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OBJECTIVES: Progress on health equity will require a robust metric. The aim of this article is to propose a new health equity metric that is distinct from existing measures and that allows meaningful comparisons across time and place, is calculable using health data typically available, and measures health equity across all major forms of social exclusion. STUDY DESIGN: A cross-sectional study. METHODS: The new health equity measure was calculated using data included from all 50 states and the District of Columbia in the 2017 Behavioral Risk Factor Surveillance Survey, collected by the US Centers for Disease Control and Prevention. The total sample size was 287,602. State-specific sample sizes ranged from 2269 (Alaska) to 14,685 (Kansas) with a median of 4452. A Healthy Days measure was calculated as the mean number of days that the respondents reported being physically healthy and mentally healthy out of the previous 30 days. The proposed measure defines individual health disutility as the distastefulness associated with one's health falling short of optimal achievable health, instrumentalized as the median health of the most socially privileged category, that of upper-income white men. The value of the health equity metric in a population is the mean value of this distastefulness over the entire population and has a theoretical range of -∞ to 1. RESULTS: There is substantial variation across states (mean: 0.13; standard deviation: 0.15), with the District of Columbia (0.48), Minnesota (0.37), and Connecticut (0.30) showing the greatest health equity, and West Virginia (-0.26), Arkansas (-0.18), and Kentucky (-0.13) exhibiting the least. Across states, the value of the health equity metric is not correlated with the size of black-white health disparities. CONCLUSIONS: It is feasible to use a single health equity metric for consistent and objective measurement of health equity. Doing so may facilitate more rapid progress toward health equity.

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PURPOSE OF THE STUDY Decision-making in treatment of an acute compartment syndrome is based on clinical assessment, supported by invasive monitoring. Thus, evolving compartment syndrome may require repeated pressure measurements. In suspected cases of potential compartment syndromes clinical assessment alone seems to be unreliable. The objective of this study was to investigate the feasibility of a non-invasive application estimating whole compartmental elasticity by ultrasound, which may improve accuracy of diagnostics. MATERIAL AND METHODS In an in-vitro model, using an artificial container simulating dimensions of the human anterior tibial compartment, intracompartmental pressures (p) were raised subsequently up to 80 mm Hg by infusion of saline solution. The compartmental depth (mm) in the cross-section view was measured before and after manual probe compression (100 mm Hg) upon the surface resulting in a linear compartmental displacement (Δd). This was repeated at rising compartmental pressures. The resulting displacements were related to the corresponding intra-compartmental pressures simulated in our model. A hypothesized relationship between pressures related compartmental displacement and the elasticity at elevated compartment pressures was investigated. RESULTS With rising compartmental pressures, a non-linear, reciprocal proportional relation between the displacement (mm) and the intra-compartmental pressure (mm Hg) occurred. The Pearson's coefficient showed a high correlation (r2 = -0.960). The intraobserver reliability value kappa resulted in a statistically high reliability (κ = 0.840). The inter-observer value indicated a fair reliability (κ = 0.640). CONCLUSIONS Our model reveals that a strong correlation between compartmental strain displacements assessed by ultrasound and the intra-compartmental pressure changes occurs. Further studies are required to prove whether this assessment is transferable to human muscle tissue. Determining the complete compartmental elasticity by ultrasound enhancement, this application may improve detection of early signs of potential compartment syndrome. Key words: compartment syndrome, intra-compartmental pressure, non-invasive diagnostic, elasticity measurement, elastography.

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PURPOSE: Postmastectomy chest wall radiation therapy using electron-beam therapy has been reported to increase lung radiation dose and the potential for pneumonitis. These reports describe treatment with varying energy electron beams prescribed to the breast/chest wall junction. Because the tissue at risk includes dermal lymphatics and subcutaneous tissues, low-energy electron beams may reduce lung radiation dose and the incidence of pneumonitis yet preserve good local control. At the University of Louisville, patients who have undergone mastectomy are treated with 6-MeV electron beam and bolus. PATIENTS AND METHODS: From 1985 through 1998, 273 patients underwent postmastectomy radiation therapy at the University of Louisville. The chest wall was treated using 6-MeV electron beam with 5-mm bolus prescribed to the 90% isodose-line, ensuring adequate dermal lymphatic dose. Internal mammary nodes were treated with electron-beam energy sufficient to treat to depth (approximately 15 MeV). Supraclavicular nodes were treated using 6-MV photon beam. Patients' charts were reviewed with respect to complications and outcome. RESULTS: Radiation pneumonitis was confirmed in one case (0.4%). The pneumonitis resolved with prednisone treatment. Twenty patients experienced locoregional failure (7.3%), 14 of whom failed in the chest wall (5.1%). DISCUSSION: Local control in our study is excellent and comparable to results expected for postmastectomy radiation therapy as reported in the literature. We conclude that postmastectomy patients can be treated with low-energy electron beam radiation therapy, protecting underlying lung without sacrificing local disease control.

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Long QT syndrome (LQTS) is the prototype of the cardiac ion channelopathies which cause syncope and sudden death. LQT1, due to mutations of KCNQ1 (KVLQT1), is the most common form. This study describes the genotype-phenotype characteristics in 10 families with mutations of KCNQ1, including 5 novel mutations. One hundred and two families with a history of lethal cardiac events, 55 LQTS, 9 Brugada syndrome, 18 idiopathic ventricular fibrillation (IVF), and 20 acquired LQTS, were studied by single-strand conformational polymorphism (SSCP) and DNA sequence analyzes. Families found to have KCNQ1 mutations were phenotyped using ECG parameters and cardiac event history, and genotype-phenotype correlation was performed. No mutations were found in Brugada syndrome, IVF, or acquired LQTS families. Ten out of 55 LQTS families had KCNQ1 mutations and 62 carriers were identified. Mutations included G269S in domain S5; W305X, G314C, Y315C, and D317N in the pore region; A341E and Q357R in domain S6; and 1338insC, G568A and T587M mutations in the C-terminus. W305X, G314C, Q357R, 1338insC, and G568A, appeared to be novel mutations. Gene carriers were 26 +/- 19 years (32 females). Baseline QTc was 0.47 +/- 0.03 s (range 0.40-0.57 s) and 40% had normal to borderline QTc (< or = 0.46 s). Typical LQT1 T wave patterns were present in at least one affected member of each family, and in 73% of all affected members. A history of cardiac events was present in 19/62 (31%), 18 with syncope, 2 with aborted cardiac arrest (ACA) and six with sudden death (SD). Two out of 6 SDs (33%) occurred as the first symptom. No difference in phenotype was evident in pore vs. non-pore mutations. KCNQ1 mutations were limited to LQTS families. All five novel mutations produced a typical LQT1 phenotype. Findings emphasize (1) reduced penetrance of QTc and symptoms, resulting in diagnostic challenges, (2) the problem of sudden death as the first symptom (33% of those who died), and (3) genetic testing is important for identification of gene carriers with reduced penetrance, in order to provide treatment and to prevent lethal cardiac arrhythmias and sudden death.

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CONTEXT: The benefits of continuity of pediatric care remain controversial. OBJECTIVE: To determine whether there is an association between having a continuous relationship with a primary care pediatric provider and decreased risk of emergency department (ED) visitation and hospitalization. DESIGN: Retrospective cohort study. Setting and Population. We used claims data from 46 097 pediatric patients enrolled at Group Health Cooperative, a large staff-model health maintenance organization, between January 1, 1993, and December 31, 1998, for our analysis. To be eligible, patients had to have been continuously enrolled for at least a 2-year period or since birth and to have made at least 4 visits to one of the Group Health Cooperative clinics. MAIN EXPOSURE VARIABLE: A continuity of care (COC) index that quantifies the degree to which a patient has experienced continuous care with a provider. MAIN OUTCOME MEASURES: ED utilization and hospitalization. RESULTS: Compared with children with the highest COC, children with medium continuity were more likely to have visited the ED (hazard ratio [HR]: 1.28 [1.20-1.36]) and more likely to be hospitalized (HR: 1.22 [1.09-1.38]). Children with the lowest COC were even more likely to have visited the ED (HR: 1.58 [1.49-1.66]) and to be hospitalized (HR: 1.54 [1.33-1.75]). These risks were even greater for children on Medicaid and those with asthma. CONCLUSIONS: Lower continuity of primary care is associated with higher risk of ED utilization and hospitalization. Efforts to improve and maintain continuity may be warranted.

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CONTEXT: Prescribing practices for otitis media are not consistent with current evidence-based recommendations. OBJECTIVE: To determine whether point-of-care evidence delivery regarding the use and duration of antibiotics for otitis media decreases the duration of therapy from 10 days and decreases the frequency of prescriptions written. DESIGN: Randomized, controlled trial. SETTING: Primary care pediatric clinic affiliated with university training program. Intervention. A point-of-care evidence-based message system presenting real time evidence to providers based on their prescribing practice for otitis media. MAIN OUTCOME MEASURES: Proportion of prescriptions for otitis media that were for <10 days and frequency with which antibiotics were prescribed. RESULTS: Intervention providers had a 34% greater reduction in the proportion of time they prescribed antibiotics for <10 days. Intervention providers were less likely to prescribe antibiotics than were control providers. CONCLUSIONS: A point-of-care information system integrated into outpatient pediatric care can significantly influence provider behavior for a common condition.

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OBJECTIVE: To evaluate the use of positron emission tomography using [(18)F]-fluorodeoxyglucose (FDG-PET) to assess the response to neoadjuvant radiotherapy and chemotherapy in patients with locally advanced esophageal cancer. SUMMARY BACKGROUND DATA: Imaging modalities, including endoscopy, endoscopic ultrasound, computed tomography, and magnetic resonance imaging, currently used to evaluate response to neoadjuvant treatment in esophageal cancer do not reliably differentiate between responders and nonresponders. METHODS: Twenty-seven patients with histopathologically proven squamous cell carcinoma of the esophagus, located at or above the tracheal bifurcation, underwent neoadjuvant therapy consisting of external-beam radiotherapy and 5-fluorouracil as a continuous infusion. FDG-PET was performed before and 3 weeks after the end of radiotherapy and chemotherapy (before surgery). Quantitative measurements of tumor FDG uptake were correlated with histopathologic response and patient survival. RESULTS: After neoadjuvant therapy, 24 patients underwent surgery. Histopathologic evaluation revealed less than 10% viable tumor cells in 13 patients (responders) and more than 10% viable tumor cells in 11 patients (nonresponders). In responders, FDG uptake decreased by 72% +/- 11%; in nonresponders, it decreased by only 42% +/- 22%. At a threshold of 52% decrease of FDG uptake compared with baseline, sensitivity to detect response was 100%, with a corresponding specificity of 55%. The positive and negative predictive values were 72% and 100%. Nonresponders to PET scanning had a significantly worse survival after resection than responders. CONCLUSION: FDG-PET is a valuable tool for the noninvasive assessment of histopathologic tumor response after neoadjuvant radiotherapy and chemotherapy.

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In clinical cardiology, deceleration-dependent QT interval shortening is considered to be an extraordinary electrocardiographic phenomenon. We present an early premature born 4-year-old African-American girl with complications related to her premature birth, developmental delay, and several episodes of cardiac arrest. An episode of severe transient bradyarrhythmia was documented on Holter monitoring. The unique feature of the rhythm strips was paradoxical gradual shortening of the QT interval to 216 ms with accompanying transient T-waves abnormalities. The activation of the Ik, ACh due to an unusually high vagal discharge to the heart is proposed as a possible mechanism responsible for both slowing of the heart rate and shortening of the QT interval.

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AIMS: The purpose of our study was to investigate the electrical trigger modes of monomorphic ventricular tachycardia, by analysing stored intracardiac electrograms, and to identify haemodynamic or electrocardiographic predictors in patients with cardioverter-defribrillators. METHODS: We recorded 286 episodes of monomorphic ventricular tachycardia in 38 patients with at least three events. The electrical triggers were characterized by the morphology number, complexity, and coupling interval of premature depolarizations preceding the ventricular tachycardia. We also evaluated clinical and electrocardiographic data. RESULTS: We found two basic electrical trigger modes. Two hundred and sixteen events (75%) were observed to have no RR-interval variations before onset, while 70 episodes (25%) had a short-long-short sequence. These episodes invariably featured increased QT disperson. In 31 of 38 patients (82%), the ventricular tachycardias were always initiated by the same mode of onset. In eight patients, the monomorphic ventricular tachycardias were always triggered by short-long-short sequences. In seven patients, more than one onset mechanism was observed. CONCLUSIONS: Two basic modes of onset were responsible for monomorphic ventricular tachycardia: one without RR-interval variations immediately prior to onset and another characterized by short-long-short sequences and increased QT dispersion. The mechanisms were largely patient-specific and not related to cardiac diagnosis or left ventricular function.

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Charcot-Marie-Tooth disease (CMT) is the most common inherited neuropathy in humans and has been associated with a partial duplication of chromosome 17 (CMT type 1A). We have generated a transgenic rat model of this disease and provide experimental evidence that CMT1A is caused by increased expression of the gene for peripheral myelin protein-22 (PMP22, gas-3). PMP22-transgenic rats develop gait abnormalities caused by a peripheral hypomyelination, Schwann cell hypertrophy (onion bulb formation), and muscle weakness. Reduced nerve conduction velocities closely resemble recordings in human patients with CMT1A. When bred to homozygosity, transgenic animals completely fail to elaborate myelin. We anticipate that the CMT rat model will facilitate the identification of a cellular disease mechanism and serve in the evaluation of potential treatment strategies.

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Crystallization of the 1:1 molecular complex between the beta-lactamase TEM-1 and the beta-lactamase inhibitory protein BLIP has provided an opportunity to put a stringent test on current protein-docking algorithms. Prior to the successful determination of the structure of the complex, nine laboratory groups were given the refined atomic coordinates of each of the native molecules. Other than the fact that BLIP is an effective inhibitor of a number of beta-lactamase enzymes (KI for TEM-1 approximately 100 pM) no other biochemical or structural data were available to assist the practitioners in their molecular docking. In addition, it was not known whether the molecules underwent conformational changes upon association or whether the inhibition was competitive or non-competitive. All six of the groups that accepted the challenge correctly predicted the general mode of association of BLIP and TEM-1.

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OBJECTIVES: This study examined the angiographic characteristics, coronary risk factors and prognosis in young men and women with a history of myocardial infarction compared with that in older patients. BACKGROUND: There are few data regarding myocardial infarction in young adults. It is undetermined whether the development of myocardial infarction at a young age represents a form of coronary heart disease with an adverse prognosis. METHODS: Of the 8,839 patients with a history of myocardial infarction in the Coronary Artery Surgery Study (CASS), there were 294 men < or = 35 years old and 210 women < or = 45 years old. Coronary anatomy, baseline characteristics and prognosis were compared in younger and older patients. RESULTS: Young men and women more often had angiographically normal coronary arteries, nonobstructive disease < 70% stenosis and single-vessel disease than older patients (p < 0.0001). Current smoking was more frequent in young patients (p < 0.0001). Hypertension and diabetes were more frequent in both older men and women, whereas a positive family history of premature coronary disease was significantly more prevalent only in young men. The survival rate at 7 years was improved for young men compared with that in older men (84% vs. 75%, p = 0.0094) and for young women compared with that in older women (90% vs. 77%, p = 0.0004). When multivariate analysis was applied to the data, the survival advantage for young patients remained after adjustment. CONCLUSIONS: Young patients with a myocardial infarction have a favorable prognosis compared with that in older patients.

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BACKGROUND: Brain peptides alter most gastrointestinal functions, but their effects on gallbladder motility have not been examined in detail. METHODS: Studies were conducted in awake, male beagle dogs. RESULTS: Of 30 brain peptides evaluated, thyrotropin-releasing hormone (TRH) and calcitonin gene-related peptide (CGRP) inhibited CCK- and meal-induced gallbladder contraction. These responses were abolished by ganglionic blockade. Truncal vagotomy prevented the central inhibitory action of TRH but not that of CGRP, whereas noradrenergic blockade prevented the central inhibitory action of CGRP but not that of TRH. Muscarinic blockade did not prevent the relaxing effect of cerebral TRH but pretreatment with the vasoactive intestinal peptide (VIP) antagonist, (4Cl-D-Phe6-Leu17)VIP, significantly attenuated gallbladder relaxation induced by cerebral TRH: the combination of both VIP and muscarinic antagonists abolished TRH-induced gallbladder relaxation. alpha-Adrenergic receptor blockade but neither beta-adrenergic blockade nor adrenalectomy abolished gallbladder relaxation induced by cerebral CGRP. Intravenous infusion of VIP and norepinephrine inhibited CCK-induced gallbladder contraction and these responses were abolished dose dependently by intravenous infusion of (4Cl-D-Phe6-Leu17)VIP and phentolamine, respectively. CONCLUSIONS: Cerebral TRH inhibits canine gallbladder contraction by stimulation of vagal outflow and subsequent release of VIP acting via its specific receptor whereas cerebral CGRP inhibits gallbladder contraction by stimulation of sympathetic, noradrenergic outflow via alpha-adrenergic receptors.

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The central nervous system effects of thyrotropin-releasing hormone (TRH) and calcitonin gene-related peptide (CGRP) on exocrine pancreatic secretion were studied in freely moving rats. TRH (0.05-0.5 nmol) significantly stimulated, whereas CGRP (0.1-1.0 nmol) significantly inhibited, volume, protein, and bicarbonate secretion. Pretreatment of the animals with the ganglionic blocking agent chlorisondamine abolished the pancreatic responses produced by both peptides. In contrast, vagotomy abolished the stimulatory effect of TRH, whereas noradrenergic blockade with bretylium or phentolamine abolished the inhibitory effect of CGRP. Atropine significantly attenuated, but the vasoactive intestinal peptide (VIP) antagonist [D-p-Cl-Phe6, Leu17]VIP completely abolished the stimulatory effect of TRH. Pancreatic secretory responses stimulated by cerebral TRH or by peripheral VIP were inhibited dose dependently by peripheral [D-p-Cl-Phe6,Leu17]VIP. Inhibition of pancreatic secretion induced by cerebral CGRP or by peripheral norepinephrine was prevented by intravenous phentolamine. These results indicate 1) cerebral TRH stimulates and cerebral CGRP inhibits exocrine pancreatic secretion in freely moving rats; 2) the effects of TRH are mediated by vagal efferents, and the primary peripheral transmitter appears to be VIP acting on VIP receptors, whereas muscarinic efferents are less important; and 3) the effects of CGRP are mediated by sympathetic noradrenergic efferents via alpha-adrenergic receptors.

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Gastrointestinal secretory and motor responses are profoundly altered during stress; but the effects of stress and its mediator(s) on the two major gut functions, exocrine pancreatic secretion and gallbladder motility, are unknown. We therefore developed two animal models that allowed us to examine the effects of acoustic stress on canine gallbladder contraction and restraint stress on rat exocrine pancreatic secretion. Acoustic stress inhibited cholecystokinin-8 (CCK)- and meal-induced gallbladder contraction, and restraint stress inhibited basal and CCK/secretin-stimulated pancreatic secretion. These inhibitory responses were mimicked by cerebral injection of corticotropin-releasing factor (CRF) and abolished by the CRF antagonist, alpha-helical CRF-(9-41). The effects of stress and exogenous CRF were simulated by intravenous infusion of norepinephrine but prevented by ganglionic, noradrenergic, and alpha-adrenergic but not beta-adrenergic receptor blockade. Vagotomy, adrenalectomy, and--in rats--hypophysectomy did not alter the effects produced by stress and CRF. These results indicate that endogenous CRF released in response to different stressors in distinct species inhibits canine gallbladder contraction and murine exocrine pancreatic secretion via activation of sympathetic efferents. Release of norepinephrine appears to be the final common pathway producing inhibition of biliary and pancreatic digestive function during stress mediated by cerebral CRF.

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We hypothesized that developmental increases in both ventricular end-diastolic pressure (EDP) and the maximum time derivative of pressure (dP/dt) observed in stage 12 to 29 chick embryos are the result of observed cardiac cycle length (CL) decrease (heart rate increase). To test this hypothesis, we evaluated EDP and dP/dt changes that occur during acute CL alterations in the Hamburger-Hamilton stage 24 chick embryo (n = 18). Ventricular pressure measurements were obtained with a servo-null pressure system and digitally recorded at 500 samples/s. A 1-mm steel probe, heated (decrease CL) or cooled (increase CL), was applied to the sinus venosus. The average baseline CL was 454 ms. The heart rate perturbation resulted in CL that varied over a range of 200-2966 ms, assimilating the range of CL change observed during development. Changes in EDP ranged from 0.014 to 0.130 kPa (baseline = 0.061 kPa) and maximum dP/dt ranged from 0.33 to 13.33 kPa/s (baseline = 5.99) kPa/s). In each study, EDP varied directly with CL (R2 = 0.70). Conversely, maximum dP/dt changes were inversely related to CL alterations (R2 = 0.54). Thus, we found that there is a direct relationship between changes in CL and EDP in the stage 24 chick embryo, whereas CL and dP/dt vary inversely. During cardiac development, observed increases in maximum dP/dt may be attributed to CL decreases. In contrast, developmental increases in EDP cannot be explained by CL decrease and must be accounted for by maturational changes in cardiac function in the chick embryo.

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Bedside pulmonary artery catheterization has proven to be an important addition to the clinical assessment of critically ill patients. Properly used, the procedure may provide hemodynamic information that is not apparent from physical examination or radiography. It may be safely accomplished through various venous routes, but care must be taken to avoid potential complications.

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