apolipoprotein cluster and their use should allow the mapping of mutations responsible for high serum cholesterol levels.

Adult↗
PubMed1986

Conditioning exercise decreases premenstrual symptoms. A prospective controlled three month trial.

Conditioning exercise decreased premenstrual symptoms during 3 months of a prospective controlled training study. Eight women with normal ovulatory menstrual cycles began a running exercise training programme while completing intensity-graded questionnaires concerning molimina. Six sedentary control women followed the same protocol for 3 months but did not exercise. Oral basal temperatures evaluated by mean temperature analysis were obtained for all cycles. Exercise distance and time, average exercise heart rate, basal and maximal heart rate and body weights were recorded prospectively and evaluated during the control (0) and 3rd month of the study. Mid-luteal phase progesterone and estrogen levels were sampled during the analyzed cycles for the exercise group. Molimina did not change over 3 months time in the control group. The exercise group, after increasing distance run to 51.0 +/- 18.1 km/cycle at 3 months, showed decreases in overall molimina (scores on a 9-point scale) 6.5 +/- 1.8 to 3.5 +/- 0.9, p less than 0.01). Breast symptoms decreased from 8.3 +/- 0.7, p less than 0.005. Fluid symptoms also decreased from 7.3 +/- 1.8 to 5.5 +/- 0.9, p less than 0.025. Menstrual cycle intervals, luteal lengths, body weights and mid-luteal estrogen and progesterone levels were normal and unchanged. Moderate exercise training without major weight, hormonal or menstrual cycle alteration significantly decreased premenstrual symptoms.

Adult↗
PubMed1988

Enhanced neutrophil chemiluminescence in familial Mediterranean fever.

Familial Mediterranean Fever is a disorder of unknown cause characterized by recurrent, self-limited paroxysms of serosal inflammation. Although the neutrophil is the predominant cell involved, no cellular abnormalities are known. Chemiluminescence was studied in neutrophils from 20 asymptomatic patients with this disease and 21 healthy controls to evaluate the oxidative response to formyl-methionyl-leucyl-phenylalanine (f-met-leu-phe). In a subset of patients with familial Mediterranean fever, neutrophils but not monocytes were shown to have significantly enhanced chemiluminescence compared to controls. The enhanced responsiveness of neutrophils to f-met-leu-phe in this disease was found to occur at a postreceptor level. Receptor binding assays demonstrated no differences in binding affinity and receptor number between patients and controls. In addition, a similar enhancement in chemiluminescence was observed with an alternative stimulus (zymosan). In contrast to chemiluminescence, chemotaxis induced by f-met-leu-phe was not enhanced in patients with familial Mediterranean fever. The enhanced neutrophil chemiluminescence may identify a subclinical inflammatory state in attack-free patients with familial Mediterranean fever, as enhanced chemiluminescence is also observed in chronic inflammatory diseases with active inflammation.

Chemotaxis, Leukocyte↗
PubMed1989

Spironolactone with physiological female steroids for presurgical therapy of male-to-female transsexualism.

The clinical and hormonal response to 12-month therapy with the antiandrogen, spironolactone, in conjunction with near-physiologic doses of female gonadal steroids in 50 transsexual males, is presented. An unselected referred series of 61 men with the psychiatric diagnosis of transsexualism was treated; 10 subjects who had received previous gonadal surgery and 1 man with Klinefelter's syndrome were excluded. Twenty-seven conventionally treated (CT; high-dose estrogen), age 34.4 +/- 10.5 years, mean +/- SD, and 23 untreated patients (SPS), age 30.7 +/- 6.2 years, were studied. Following the initial visit, all 50 were begun on spironolactone and low-dose female hormone therapy. Despite high-dose estrogen treatment for more than 2 years, the mean testosterone (T) level for the CT group was not in the female range (169 +/- 193 ng/dl; normal 20-80). Spironolactone, in doses of 200-600 mg/day, lowered T to the female range in both groups after 12 months (CT 87 +/- 111 and SPS 49 +/- 41 ng/dl). This was achieved in the CT group despite decreases in estrogen dose and discontinuation of parenteral therapy. SPS subjects experienced significant decreases in plasma T (642 +/- 236 to 49 +/- 41 ng/dl, p less than 0.001). Systolic blood pressure dropped (128 +/- 14 to 121 +/- 14 mm Hg, p less than 0.05). The clinical response, including decreased male pattern hair, breast development, feminization, and lack of erections was excellent in most subjects.

Adult↗
PubMed1987

Analbuminaemia: a natural model of metabolic compensatory systems.

Important clinical signs are usually not present in analbuminaemia, a congenital condition inherited as an autosomal recessive trait, but several biochemical alterations in proteins, cholesterol, phospholipids and plasma beta lipoproteins have been observed. We studied two sibs, R.U. and R.R., with this disease and observed a striking increase in the variables mentioned above as well as a high LDL fraction with concomitant increase in apo B; increases in HDL3 and apo A-I and A-II levels were also observed. The lipoproteins, however, were not altered in morphology but showed a slight increase in lipid/protein ratio. Post-heparin lipolytic activity was normal in the male patient and reduced in the female while LCAT enzyme activity instead was increased in both. Fatty acids bound to phospholipids and serum cholesterol were mostly monounsaturated. Free fatty acid concentration was normal and they appeared mostly bound to the LDL and HDL3 fractions, which are increased in this disease and appear to replace albumin in one of its main carrier functions.

Apoproteins↗
PubMed1996

Increased substance P receptor expression by blood vessels and lymphoid aggregates in Clostridium difficile-induced pseudomembranous colitis.

Pseudomembranous colitis is most often caused by toxins secreted by Clostridium difficile following bowel flora overgrowth after antibiotic use. The secretory and inflammatory effects observed in C. difficile toxin A-induced enterocolitis in the rat ileum are inhibited by CP-96,345, a substance P (SP) receptor antagonist. To determine if SP plays a role in the pathogenesis of human pseudomembranous colitis, SP receptor distribution was examined in a toxin A-positive specimen of bowel. Quantitative receptor autoradiography was used to examine SP receptors in tissue from a patient who tested positive for C. Difficile toxin. SP receptors were massively increased in small blood vessels and lymphoid aggregates in the pseudomembranous colitis bowel in comparison to control specimens. The SP binding was saturable and exhibited similar affinities for SP and CP-96,345. SP may contribute to the inflammatory response in pseudomembranous colitis via a massive increase in SP receptor antagonists may offer a novel therapeutic intervention for pseudomembranous colitis.

Adult↗
PubMedDate not supplied

Treatment of hypertension and adherence to treatment guidelines in clinical practice: an Italian study.

Despite the results from clinical trials in patients with hypertension and the development of a long list of guidelines for the management of hypertension, many physicians and other healthcare professionals still manage hypertension using approaches that clearly diverge at least partially from the recommendations of these guidelines. Whatever the underlying reasons for physicians' failure to adhere to these guidelines, it is one of the main causes of the high percentage of treated patients with uncontrolled hypertension. This article is a report of the outcomes of a project designed to identify specific discrepancies between hypertension guidelines and clinical practice in Italy then guide the physicians to reach a consensus on hypertension management through discussions with their peers. A total of 1120 internists from all 20 regions in Italy were recruited to participate in workshops conducted between June 2002 and July 2004. They were divided into 57 groups to discuss at least 7 key topics, including the blood pressure level at which to start drug therapy, target-organ damage, isolated systolic hypertension, pulse pressure, clinical trials, generic drugs, and fixed combination drug therapy. The project findings confirmed that the vast majority of internists agree with the guidelines but do not adhere to them completely in clinical practice. Through open discussions that allowed them to identify common viewpoints, the participants may have developed a better awareness of and insight into the guidelines for hypertension management. Hopefully this strategy for group participation will lead to improvements in the management of hypertension throughout Italy.

Guideline Adherence↗
PubMed2006

Levels of vancomycin in the cerebral interstitial fluid after severe head injury.

OBJECTIVE: To evaluate the concentrations of vancomycin in the cerebral interstitial fluid after intravenous administration by multiple boli. DESIGN: Prospective non randomized study SETTING: University hospital general ICU. PATIENTS: Four patients undergone to craniotomy for evacuation of cerebral posttraumatic hemorrhage, who developed pneumonia 4-7 days from the injury METHODS: Two microdialysis catheters were placed in each patient: one in the edematous brain surrounding the focal lesion and one in the subcutaneous tissue of abdomen. Levels of vancomycin were measured in serum and in the microdialysates samples. RESULTS: Plasmatic concentration of 10-15 microg/ml in the trough level was obtained after four administrations of vancomycin. Levels of vancomycin in the subcutaneous tissue was above minimum inhibitory concentrations in all patients after the second administration. Mean serum/brain ratio was 8%. Cerebral interstitial concentration of vancomycin was never above minimum inhibitory concentrations; its maximum value was 1.2 microg/ml. CONCLUSIONS: In edematous brain close to a posttraumatic hemorrhage the levels of vancomycin do not differ from that in healthy subjects. At these plasmatic concentrations cerebral interstitial levels of vancomycin were insufficient while subcutaneous interstitial levels were effective for clinical use.

Adult↗
PubMed2004

Percutaneous placement of peritoneal port-catheter in oncologic patients.

The aim of this paper is to describe the technique of percutaneous ultrasound (US)-guided placement of a peritoneal port-catheter in an interventional radiological setting. Nineteen patients with peritoneal carcinomatosis were selected for intraperitoneal port-catheter placement in order to perform intracavitary receptor-immuno- or radio-immunotherapy with Ytrium-90. All the procedures were performed percutaneously under US and fluoro guidance; the insertion site for catheters was chosen according to abdominal conditions and US findings: all devices were implanted at the lower abdominal quadrants. All patients were followed up with CT and US according to the therapy protocol. The procedure was successfully completed in 15/19 patients, in 4 being contraindicated by peritoneal adhesions. No procedure-related complications and device occlusions during therapy were observed; one catheter displaced 7 months later the placement. In our experience, this procedure was feasible, reliable and easy to perform, allowing the correct administration of the planned intracavitary therapy. Peritoneal adhesions are the main limitation of peritoneal port placement.

Adult↗
PubMed2026

Silicon-mediated alleviation of mercury toxicity requires coordinated regulation of antioxidant defense, metal homeostasis, and nodule function in mung bean.

Mercury (Hg) contamination and accumulation in agricultural soil represent a major hazardous environmental concern, posing serious threats to living organisms, including plants. Silicon (Si) has been widely recognized to mitigate heavy metal (loid) toxicity; however, the underlying mechanism of Si-mediated mitigation of Hg-stress in mung bean remains unclear. In this study, we addressed this research gap by thoroughly examining the potential effects of Si supplementation on Hg-stressed mung bean plants, with particular emphasis on investigating the possible effects of Si on plant biomass, nodulation traits, antioxidant defense, and expression of metal-transporter and detoxification genes. Our findings demonstrated that Hg stress significantly impaired plant growth by inducing oxidative stress and reducing biological nitrogen fixation efficiency whereas Si application significantly alleviated the Hg-induced toxicity. Specifically, Si increased shoot dry biomass by +113% (2.13-fold), root dry biomass by +60% (1.60-fold), nodule number by +152% (2.52-fold), and nodule dry weight by +273% (3.73-fold) under Hg stress compared to Hg treated plants only. Furthermore, Si enhanced antioxidant defense system, restricted the uptake and accumulation of Hg in different plant tissues, and regulated the expression of genes related to metal transport and detoxification, contributing to improved nodulation and nitrogen fixation under Hg stress. Overall, our findings demonstrate that Si application mitigates the Hg-induced toxicity in mung bean plants by enhancing antioxidant defense, improving nitrogen fixation, regulation of genes involved in metal transport and detoxification, and limiting Hg accumulation.

Vigna radiata↗
PubMed2005

Inhibition of Clostridium difficile toxin A-induced colitis in rats by APAZA.

A new compound, APAZA, consisting of a molecule of 5-aminosalicylic acid linked to one molecule of 4-aminophenylacetic acid by an azo bond, was testedfor its ability to inhibit acute colitis in rats caused by Clostridium difficile toxin A. When administered chronically for 5 days in drinking water, APAZA significantly inhibited toxin A-induced myeloperoxidase activity, luminal fluid accumulation, and structural damage to the colon at doses of from 1 to 100 mg/kg x day. For comparison, sulfasalazine was administered in identical doses and was found to significantly inhibit toxin A-induced colitis only at the dose of 100 mg/kg x day. When 4-aminophenylacetic acid alone was administered chronically in drinking water, it also inhibited toxin A-induced colonic inflammation at a dose of 100 mg/kg x day. In order to determine if 4-aminophenylacetic acid has a direct anti-inflammatory effect on the colon rather than a systemic effect, 4-aminophenylacetic acid was administered acutely to surgically prepared isolated colonic segments by intraluminal injection in anesthetized rats 30 min before toxin A was injected. 4-Aminophenylacetic acid strongly and significantly inhibited toxin A-induced colitis in this experiment at doses as low as 10 microg/segment. It is concluded that APAZA is a potent inhibitor of toxin A-induced colonic inflammation in rats and that its constituent, 4-aminophenylacetic acid, is responsible for this increased protection against colitis compared to the 5-aminosalicylic acid component of sulfasalazine.

Analysis of Variance↗