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At least 1,063 records · Page 59Linked to original sources
PubMed2003

Effect of a standardized grape seed extract on low-density lipoprotein susceptibility to oxidation in heavy smokers.

The aim of our study was to evaluate the effect of a standardized formulation of a polyphenolic extract of grapes (Leucoselect-Phytosome [LP]) on low-density lipoprotein (LDL) susceptibility to oxidation in a group of heavy smokers. A randomized, double-blind, crossover study was undertaken in 24 healthy male heavy smokers, aged > or = 50 years. Enrolled subjects were given 2 capsules twice daily for 4 weeks (phase 1). Each capsule contained 75 mg of a grape procyanidin extracts and soy-phosphatidlcholine or placebo consisiting of 75 mg lactose and soy-phosphatidlcholine. A wash out period of 3 weeks was then followed by 4 weeks of the opposite treatment (phase 2). Blood samples were taken at baseline and at the end of each phase and assayed for plasma lipids and LDL susceptibility to oxidation. Compliance was good, and no adverse effects were recorded. Subjects did not show significant modification of total cholesterol (TC), triglycerides (TG), high-density lipoprotein-cholesterol (HDL-C) and LDL-C during LP treatment. Among oxidative indices, thiobarbituric acid reactive substances (TBARS) concentration was significantly reduced in subjects taking LP (-14.7% +/- 21.1% v +5.0% +/- 18.1%, P <.01), and the lag phase prolonged (+15.4% +/- 24.4% v -0.1% +/- 16.0%, P <.05) compared with placebo and basal values. The antioxidant potential of grape seed extract polyphenols may prove effective in a model of oxidative stress (smoking); however more investigational data are needed before use in wider clinical settings.

Antioxidants↗
PubMed2003

The role of the amino-terminal domain of tachykinins in neurokinin-1 receptor signaling and desensitization.

Neurokinin A (NKA) has previously been shown to be a full agonist of the neurokinin-1 receptor (NK-1R) but is only able to cause partial homologous desensitization of the receptor compared to substance P (SP). NKA and SP share the same amino acid sequence at their C-terminal active site domains but differ in structure at their N-terminal domains. These observations have led to the proposal that the N-terminal domains of tachykinin peptides affect the desensitization but not the agonist activities of the peptides. Some of the preprotachykinin proteins contain SP and the NKA-like tachykinins neuropeptide K (NPK) and neuropeptide gamma (NPgamma), which contain NKA at their C-terminals and are N-terminally extended. In this study, the abilities of NKA, NPK, and NPgamma to stimulate NK-1R second messenger (IP(3)) signaling and rapid homologous desensitization of the NK-1R were examined. In addition, a similar analysis was performed using several nonmammalian tachykinin peptides in order to obtain additional insight into the role of the tachykinin N-terminal domain in these NK-1R functions. NPK and NPgamma were found, like NKA, to be full agonists of rat NK-1R IP(3) signaling but, unlike NKA, were also able to cause full rapid homologous desensitization of the receptor. The extended N-terminal domains of NPK and NPgamma thus increase the desensitization activities of these NKA-like peptides. Of the nonmammalian tachykinins tested, all were full agonists but kassinin and eledoisin had only partial homologous desensitization activity, suggesting that the N-terminal structures of these peptides also differentially affect agonist versus desensitization activities of the NK-1R.

Amino Acid Sequence↗
PubMed2002

Characterization of B-1b cells as antigen presenting cells in the immune response to gp43 from Paracoccidioides brasiliensis in vitro.

Antigen presentation is an essential stage in the development of immune response to a specific antigen. This response can lead to the production of antibodies and/or effector T lymphocyte activation. Macrophages, dendritic cells and B-lymphocytes, among others, act as antigen presenting cells. B-lymphocytes capture antigenic particles through a surface receptor of IgM nature. The interaction IgM-antigen leads to endocytosis of the complex and antigen processing which culminates in presentation of the antigen on the cell surface associated with a class II MHC molecule. At least three B cell subsets, B-1a (Ly-1B), B-1b and B-2, are present in the mouse periphery. B-1a and B1-b cells represent a small population in the adult spleen and are abundant in the peritonial and pleural cavities. It has been demonstrated in our laboratory that B-1b cells spontaneously proliferated in stationary cultures of adherent peritonial cells. Further, that these cells migrate to a non-specific inflammatory focus. Based on these findings, we investigated whether these cells are antigen presenting cells in vitro using as antigenic stimulus gp43 from Paracoccidioides brasiliensis. Results showed that B1-b cells express constitutively high levels of class II MHC and costimulatory molecules inducing an efficient proliferation of gp43 sensitized T lymphocytes.

Animals↗
PubMed2003

Cost of strategies after myocardial infarction (COSTAMI): a multicentre, international, randomized trial for cost-effective discharge after uncomplicated myocardial infarction.

AIMS: Risk stratification after uncomplicated acute myocardial infarction is mostly applied by either symptom-limited post discharge exercise electrocardiography or pre-discharge submaximal exercise test. Aim of the present study was to determine if early pharmacological stress echocardiography and discharge within 24 hours of the test in cases without induced myocardial ischemia leads to lower costs and similar clinical outcome during 1 year follow up when compared to clinical evaluation and exercise electrocardiography after discharge. METHODS AND RESULTS: Four-hundred fifty-eight patients from 10 participating centers with a recent uncomplicated myocardial infarction were randomized to pharmacological stress echocardiography on day 3-5 followed by early discharge in the case of negative test result (early discharge strategy) (n=233) or clinical evaluation with hospital discharge on day 7-9 and symptom-limited post-discharge exercise electrocardiography at 2-4 weeks after myocardial infarction (usual care strategy) (n=225). At 1 year follow up there were 63 events (4 deaths, 9 non fatal reinfarctions, 50 chest pains requiring hospitalization) in patients randomized to early discharge, and 69 events (6 deaths, 13 reinfarctions, 50 chest pains requiring hospitalization) in usual care (p=ns). Total median individual costs calculated on the basis of hospitalizations, investigations and interventions during 1 year follow up were 3561 for early discharge strategy vs 3850 for usual care strategy (p<0.05). CONCLUSIONS: Early pharmacological stress echocardiography followed by early discharge in case of negative test result gives similar clinical outcome and lower costs after uncomplicated myocardial infarction than clinical evaluation and delayed post-discharge symptom-limited exercise electrocardiography.

Cardiotonic Agents↗
PubMed2001

The capsaicin VR1 receptor mediates substance P release in toxin A-induced enteritis in rats.

The mechanism by which Clostridium difficile toxin A causes substance P (SP) release and subsequent inflammation in the rat ileum is unknown. Pretreatment with the vanilloid receptor subtype 1 (VR1) antagonist, capsazepine, before toxin A administration significantly inhibited toxin A-induced SP release and intestinal inflammation. Intraluminal administration of the VR1 agonist capsaicin caused intestinal inflammation similar to the effects of toxin A. Pretreatment with capsazepine before capsaicin administration also significantly inhibited capsaicin-induced intestinal inflammation. These results suggest that intraluminal toxin A causes SP release from primary sensory neurons via stimulation of VR1 receptors resulting in intestinal inflammation.

Acute-Phase Reaction↗
PubMed1999

Monitor peptide binding sites are expressed in the rat liver and small intestine.

125I-monitor peptide binding was performed using frozen sections of the rat liver and gut and visualized using autoradiography. Saturable binding was observed in unidentified single cells in the liver and in the mucosa of the small intestine. Epidermal growth factor (EGF) and GTPgammaS did not inhibit 125I-monitor peptide binding indicating that the binding sites are not EGF receptors or G protein-coupled receptors. The liver binding site exhibited an affinity 3.7-4.4-fold higher than those in the small intestine. It has been established that intraluminal monitor peptide releases cholecystokinin from the small intestine. The present results indicate that monitor peptide may also have liver associated functions.

Animals↗
PubMed2000

Extrinsic surgical denervation inhibits Clostridium difficile toxin A-induced enteritis in rats.

Clostridium difficile enteritis is caused by toxin A (TA) which stimulates substance P release and subsequent receptor activation. This receptor stimulation results in secretion, inflammation, and structural damage. However, it is unclear as to which subset of neurons is required to initiate substance P release following toxin stimulation. Five centimeter ileal segments were surgically denervated. After 10 days, three ileal loops were constructed in each rat: the denervated loop was injected intraluminally with 5 microg of TA and two intact loops were injected with TA or vehicle, respectively. Ileal secretion, myeloperoxidase activity, and histology were then assessed. Denervated ileal loops injected with TA had a 75% reduction in ileal secretion (P < 0.001), 92% reduction in myeloperoxidase activity (P < 0.01) and 96% reduction in histologic damage (P < 0.001) compared to innervated loops. There were no significant differences between the denervated loops injected with TA and those injected with vehicle. Extrinsic surgical denervation results in protection of ileal loops from TA enteritis. Furthermore, these results exclude the participation of intrinsic enteric nerves in TA-induced ileal damage. Finally, this suggests that extrinsic primary sensory neurons mediate the effects of intraluminal TA in the ileum.

Animals↗
PubMed2004

Risk of hospitalization for upper gastrointestinal tract bleeding.

OBJECTIVE: This study evaluates the hospitalization risk for upper gastrointestinal bleeding (UGIB) with reference to the clinical characteristics of patients and drugs taken before admission. METHODS: This study is based on the GIFA (Italian Group for the Pharmacosurveillance in the Elderly) database. Cases with an ICD-9 code of esophagus, stomach or duodenum bleeding, or acute esophago-gastroduodenal disease associated with anemia have been classified as UGIB. Sex, age, year of observation, drugs taken at home, comorbidity, smoking, alcohol, and use of gastroprotectants have been also taken into account. Statistical analysis has been conducted using multivariate logistic regression models. RESULTS: 32,388 patients have been enrolled, 940 of which presented UGIB. Age, comorbidity, use of smoke and alcohol, hospitalization duration, and mortality during hospitalization were significantly higher in UGIB than nonUGIB patients. Increased UGIB risk has been found in patients taking NSAIDs (both when aspirin was included or excluded), acetaminophen, constipating agents, iron, ethacrynic acid, propranolol. Reduced UGIB risk has been found in patients taking nitrates. CONCLUSIONS: UGIB risk appears to correlate with clinical characteristics of the patient: it increases with age, comorbidity, and smoke and alcohol consumption. Among drugs, NSAIDs are associated with the highest UGIB risk, while nitrates with a reduction of risk.

Aged↗
PubMed2004

Endothelial function and postprandial lipemia.

It is widely recognised that post-prandial lipoproteins play a role in the development of atherosclerosis, but the mechanisms underlying this role are unclear. An attractive working hypothesis is that the pathogenetic link is endothelial dysfunction. The available data seem to corroborate this theory and recognise triggering by oxidative stress, but some of the evidence is still contradictory.

Animals↗
PubMedDate not supplied

Anatomic consideration for standard and modified techniques of cervical lateral mass screw placement.

BACKGROUND CONTEXT: Posterior screw placement techniques have been previously described. Each technique differs with respect to starting point, lateral angulation and sagittal orientation. PURPOSE: To examine the potential for injury to critical anatomic structures, such as nerve roots and vertebral arteries, during posterior cervical screw placement and to determine safe screw placement. STUDY DESIGN/SETTING: An anatomic study was conducted to determine the optimal screw angulation for posterior cervical lateral mass screws. SPECIMEN SAMPLE: Ten fresh-frozen human cadaveric cervical spine specimens were used, consisting of four females and six males, ranging in age from 32 to 68 years. OUTCOME MEASURES: Angular measurements and distance from nerve root and vertebral arteries were measured with a single caliper and recorded. One millimeter of proximity to a vital structure was considered a violation of that structure. METHODS: Ten fresh-frozen human cadaveric cervical spine specimens were instrumented from C2 to C7 by a single surgeon. Kirschner wires (2.0 mm) were used to reproduce the Roy-Camille, Anderson and Magerl screw trajectories. The wire was drilled through each lateral mass, simulating overdrill error. Each technique was instrumented according to the original description and with additional modifications. The modification consisted of varying the angle of screw placement in the axial plane of the original description from 0 to 30 degrees. Distances to the closest neurovascular structures were averaged for all assays. RESULTS: The Magerl technique is safe at the standard position and modified positions of 20 degrees and 30 degrees from C3-C6. The Roy-Camille technique frequently violates neurovascular structures below C3, especially the nerve root with more lateral screw angulation. The standard technique is noted to have good bone purchase only at C2 and C3. The Anderson technique is safe at 20 degrees and 30 degrees modified positions from C3-C7. Posterior screw placement at the C7 vertebral level was safe only with a modified Anderson technique of 20 degrees and 30 degrees of lateral screw angulation. CONCLUSIONS: The present study indicates that there are significant differences of potential neurovascular injury, which is dependent on the technique used for screw entry, the level instrumented and the angle of screw trajectory in the parasagittal plane.

Adult↗
PubMed1976

Complete amino acid sequence of the myoglobin from the Atlantic bottlenosed dolphin, Tursiops truncatus.

The complete amino acid sequence of the major component myoglobin from the Atlantic bottlenosed dolphin, Tursiops truncatus, was determined by specific cleavage of the protein to obtain large peptides that are readily degraded by the automatic sequencer. Three easily separable peptides were obtained by cleaving the protein with cyanogen bromide at the 2 methionine residues and 4 peptides were obtained by cleaving the methyl acetimidated protein with trypsin at the 3 arginine residues. By subjecting 4 of these peptides and the apomyoglobin to automatic Edman degradation, over 80% of the covalent structure of the protein was obtained. The remainder of the primary structure was determined by further digestion of the central cyanogen bromide peptide with trypsin and staphylococcal protease. This myoglobin differs from that of the sperm whale, Physter catodon, at 15 positions, from that of the California gray whale, Eschrichtius gibbosus, at 14 positions, from that of the common porpoise, Phocoena phocoena, at 6 positions, and from the myoglobin of the Black Sea dolphin, Delphinus delphis and the Amazon River dolphin, Inia goeffrensis, at 5 and 7 positions, respecitvely. All substitutions observed in this sequence fit easily into the tertiary structure of sperm whale myoglobin.

Amino Acid Sequence↗
PubMed2004

Coordinate dual-gene transgenesis by lentiviral vectors carrying synthetic bidirectional promoters.

Transferring multiple genes into the same cell allows for the combination of genetic correction, marking, selection and conditional elimination of transduced cells or the reconstitution of multisubunit components and synergistic pathways. However, this cannot be reliably accomplished by current gene transfer technologies. Based on the finding that some cellular promoters intrinsically promote divergent transcription, we have developed synthetic bidirectional promoters that mediate coordinate transcription of two mRNAs in a ubiquitous or a tissue-specific manner. Lentiviral vectors incorporating the new promoters enabled efficient dual gene transfer in several tissues in vivo after direct delivery or transgenesis, and in a human gene therapy model. Because divergent gene pairs, likely transcribed from shared promoters, are common in the genome, the synthetic promoters that we developed may mimic a well-represented feature of transcription. Vectors incorporating these promoters should increase the power of gene function studies and expand the reach and safety of gene therapy.

Antigens, CD34↗
PubMed1997

Mutational analysis of the interacting cell death regulators CED-9 and CED-4.

The genes ced-3, ced-4 and ced-9 are central components in the cell death pathway of the nematode C. elegans. Ced-9, which functions to inhibit cell death, is homologous to the Bcl-2 family of mammalian anti-apoptotic genes. The ced-3 gene encodes a protein homologous to the caspases, a family of cysteine proteases involved in the execution of programmed cell death. It has recently been demonstrated that CED-4, an inducer of apoptosis for which no mammalian equivalent has been reported, can interact with CED-9 and Bcl-x(L). Here we confirm that CED-9 and CED-4 interact and using a series of deletion mutants, demonstrate that only short N-terminal deletions are tolerated in each molecule without loss-of-interaction. Two loss-of-function point mutations in different regions of CED-4 also lead to a significant loss of interaction suggesting further that the relevant interaction domains are not short linear sequences, but rather, are formed by more complex structural determinants in each molecule. Furthermore, we demonstrate that CED-4 not only interacts with Bcl-x(L) but also with its homologue, Bcl-2, and that the unstructured loop region present in Bcl-x(L) and Bcl-2 can regulate the CED-4 interaction. Lastly, we show that a BH3 peptide that can inhibit Bcl-2 family interactions also inhibits the interaction between Bcl-x(L) and CED-4.

Journal Article↗
PubMed1999

Loss of the exon encoding the juxtamembrane domain is essential for the oncogenic activation of TPR-MET.

TPR-MET, a transforming counterpart of the c-MET proto-oncogene detected in experimental and human cancer, results from fusion of the MET kinase domain with a dimerization motif encoded by TPR. In this rearrangement the exons encoding the Met extracellular, transmembrane and juxtamembrane domains are lost. The juxtamembrane domain has been suggested to be a regulatory region endowed with negative feedback control. To understand whether its absence is critical for the generation of the Tpr-Met transforming potential, we produced a chimeric molecule (Tpr-juxtaMet) with a conserved juxtamembrane domain. The presence of the domain (aa 962-1009) strongly inhibited Tpr-Met dependent cell transformation. Cell proliferation, anchorage-independent growth, motility and invasion were also impaired. The enzymatic behavior of Tpr-Met and Tpr-juxtaMet was the same, while Tpr-juxtaMet ability to associate cytoplasmic signal transducers and to elicit downstream signaling was severely impaired. These data indicate that the presence of the juxtamembrane domain counterbalances the Tpr-Met transforming potential and therefore the loss of the exon encoding the juxtamembrane domain is crucial in the generation of the active TPR-MET oncogene.

Adaptor Proteins, Signal Transducing↗
PubMed1994

Agonist-induced internalization of the substance P (NK1) receptor expressed in epithelial cells.

Internalization of the NK1 receptor (NK1R) and substance P was observed in cells transfected with cDNA encoding the rat NK1R by using anti-receptor antibodies and cyanine 3-labelled substance P (cy3-substance P). After incubation at 4 degrees C, NK1R immunoreactivity and cy3-substance P were confined to the plasma membrane. Within 3 min of incubation at 37 degrees C, NK1R immunoreactivity and cy3-substance P were internalized into small intracellular vesicles located beneath the plasma membrane. Fluorescein isothiocyanate-labelled transferrin and cy3-substance P were internalized into the same vesicles, identifying them as early endosomes. After 60 min at 37 degrees C, NK1R immunoreactivity was detected in larger, perinuclear vesicles. Internalization of 125I-labelled substance P was studied by using an acid wash to dissociate cell-surface label from that which has been internalized. Binding reached equilibrium after incubation for 60 min at 4 degrees C with no detectable internalization. After 10 min incubation at 37 degrees C, 83.5 +/- 1.0% of specifically bound counts were internalized. Hyperosmolar sucrose and phenylarsine oxide, which are inhibitors of endocytosis, prevented internalization of 125I-labelled substance P and accumulation of NK1R immunoreactivity into endosomes. Acidotropic agents caused retention of 125I-labelled substance P within the cell and inhibited degradation of the internalized peptide. Continuous incubation of cells with substance P at 37 degrees C reduced 125I-substance P binding at the cell surface. Therefore, substance P and its receptor are internalized into early endosomes within minutes of binding, and internalized substance P is degraded. Internalization depletes NK1Rs from the cell surface and may down-regulate the response of a cell to substance P.

Amino Acid Sequence↗
PubMed1997

Characterization of the hydrolytic activity of a polyclonal catalytic antibody preparation by pH-dependence and chemical modification studies: evidence for the involvement of Tyr and Arg side chains as hydrogen-bond donors.

The hydrolyses of 4-nitrophenyl 4'-(3-aza-2-oxoheptyl)phenyl carbonate and of a new, more soluble, substrate, 4-nitrophenyl 4'-(3-aza-7-hydroxy-2-oxoheptyl)phenyl carbonate, each catalysed by a polyclonal antibody preparation elicited in a sheep by use of an analogous phosphate immunogen, were shown to adhere closely to the Michaelis-Menten equation, in accordance with the growing awareness that polyclonal catalytic antibodies may be much less heterogeneous than had been supposed. The particular value of studies on polyclonal catalytic antibodies is discussed briefly. Both the kcat and kcat/K(m) values were shown to increase with increase in pH across a pKa of approx. 9. Group-selective chemical modification studies established that the side chains of tyrosine and arginine residues are essential for catalytic activity, and provided no evidence for the involvement of side chains of lysine, histidine or cysteine residues. The combination of evidence from the kinetic and chemical modification studies and from studies on the pH-dependence of binding suggests that catalysis involves assistance to the reaction of the substrate with hydroxide ions by hydrogen-bond donation at the reaction centre by tyrosine and arginine side chains. This combination of hydrogen-bond donors appears to be a feature common to a number of other hydrolytic catalytic antibodies. High-pKa acidic side chains may be essential for the effectiveness of catalytic antibodies that utilize hydroxide ions.

Animals↗
PubMed1998

Protein tyrosine phosphatase PTP-S binds to the juxtamembrane region of the hepatocyte growth factor receptor Met.

We reported previously that a protein tyrosine phosphatase (PTP) activity is associated with the immunoprecipitated hepatocyte growth factor (HGF) receptor, also known as Met. The activity increased reversibly when Met was stimulated by HGF and decreased when Met was inactivated by PMA. To identify the PTP-binding region, we used deletion mutants of the receptor beta-subunit. The PTP activity did not associate with Tpr-Met, a construct containing residues 1010-1390 of Met fused to Tpr. In contrast, PTP activity was present when the expressed protein contained the full juxtamembrane region (residues 956-1390 of Met) or part of this region (residues 957-1390 or 995-1390), indicating that the PTP-binding region is between residues 995 and 1009. This region includes Tyr1003, a site involved in Met downstream signalling. Incubation of Met immunoprecipitated from GTL-16 cells with an 8-mer phosphopeptide derived from residues 1003-1010 induced a marked decrease in the associated PTP activity, suggesting that the peptide reproduced the PTP-binding region. Mutation of Glu, Asp or Arg at positions -4, -1 or +1 respectively relative to Tyr1003 in a 9-mer peptide (residues 999-1007) abolished the ability of the peptide to decrease the PTP activity associated with Met. Phosphorylation of Tyr1003 was not required for PTP binding, since: (1) both phospho- and dephospho-peptides on a solid bead bound PTP activity from a GTL-16 cell extract, and (2) PTP activity was associated with a Met deletion mutant lacking residues 1-955 in which Tyr1003 had been changed into Phe. In order to partially purify the PTP from the GTL-16 cell extract, an affinity column was prepared using the Met-derived peptide comprising residues 998-1007. Less than 0.1% of the total cellular PTP was retained by the column, and was eluted with low salt concentrations. Using antibodies, this PTP was identified as PTP-S, a soluble PTP present in epithelial cells and fibroblasts.

3T3 Cells↗