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| 1 | Methane production and small intestinal bacterial overgrowth in children living in a slum显示文摘AIM:To analyze small intestinal bacterial overgrowth in school-aged children and the relationship between hydrogen and methane production in breath tests.METHODS:This transversal study included 85 children residing in a slum and 43 children from a private school,all aged between 6 and 10 years,in Osasco,Brazil.For characterization of the groups,data regarding the socioeconomic status and basic housing sanitary conditions were collected.Anthropometric data was obtained in children from both groups.All children completed the hydrogen(H 2) and methane(CH 4) breath test in order to assess small intestinal bacterial overgrowth(SIBO).SIBO was diagnosed when there was an increase in H 2 ≥ 20 ppm or CH 4 ≥ 10 ppm with regard to the fasting value until 60 min after lactulose ingestion.RESULTS:Children from the slum group had worse living conditions and lower nutritional indices than children from the private school.SIBO was found in 30.9%(26/84) of the children from the slum group and in 2.4%(1/41) from the private school group(P = 0.0007).Greater hydrogen production in the small intestine was observed in children from the slum group when compared to children from the private school(P = 0.007).A higher concentration of hydrogen in the small intestine(P < 0.001) and in the colon(P < 0.001) was observed among the children from the slum group with SIBO when compared to children from the slum group without SIBO.Methane production was observed in 63.1%(53/84) of the children from the slum group and in 19.5%(8/41) of the children from the private school group(P < 0.0001).Methane production was observed in 38/58(65.5%) of the children without SIBO and in 15/26(57.7%) of the children with SIBO from the slum.Colonic production of hydrogen was lower in methaneproducing children(P = 0.017).CONCLUSION:Children who live in inadequate environmental conditions are at risk of bacterial overgrowth and methane production.Hydrogen is a substrate for methane production in the colon. | Carolina Santos Mello Soraia Tahan Lígia Cristina FL Melli Mirian Silva do Carmo Rodrigues Ricardo Martin Pereira de Mello Isabel Cristina Affonso Scaletsky Mauro Batista de Morais | 2012 | World Journal of Gastroenterology2012，18，41： | 3 |
| 2 | Mangiferin,a natural xanthone,accelerates gastrointestinal transit in mice involving cholinergic mechanism显示文摘AIM:To investigate the effects of mangiferin on gastrointestinal transit(GIT) in normal and constipated mice,together with the possible mechanism.METHODS:Intragastrically-administered charcoal mealwas used to measure GIT in overnight starved Swiss mice.In the first experiments,mangiferin(3 mg/kg,10 mg/kg,30 mg/kg,and 100 mg/kg,po) or tegaserod(1 mg/kg,ip) were administered 30 min before the charcoal meal to study their effects on normal transit.In the second series,mangiferin(30 mg/kg) was tested on delayed GIT induced by several different pharmacological agonists(morphine,clonidine,capsaicin) or antagonists(ondansetron,verapamil,and atropine) whereas in the third series,mangiferin(30 mg/kg,100 mg/kg and 300 mg/kg) or tegaserod(1 mg/kg) were tested on 6 h fecal pellets outputted by freely fed mice.The ratio of wet to dry weight was calculated and used as a marker of fecal water content.RESULTS:Mangiferin administered orally significantly(P < 0.05) accelerated GIT at 30 mg/kg and 100 mg/kg(89% and 93%,respectively),similarly to 5-hydroxytryptamine4(5-HT4) agonist tegaserod(81%) when compared to vehicle-treated control(63%).Co-administered mangiferin(30 mg/kg) totally reversed the inhibitory effect of opioid agonist morphine,5-HT3-receptor antagonist ondansetron and transient receptor potential vanilloid-1 receptor agonist capsaicin on GIT,but only to a partial extent with the GIT-delay induced by 2-adrenoceptor agonist clonidine,and calcium antagonist verapamil.However,co-administered atropine completely blocked the stimulant effect of mangiferin on GIT,suggesting the involvement of muscarinic acetylcholine receptor activation.Although mangiferin significantly enhanced the 6 h fecal output at higher doses(245.5 ± 10.43 mg vs 161.9 ± 10.82 mg and 227.1 ± 20.11 mg vs 161.9 ± 10.82 mg of vehicle-treated control,at 30 and 100 mg/kg,P < 0.05,respectively),the effect of tegaserod was more potent(297.4 ± 7.42 mg vs 161.9 ± 10.82 mg of vehicle-treated control,P < 0.05).Unlike tegaserod,which showed an enhanced water content in fecal pellets(59.20% ± 1.09% vs 51.44% ± 1.19% of control,P < 0.05),mangiferin evidenced no such effect,indi-cating that it has only a motor and not a secretomotor effect.CONCLUSION:Our data indicate the prokinetic action of mangiferin.It can stimulate the normal GIT and also overcome the drug-induced transit delay,via a cholinergic physiological mechanism. | Talita Cavalcante Morais Synara Cavalcante Lopes Karine Maria Martins Bezerra Carvalho Bruno Rodrigues Arruda Francisco Thiago Correia de Souza Maria Teresa Salles Trevisan Vietla Satyanarayana Rao Flávia Almeida Santos | 2012 | World Journal of Gastroenterology2012，18，25： | 3 |
| 3 | Calcium potentiates the effect of estradiol on PGF2α production in the bovine endometrium显示文摘Background: Estradiol(E2) is required for luteolysis in cows and its injection stimulates prostaglandin F2α(PGF2α)release. The main goal of our study was to investigate the ability of endometrial explants and cells treated with E2 and the calcium ionophore(CI) A23187 to synthesize PGF2α.Results: Treatment with E2 in vivo resulted in a 48.4% increase of PGF2α production by endometrial explants treated in vitro with A23187. Production of PGF2α was better stimulated with A23187 at concentrations of 10-6and10-5mol/L compared with other concentrations used. The concentration of PGF2α for untreated bovine endometrial cell cultures was 33.1 pg/m L, while for cultures treated with E2, A23187, or a combination of E2 and A23187, the PGF2α concentration was 32.5, 92.4 and 145.6 pg/m L, respectively.Conclusions: Treatment with A23187 tended to stimulate PGF2α production. In the presence of E2, A23187 significantly stimulated PGF2α synthesis. It appears that A23187 potentiates the effects of E2 with respect to synthesis of endometrial PGF2α in cattle. | Claudia Maria Bertan Membrive Pauline Martins da Cunha Flávio Vieira Meirelles Mario Binelli | 2015 | Journal of Animal Science and Biotechnology2015，6，2： | 2 |
| 4 | Murine model to study brain,behavior and immunity during hepatic encephalopathy显示文摘AIM:To propose an alternative model of hepatic encephalopathy(HE) in mice,resembling the human features of the disease.METHODS:Mice received two consecutive intraperitoneal injections of thioacetamide(TAA) at low dosage(300 mg/kg).Liver injury was assessed by serum transaminase levels(ALT) and liver histology(hematoxylin and eosin).Neutrophil infiltration was estimated by confocal liver intravital microscopy.Coagulopathy was evaluated using prolonged prothrombin and partial thromboplastin time.Hemodynamic parameters were measured through tail cuff.Ammonia levels were quantified in serum and brain samples.Electroencephalography(EEG) and psychomotor activity score were performed to show brain function.Brain edema was evaluated using magnetic resonance imaging.RESULTS:Mice submitted to the TAA regime developed massive liver injury,as shown by elevation of serum ALT levels and a high degree of liver necrosis.An intense hepatic neutrophil accumulation occurred in response to TAA-induced liver injury.This led to mice mortality and weight loss,which was associated with severe coagulopathy.Furthermore,TAA-treated mice presented with increased serum and cerebral levels of ammonia,in parallel with alterations in EEG spectrum and discrete brain edema,as shown by magnetic resonance imaging.In agreement with this,neuropsychomotor abnormalities ensued 36 h after TAA,fulfilling several HE features observed in humans.In this context of liver injury and neurological dysfunction,we observed lung inflammation and alterations in blood pressure and heart rate that were indicative of multiple organ dysfunction syndrome.CONCLUSION:In summary,we describe a new murine model of hepatic encephalopathy comprising multiple features of the disease in humans,which may provide new insights for treatment. | Lindisley Ferreira Gomides Pedro Elias Marques Bruno Engler Faleiros Rafaela Vaz Pereira Sylvia Stella Amaral Thais Reis Lage Gustavo Henrique Souza Resende Patricia Alves Maia Guidine Giselle Foureaux Fabíola Mara Ribeiro Fabiana Paiva Martins Marco Antonio Peliky Fontes Anderson José Ferreira Remo Castro Russo Mauro Martins Teixeira Márcio Flávio Moraes Antonio Lúcio Teixeira Gustavo Batista Menezes | 2014 | World Journal of Hepatology2014，6，4： | 2 |
| 5 | Acute kidney injury and electrolyte disorders in COVID-19显示文摘Acute kidney injury(AKI)and electrolyte disorders are important complications of hospitalized coronavirus disease 2019(COVID-19)patients.AKI is thought to occur due to multiple pathophysiological mechanisms,such as multiple organ dysfunction(mainly cardiac and respiratory),direct viral entry in the renal tubules,and cytokine release syndrome.AKI is present in approximately one in every ten hospitalized COVID-19 patients.The incidence rates of AKI increase in patients who are admitted to the intensive care unit(ICU),with levels higher than 50%.Additionally,renal replacement therapy(RRT)is used in 7%of all AKI cases,but in nearly 20%of patients admitted to an ICU.COVID-19 patients with AKI are considered moderate-to-severe cases and are managed with multiple interdisciplinary conducts.AKI acts as a risk factor for mortality in severe acute respiratory syndrome coronavirus 2 infection,especially when RRT is needed.Electrolyte disorders are also common manifestations in hospitalized COVID-19 patients,mainly hyponatremia,hypokalemia,and hypocalcemia.Hyponatremia occurs due to a combination of syndrome of inappropriate secretion of antidiuretic hormone and gastrointestinal fluid loss from vomiting and diarrhea.When it comes to hypokalemia,its mechanism is not fully understood but may derive from hyperaldosteronism due to renin angiotensin aldosterone system overstimulation and gastrointestinal fluid loss as well.The clinical features of hypokalemia in COVID-19 are similar to those in other conditions.Hypocalcemia is the most common electrolyte disorder in COVID-19 and seems to occur because of vitamin D deficiency and parathyroid imbalance.It is also highly associated with longer hospital and ICU stay. | Gabriel Martins Nogueira Noel Lucas Oliveira Rodrigues Silva Ana Flávia Moura Marcelo Augusto Duarte Silveira JoséA Moura-Neto | 2022 | World Journal of Virology2022，11，5： | 2 |
| 6 | Metabolic activation of carcinogens and expression of various cytochromes P450 in human prostate tissue显示文摘 | Williams JA Martin FL Muir GH | 2000 | Carcinogenesis2000，21，9： | 1 |
| 7 | Perfluorooctanoic acid induces gene promoter hypermethylation of glutathione-S- transferase Pi in human liver L02 cells显示文摘 | Tian M Peng S Martin FL | 2012 | Toxicology2012，296，13： | 1 |
| 8 | The major genetic determinants of HIV-1control affect HLA class I peptide presentation显示文摘 | International HIV Controllers Study Pereyra F Jia X McLaren P J Telenti A de Bakker P I Walker B D Ripke S Brumme C J Pulit S L Carrington M Kadie C M Carlson J M Heckerman D Graham R R Plenge R M Deeks S G Gianniny L Crawford G Sullivan J Gonzalez E Davies L Camargo A Moore JM Beattie N Gupta S Crenshaw A Burtt N P Guiducci C Gupta N Gao X Qi Y Yuki Y Piechocka-Trocha A Cutrell E Rosenberg R Moss K L Lemay P O'Leary J Schaefer T Verma P Toth I Block B Baker B Rothchild A Lian J Proudfoot J Alvino D M Vine S Addo M M Allen T M Altfeld M Henn M R Le Gall S Streeck H Haas D W Kuritzkes D R Robbins G K Shafer R W Gulick R M Shikuma C M Haubrich R Riddler S Sax P E Daar E S Ribaudo H J Agan B Agarwal S Ahern R L Allen B L Altidor S Altschuler E L Ambardar S Anastos K Anderson B Anderson V Andrady U Antoniskis D Bangsberg D Barbaro D Barrie W Bartczak J Barton S Basden P Basgoz N Bazner S Bellos N C Benson A M Berger J Bernard N F Bernard A M Birch C Bodner S J Bolan R K Boudreaux E T Bradley M Braun J F Brndjar J E Brown S J Brown K Brown S T Burack J Bush LM Cafaro V Campbell O Campbell J Carlson R H Carmichael J K Casey K K Cavacuiti C Celestin G Chambers S T Chez N Chirch L M Cimoch P J Cohen D Cohn LE Conway B Cooper D A Cornelson B Cox D T Cristofano M V Cuchural G Jr Czartoski J L Dahman J M Daly J S Davis B T Davis K Davod S M DeJesus E Dietz C A Dunham E Dunn M E Ellerin T B Eron J J Fangman J J Farel C E Ferlazzo H Fidler S Fleenor-Ford A Frankel R Freedberg K A French N K Fuchs JD Fuller J D Gaberman J Gallant J E Gandhi R T Garcia E Garmon D Gathe J C Jr Gaultier C R Gebre W Gilman F D Gilson I Goepfert P A Gottlieb M S Goulston C Groger R K Gurley T D Haber S Hardwicke R Hardy W D Harrigan P R Hawkins T N Heath S Hecht F M Henry W K Hladek M Hoffman R P Horton J M Hsu R K Huhn G D Hunt P Hupert M J Illeman M L Jaeger H Jellinger R M John M Johnson J A Johnson K L Johnson H Johnson K Joly J Jordan W C Kauffman C A Khanlou H Killian R K Kim A Y Kim D D Kinder C A Kirchner J T Kogelman L Kojic E M Korthuis P T Kurisu W Kwon D S LaMar M Lampiris H Lanzafame M Lederman M M Lee D M Lee J M Lee M J Lee E T Lemoine J Levy J A Llibre J M Liguori M A Little S J Liu A Y Lopez A J Loutfy M R Loy D Mohammed D Y Man A Mansour M K Marconi V C Markowitz M Marques R Martin J N Martin H L Jr Mayer K H McElrath M J McGhee T A McGovern B H McGowan K McIntyre D Mcleod GX Menezes P Mesa G Metroka CE Meyer-Olson D Miller A O Montgomery K Mounzer K C Nagami E H Nagin I Nahass R G Nelson M O Nielsen C Norene D L O'Connor D H Ojikutu B O Okulicz J Oladehin O O Oldfield E C Olender S A Ostrowski M Owen WF Jr Pae E Parsonnet J Pavlatos A M Perlmutter A M Pierce M N Pincus J M Pisani L Price L J Proia L Prokesch R C Pujet H C Ramgopal M Rathod A Rausch M Ravishankar J Rhame F S Richards C S Richman D D Rodes B Rodriguez M Rose R C 3rd Rosenberg E S Rosenthal D Ross P E Rubin D S Rumbaugh E Saenz L Salvaggio M R Sanchez WC Sanjana V M Santiago S Schmidt W Schuitemaker H Sestak P M Shalit P Shay W Shirvani V N Silebi V I Sizemore J M Jr Skolnik P R Sokol-Anderson M Sosman J M Stabile P Stapleton J T Starrett S Stein F Stellbrink H J Sterman FL Stone V E Stone D R Tambussi G Taplitz R A Tedaldi E M Telenti A Theisen W Torres R Tosiello L Tremblay C Tribble M A Trinh P D Tsao A Ueda P Vaccaro A Valadas E Vanig T J Vecino I Vega V M Veikley W Wade B H Walworth C Wanidworanun C Ward D J Warner D A Weber R D Webster D Weis S Wheeler D A White D J Wilkins E Winston A Wlodaver C G van't Wout A Wright D P Yang O O Yurdin D L Zabukovic B W Zachary K C Zeeman B Zhao M | 2010 | Science2010，330，6010： | 1 |
| 9 | CYP1B1 and hormone-in- duced cmcer显示文摘 | Gajjar K Martin-Hirsch PL Martin FL | 2012 | Cancer Letters2012，324，1： | 1 |
| 10 | B-type natriuretic peptide:beyond a diagnostic显示文摘 | Martin FL Chen HH Cataliotti A | 2008 | Heart Fail Clin2008，4，4： | 1 |
| 11 | A novel atrial natriuretic peptide based ther- apeutic in experimental angiotensin II mediated acute hypertension 显示文摘 | McKie PM Cataliotti A Boerrigter G Chen HH Sangaralingham SJ Martin FL | 2010 | Hypertension2010，56，6： | 1 |
| 12 | Alpha-synuelein and the pathogenesis of Parkinson's disease显示文摘 | Martin FL Willamson SJ Paleologou KE | 2004 | Protein Pept Lett2004，11，3： | 1 |
| 13 | Oral human brain natriuretic peptide activates cyclic guanosine 3′,5′-monophosphate and decreases mean arterial pressure 显示文摘 | Cataliotti A Schirger JA Martin FL | 2005 | Circulation2005，112，6： | 1 |
| 14 | CYP1 B1 and hormone-induced cancer 显示文摘 | Gajjar K Martin-Hirsch PL Martin FL | 2012 | Cancer Lett2012，324，： | 1 |
| 15 | Metabolic activation of carcinogens and expression of various cytochromes P450 in human prostate tissue显示文摘 | Williams JA Martin FL Muir GH | 2000 | Carcinogenesis2000，21，9： | 1 |
| 16 | Low-dose nesiritide in human anterior myocardial infarction suppresses aldoste- tone and preserves ventricular function and structure : a proof of concept study 显示文摘 | Chen HH Martin FL Gibbons R J | 2009 | Heart2009，95，16： | 1 |
| 17 | Diffusion-Weighted Magnetic Resonance Imaging for the Evaluation of Musculoskeletal Tumors显示文摘 | Flávia Martins Costa Elisa Carvalho Ferreira Evandro Miguelote Vianna | 2011 | Magnetic Resonance Imaging Clinics of North America2011，，1： | 1 |
| 18 | B-type natriuretic pep-tide:beyond a diagnostic显示文摘 | Martin FL Chen HH Cataliotti A et a1 | | 0，，4： | 1 |
| 19 | CYP 1B 1 and hormone-induced cancer显示文摘 | Gajjar K Martin-Hirsch PL Martin FL | 2012 | Cancer Lett2012，324，1： | 1 |
| 20 | α,β-amyrin, a natural triterpenoid ameliorates L-arginine-induced acute pancreatitis in rats显示文摘AIM: To study the benef icial effects of triterpene α,β-amyrin and the underlying mechanisms in an experimental pancreatitis model. METHODS: Acute pancreatitis was induced in five groups of rats (n = 8) by L-arginine (2 × 2.5 g/kg, intraperitoneal, 1 h apart) and 1 h later, they received a single oral dose of α,β-amyrin (10, 30 and 100 mg/kg),methylprednisolone (30 mg/kg) and vehicle (3% Tween 80). A saline (0.9% NaCl) treated group served as a normal control. Efficacy was assessed at 24 h by determination of serum levels of amylase, lipase and proinflammatory cytokines [tumor necrosis factor (TNF)-α and interleukin (IL)-6], pancreatic myeloperoxidase (MPO) activity, lipid peroxidation [thiobarbituric acid reactive substances (TBARS)], nitrate/nitrite levels, and the wet weight/body weight ratio. Tissue histology and the immunoreactivity for TNF-α and inducible nitric oxide synthetase (iNOS) were performed. RESULTS: α,β-amyrin and methylprednisolone treatments significantly (P < 0.05) attenuated the L-arginine-induced increases in pancreatic wet weight/body weight ratio, and decreased the serum levels of amylase and lipase, and TNF-α and IL-6, as compared to the vehicle control. Also, pancreatic levels of MPO activity, TBARS, and nitrate/nitrite were signifi cantly lower. Histological f indings and TNF-α and iNOS immunostaining further confirmed the amelioration of pancreatic injury by α,β-amyrin. CONCLUSION: α,β-amyrin has the potential to combat acute pancreatitis by acting as an anti-in? ammatory and antioxidant agent. | Caroline Mouro Melo Karine Maria Martins Bezerra Carvalho Julliana Catharina de Sousa Neves Talita Cavalcante Morais Vietla Satyanarayana Rao Flávia Almeida Santos Gerly Anne de Castro Brito Mariana Helena Chaves | 2010 | World Journal of Gastroenterology2010，16，34： | 1 |
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