tbuckley/cabot-search huggingface dataset:
Right ventricular volume characteristics in ventricular septal defect.
Authors: T P Graham, G F Atwood, R J Boucek, D Cordell, R C Boerth
Journal: Circulation (1976)

Right and left ventricular volume characteristics were determined from biplane cineangiocardiography in 37 patients with isolated ventricular septal defects. Patients were divided into three categories as determined by the degree of left-to-right shunt: small shunt-less than 35% of pulmonary blood flow (N=9); moderate shunt-35-49% (N=8), and large shunt-greater than 50% (N=20). Right ventricular (RV) end-diastolic volume was increased above normal in 15 of 20 studies performed in patients with large left-to-right shunts and averaged 159 +/- 10% of normal (P less than 0.001). In contrast, only one of the patients in the small shunt group and only half of the patients in the moderate shunt group showed increases in RV end-diastolic volume. The increase in RV volume was proportional to the corresponding increase in left ventricular end-diastolic volume, with the right ventricle ranging from 48 to 116% of LV end-diastolic volume (average 83%). Right ventricular ejection fraction was normal in all patient groups. Right ventricular outpur was increased commensurate with the increases in the RV end-diastolic volume. These data indicate that substantial augmentation in RV end-diastolic volume does occur in patients with isolated ventricular septal defects and large left-to-right shunts. These data can be explained by the significant diastolic and "isovolumic" shunting from left ventricle to right ventricle which occurs in these patients.
Role of the inflammasome in inflammatory responses and subsequent injury after hepatic ischemia-reperfusion injury
Authors: Yoshiyuki Inoue, Yoshikazu Yasuda, Masafumi Takahashi
Journal: Hepatology (2013)

We read with great interest the article by Kamo et al.1 in which the authors showed that after hepatic ischemia-reperfusion (I/R) injury, inflammasome activation mediated by apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) leads to interleukin-1β (IL-1β) production and subsequently promotes high mobility group box 1(HMGB1) induction, which triggers a Toll-like receptor 4 (TLR4)-driven inflammatory response. Consistent with their findings, we recently showed that ASC-mediated inflammasome activation plays an essential role in the initial inflammatory response after myocardial I/R injury.2 Recently, it has been shown that inflammasome components such as ASC and NLR family pyrin domain containing 3 (NLRP3) can function independently of inflammasomes. Shigeoka et al.3 showed that mice deficient in NLRP3 but not ASC or caspase-1 had reduced renal I/R. Because the inflammasome is defined as a molecular platform that induces caspase-1 activation, they concluded that an NLRP3-dependent and inflammasome-independent pathway contributed to the development of I/R injury in the kidney. Similar to their findings, we observed that hepatic I/R injury was significantly ameliorated in mice deficient for NLRP3 but not ASC. This was inconsistent with the finding of Kamo et al.1 Although the reason for this discrepancy is unclear, the differences between our study and Kamo et al.'s study are the hepatic I/R protocol used and the extent of injury. We subjected C57BL/6 wild-type mice to hepatic I/R with 60 minutes ischemia of the left lateral and median lobes (i.e., interruption of the hepatic artery and portal vein) followed by a 6-hour reperfusion, whereas Kamo et al.1 subjected mice to I/R with 90 minutes ischemia followed by a 6-hour reperfusion. Serum alanine transaminase (ALT) levels increased to ∼5,000 IU/mL in our model and 33,000 IU/mL in the model of Kamo et al. Moreover, regarding the role of IL-1β, Kato et al.4 reported that there was no difference in serum ALT levels between wild-type and IL-1 receptor-deficient mice after hepatic I/R injury and suggested a limited role of IL-1β in causing hepatic I/R injury. We agree with the authors' conclusion that the inflammasome plays a substantial role in hepatic I/R injury; however, the contribution of the inflammasome depends on the extent of injury and status of inflammatory responses; therefore, researchers should be aware of experimental disease conditions to discern the precise role of the inflammasome. Yoshiyuki Inoue, M.D.1,2 Yoshikazu Yasuda, M.D., Ph.D.2 Masafumi Takahashi, M.D., Ph.D.1 1Division of Inflammation Research, Center for Molecular Medicine, Tochigi, Japan 2Department of Surgery, Jichi Medical University, Tochigi, Japan
Bacteria in the respiratory tract and wheeze in children
Authors: J. P. Armann, E. v. Mutius
Journal: BMJ (2010)

Colonisation is more common in symptomatic children, but causation is not established

In the linked cohort study (doi:10.1136/bmj.c4978), Bisgaard and colleagues assess the association between wheezy symptoms in young children and the presence of bacteria in the airway.1 Lower respiratory tract illnesses presenting with cough, shortness of breath, or wheeze are common in preschool years.2 It has been proposed that, for the management of preschool wheeze, a distinction is made between episodic and multiple trigger wheeze.3 Episodic wheeze is defined as wheeze in discrete episodes of up to two to four weeks’ duration, usually triggered by a viral infection, and with the child being well in between. In multi-trigger wheeze, the child has distinct episodes of wheeze but also has intermittent symptoms, such as cough and wheeze at night or in response to exercise, crying, laughter, mist, and cold air, between these episodes. Viral infections are again the most common triggers, but multi-trigger wheeze is often associated with allergic features, and many children with preschool multi-trigger wheeze progress to chronic asthma. Current guidelines recommend the use of bronchodilators for wheezing episodes.3 Children with multi-trigger wheeze may also benefit from inhaled corticosteroids and leukotriene receptor agonists. Antibiotics have …
Reply from Authors re: Maurizio Brausi. Are New Technologies for Detection and Treatment of Non–Muscle-Invasive Bladder Cancer (NMIBC) So Important? A Plea For Adoption by Teaching Programs to Improve Results After Standard White Light Transurethral Resection of NMIBC. Eur Urol 2012;61:914–6
Authors: Angelo Naselli, Paolo Puppo
Journal: European Urology (2012)
Cocaine Abuse and Endocarditis
Authors: Paul Devenyi
Journal: Annals of Internal Medicine (1988)

Letters and Corrections1 July 1988Cocaine Abuse and EndocarditisPaul Devenyi, MD, Michael A. McDonough, MB, BSPaul Devenyi, MDSearch for more papers by this author, Michael A. McDonough, MB, BSSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-109-1-82 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editor: The paper of Chambers and colleagues (1) was interesting and intriguing. The authors provide evidence for a statistically compelling association between intravenous cocaine use and the risk for endocarditis. They speculate that this risk is not related to intravenous drug use by itself, but rather to some inherent properties peculiar to cocaine. The latter point is argued mainly on the basis of intravenous heroin use not having made an independent contribution to the risk for endocarditis.Information about injection technique and sharing or not sharing equipment is conspicuously lacking. Such information is an important independent variable to...Reference1. ChambersMorrisTäuberModin HDMG. Cocaine use and the risk for endocarditis in intravenous drug users. Ann Intern Med. 1987;106:833-6. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Addiction Research Foundation University of Toronto Toronto, Ontario M5S 2S1 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByMechanical Thrombectomy for Large Vessel Occlusions in Cocaine Associated Acute Ischemic Stroke: Small Case Series and Review of the Literature“Cocaine-Related” Deaths: Media Coverage in the War on DrugsCocaine-induced heart diseasesEndocarditis in Intravenous Drug AbusersCardiovascular effects of adolescent drug abuse 1 July 1988Volume 109, Issue 1Page: 82-83KeywordsCocaineDrugsEndocarditisHeroin use Issue Published: 1 July 1988 PDF DownloadLoading ...
Hemoglobin-mediated oxidant damage to the central nervous system requires endogenous ascorbate.
Authors: S M Sadrzadeh, J W Eaton
Journal: Journal of Clinical Investigation (1988)

Hemorrhage within the central nervous system (CNS) may be associated with subsequent development of seizure states or paralysis. Prior investigations indicate that hemoglobin, released from extravasated erythrocytes, may be toxic to the CNS by promoting peroxidation of lipids and inhibition of Na,K-ATPase. These deleterious effects are blocked both in vitro and in vivo by the Fe3+ chelator, desferrioxamine, indicating the involvement of free iron derived from hemoglobin. We now report that the Fe2+ chelator, ferene, also inhibits methemoglobin- and ferric iron-mediated CNS lipid oxidation, reflecting the reduction of Fe3+ by some component of the CNS. This reduction is apparent in the accumulation of the highly chromophoric ferene: Fe2+ chelate after the addition of Fe3+ salts to supernatants of murine brain homogenates. Because large amounts of ascorbic acid occur in mammalian CNS, we suspected that this reducing substance might be responsible. Indeed, the peroxidative effects of hemoglobin and iron on murine brain are blocked by washing of CNS membranes or by preincubation of crude homogenates with ascorbate oxidase. Furthermore, the addition of ascorbate to washed CNS membranes fully restores hemoglobin/iron-driven peroxidation. We conclude that posthemorrhagic CNS dysfunction may stem from damaging redox reactions between hemoglobin iron, ascorbic acid, and oxidizable components of the nervous system.
Birth Control in America: The Career of Margaret Sanger
Authors: Marjorie C. Meehan
Journal: JAMA (1970)

While we discuss the relative merits of various contraceptive methods, and the difficulty in educating "backward" people to limit population growth, we may forget that only a few decades ago it was illegal and generally considered immoral to give any information about birth control. As late as 1932, the AMA executive committee refused a proposal to conduct a study of contraception because it was a controversial subject. The gradual acceptance of birth control in the United States is largely due to the efforts of a few people, especially Margaret Sanger. Mrs. Sanger, a nurse married to an architect, after a few years of sub-urban domesticity, became involved with a group of radicals, including Eugene Debs, John Reed, and Emma Goldman. She crusaded for various causes, but after witnessing a death from attempted abortion, decided to devote all her efforts to the emancipation of women and the dissemination of birth control
Novel insights into human intestinal epithelial cell proliferation in health and disease using confocal microscopy.
Authors: T C Savidge, J A Walker-Smith, A D Phillips
Journal: Gut (1995)

Measurement of intestinal epithelial cell proliferation has provided important information concerning tissue responses in neoplasia, enteropathy, and adaptation. This study reexamined current concepts regarding intestinal proliferation by using a novel confocal microscopical technique to map mitotic figures accurately within the intact three dimensional framework of the crypts of Lieberkühn. The ability of confocal microscopy to simultaneously measure crypt morphology and internal detail, without disrupting spatial cell arrangements, has provided important new data. These question the ability of existing methods to accurately measure and interpret proliferative changes in the gut. This work investigates intestinal proliferation in children with coeliac disease, a well defined hyperproliferative disorder, in comparison with the healthy intestine. These results show that crypt cell division occurs with an equal probability in health and disease. In addition, increased crypt cell production rates are largely caused by a change in crypt size rather than a change in cell cycle time or crypt growth fraction and, as such, alter our understanding of kinetic responses in gastrointestinal disease.
Prenatal Magnesium Sulfate Exposure and the Risk for Cerebral Palsy or Mental Retardation Among Very Low-Birth-Weight Children Aged 3 to 5 Years
Authors: Diana E. Schendel
Journal: JAMA (1996)

To examine the relationship between prenatal magnesium sulfate exposure and the risk for cerebral palsy (CP) or mental retardation (MR) among very low-birth-weight (VLBW; <1500 g) children. Secondarily, to investigate the effect of prenatal magnesium sulfate exposure on VLBW infant mortality.Cohort study with follow-up to 1 year of age; a subset followed up to 3 to 5 years.Twenty-nine Georgia counties, including the 5-county Atlanta metropolitan area.All VLBW births (N=1097) occurring during 2 years (1986-1988); all metropolitan Atlanta VLBW neonates who survived infancy (N=519).Infant mortality as determined from vital statistics records. Development of CP or MR by 3 to 5 years of age among metropolitan Atlanta VLBW survivors as determined from the Metropolitan Atlanta Developmental Disabilities Surveillance Program.For the entire cohort, there was no association between prenatal magnesium sulfate exposure and infant mortality (adjusted rate ratio, 1.02; 95% confidence interval [CI], 0.83-1.25). Among Atlanta-born survivors, those exposed to magnesium sulfate had a lower prevalence of CP or MR than those not exposed (CP: magnesium sulfate, 0.9%, no magnesium sulfate, 7.7%, crude odds ratio [OR], 0.11, 95% CI, 0.02-0.81; MR: magnesium sulfate, 1.8%, no magnesium sulfate, 5.8%, crude OR, 0.30, 95% CI, 0.07-1.29). Multivariable adjustment had no appreciable effect on the ORs for CP or MR, but the CIs included 1.0.A reduced risk for CP, and possibly MR, among VLBW children is associated with prenatal magnesium sulfate exposure. The reduced risk for childhood CP or MR does not appear to be due to selective mortality of magnesium sulfate-exposed infants.
Localised intratesticular abscess complicating epididymo-orchitis: the use of scrotal ultrasonography in diagnosis and management.
Authors: K M Desai, J C Gingell, J M Haworth
Journal: BMJ (1986)

Are families of diabetic children adequately taught?Education is an integral part ofcaring for patients with diabetes.We report a study of the knowledge of the families of children with diabetes attending five clinics in the north of England.
Axons mediate the distribution of arylsulfatase a within the mouse hippocampus upon gene delivery
Authors: Tonia Luca, Maria I. Givogri, Laura Perani, Francesca Galbiati, Antonia Follenzi, Luigi Naldini, Ernesto R. Bongarzone
Journal: Molecular Therapy (2005)

Axonal transport of the lysosomal enzyme arylsulfatase A (ARSA) may be an additional mechanism of enzyme distribution after in vivo brain gene transfer in an animal model of metachromatic leukodystrophy (MLD). Direct molecular demonstration of the movement of this lysosomal enzyme within axonal networks was missing. We generated lentiviral vectors carrying the ARSA cDNA tagged with hemagglutinin or the green fluorescent protein and examined the subcellular localization and anatomical distribution of the tagged enzymes within the MLD hippocampus after in vivo lentiviral gene transfer. The use of tagged ARSA allowed direct real-time observation and tracking of axon-dendritic transport of the enzyme after lentiviral gene therapy. Tagged ARSA was expressed in transduced pyramidal, granule, and hilar neurons within the lentiviral-injected side and was robustly contained in vesicles within ipsilateral axon-dendritic processes as well as in vesicles associated with contralateral axons and commissural axons of the ventral hippocampal commissure. Axonal transport of tagged ARSA led to the correction of hippocampal defects in long-term treated MLD mice, which was accompanied by enzyme uptake in nontransduced contralateral neurons, enzyme accumulation within the lysosomal compartment, and clearance of sulfatide storage deposits in this region of the MLD brain. These results contribute to the understanding of the mechanisms of distribution of lysosomal enzymes within the mammalian brain after direct gene therapy, demonstrating the use of neural processes for enzyme transport.
Reactivity to endothelium-dependent and -independent vasoactive substances is maintained in coronary resistance vessels of the failing hamster heart
Authors: M VERONNEAU, M TANGUAY, T FONTAINE, G JASMIN, L DUMONT
Journal: Cardiovascular Research (1997)

Objectives: Several studies suggest that regulation of coronary vasomotion is abnormal in heart failure, but controversies exist as to whether an altered endothelium-dependent dilation of the coronary vasculature contributes to these abnormalities. In the present study we evaluated the coronary reactivity to endothelium-dependent and -independent vasoactive substances in a model of chronic heart failure. Methods: Isolated hearts from > 200-day-old cardiomyopathic hamsters (UM-X7.1) and age-matched normal Syrian hamsters were mounted on a Langendorff apparatus and retrogradely perfused at constant pressure (100 mmHg). Heart rate, left ventricular developed pressure (LVP) and coronary flow (CF) were measured. A first group of normal and failing hearts were challenged with increasing doses of acetylcholine (Ach), 1–1000 nM, and sodium nitroprusside (SNP), 0.01-10μM. A second group was challenged with Ach (100 nM) and SNP (1 μM) before and during infusion of the NO synthase inhibitor, N G -nitro- l -arginine methyl ester ( l -NAME). Finally, normal and failing hearts were challenged with Ach (100 nM) before and during infusion of indomethacin (10 μM) or tetraethylammonium (1 mM). Results: Myocardial contractility and coronary flow were significantly impaired in failing hearts (LVP = 32 ± 5 vs. 50 ± 4 mmHg in normal hearts; CF = 4.7 ± 0.6 vs. 6.7 ± 0.6 ml/min in normal hearts). Coronary flow increases with increasing doses of Ach (EC 50 = 84 ± 15 nM for failing hearts and 100 ± 3 nM for normal hearts, P = ns). At concentrations exceeding the EC 50 , failing hearts were more sensitive to the coronary dilator effects of Ach. The reduction in coronary flow elicited by l -NAME was similar in normal (−41 ± 2%) and failing hearts (−40 + 3%); in both normal and failing hearts, the acetylcholine vasodilator response was not significantly affected by l -NAME. Indomethacin infusion resulted in a slight increase in coronary flow and significantly reduced the coronary dilator effects of acetylcholine. Tetraethylammonium had no significant effects on basal coronary perfusion of normal and failing hearts. However, in the latter group, acetylcholine vasodilator response was significantly attenuated. Conclusion: Results obtained in isolated failing hamster hearts allow us to conclude that (1) significant coronary dysfunctions are present in this model of chronic heart failure, (2) neither the NO-synthase nor the cyclo-oxygenase pathway contributes to these coronary dysfunctions, and (3) an adequate coronary vasodilator response appears to be present in this model of chronic heart failure.
Cardiovascular effects of sildenafil in experimental ischemia–reperfusion (reply to “Sildenafil-induced cardioprotection in rabbits, by Kukreja, R.C., Ockaili, R., Salloum, F., Xi, L.”)
Authors: T Reffelmann
Journal: Cardiovascular Research (2003)

In their letter to the editor, Kukreja, Ockaili, Salloum and Xi comment on our recently published study in which intravenous application of 1.45 or 0.7 mg/kg sildenafil 30 min prior to coronary artery occlusion did not reduce myocardial infarct size in an experimental rabbit model of 30 min ischemia followed by 180 min of reperfusion [1].Since our results contrast with a recent investigation by this research group [2] that described pronounced infarct size reduction after pretreatment with sildenafil in a very similar model, the authors are ''puzzled by our negative findings''.Indeed, we appreciate the editorial decision from Cardiovascular Research to publish our results, as in these days publication bias in favor of positive results occasionally makes it difficult to publish ''negative findings''.We believe that the constructive debate, initiated by Kukreja et al. in this letter to the editor, may encourage this editorial policy.When comparing the mentioned investigations by Ockaili et al. [2] with our study, again-and we think that the extensive work from Dr. Kukreja's group on delayed cardioprotective effects of sildenafil [2,3] should be clearly differentiated from acute effects-we must reiterate the very similar study design in Ockaili's and our investigations.The only noticeable differences are the use of atropine when initiating anesthesia, the slightly lower body temperature in Ockaili's study, the use of pentobarbital for maintenance of anesthesia, and the higher infarct size in the control group in our study.Additionally, for preparation of a sildenafil solution, Ockaili et al. crushed Viagra tablets and dissolved them in saline, while we used the pure powder of sildenafil citrate.Whether these subtle differences in the study proto-
Sensitivity of end-systolic pressure-dimension and pressure-volume relations to the inotropic state in humans.
Authors: K M Borow, A Neumann, J Wynne
Journal: Circulation (1982)

The value for the slope of the left ventricular (LV) end-systolic pressure-dimension and pressure-volume relations has been proposed as a quantitative measure of the LV inotropic state. This measure of LV inotropic state is attractive because it is independent of preload and incorporates afterload. To investigate the sensitivity of the slope of these relations to alterations in contractile state, 10 normal subjects were studied using M-mode echocardiographic, phonocardiographic and indirect carotid pulse recordings during infusion of methoxamine to alter end-systolic pressure and during infusion of dobutamine (5 micrograms/kg/min) to increase LV inotropic state. Heart rate was maintained within a narrow range for each subject. End-systolic volume was calculated from end-systolic echocardiographic dimension by standard methods. End-systolic pressure was estimated from the dicrotic notch pressure determined from a calibrated carotid pulse recording; peak systolic pressure was also measured. Regardless of the method of approximating end-systolic pressure, the positive inotropic intervention caused a leftward shift in the end-systolic pressure-dimension and pressure-volume lines. With the dobutamine infusion, the value for the slope of the end-systolic pressure-dimension relation increased by 25% (range 16-46%, p less than 0.001), while the slope of the end-systolic pressure-volume relation increased by 55% (range 37-85%, p less than 0.001). In all cases, the curves were linear and became steeper with the positive inotropic intervention. In contrast, the value of the slope of the peak systolic pressure-end-systolic dimension relation showed a variable response to the dobutamine infusion (mean change 13%, range -77% to 73%; NS). Although the position of the peak systolic pressure-end-systolic dimension curve is consistently shifted with an alteration in inotropic state, the values of the slope of these curves are not reliable indicators of change in LV contractility. The values for the slope of the line relating end-systolic pressure (estimated by dicrotic notch pressure) to end-systolic dimension or volume, however, are highly sensitive to a change in inotropic state in human subjects.
LTB4 promotes insulin resistance in obese mice by acting on macrophages, hepatocytes and myocytes
Authors: Pingping Li, Da Young Oh, Gautam Bandyopadhyay, William S Lagakos, Saswata Talukdar, Olivia Osborn, Andrew Johnson, Heekyung Chung, Rafael Mayoral, Michael Maris, Jachelle M Ofrecio, Sayaka Taguchi, Min Lu, Jerrold M Olefsky
Journal: Nature Medicine (2015)