tbuckley/cabot-search huggingface dataset:
Right and left heart failure in severe H1N1 influenza A infection
Authors: S.M. Brown, J. Pittman, R.R. Miller, K.D. Horton, B. Markewitz, E. Hirshberg, J. Jones, C.K. Grissom
Journal: European Respiratory Journal (2010)

Influenza infection can affect cardiac function. The recent pandemic of H1N1 influenza A provided an opportunity to study echocardiographic findings in critically ill infected patients. We hypothesised that critically ill patients with H1N1 infection would have a higher incidence of right and left heart failure than is seen in unselected populations of patients with septic shock and/or acute respiratory distress syndrome (ARDS). We retrospectively studied all patients admitted to four intensive care units at three hospitals in Salt Lake County, UT, USA, with laboratory-confirmed H1N1 infection in whom a clinical echocardiogram was available. 23 out of 48 patients had qualifying echocardiograms. Right ventricular (RV) dilatation (50–80%) and at least moderate systolic impairment (23%) were common, higher than the range described in general populations with ARDS. Left ventricular systolic dysfunction was present in 17% of patients. No single echocardiographic parameter was associated with 28-day mortality or ventilator-free days to 28 days. Critically ill patients with H1N1 infection frequently exhibit right heart dilatation and failure. RV basal dilatation was extremely common. These patients have less left heart failure than expected on the basis of prior descriptions of influenza myopericarditis or of general populations of septic patients.
Burden of non-communicable diseases in South Asia: Evidence for epidemic of coronary heart disease in India is weak
Authors: Naseer Ahmad, Raj Bhopal
Journal: BMJ (2004)

EDITOR—India is widely believed to be on the verge of an epidemic of coronary heart disease, as expressed by Ghaffar et al in their clinical review.1 2 We believe this assumption to be based on weak evidence.

We found one meta-analysis, reporting a ninefold increase in urban India (1-9%) and twofold increase (2-4%) in rural India between the 1960s …
Distribution of Excitation Frequencies on the Epicardial and Endocardial Surfaces of Fibrillating Ventricular Wall of the Sheep Heart
Authors: Alexey V. Zaitsev, Omer Berenfeld, Sergey F. Mironov, José Jalife, Arkady M. Pertsov
Journal: Circulation Research (2000)

Abstract —Tissue heterogeneities may play an important role in the mechanism of ventricular tachycardia (VT) and fibrillation (VF) and can lead to a complex spatial distribution of excitation frequencies. Here we used optical mapping and Fourier analysis to determine the distribution of excitation frequencies in &gt;20 000 sites of fibrillating ventricular tissue. Our objective was to use such a distribution as a tool to quantify the degree of organization during VF. Fourteen episodes of VT/VF were induced via rapid pacing in 9 isolated, coronary perfused, and superfused sheep ventricular slabs (3×3 cm 2 ). A dual-camera video-imaging system was used for simultaneous optical recordings from the entire epi- and endocardial surfaces. The local frequencies of excitation were determined at each pixel and displayed as dominant frequency (DF) maps. A typical DF map consisted of several (8.2±3.6) discrete areas (domains) with a uniform DF within each domain. The DFs in adjacent domains were often in 1:2, 3:4, or 4:5 ratios, which was shown to be a result of an intermittent Wenckebach-like conduction block at the domain boundaries. The domain patterns were relatively stable and could persist from several seconds to several minutes. The complexity in the organization of the domains, the number of domains, and the dispersion of frequencies increased with the rate of the arrhythmia. Domain patterns on the epicardial and endocardial surfaces were not correlated. Sustained epicardial or endocardial reentry was observed in only 3 episodes. Observed frequency patterns during VT/VF suggest that the underlying mechanism may be a sustained intramural reentrant source interacting with tissue heterogeneities.
OP37 * BENIGN MENINGIOMA AND QUALITY OF LIFE: WHAT INFLUENCE DOES EPILEPSY HAVE ON QUALITY OF LIFE?
Authors: M. Tanti, A. G. Marson, M. D. Jenkinson
Journal: Neuro-Oncology (2014)

INTRODUCTION: Epilepsy is known to impair quality of life (QoL) but the impact of epilepsy on QoL in meningioma population is not certain. The aim of this cross-sectional postal study was to investigate the effects of benign meningioma and epilepsy on QoL. METHOD: Three patient groups were recruited: (1) meningioma without epilepsy; (2) meningioma with epilepsy; and (3) epilepsy without meningioma. Three QoL questionnaires were used: (a) Sf-36; (b) Fact-Br; and (c) the Liverpool Adverse Events Profile (LAEP). Mean scores of each scale were compared between meningioma patients with and without epilepsy, and between epilepsy patients with and without meningioma. Regression models identified factors that correlated with poor QoL. RESULTS: There were 229 participants (mean age 59.9 ± 12.2 years); 109 meningioma, 56 meningioma and epilepsy, and 64 epilepsy without meningioma. QoL was impaired in the meningioma with epilepsy group compared to the meningioma without epilepsy group in all questionnaires; but only the Fact-Br was significantly impaired (t-test; p = 0.012). Antiepileptic drugs (AEDs) significantly impaired QoL in the regression analyses, while seizures were less influential. QoL was impaired in the epilepsy without meningioma group compared to the meningioma and epilepsy group, but this difference was not significant (t-test; p = 0.44). Increased seizure frequency and AEDs (particularly Levetiracetam) significantly impaired QoL in the regression analyses. CONCLUSION: In meningioma, epilepsy has a minor impact on QoL; but AEDs significantly impair QoL and this has potential implications for seizure management. Meningioma patients with epilepsy have comparable QoL to epilepsy patients without meningioma.
Randomized, Double-Blind Trial of Simultaneous Right and Left Atrial Epicardial Pacing for Prevention of Post–Open Heart Surgery Atrial Fibrillation
Authors: Emile G. Daoud, Reza Dabir, Michelle Archambeau, Fred Morady, S. Adam Strickberger
Journal: Circulation (2000)

Background —The purpose of this study was to assess simultaneous right and left atrial pacing as prophylaxis for postoperative atrial fibrillation. Methods and Results —In a double-blind, randomized fashion, 118 patients who underwent open heart surgery were assigned to right atrial pacing at 45 bpm (RA-AAI; n=39), right atrial triggered pacing at a rate of ≥85 bpm (RA-AAT; n=38), or simultaneous right and left atrial triggered pacing at a rate of ≥85 bpm (Bi-AAT; n=41). Holter monitoring was performed for 4.8±1.4 days after surgery to assess for episodes of atrial fibrillation lasting &gt;5 minutes. The prevalence of postoperative atrial fibrillation was significantly less in the patients randomized to biatrial AAT pacing when compared with the other 2 pacing regimens ( P =0.02). An episode of atrial fibrillation occurred in 4 (10%) of 41 patients in the Bi-AAT group compared with 11 (28%) of 39 patients in the RA-AAI group ( P =0.03 versus Bi-AAT) and 12 (32%) of 38 patients in the RA-AAT group ( P =0.01 versus Bi-AAT). There was no difference in the occurrence of atrial fibrillation between the right atrial AAI and AAT groups ( P =0.8). There was no significant difference among the 3 groups with regard to the number of postoperative hospital days (7.3±4.2 days), morbidity (5.1%), or mortality rate (2.5%). Conclusions —Simultaneous right and left atrial triggered pacing is well tolerated and significantly reduces the prevalence of post–open heart surgery atrial fibrillation.
Renal Failure Associated with Cancer and Its Treatment
Authors: Benjamin D. Humphreys, Robert J. Soiffer, Colm C. Magee
Journal: Journal of the American Society of Nephrology (2004)

Kidney disease frequently complicates malignancy and its treatment. The spectrum of disease in this setting includes acute renal failure (ARF), chronic renal failure, and tubular disorders. Fortunately, these complications are often preventable or reversible with prompt diagnosis and treatment. This
Abnormalities of renal perfusion and the renal pressor system in dogs with chronic aortic coarctation.
Authors: S P Bagby, W J McDonald, D W Strong, G A Porter, W M Bennett, L I Bonchek
Journal: Circulation Research (1975)

To clarify the role of the renin-angiotensin system in coarctation hypertension, 2-year-old inbred dogs with chronic neonatally induced thoracic aortic coarctation were subjected to 6 days of rigorous salt restriction. The following parameters were then measured: glomerular filtration rate, renal plasma flow, plasma renin activity, plasma renin concentration, renin reactivity, and renin substrate concentration. Glomerular filtration rate and renal plasma flow were significantly lower in salt-restricted coarcted dogs: 3.0 +/- 0.2 and 9.0 +/- 1.5 ml/min kg-1, respectively, compared with values of 4.0 +/- 0.2 (P less than 0.005) and 13.2 +/- 0.6 (P less than 0.025) ml/min kg-1 in salt-restricted controls. Plasma renin activity was abnormally high in experimental dogs: 13.5 +/- 2.5 vs. 4.5 +/- 1.5 ng angiotensin I/ml hour-1 in controls (P less than 0.005). In addition, a significant elevation of renin reactivity (indicating a relative increase in circulating accelerators or a relative decrease in inhibitors of the renin reaction) was apparent in the plasma of coarcted dogs. Plasma renin concentration was elevated but to an insignificant degree in coarcted dogs, and renin substrate concentration was comparable with that of controls. The impaired renal perfusion and abnormal elevation of plasma renin activity during salt restriction is analogous to clinical and experimental observations in hypertensive states associated with total renal underperfusion and supports a major role for the renal pressor system in the pathogenesis of coarctation hypertension. The insignificant elevation of plasma renin concentration is not incompatible with this view. The demonstration of increased renin reactivity in coarctation hypertension provides additional evidence that acceleration of the renin reaction is common to all hypertensive states.
HIF-2α, but not HIF-1α, promotes iron absorption in mice
Authors: Maria Mastrogiannaki, Pavle Matak, Brian Keith, M. Celeste Simon, Sophie Vaulont, Carole Peyssonnaux
Journal: Journal of Clinical Investigation (2009)

HIF transcription factors (HIF-1 and HIF-2) are central mediators of cellular adaptation to hypoxia. Because the resting partial pressure of oxygen is low in the intestinal lumen, epithelial cells are believed to be mildly hypoxic. Having recently established a link between HIF and the iron-regulatory hormone hepcidin, we hypothesized that HIFs, stabilized in the hypoxic intestinal epithelium, may also play critical roles in regulating intestinal iron absorption. To explore this idea, we first established that the mouse duodenum, the site of iron absorption in the intestine, is hypoxic and generated conditional knockout mice that lacked either Hif1a or Hif2a specifically in the intestinal epithelium. Using these mice, we found that HIF-1alpha was not necessary for iron absorption, whereas HIF-2alpha played a crucial role in maintaining iron balance in the organism by directly regulating the transcription of the gene encoding divalent metal transporter 1 (DMT1), the principal intestinal iron transporter. Specific deletion of Hif2a led to a decrease in serum and liver iron levels and a marked decrease in liver hepcidin expression, indicating the involvement of an induced systemic response to counteract the iron deficiency. This finding may provide a basis for the development of new strategies, specifically in targeting HIF-2alpha, to improve iron homeostasis in patients with iron disorders.
Is lung transplantation a cause of sleep apnea hypopnea syndrome? Preliminary data
Authors: Inés Escribano Gimeno, María Josefa Díaz de Atauri, Trinidad Díaz Cambriles, Alicia De Pablo Gafas, Virginia Pérez Gonzalez, Angel Lόpez Encuentra
Journal: European Respiratory Journal (2011)

Aims:  To analyze the presence of Sleep Apnea Hypopnea Syndrome (SAHS) in a cohort of patients before and after lung transplantation (LT).   Methods:  All consecutive LT recipients with at least 2 polysomnographies (PSG) during one-year post-LT follow up have been included. The study was done in a tertiary hospital. Period of study: September 2008-February 2011. Anthropomorphic measurements, Epworth scale and PSG (before LT, 6 and after 12 months post-LT) were performed. Data about type and cumulative dose of immunosuppressive drugs were collected. SAHS was defined as an apnea-hypopnea index (AHI) ≥ 10/hour.   Results:  Ten patients were included, 60% males, with a median age of 53.5 (range 15 to 63) years. 4 LT were unilateral and 6 bilateral. The SAHS prevalence was 30% (n=3) pre-LT, 80% (n=8) at the first PSG after LT, and 40% (n=4) at the second one. There were significant differences between mean AHI in the pre-LT sleep study and AHI in the first study after LT, but not with the one after 12 month of follow up. The data are shown in the figure:  Considering AHI values and SAHS presence there were not found any statistical relationship among them and the variables analyzed that could explains the SAHS prevalence progression in LT recipients.   Conclusions:  The prevalence of SAHS is higher in the patients listed for LT compared with general population. It increases during the first months after LT and decreases over the time.
Inducible Cardiac-Restricted Expression of Enteroviral Protease 2A Is Sufficient to Induce Dilated Cardiomyopathy
Authors: Dingding Xiong, Toshitaka Yajima, Byung-Kwan Lim, Antine Stenbit, Andrew Dublin, Nancy D. Dalton, Daphne Summers-Torres, Jeffery D. Molkentin, Herve Duplain, Rainer Wessely, Ju Chen, Kirk U. Knowlton
Journal: Circulation (2006)

Enterovirus infection is a cause of cardiomyopathy. We previously demonstrated that enteroviral protease 2A directly cleaves the cytoskeletal protein dystrophin. However, the direct effect of protease 2A in enteroviral cardiomyopathy is less clear because other viral proteins are also expressed with viral infection.A transgenic mouse with inducible cardiac-restricted expression of enteroviral protease 2A was generated. In the transgenic mouse, a tamoxifen-regulated Cre-loxP system, MerCreMer (MCM), was used to induce genetic recombination in cardiac myocytes, which led to protease 2A expression. Protease 2A and MCM double transgenic (2AxMCM) mice were treated with tamoxifen; the controls included 2AxMCM mice treated with diluents for tamoxifen and tamoxifen-treated MCM littermates. Protease 2A activity was significantly induced after tamoxifen in the 2AxMCM mice compared with controls. Echocardiographic analysis demonstrated an increase in left ventricular end-diastolic and end-systolic chamber size, with decreased fractional shortening in tamoxifen-treated 2AxMCM mice. There was an increase in heart weight-to-body weight ratio in 2AxMCM mice treated with tamoxifen. Only a small increase in interstitial fibrosis and inflammation was found in tamoxifen-treated 2AxMCM mice; however, ultrastructural analysis demonstrated myofibrillar collapse with abnormalities of intercalated discs and sarcolemmal membranes. Evans blue dye-positive myocytes with disruption of dystrophin were present in 2AxMCM mice treated with tamoxifen. Disruption of dystrophin was also found in cultured myocytes isolated from 2AxMCM mice with Cre in the nucleus.Protease 2A has a significant role in enteroviral cardiomyopathy and alone is sufficient to induce dilated cardiomyopathy, which is associated with disruption of the sarcolemmal membrane and cleavage of dystrophin with protease 2A expression.
Evidence of Tubular Hypoxia in the Early Phase in the Remnant Kidney Model
Authors: Krissanapong Manotham, Tetsuhiro Tanaka, Makiko Matsumoto, Takamoto Ohse, Toshio Miyata, Reiko Inagi, Kiyoshi Kurokawa, Toshiro Fujita, Masaomi Nangaku
Journal: Journal of the American Society of Nephrology (2004)

ABSTRACT. The remnant kidney model is a mainstay in the study of progressive renal disease. The earliest changes in this model result from glomerular hemodynamic alterations. Given that progressive renal disease is the result of subsequent interstitial damage initiated by undetermined pathogenic factors, the authors investigated the role of hypoxia as a pathogenic factor in tubulointerstitial damage after renal ablation in rats. Cortical tissue hypoxia in the early phase (4 and 7 d) in remnant kidney rats, sham-operated rats, and animals treated with the angiotensin II receptor blocker (ARB) olmesartan (10 mg/kg per d) was assessed by uptake of a hypoxic probe, pimonidazole, expression of HIF-1α, and by increased transcription of hypoxia-responsive genes. Physiologic perfusion status of the postglomerular peritubular capillary network was evaluated by lectin perfusion and Hoechst 33342 diffusion techniques. Results showed that the number of hypoxic tubules was markedly increased 4 and 7 d after nephron loss. These findings antedated any histologic evidence of tubulointerstitial damage. The hypoxic state persisted until interstitial damage developed. These results were confirmed using HIF-1α immunoprecipitation and increase of hypoxia-responsive genes. Pathologic studies of the vasculature demonstrated significant functional changes that generated a hypoxic milieu. ARB treatment prevented vascular changes and ameliorated tubular hypoxia. These results suggest that the initial tubulointerstitial hypoxia in remnant kidney model plays a pathogenic role in the subsequent development of tubulointerstitial injury. The initial hypoxia in this model was dependent on activation of the renin-angiotensin system and hemodynamic alterations after nephron loss.
EFFECT OF SMALL DOSES OF X-RAYS ON HYPERTROPHIED TONSILS AND OTHER LYMPHOID STRUCTURES OF THE NASOPHARYNX
Authors: James B. Murphy, William D. Witherbee, Stuart L. Craig, Raymond G. Hussey, Ernest Sturm
Journal: The Journal of Experimental Medicine (1921)

46 individuals with tonsils both hypertrophied and otherwise pathologically altered and some of whom had in addition adenoid masses and lymphoid deposits posterior to the pillars of the fauces, were given exposures to x-rays. In all but four cases the treatment was followed by marked atrophy of the tonsils and the other lymphoid deposits, attended by an opening and drainage of the tonsillar crypts. As this process progressed the previously enlarged tonsils assumed a smooth and normal appearance and the hemolytic bacteria—streptococci and staphylococci chiefly—which were often present in the affected tonsil disappeared usually within 4 weeks of the treatment.
SUB-ACUTE OTITIS MEDIA
Authors: A. L. Yates
Journal: BMJ (1931)

_fEDCLJORA After-treatment 'Whether in the after-treatment of the case the medical attendant favours the so-called dry method of mopping out, or the method of frequent washing out by syringing, irrigations must be employed if the discharge becomes tenacious, and even when discharge is free occasional re- lapse and disappointment can be overcome by a thorough but gently performed wash-out with a mild isotonic saline or alkaline lotion.Kerrison" strongly advocates washing out almost immediately after paracentesis, to avoid gumming up of the incision by blood clot or fibrin.In the later stage, too, irrigations with a mild mercurial lotion and the use of the suction speculum may result in resolu- tion and avoid further operation as the time approaches to suggest drainage through the mastoid, namely, in three to six weeks. Differential Diagnosis from Other Causes ofAcute Earache Acute pain felt in the ear may be caused by troubles at
The Critical Role of Dysregulated FOXM1–PLAUR Signaling in Human Colon Cancer Progression and Metastasis
Authors: Dawei Li, Ping Wei, Zhihai Peng, Chen Huang, Huamei Tang, Zhiliang Jia, Jiujie Cui, Xiangdong Le, Suyun Huang, Keping Xie
Journal: Clinical Cancer Research (2012)

The mammalian Forkhead Box (Fox) transcription factor FOXM1 is implicated in tumorigenesis including mouse intestinal cancer. However, the clinical significance of FOXM1 signaling in human colorectal cancer pathogenesis remains unknown.We investigated FOXM1 expression in 203 cases of primary colon cancer and matched normal colon tissue specimens and explored the underlying mechanisms of altered FOXM1 expression and the impact of this altered expression on colon cancer growth and metastasis using in vitro and animal models of colon cancer.We found weak expression of FOXM1 protein in the colon mucosa, whereas we observed strong FOXM1 expression in tumor-cell nuclei of colon cancer and lymph node metastases. A Cox proportional hazards model revealed that FOXM1 expression was an independent prognostic factor in multivariate analysis. Experimentally, overexpression of FOXM1 by gene transfer significantly promoted the growth and metastasis of colon cancer cells in orthotopic mouse models, whereas knockdown of FOXM1 expression by siRNA did the opposite. Promotion of colon tumorigenesis by FOXM1 directly and significantly correlated with activation of urokinase-type plasminogen activator receptor (PLAUR) expression and elevation of invasion and metastasis.Given the importance of FOXM1 in regulation of the expression of genes key to cancer biology, dysregulated expression and activation of FOXM1 may play important roles in colon cancer progression and metastasis.
Notch1 counteracts WNT/β-catenin signaling through chromatin modification in colorectal cancer
Authors: Hyun-A Kim, Bon-Kyoung Koo, Ji-Hoon Cho, Yoon-Young Kim, Jinwoo Seong, Hee Jin Chang, Young Min Oh, Daniel E. Stange, Jae-Gahb Park, Daehee Hwang, Young-Yun Kong
Journal: Journal of Clinical Investigation (2012)

Crosstalk between the Notch and wingless-type MMTV integration site (WNT) signaling pathways has been investigated for many developmental processes. However, this negative correlation between Notch and WNT/β-catenin signaling activity has been studied primarily in normal developmental and physiological processes in which negative feedback loops for both signaling pathways are intact. We found that Notch1 signaling retained the capability of suppressing the expression of WNT target genes in colorectal cancers even when β-catenin destruction by the adenomatous polyposis coli (APC) complex was disabled. Activation of Notch1 converted high-grade adenoma into low-grade adenoma in an Apcmin mouse colon cancer model and suppressed the expression of WNT target genes in human colorectal cancer cells through epigenetic modification recruiting histone methyltransferase SET domain bifurcated 1 (SETDB1). Extensive microarray analysis of human colorectal cancers also showed a negative correlation between the Notch1 target gene, Notch-regulated ankyrin repeat protein 1 (NRARP), and WNT target genes. Notch is known to be a strong promoter of tumor initiation, but here we uncovered an unexpected suppressive role of Notch1 on WNT/β-catenin target genes involved in colorectal cancer.