bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of non-invasive calibration of radial waveforms on error in transfer-function-derived central aortic waveform characteristics
Authors: HOPE Sarah A. , MEREDITH Ian T. , CAMERON James D. 
Published: July 2004

Transfer function techniques are increasingly used for non-invasive estimation of central aortic waveform characteristics. Non-invasive radial waveforms must be calibrated for this purpose. Most validation studies have used invasive pressures for calibration, with little data on the impact of non-invasive calibration on transfer-function-derived aortic waveform characteristics. In the present study, simultaneous invasive central aortic (Millar Mikro-tip® catheter transducer) and non-invasive radial (Millar® Mikro-tip® tonometer) pressure waveforms and non-invasive brachial pressures (Dinamap®) were measured in 42 subjects. In this cohort, radial waveforms were calibrated to both invasive and non-invasive mean and diastolic pressures. From each of these, central waveforms were reconstructed using a generalized transfer function obtained by us from a previous cohort [Hope, Tay, Meredith and Cameron (2002) Am. J. Physiol. Heart Circ. Physiol. 283, H1150–H1156]. Waveforms were analysed for parameters of potential clinical interest. For calibrated radial and reconstructed central waveforms, different methods of calibration were associated with differences in pressure (P&lt;0.001), but not time parameters or augmentation index. Whereas invasive calibration resulted in little error in transfer function estimation of central systolic pressure (difference −1±8 mmHg; P=not significant), non-invasive calibration resulted in significant underestimation (7±12 mmHg; P&lt;0.001). Errors in estimated aortic parameters differed with non-invasively calibrated untransformed radial and transfer-function-derived aortic waveforms (all P&lt;0.01), with smaller absolute errors with untransformed radial waveforms for most pressure parameters [systolic pressure, 5±16 and 7±12 mmHg; pulse pressure, 0±16 and 4±12 mmHg (radial and derived aortic respectively)]. When only non-invasive pressures are accessible, analysis of untransformed radial waveforms apparently produces smaller errors in the estimation of central aortic systolic pressure, and other waveform parameters, than using a generalized transfer function.
Probucol aggravates long QT syndrome associated with a novel missense mutation M124T in the N-terminus of HERG
Authors: HAYASHI Kenshi , SHIMIZU Masami , INO Hidekazu , YAMAGUCHI Masato , TERAI Hidenobu , HOSHI Naoto , HIGASHIDA Haruhiro , TERASHIMA Nariaki , UNO Yoshihide , KANAYA Honin , MABUCHI Hiroshi 
Published: July 2004

Patients with LQTS (long QT syndrome) with a mutation in a cardiac ion channel gene, leading to mild-to-moderate channel dysfunction, may manifest marked QT prolongation or torsade de pointes only upon an additional stressor. A 59-year-old woman had marked QT prolongation and repeated torsade de pointes 3 months after initiation of probucol, a cholesterol-lowering drug. We identified a single base substitution in the HERG gene by genetic analysis. This novel missense mutation is predicted to cause an amino acid substitution of Met124→Thr (M124T) in the N-terminus. Three other relatives with this mutation also had QT prolongation and one of them had a prolonged QT interval and torsade de pointes accompanied by syncope after taking probucol. We expressed wild-type HERG and HERG with M124T in Xenopus oocytes and characterized the electrophysiological properties of these HERG channels and the action of probucol on the channels. Injection of the M124T mutant cRNA into Xenopus oocytes resulted in expression of functional channels with markedly smaller amplitude. In both HERG channels, probucol decreased the amplitude of the HERG tail current, decelerated the rate of channel activation, accelerated the rate of channel deactivation and shifted the reversal potential to a more positive value. The electrophysiological study indicated that QT lengthening and cardiac arrhythmia in the two present patients were due to inhibition of IKr (rapidly activating delayed rectifier K+ current) by probucol, in addition to the significant suppression of HERG current in HERG channels with the M124T mutation.
Randomized double-blind placebo-controlled study of an angiotensin immunotherapeutic vaccine (PMD3117) in hypertensive subjects
Authors: BROWN Morris J. , COLTART John , GUNEWARDENA Kulasiri , RITTER James M. , AUTON Timothy R. , GLOVER James F. 
Published: July 2004

Immunization against components of the renin–angiotensin system offers a potential alternative to daily medication in some patients with hypertension or heart failure. Our primary objective was to determine whether a sustained antibody titre to Ang I (angiotensin I) can be achieved in hypertensive patients. The secondary objective was to determine whether the antibodies block the renin system. Patients (n=27) with essential hypertension responsive to an ACEi (angiotensin-converting enzyme inhibitor) or ARB (angiotensin blocker) were randomly assigned to receive three or four injections of the Ang I vaccine PMD3117 or aluminium hydroxide (Alhydrogel™) over a 6 week period. Antibody titre was measured prior to each injection and every 30 days until disappearance. Indices of renin blockade were changes in renin and aldosterone (blood and urine) and a within-patient comparison of the pre- and post-vaccination rise in 24 h ambulatory blood pressure after 2 weeks of withdrawal of ACEi or ARB. The anti-(Ang I) antibody titre rose from the second injection in both regimes and peaked on day 64. Median half-life was 85 (95% CI, 44 and 153) days (where CI is confidence interval). Vaccination did not influence blood pressure, but significantly blunted the fall in plasma renin following withdrawal of ACEi or ARB. At 42 days after the first injection, aldosterone excretion was decreased by PMD3117 to 6 (95% CI, 1 and 31)% of values in patients receiving Alhydrogel™ (P=0.012). In patients with essential hypertension, PMD3117 generated a prolonged antibody response to Ang I. Biochemical measurements show evidence of blockade of the renin system, but higher titres will be required to achieve a decrease in blood pressure.
Testosterone-induced coronary vasodilatation occurs via a non-genomic mechanism: evidence of a direct calcium antagonism action
Authors: JONES Richard D. , ENGLISH Kate M. , JONES T. Hugh , CHANNER Kevin S. 
Published: July 2004

Testosterone decreases myocardial ischaemia in men with coronary artery disease via a coronary vasodilatory action. However, long-term therapy may increase the risk of prostatic carcinoma via activation of the nuclear AR (androgen receptor). In the present study, we have investigated the mechanism of testosterone-induced vasodilatation using isolated rat coronary arteries and thoracic aortae from control and AR-deficient testicular-feminized mice. Vasodilatation induced by testosterone, T-3-OCMO [testosterone 3-(O-carboxymethyl)oxime] or T-3-OCMO conjugated to BSA was initially measured in preconstricted vessels that had undergone endothelial denudation or incubation with flutamide (10 μM). Cellular fluorescence was also measured in primary aortic SMCs (smooth muscle cells) following exposure to the above fluorescent-labelled agents. Subsequently, vessels were incubated with testosterone (100 μM) or vehicle prior to constriction with KCl (1–100 mM). Testosterone-induced vasodilatation was unaffected by endothelial denudation, flutamide treatment, AR deficiency or conjugation to BSA. Cells exposed to T-3-OCMO–BSA (10 μM) had a higher fluorescence than control cells (32.8±4.5 compared with 14.5±1.8 arbitrary units respectively; P&lt;0.01). Incubation with testosterone (100 μM) reversibly attenuated coronary vasoconstriction to KCl (1–100 mM; 0.08±0.09 compared with 0.79±0.08 mN/mm respectively; P&lt;0.0001). Testosterone-induced vasodilatation is independent of the vascular endothelium and nuclear AR, and is initiated at the SMC membrane, which contains testosterone binding sites. A direct calcium antagonistic action is implicated.
Factors influencing heart rate variability power spectral analysis during controlled breathing in patients with chronic heart failure or hypertension and in healthy normotensive subjects
Authors: PICCIRILLO Gianfranco , MAGRÌ Damiano , NASO Camilla , di CARLO Silvia , MOISÈ Antonio , DE LAURENTIS Tiziana , TORRINI Alessia , MATERA Sabrina , NOCCO Marialuce 
Published: July 2004

A decreased LFP (low-frequency power) spectral component of HRV [HR (heart rate) variability] is a risk factor for sudden death in patients with CHF (chronic heart failure). In the present study, we evaluated factors (age, arterial pressures and HR) influencing LFP and HFP (high-frequency power) components in short-term recordings during controlled breathing in patients with CHF or hypertension, and healthy normotensive subjects. In patients with CHF, we also compared LFP values with known markers of sudden death [NYHA (New York Heart Association) class, HR and ejection fraction]. All HRV measures were significantly lower in patients with CHF than in hypertensive and normotensive subjects (P&lt;0.001), and in hypertensive than in normotensive subjects (P&lt;0.05). Stepwise multiple regression analysis showed that, in patients with CHF, LFP was inversely associated with NYHA class (β=−0.5, P&lt;0.0001) and HR (β=−0.2, P=0.001) and was positively associated with ejection fraction (β=0.28, P&lt;0.0001). In patients with CHF, LFP remained unchanged with age. In normotensive and hypertensive subjects, HFP decreased with age, but in patients with CHF it did not. In the ≥60&lt;70 and ≥70 years of age subgroups, we found no difference between HFP in the three groups studied. Hence, in normotensives and hypertensives, LFP tended to diminish with age (β=−0.4, P&lt;0.0001 in normotensives; β=−0.4, P&lt;0.001 in hypertensives) and was inversely associated with HR (β=−0.2, P=0.002 in normotensives; β=−0.3, P=0.002 in hypertensives). Conversely, in patients with CHF, LFP is predominantly influenced by NYHA class, HR and ejection fraction, but not by age. LFP might therefore increase the sensitivity of factors already used in stratifying the risk of sudden death in patients with CHF.
Lack of effect of oral glucose loading on conduit vessel endothelial function in healthy subjects
Authors: SIAFARIKAS Aris , WATTS Katie , BEYE Petra , JONES Timothy W. , DAVIS Elizabeth A. , GREEN Daniel J. 
Published: July 2004

The aim of the present study was to investigate the impact of an oral glucose load on circulating insulin and glucose levels and arterial function in healthy non-diabetic subjects. Thirty-nine non-obese, healthy subjects (24 female, 15 male), aged 21.0±1.8 years of age, were randomly assigned to undergo either an OGTT (oral glucose tolerance test; 75 g of glucose) or administration of a placebo. Analyses of lipids, liver function and HbA1c (glycated haemoglobin) at baseline revealed results which were within the standard reference range. Insulin and glucose levels as well as vascular function [FMD (flow-mediated dilation)] were measured at 0, 60 and 120 min. Compared with baseline, the control subjects did not exhibit any significant changes in glucose or insulin levels, whereas, in the OGTT group, blood glucose levels at both 60 (5.4±1.7 mmol/l) and 120 (5.0±1.1 mmol/l) min increased significantly relative to baseline (4.1±0.4 mmol/l; both P&lt;0.001) and, similarly, insulin levels were higher at both 60 (30.1±21.3 m-units/l) and 120 (34.9±23.6 m-units/l) min compared with baseline (4.7±4.3 m-units/l; both P&lt;0.001). Although blood glucose and insulin levels changed, FMD did not significantly differ between time-points or between groups. In summary, despite significantly elevated glucose and insulin concentrations in these subjects, we observed no change in vascular function, suggesting that acute elevations of glucose and insulin within the clinically normal range are not associated with impaired vascular function in vivo.
Renal aluminium handling in the rat: a micropuncture assessment
Authors: SHIRLEY David G. , WALTER Mary F. , WALTER Stephen J. , THEWLES Andrew , LOTE Christopher J. 
Published: July 2004

Uncertainties exist over the glomerular filtration of aluminium and virtually nothing is known about its segmental handling along the nephron. The present study has used micropuncture, combined with electrothermal atomic absorption spectroscopy, to determine directly the aluminium content of glomerular filtrate and of late PCTs (proximal convoluted tubules) and early distal tubules in anaesthetized Munich–Wistar rats infused with three different doses of aluminium citrate (plasma aluminium concentrations, 2.9±0.1, 5.2±0.4 and 10.0±0.9 μg·ml−1 respectively). Aluminium filtration into Bowman's space was found to be considerably greater than that predicted by an in vitro filtration system: in all three groups it was essentially filtered freely. No significant aluminium reabsorption took place along the PCT, but with every dose the FDAl (fractional delivery of aluminium; tubular fluid:plasma aluminium/inulin concentration ratio) was lower at the early distal site than at the late PCT (P&lt;0.001 in each case), indicating net aluminium reabsorption in the loop of Henle. This reabsorption amounted to 19–26% of the filtered aluminium load. In the low- and medium-dose groups, there was no significant difference between FDAl at the early distal site and that in the final urine; however, in the high-dose group, FDAl in the urine (1.02±0.06) exceeded that at the early distal tubule (0.75±0.04; P&lt;0.001), suggesting aluminium secretion in the distal nephron. The results indicate that aluminium loads, when complexed with citrate, are excreted efficiently owing to a combination of glomerular filtration and minimal reabsorption.
Pathophysiology of acute lung injury in combined burn and smoke inhalation injury
Authors: ENKHBAATAR Perenlei , TRABER Daniel L. 
Published: July 2004

In the U.S.A., more than 1 million burn injuries occur every year. Although the survival from burn injury has increased in recent years with the development of effective fluid resuscitation management and early surgical excision of burned tissue, the mortality of burn injury is still high. In these fire victims, progressive pulmonary failure and cardiovascular dysfunction are important determinants of morbidity and mortality. The morbidity and mortality increases when burn injury is associated with smoke inhalation. In the present review, we will describe the pathophysiological aspects of acute lung injury induced by combined burn and smoke inhalation and examine various therapeutic approaches.
MR imaging of displaced meniscal tears of the knee: Importance of a “disproportional posterior horn sign”
Authors: Chen H.C. , Hsu C.Y. , Shih T.T.F. , Huang K.M. , Li Y.W. 
Published: July 2004

Purpose: Meniscal tears associated with displaced fragments are clinically significant. We propose the "disproportional posterior horn sign" as a supportive criterion to identify a posterocentrally displaced meniscal fragment on MR imaging studies. If the meniscal posterior horn in the central portion appears larger than that in the peripheral section, it is considered positive for "disproportional posterior horn sign". Material and Methods: MR images obtained in 42 patients with 43 lesions, confirmed to have displaced meniscal tears, were included in this study. The MR images were retrospectively evaluated for the presence of the "disproportional posterior horn sign", as well as the other known signs. Results: The "disproportional posterior horn sign" was seen in 9 (20.9%) of 43 lesions, including 1 lateral discoid meniscal tear, 5 lateral meniscal tears and 3 medial meniscal tears. Five of them also had other signs of a displaced meniscal fragment. However, the remaining 4 cases only exhibited the "disproportional posterior horn sign". For the other MR signs, the "absent bow tie sign" was detected in 40 (93%) of 43 lesions, the "flipped meniscus sign" in 27 (62.8%) of 43 lesions, the "double posterior cruciate ligament sign" in 17 (39.5%) of 43 lesions and the "notch fragment sign" in 22 (51.2%) of 43 lesions. Conclusion: The "disproportional posterior horn sign" is helpful in demonstrating a posterocentrally displaced meniscal fragment, especially when other characteristic signs are unremarkable or absent.
Classification and Consequences of Errors in Otolaryngology
Authors: Shah Rahul K. , Kentala Erna , Healy Gerald B. , Roberson David W. 
Published: July 2004

AbstractObjective: To develop a preliminary classification system for errors in otolaryngology.Methods: A retrospective, anonymous survey was distributed to 2,500 members of the American Academy of Otolaryngology–Head and Neck Surgery (AAO‐HNS). Respondents were asked whether an error had occurred in their practice in the last 6 months, and if so, to describe the error, its consequences, and any corrective action taken.Results: There were 466 (18.6%) responses. Two hundred ten (45% of respondents) otolaryngologists reported 216 errors. A classification system for errors in otolaryngology was developed. Errors were classified as related to history and physical (1.4%), differential or final diagnosis (1.4%), testing (10.4%), surgical planning (9.9%), wrong‐site surgery (6.1%), anesthesia‐related (3.3%), wrong drug/dilution on the surgical field (3.8%), technical (19.3%), retained foreign body (0.9%), equipment‐related (9.4%), postoperative care (8.5%), medical management (13.7%), nursing/ancillary (0.5%), administrative (6.6%), communication (3.8%), and miscellaneous (0.9%). There were 78 cases of major morbidity and 9 deaths. If these data are representative, there may be more than 2,600 episodes of major morbidity and more than 165 deaths related to medical error in otolaryngology patients annually.Conclusions: Human error in otolaryngology occurs in all practice components, including diagnostic, treatment, surgical, communication, and administrative. Types of errors reported by otolaryngologists differ from those reported by other specialists. Error classification systems may need to reflect each specialty's realm of practice. Errors in otolaryngology cause appreciable morbidity and mortality. Quantitative study of errors and the development of targeted prevention and amelioration strategies should be a high priority.
Diagnosis and Surgical Management of Nasopalatine Duct Cysts
Authors: Elliott Kimberly A. , Franzese Christine B. , Pitman Karen T. 
Published: July 2004

AbstractObjectives/Hypothesis: Nasopalatine duct cysts are the most common cystic lesion of nonodontogenic origin of the maxilla. The purposes of the study were to review the epidemiology and clinical presentation, to describe the radiographic and pathological findings, and to discuss surgical management of this entity.Study Design: Case presentations of two patients with nasopalatine duct cysts at a tertiary care institution with a review of the English medical literature from January 1960 to the present.Methods: A 69‐year‐old man presented with an asymptomatic swelling of the premaxilla, and a 17‐year‐old woman presented with a painful swelling of the hard palate. A computed tomography scan, fine‐needle aspiration, and preoperative workup were obtained in both cases. Literature was reviewed with respect to epidemiology, etiology, presentation, diagnostic studies, operative management, and recurrence rates.Results: Computed tomography scan demonstrated midline ovoid cystic lesions in both cases. Fine‐needle aspiration of both lesions revealed no evidence of malignancy. Surgical treatment consisted of enucleation in the first case and marsupialization in the second case. Both patients did well with no evidence of recurrence. Nasopalatine duct cyst presents in the fourth to sixth decades of life with a male predilection. Recurrence rates range from 0% to 11%.Conclusion: Nasopalatine duct cyst occurs in approximately 1% of the population. Presentation may be asymptomatic or include swelling, pain, and drainage from the hard palate. A well‐circumscribed, round, ovoid, or heart‐shaped radiolucency is seen on computed tomography. Pathological findings reveal squamous or respiratory cell types, or a combination of these, infiltrated by inflammatory cells. Enucleation is the preferred treatment with low recurrence rates.
Respiratory Retraining of Refractory Cough and Laryngopharyngeal Reflux in Patients With Paradoxical Vocal Fold Movement Disorder
Authors: Murry Thomas , Tabaee Abtin , Aviv Jonathan E. 
Published: July 2004

AbstractObjectives/Hypothesis: The objective was to describe a case series of patients with refractory cough and paradoxical vocal fold movement disorder treated with respiratory retraining therapy.Study Design: Retrospective review of a case series in a tertiary medical care center.Methods: Five patients with laryngopharyngeal reflux were identified with refractory cough and paradoxical fold movement disorder on transnasal fiberoptic laryngoscopy by a greater than 50% reduction in airway during inspiration. The were four women and one man (age range, 42–67 y). All patients had normal forced vital capacity and forced expiratory flow but decreased ratio of forced inspiratory volume at 0.5 seconds (FIV0.5) to forced inspiratory vital capacity (FIVC) before starting therapy. All patients were treated with more than 6 months of twice‐daily proton pump inhibitor therapy with improvement in reflux symptoms but persistent and severe daytime cough. They were subsequently treated with respiratory retraining therapy. Patients were asked to rate subjectively the severity of cough at the onset and conclusion of therapy. All patients underwent pulmonary function testing before and after therapy. Long‐term follow‐up ranged from 5 to 17 months.Results: Patients received two to seven sessions of respiratory retraining therapy. The mean severity score changed from 9.2 before therapy to 1.3 after therapy. All patients subjectively described an improvement in the severity of their cough. Transnasal flexible laryngoscopy demonstrated improvement in paradoxical vocal fold movement, and pulmonary function testing showed improvement in the FIV0.5/FIVC ratio.Conclusion: Patients with laryngopharyngeal reflux and refractory cough in the absence of pulmonary disease should be evaluated for paradoxical vocal fold movement disorder. Respiratory retraining therapy may represent an effective therapy for cough in the absence of relief from standard management of laryngopharyngeal reflux.