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排序方式: 共有67条查询结果,搜索用时 31 毫秒
1.
Valentina Kutyifa MD PhD Scott McNitt MS Bronislava Polonsky MS Charles Lowenstein MD Kris Cutter MS Coeli Lopes PhD Wojciech Zareba MD PhD Arthur J. Moss MD 《Annals of noninvasive electrocardiology》2018,23(3)
Background
A comprehensive report on the clinical course of the three major genotypes of the long QT syndrome (LQTS) in a large U.S. patient cohort is lacking.Methods
Our study consisted of 1,923 U.S. subjects from the Rochester‐based LQTS Registry with genotype‐positive LQT1 (n = 879), LQT2 (n = 807), and LQT3 (n = 237). We evaluated the risk of a first cardiac event (syncope, aborted cardiac arrest, or sudden cardiac death, whichever occurred first) from birth through age 50 years. Cox proportional hazards regression models incorporating clinical covariates were used to assess genotype‐specific risk of cardiac events.Results
For all three genotypes, the cumulative probability of a first cardiac event increased most markedly during adolescence. Multivariate analysis identified proband status and QTc > 500 ms as predictors of cardiac events in all three genotypes, and males <14 years and females >14 years as predictors of cardiac events in LQT1 and LQT2 only. Beta‐blockers significantly reduced the risk of cardiac events in LQT1 (HR: 0.49, p = .002) and LQT2 patients (HR: 0.48, p = .001). A trend toward beta‐blocker benefit in reducing cardiac events was found in LQT3 females (HR: 0.32, p = .078), but not in LQT3 males (HR: 1.37, p = .611).Conclusion
Risk factors and outcomes in LQTS patients varied by genotype. In all three genotypes, proband status and prolonged QTc were risk factors for cardiac events. Younger males and older females experienced increased risk in LQT1 and LQT2 only. Beta‐blockers were most effective in reducing cardiac events in LQT1 and LQT2, with a potential benefit in LQT3 females.2.
3.
Andrew A. Young William Vine Bronislava R. Gedulin Richard Pittner Susan Janes Laura S.L. Gaeta Amy Percy Candace X. Moore Joy E. Koda Timothy J. Rink Kevin Beaumont 《Drug development research》1996,37(4):231-248
The pancreatic β-cell hormone, amylin, is absent or reduced in individuals with type I diabetes mellitus and in many insulin-treated patients with type II diabetes. Amylin replacement therapy may be beneficial in these individuals, but the pharmaceutically inconvenient physicochemical properties of native human amylin led to the development instead of the amylin agonist, [Pro25,28,29]human amylin, or pramlintide (formerly designated AC137). Here we compare for rat amylin, human amylin and pramlintide, receptor binding and biological actions in rats in vivo and in rat soleus muscle. In the rat, the spectrum of actions and pharmacokinetic and pharmacodynamic properties of pramlintide are either very similar to, or indistinguishable from, those of rat or human amylin. © 1996 Wiley-Liss, Inc. 相似文献
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Andrew A. Young Ming-Wei Wang Bronislava Gedulin Timothy J. Rink Richard Pittner Kevin Beaumont 《Metabolism: clinical and experimental》1995,44(12)
During the development of synthetic calcitonins for therapeutic use in bone disease, a “diabetogenic” (hyperglycemic) effect was observed, particularly with salmon calcitonin. The effect was attributed by some to inhibition of insulin secretion. We have recently reported high-affinity (28 pmol/L) amylin-binding sites in certain areas of rat brain, and found that these sites also bind salmon but not rat calcitonin with comparable high affinity. Rat amylin and salmon calcitonin have been determined to have significant structural homology. In vitro and in vivo studies indicate that rat amylin can exert calcitonin-like effects on osteoclasts and on plasma calcium. Here we report that salmon calcitonin mimics the actions of rat amylin on skeletal muscle glycogen metabolism in vitro; it stimulates glycogenolysis and inhibits incorporation of radiolabeled glucose into glycogen (50% effective concentration [EC50], 0.4 ± 0.11 nmol/L log and 8.4 ± 0.05 nmol/L log, respectively). In anesthetized rats salmon calcitonin, like rat amylin, rapidly increases plasma lactate concentration, followed by a slower increase in glucose concentration. Like amylin, salmon calcitonin also inhibits the insulin response to 2 mmol infused glucose (insulin increments suppressed by 52% and 57% at 10 minutes for salmon calcitonin and amylin). Other shared actions, such as suppression of appetite, stimulation of renin secretion, inhibition of gastric acid secretion, and inhibition of gastric emptying, further affirm our proposal that the exogenous peptide, salmon calcitonin, is a mimic of endogenous amylin in the rat. 相似文献
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Daniela Knafelz Fabio Panetta Lidia Monti Fiammetta Bracci Bronislava Papadatou Giuliano Torre Luigi Dall’Oglio Antonella Diamanti 《World journal of gastroenterology : WJG》2013,19(31):5204-5206
It is reported that a pancreatic disease may precede the diagnosis of inflammatory bowel disease(IBD) both in children and in adults.Idiopathic chronic pancreatitis,however,occasionally co-exists with the IBD,mainly at pediatric age.We report a case of a patient who progressively developed the features of a chronic pancreatitis,before the diagnosis of Crohn’s Disease(CD).Ten months after the onset of the first episode of pancreatitis the patient developed bloody diarrhea,mucus stools and biochemical findings of inflammation.The colonoscopy revealed a diffuse colitis without involvement of the last loop and the gastroscopy showed inflammation of the iuxta-papillary area.The histological findings confirmed the diagnosis of CD that involved the colon and the duodenum.In conclusion,in children the idiopathic chronic pancreatitis may be an unusual presentation of CD.Thus,if other known cause of chronic pancreatitis are not found,a not invasive work up to exclude the IBD should be warranted.An early coincidental diagnosis of the IBD may delay the progression of the pancreatic disease. 相似文献
7.
Ivan Gut Ylva Terelius Emil Frantík Igor Linhart Pavel Souček Bronislava Filipcová Hana Klučková 《Archives of toxicology》1993,67(4):237-243
Benzene (B), toluene (T), ethylbenzene (EB), styrene (S) and xylene isomers (oX, mX, pX) are important environmental pollutants and B is a proved human carcinogen. Their inhalation by male Wistar rats (4 mg/1,20 h/day, 4 days) caused cytochrome P450 (P450) induction. The degree of P450 2B1 induction increased and that of 2E1 decreased in the series B, T, EB, S, oX, mX and pX, as estimated by Western blots, while neither solvent was as effective for 2B1 induction as phenobarbital and B was more effective for 2E1 than ethanol. The levels of several other P450s decreased after exposure to these solvents, B being most effective. Exposure to these solvents increased in vitro hepatic microsomal oxidation of B and aniline (AN) (2E1 substrates) 3 to 6-fold, indicating induction of this P450. T oxidation was increased 2 to 4-fold and chlorobenzene (ClB) oxidation 3-fold. Sodium phenobarbital (PB, 80 mg/kg/day, 4 days, i.p.) did not increase ethylmorphine (EM) and benzphetamine (BZP) demethylation (2B1 substrates), neither of the B derivatives did so, and oX decreased it; however, pentoxyresorufin O-dealkylation was well related to the immunochemically detected 2B1 levels in control, PB and B microsomes. PB did not increase B, but increased T and C1B oxidation 2–4 and 3-fold, respectively, indicating possible 2B1 role in their oxidation. B oxidation after various inducers was related to immunochemical 2E1 levels, T and C1B oxidation to both 2B1 and 2E1 and AN oxidation to 2E1 and 1A2 levels. Very efficient B oxidation by 2E1 at low B levels indicates that induction of 2E1 may contribute to B myelotoxicity in vivo more than any other P450 enzyme tested, especially considering the fact that B is the most efficient inducer of its metabolism. 相似文献
8.
Adams SH Lei C Jodka CM Nikoulina SE Hoyt JA Gedulin B Mack CM Kendall ES 《The Journal of nutrition》2006,136(1):195-201
In rodents, weight reduction after peptide YY[3-36] (PYY[3-36]) administration may be due largely to decreased food consumption. Effects on other processes affecting energy balance (energy expenditure, fuel partitioning, gut nutrient uptake) remain poorly understood. We examined whether s.c. infusion of 1 mg/(kg x d) PYY[3-36] (for up to 7 d) increased metabolic rate, fat combustion, and/or fecal energy loss in obese mice fed a high-fat diet. PYY[3-36] transiently reduced food intake (e.g., 25-43% lower at d 2 relative to pretreatment baseline) and decreased body weight (e.g., 9-10% reduction at d 2 vs. baseline) in 3 separate studies. Mass-specific metabolic rate in kJ/(kg x h) in PYY[3-36]-treated mice did not differ from controls. The dark cycle respiratory quotient (RQ) was transiently decreased. On d 2, it was 0.747 +/- 0.008 compared with 0.786 +/- 0.004 for controls (P < 0.001); light cycle RQ was reduced throughout the study in PYY[3-36]-treated mice (0.730 +/- 0.006) compared with controls (0.750 +/- 0.009; P < 0.001). Epididymal fat pad weight in PYY[3-36]-treated mice was approximately 50% lower than in controls (P < 0.01). Fat pad lipolysis ex vivo was not stimulated by PYY[3-36]. PYY[3-36] decreased basal gallbladder emptying in nonobese mice. Fecal energy loss was negligible ( approximately 2% of ingested energy) and did not differ between PYY[3-36]-treated mice and controls. Thus, negative energy balance after PYY[3-36] administration in diet-induced obese mice results from reduced food intake with a relative maintenance of mass-specific energy expenditure. Fat loss and reduced RQ highlight the potential for PYY[3-36] to drive increased mobilization of fat stores to help meet energy requirements in this model. 相似文献
9.
Cost-effectiveness of screening BRCA1/2 mutation carriers with breast magnetic resonance imaging 总被引:8,自引:0,他引:8
Plevritis SK Kurian AW Sigal BM Daniel BL Ikeda DM Stockdale FE Garber AM 《JAMA》2006,295(20):2374-2384
Context Women with inherited BRCA1/2 mutations are at high risk for breast cancer, which mammography often misses. Screening with contrast-enhanced breast magnetic resonance imaging (MRI) detects cancer earlier but increases costs and results in more false-positive scans. Objective To evaluate the cost-effectiveness of screening BRCA1/2 mutation carriers with mammography plus breast MRI compared with mammography alone. Design, Setting, and Patients A computer model that simulates the life histories of individual BRCA1/2 mutation carriers, incorporating the effects of mammographic and MRI screening was used. The accuracy of mammography and breast MRI was estimated from published data in high-risk women. Breast cancer survival in the absence of screening was based on the Surveillance, Epidemiology and End Results database of breast cancer patients diagnosed in the prescreening period (1975-1981), adjusted for the current use of adjuvant therapy. Utilization rates and costs of diagnostic and treatment interventions were based on a combination of published literature and Medicare payments for 2005. Main Outcome Measures The survival benefit, incremental costs, and cost-effectiveness of MRI screening strategies, which varied by ages of starting and stopping MRI screening, were computed separately for BRCA1 and BRCA2 mutation carriers. Results Screening strategies that incorporate annual MRI as well as annual mammography have a cost per quality-adjusted life-year (QALY) gained ranging from less than $45 000 to more than $700 000, depending on the ages selected for MRI screening and the specific BRCA mutation. Relative to screening with mammography alone, the cost per QALY gained by adding MRI from ages 35 to 54 years is $55 420 for BRCA1 mutation carriers, $130 695 for BRCA2 mutation carriers, and $98 454 for BRCA2 mutation carriers who have mammographically dense breasts. Conclusions Breast MRI screening is more cost-effective for BRCA1 than BRCA2 mutation carriers. The cost-effectiveness of adding MRI to mammography varies greatly by age. 相似文献
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