Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mentha piperita or peppermint is currently used for alleviating nausea, flatulence, and vomiting. In the present investigation, we evaluated the chemopreventive, antigenotoxic, and antioxidative effects of an aqueous extract of Mentha piperita leaves. One-day-old Swiss albino mice were treated with a single subcutaneous injection of 0.5 mg benzo[a]pyrene (BP) and then given either water or a Mentha extract (ME; 1 g/kg body weight) by gavage starting at 3 weeks of age (weaning). The mice were killed at 9 weeks of age and tested for lung tumor incidence (chemoprevention); bone marrow micronucleus and chromosome aberration frequency (antigenotoxicity); and levels of liver and lung sulfhydral groups, superoxide dismutase (SOD) and catalase (CAT) activity, and lipid peroxidation (LPO) (antioxidative properties). The ME treatment resulted in a significant reduction in the number of lung adenomas from an incidence of 67.92% in animals given only BP to 26.31%, an inhibition of 61.26%. Tumor multiplicity was 1.22 in the BP-alone group and 1.15 in the BP + ME group. In addition, compared with the animals in the BP-alone group, ME reduced the frequency of chromosomal aberrations and micronuclei in bone marrow cells and decreased the levels of LPO and increased reduced glutathione content, and SOD and CAT activities in liver as well as lung. The results of this study indicate that ME is chemopreventive and antigenotoxic when given subsequent to an initiating dose of BP in newborn Swiss albino mice. The chemopreventive action and antigenotoxic effects observed in the present study may be due to the antioxidative properties of ME.
Environ Mol Mutagen 2006 Apr
PMID:Modulatory effects of Mentha piperita on lung tumor incidence, genotoxicity, and oxidative stress in benzo[a]pyrene-treated Swiss albino mice. 1761 39

Crimean-Congo hemorrhagic fever virus (CCHFV) is an important human pathogen, which is the cause of a tick-borne illness occurring in many areas of Africa, Asia, and Europe. CCHF is characterized by a sudden onset of high fever, chills, and severe headache. Other symptoms can include gastrointestinal disorders, such as nausea, vomiting, and diarrhea. In severe cases, hemorrhagic manifestations can occur and often present as large areas of ecchymosis, rather than frank bleeding. Exposure to ticks, particularly those in the genus Hyalomma, or direct contact with virus-infected animals or people are considered the major risk factors. Studies on CCHFV are impeded by the biocontainment needed for their manipulation. However, the increasing worldwide medical awareness, the enormous interest of the media in hemorrhagic fever diseases, and their potential to be used as a bioweapon, have greatly spurred on research on this important virus, as evidenced by many new developments including the development of a reverse genetics system which should greatly enhance future research with this virus.
Curr Mol Med 2005 Dec
PMID:Crimean-Congo hemorrhagic fever virus. 1637 10

This chapter briefly describes the physiological neural mechanisms by which diverse neurotransmitter receptor systems control several aspects of gastrointestinal functions such as motility, secretion, feeding, and emesis. The current techniques used to study the effects of cannabinoids on these gastrointestinal functions are then sequentially described, starting with isolated gastrointestinal muscle preparations and ultimately evolving to whole animal models. Both delta9-tetrahydrocannibinol (delta9-THC) and well-studied representatives of other classes of exogenous cannabinoid CB1/CB2 receptor agonists inhibit gastrointestinal motility, peristalsis, defecation, and secretions via cannabinoid CB1 receptors since the CB1 (SR141716A)- and not the CB2 (SR144528)-receptor antagonist reverses these effects in a dose-dependent manner. In addition, exogenous cannabinoids inhibit vomiting produced by diverse emetic stimuli in a SR141716A-sensitive manner in different animal models of emesis. Often these cannabinoids produce hyperphagic effects under laboratory conditions in most human and animal models of feeding. Administration of SR141716A by itself can produce effects opposite to cannabinoid agonists (e.g., increases in gastrointestinal motility and secretions, hyperphagia and vomiting), which suggests an important role for endocannabinoids in these gastrointestinal functions. Indeed, the presence of cannabinoid CB1 receptor markers, endocannabinoids such as anandamide and 2-arachidonoylglycerol (2-AG), their metabolic enzymes, and an endocannabinoid reuptake system have been confirmed in the gastrointestinal tract (GIT). The well-studied endocannabinoid anandamide also seems to reduce both gastrointestinal motility and secretion while producing hyperphagia. On the other hand, while the less well-investigated endocannabinoid 2-AG is a potent emetogen, anandamide may possess weak antiemetic activity.
Methods Mol Med 2006
PMID:Methods evaluating cannabinoid and endocannabinoid effects on gastrointestinal functions. 1650 8

Trichothecenes are secondary metabolites produced by several fungi of the Fusarium genus during their growth period. They inhibit protein biosynthesis in eukaryotic cells resulting in numerous toxic effects such as diarrhea, vomiting, and gastro-intestinal inflammation. Considering its occurrence in food and feedstuff, deoxynivalenol (DON) is one of the most important trichothecenes. We report the synthesis of stable isotope labeled 15-d(1)-deoxynivalenol (15-d(1)-DON) from its natural precursor 3-acetyldeoxynivalenol (3-AcDON) as starting material. Furthermore, a method for the analysis of DON and 3-AcDON using HPLC-MS/MS with stable isotope labeled 15-d(1)-DON and 3-d(3)-AcDON as internal standards has been developed. In total, 18 cereal product samples were analyzed with contamination levels ranging from 10-301 microg/kg for DON and 5-14 microg/kg for 3-AcDON. This is the first report of an isotope dilution MS method for the analysis of type B-trichothecenes.
Mol Nutr Food Res 2006 Mar
PMID:Stable isotope dilution analysis of the Fusarium mycotoxins deoxynivalenol and 3-acetyldeoxynivalenol. 1652 Nov 58

The neuronal ceroid lipofuscinoses (NCLs) are inherited lysosomal storage diseases characterized by progressive neuropathy and the accumulation of autofluorescent cytoplasmic granules. Clinical signs of a new canine NCL began in a 9-month-old male Dachshund with vomiting, mental dullness, and loss of previously learned commands and rapidly progressed to include disorientation, ataxia, visual deficits, generalized myoclonic seizures, and death at 12 months of age. Neurons throughout the CNS contained autofluorescent storage granules that stained with periodic acid-Schiff and Luxol fast blue stains. Electron microscopy revealed that the storage granule contents consisted of curvilinear-appearing material characteristic of human late infantile NCL caused by CLN2 mutations. Nucleotide sequence analysis of canine TPP1, the ortholog of human CLN2, revealed a single nucleotide deletion in exon 4 which predicted a frame shift with a premature stop codon. Brain tissue from the affected dog lacked detectable activity of the tripeptidyl-peptidase enzyme encoded by TPP1, whereas the specific activities of 15 other lysosomal enzymes were higher than those in the brains of three control dogs. The affected Dachshund was homozygous for the mutant c.325delC allele, his sire and dam were heterozygotes, and 181 unrelated dogs, including 77 Dachshunds, were all homozygous for the wild-type allele. A DNA assay that detects the mutant allele will help Dachshund breeders avoid producing affected puppies in future generations. Furthermore, this Dachshund NCL may prove to be a useful model for studying the pathogenesis of neurodegeneration in human late infantile NCL and for evaluating novel therapeutic interventions for this disease.
Mol Genet Metab 2006 Nov
PMID:A frame shift mutation in canine TPP1 (the ortholog of human CLN2) in a juvenile Dachshund with neuronal ceroid lipofuscinosis. 1662 47

CG7870 is a replication-selective oncolytic adenovirus genetically engineered to replicate preferentially in prostate tissue. In a previous phase I/II clinical trial of intraprostatic delivery of CG7870 for locally recurrent prostate cancer this virus was well tolerated. In this phase I study CG7870 was administered as a single intravenous infusion in a group-sequential dose escalation design (1 x 10(10) to 6 x 10(12) viral particles (vp)) to 23 patients with hormone-refractory metastatic prostate cancer. Flulike symptoms (fever, fatigue, rigors, nausea, and/or vomiting) were the most common adverse events. Three therapy-related grade 3 adverse events were reported, one of which (fatigue) was serious. At doses greater than 10(12) vp all five patients experienced asymptomatic grade 1 to 2 transaminitis and/or isolated d-dimer elevations starting on day 2 through 8; dose escalation was therefore halted at 6 x 10(12) vp. All tested patients had CG7870 genomes present in the peripheral blood for at least 90 minutes after infusion; patients in the highest dose group had persistence of genomes through 29 days. A "secondary" or "delayed" peak in plasma CG7870 genome copies (defined as a >10-fold increase in CG7870 genomes from nadir concentration) suggestive of active viral replication and shedding into the bloodstream was detected in 16/23 (70%) patients. CG7870 was detected in the saliva of 3 patients, whereas all urine samples tested negative. All patients developed antibodies to CG7870. Dose-related increases in interleukins 6 and 10 (IL-6, IL-10) blood levels were detected. The peak IL-6 concentration after CG7870 treatment was associated with a transient, asymptomatic decrease in blood pressure. No partial or complete prostate-specific antigen (PSA) responses were observed; however, 5 patients had a decrease in serum PSA of 25% to 49% following a single treatment, including 3 of 8 patients at the highest dose levels.
Mol Ther 2006 Jul
PMID:A phase I trial of intravenous CG7870, a replication-selective, prostate-specific antigen-targeted oncolytic adenovirus, for the treatment of hormone-refractory, metastatic prostate cancer. 1669 Mar 59

Isovaleric acidemia (IVA), a rare recessive autosomal disorder, is caused by isovaleryl-CoA dehydrogenase (IVD) deficiency. IVA may present with symptoms during the acute stage of severe metabolic acidosis, ketosis, vomiting, and altered mental status. With the help of newborn screening (NBS) by tandem mass spectrometry (MS/MS), IVA can now be diagnosed presymptomatically. According to statistic data, the incidence of IVA in Taiwan was about 1/365,000. In this study, six IVA patients from five families were investigated and followed-up clinically. As for the timing, two patients were found before MS technique introduced to Taiwan, the others were identified after MS/MS applied to NBS. The blood level of C5-carnitine in our patients was 7.43-18.96 microM (with upper limit in our laboratory <0.51 microM) and all of their urines contained raised amounts of 3-hydroxyisovaleric acid and isovalerylglycine. Molecular analysis of their IVD gene revealed six mutation profiles, among which the 149G-->A (Arg21His) and 1174 C-->T (Arg363Cys) mutations have been reported previously, while the other four mutations, 386A-->G (His100Arg), 347C-->T (Ser87Phe), 1007G-->A (Cys307Tyr) and 1199A-->G (Tyr371Cys), were first reported. Specially, we found 1199A-->G (Tyr371Cys) mutated was a common recurring missense mutation in our population (4 in 10 mutant alleles).
Mol Genet Metab 2007 Feb
PMID:Genetic mutation profile of isovaleric acidemia patients in Taiwan. 1702 10

The accurate and timely diagnosis of pertussis continues to be challenging. The widespread use of pertussis vaccines has dramatically altered the epidemiology and clinical presentation of pertussis disease, such that many cases do not present with the hallmark symptoms, such as inspiratory whoop, post-tussive vomiting and paroxysmal cough. A variety of laboratory tools are available to aid in the diagnosis of pertussis, including culture, direct fluorescent antibody testing, PCR, and paired and single serology techniques. This article reviews the strengths and limitations, including the sensitivity and specificity, of each of these diagnostic tools.
Expert Rev Mol Diagn 2006 Nov
PMID:Diagnosis of pertussis: a historical review and recent developments. 1714 Mar 72

To date, the primary treatments for Alzheimer's disease with proven efficacy have been acetylcholinesterase inhibitors that prevent the hydrolysis of acetylcholine (ACh) in the synaptic cleft, thereby prolonging its activity. Although these agents have some benefit in alleviating cognitive impairment, they have limited clinical utility because of insufficient efficacy and marginal tolerability. Within the last decade, there has been much experimental support for the use of therapeutics that directly target nicotinic ACh receptors (nAChRs) to improve cognitive function and slow neurodegenerative disease progression. These findings have spurred considerable research efforts to develop ligands selective for nAChRs, such as ABT-418 (Arneric et al., 1995), SIB-1553 (Bontempi et al., 2001), TC-2403 (Lippiello et al., 1996), and TC-2559 (Bencherif et al., 2000). There is abundant evidence that nAChR modulators have the potential to alleviate cognitive impairment in demented states. In addition to improving cognitive function, a large body of research implicates a role for nAChRs in neuroprotection, suggesting potential for disease modification. An impact of nAChR agonists on disease progression would provide an advantage over currently available treatments for memory loss. The profile of previous nAChR-targeted clinical candidates has not been adequate to warrant further development owing to poor oral bioavailability, side effects, and/or lack of efficacy. Thus, a challenge in nAChR drug design and development has been the reduction of undesirable effects that result from activity at specific nAChRs in the CNS and PNS, including cardiovascular toxicity, emesis, seizures, and hypothermia.
J Mol Neurosci 2006
PMID:Ispronicline: a novel alpha4beta2 nicotinic acetylcholine receptor-selective agonist with cognition-enhancing and neuroprotective properties. 1719 10

Converging evidence has suggested that anandamide (AEA), an endogenous agonist of cannabinoid (CB) receptors, can directly interact with certain types of ligand-gated ion channels (LGICs). However, little is known about the molecular and cellular mechanisms of AEA-induced direct effects on LGICs. Here, we report that AEA inhibited the function of serotoningated ion channels (5-HT(3A)) expressed in Xenopus laevis oocytes and human embryonic kidney 293 cells in a manner that was dependent on the steady-state receptor density at the cell surface. The magnitude of AEA inhibition was inversely correlated with the expression levels of receptor protein and function. With increasing surface receptor expression, the magnitude of AEA inhibition decreased. Consistent with this idea, pretreatment with actinomycin D, which inhibits transcription, decreased the amplitude of current activated by maximal concentrations of 5-hydroxytryptamine (5-HT) and increased the magnitude of AEA inhibition. AEA did not significantly alter 5-HT(3A) receptor trafficking. However, AEA accelerated 5-HT(3A) receptor desensitization time in a concentration-dependent manner without significantly changing receptor activation and deactivation time. The desensitization time was correlated with the AEA-induced inhibiting effect and mean 5-HT current density. Applications of 5-hydroxyindole and nocodazole, a microtubule disruptor, significantly slowed 5-HT(3A) receptor desensitization and reduced the magnitude of AEA inhibition. These observations suggest that 5-HT(3) receptor density at the steady state regulates receptor desensitization kinetics and the potency of AEA-induced inhibiting effect on the receptors. The inhibition of 5-HT(3) receptors by AEA may contribute to its physiological roles in control of pain and emesis.
Mol Pharmacol 2008 Feb
PMID:Anandamide inhibition of 5-HT3A receptors varies with receptor density and desensitization. 1799 12


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