288 Anti-TNF Withdrawal in IBD: Relapse and Recapture Rates and Predictive Factors From 160 Patients in a Pan-UK Study
Nicholas A. KennedyBenjamin D. WarnerEmma JohnstonLucy FlandersPhilip HendyNik S. DingRichard HarrisAdam S. FadraCatriona BasquillChristopher A LambFiona CameronAbhey SinghJoy MasonChristos ChristodoulouCatherine StansfieldEmma NowellUmesh BasavarajuDavid C. WilsonJohn ThomsonSimon LalMiles ParkesRichard K. RussellIan GoodingTariq AhmadDaniel R. GayaJohn MansfieldStephen MannJames O. LindsayJ GordonAilsa HartSara McCartneyPeter M. IrvingJack SatsangiCharlie W. Lees
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Mark and recapture
Biologists often estimate separate survival and movement rites from radiotelemetry and markrecapture data from the same study population.We describe a method for combining these data types in a single model to obtain joint, potentially less biased estimates of survival and movement that use all available data.We furnish an example using wood thrushes (Hylocichla mustelina) captured at the Piedmont National Wildlife Refuge in central Georgia in 1996.The model structure allows estimation of survival and capture probabilities, as well as estimation of movements away from and into the study area.In addition, the model structure provides many possibilities for hypothesis testing.Using the combined model structure, we estimated that weekly survival of wood thrushes was 0.989 ?0.007 (-SE).Survival rates of banded and radiomarked individuals were not different (&[Sradioed, Sbanded] = log[Sradioed/Sbanded] = 0.0239, 95% CI = -0.0196 to 0.0486).Fidelity rates (weekly probability of remaining ih a stratum) did not differ between geographic strata (4 = 0.911 ?0.020; a&["11, •22] = 0.0161, 95% CI = -0.0309 to 0.0631), and recapture rates (p = 0.097 + 0.016) of banded and radiomarked individuals were not different (&[Pradioed, Pbandedl = 0.145, 95% CI = -0.510 to 0.800).Combining these data types in a common model resulted in more precise estimates of movement and recapture rates than separate estimation, but ability to detect stratum or mark-specific differences in parameters was weak.We conducted simulation trials to investigate the effects of varying study designs on parameter accuracy and statistical power to detect important differences.Parameter accuracy was high (relative bias [RBIAS] <2%) and confidence interval coverage close to nominal, except for survival estimates of banded birds for the "off study area" stratum, which were negatively biased (RBIAS -7 to -15%) when sample sizes were small (5-10 banded or radioed animals "released" per time interval).To provide adequate data for useful inference from this model, study designs should seek a minimum of 25 animals of each marking type observed (marked or observed via telemetry) in each time period and geographic stratum.
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USE AND LIMITATIONS OF THE CAPTURE-RECAPTURE METHOD IN DISEASE MONITORING WITH TWO DEPENDENT SOURCES
Capture-recapture techniques are employed increasingly to correct for underascertainment of cases in epidemiologic surveillance. A key assumption of the basic two-source capture-recapture method is the independence of sources, which is often violated in practice. This paper provides a quantitative comparison of the performance of the capture-recapture method and the traditional registration approach in disease monitoring with two dependent sources. If sources are negatively dependent, underascertainment of cases by the traditional registration approach is transformed into overestimation of case numbers with the capture-recapture method. This over-estimation can be extreme under certain conditions. Application of the capture-recapture method is therefore discouraged if negative source dependence is of concern. In other situations, the capture-recapture method can be a valuable tool to correct for underascertainment of cases. Although the correction remains imperfect if notifications from both sources are positively dependent, underestimation of case numbers is typically much less severe than with the traditional registration approach. I illustrate the findings for a broad range of registration scenarios and provide empirical examples from population-based cancer registration. I also discuss strategies that may minimize the degree of source dependence in the design and analysis of capture-recapture studies.
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Corticosterone (CORT) and other glucocorticoids cause peripheral insulin resistance and compensatory increases in β-cell mass. A prolonged high-fat diet (HFD) induces insulin resistance and impairs β-cell insulin secretion. This study examined islet adaptive capacity in rats treated with CORT and a HFD. Male Sprague-Dawley rats (age ∼6 weeks) were given exogenous CORT (400 mg/rat) or wax (placebo) implants and placed on a HFD (60% calories from fat) or standard diet (SD) for 2 weeks (N = 10 per group). CORT-HFD rats developed fasting hyperglycemia (>11 mM) and hyperinsulinemia (∼5-fold higher than controls) and were 15-fold more insulin resistant than placebo-SD rats by the end of ∼2 weeks (Homeostatic Model Assessment for Insulin Resistance [HOMA-IR] levels, 15.08 ± 1.64 vs 1.0 ± 0.12, P < .05). Pancreatic β-cell function, as measured by HOMA-β, was lower in the CORT-HFD group as compared to the CORT-SD group (1.64 ± 0.22 vs 3.72 ± 0.64, P < .001) as well as acute insulin response (0.25 ± 0.22 vs 1.68 ± 0.41, P < .05). Moreover, β- and α-cell mass were 2.6- and 1.6-fold higher, respectively, in CORT-HFD animals compared to controls (both P < .05). CORT treatment increased p-protein kinase C-α content in SD but not HFD-fed rats, suggesting that a HFD may lower insulin secretory capacity via impaired glucose sensing. Isolated islets from CORT-HFD animals secreted more insulin in both low and high glucose conditions; however, total insulin content was relatively depleted after glucose challenge. Thus, CORT and HFD, synergistically not independently, act to promote severe insulin resistance, which overwhelms islet adaptive capacity, thereby resulting in overt hyperglycemia.
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본 연구는 capture-recapture 방법을 통해 두 가지 종류의 데이터를 결합하여 장애 인구수를 추정 하는 것이다. 이를 위해 데이터가 두 가지인 경우에 활용할 수 있는 여러 capture-recapture 추정 방법에 대해 살펴보았다. 등록 장애인 명부와 2017년 장애인 실태조사를 이용하여 기존 장애인구 수 추정 방안을 검토하고 기존의 추정량과 capture-recapture 방법을 활용한 추정량을 비교하여 효율적인 추정 방안을 고찰하였다. capture-recapture 방법을 사용한 추정량은 기존 장애 인구수 추정량보다 더 작은 분산 추정값을 갖고, 보정 가중치를 사용한 추정량은 기존 장애 인구수 추정량과 같은 추정값이지만 보다 적은 평균제곱오차값을 갖는 것을 확인하였다. 이 연구를 통해 여러한 조사 데이터로부터 모집단의 크기를 추정함에 있어 capture-recapture 방법을 활용할 수 있음을 확인하였다.
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The effect of 48 h of fasting in C57B1/6J-ob/ob and +/+ mice on body weight (BW), blood glucose (BG), serum immunreactive insulin (IRI), plasma immunoreactive glucagon (IRG) and on tissue levels of cyclic adenosine monophosphate (cAMP) were studied. Both groups of mice lost weight and demonstrated a decrease in BG and IRI with fasting. However, the BG and IRI of the ob/ob animals were initially highter and remained higher than those of the 2% of their initial weight while the +/+ lost 14 %. The +/+ mice exhibited an increase in cAMP levels in skeletal muscle, fat and liver with fasting, while the ob/ob mice had increased levels of cAMP in fat, but not in muscle. They also had a paradoxical decrease in liver cAMP levels with fasting, and associated with this was the lack of stimulation of glycogenolysis. Glycogenolysis was significant in the livers of fasted +/+ mice. The plasma IRG levels of the fed ob/ob mice were significantly higher (1.8) times) than those of the fed +/+ mice. Islet cAMP levels were decreased with fasting in ob/ob mice. However, the levels were significantly higher in 48-h faster ob/ob mice compared to the fasted +/+ group. The apparent paradoxical response to fasting observed in the livers of the ob/ob mice remains unexplained.
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Abstract Dysregulation of the adipoinsular axis in male obese Zucker diabetic fatty (ZDF; fa/fa) rats, a model of type 2 diabetes, results in chronic hyperinsulinemia and increased de novo lipogenesis in islets, leading to β-cell failure and diabetes. Diazoxide (DZ; 150 mg/kg·d), an inhibitor of insulin secretion, was administered to prediabetic ZDF animals for 8 wk as a strategy for prevention of diabetes. DZ reduced food intake (P < 0.02) and rate of weight gain only in ZDF rats (P < 0.01). Plasma insulin response to glucose load was attenuated in DZ-Zucker lean rats (ZL; P < 0.01), whereas DZ-ZDF had higher insulin response to glucose than controls (P < 0.001). DZ improved hemoglobin A1c (P < 0.001) and glucose tolerance in ZDF (P < 0.001), but deteriorated hemoglobin A1c in ZL rats (P < 0.02) despite normal tolerance in the fasted state. DZ lowered plasma leptin (P < 0.001), free fatty acid, and triglyceride (P < 0.001) levels, but increased adiponectin levels (P < 0.02) only in ZDF rats. DZ enhanced β3-adrenoreceptor mRNA (P < 0.005) and adenylate cyclase activity (P < 0.01) in adipose tissue from ZDF rats only, whereas it enhanced islet β3- adrenergic receptor mRNA (P < 0.005) but paradoxically decreased islet adenylate cyclase activity (P < 0.005) in these animals. Islet fatty acid synthase mRNA (P < 0.03), acyl coenzyme A carboxylase mRNA (P < 0.01), uncoupling protein-2 mRNA (P < 0.01), and triglyceride content (P < 0.005) were only decreased in DZ-ZDF rats, whereas islet insulin mRNA and insulin content were increased in DZ-ZDF (P < 0.01) and DZ-ZL rats (P < 0.03). DZ-induced β-cell rest improved the lipid profile, enhanced the metabolic efficiency of insulin, and prevented β-cell dysfunction and diabetes in diabetes-prone animals. This therapeutic strategy may be beneficial in preventing β-cell failure and progression to diabetes in humans.
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In normal rats, females have higher circulating GH-binding protein (GHBP) levels than males, whereas in the GH-deficient dwarf (Dw) rat, there is no sexual dimorphism in plasma GHBP, suggesting that GH secretion may be involved in this difference. In order to study the relationship between gonadal steroids and GH on GHBP and GH receptor regulation, the levels of plasma GHBP, hepatic bovine GH, and human GH (hGH) binding as well as GHBP and GH receptor messenger RNA (mRNA) have now been studied in normal, Dw, hypophysectomized (Hx), or ovariectomized (Ovx) rats, subjected to different GH and gonadal steroid exposure. In normal male rats, estradiol (E2, 12.5-25 micrograms/day for 1 or 2 weeks) markedly increased plasma GHBP and hepatic hGH, and bGH binding. These effects of E2 were diminished in Dw rats, absent in Hx rats, but restored in Hx rats given exogenous hGH. Plasma GHBP rose in female rats given E2, and fell in females given the anti-estrogen tamoxifen. Ovx animals had lower plasma GHBP and hepatic GH binding which was reversed by E2, but not testosterone treatment. Continuous hGH infusions in Ovx rats restored hepatic GH binding, and increased plasma GHBP. In Dw males, hGH increased plasma GHBP and hepatic GH binding, whereas testosterone had no effect on GHBP or GH receptors and did not affect their up-regulation by hGH. Hepatic levels of GHBP-, and GH receptor mRNA transcripts showed the same trends in response to steroid or GH treatment, but the differences were rarely significant, except in Ovx animals which had higher GHBP mRNA transcripts after GH or E2 treatment. Thus E2 and GH increase both plasma GHBP and hepatic GH receptor binding. GH up-regulates GHBP in the absence of E2, whereas E2 treatment does not raise GHBP in the absence of GH. Whereas some of the effects of estrogen could be mediated via alterations in GH secretion, estrogen may also directly influence GHBP production at the liver, but only in the presence of GH.
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Plasma glucose, insulin, and FFA concentrations were determined in 15 normal subjects and 15 patients with noninsulin-dependent diabetes mellitus (NIDDM) from 0800 to 1600 h. Breakfast and lunch were consumed at 0800 and 1200 h, respectively, and plasma concentrations were measured at hourly intervals from 0800-1600 h. Plasma glucose concentrations between 0800 and 1600 h were significantly elevated in patients with NIDDM, and the higher the fasting glucose level, the greater the postprandial hyperglycemia. Hyperglycemia in patients with NIDDM was associated with plasma insulin levels that were significantly higher (P less than 0.001) than those in normal subjects, and substantial hyperinsulinemia occurred between 0800 and 1600 h in patients with mild NIDDM (fasting plasma glucose concentrations, less than 140 mg/dl). Both fasting and postprandial FFA levels were also increased in patients with NIDDM (P less than 0.001), and the greater the plasma glucose response, the higher the FFA response (r = 0.70; P less than 0.001). However, there was no significant correlation between plasma insulin and FFA concentrations. More specifically, hyperinsulinemic patients with mild diabetes (fasting plasma glucose, less than 140 mg/dl) maintained normal ambient FFA levels, while FFA concentrations were significantly elevated in patients with severe NIDDM (fasting plasma glucose, greater than 250 mg/dl), with insulin concentrations comparable to those in normal subjects. These results demonstrate that patients with NIDDM are not capable of maintaining normal plasma FFA concentrations. This defect in FFA metabolism is proportionate to the magnitude of hyperglycemia and occurs despite the presence of elevated levels of plasma insulin. These results are consistent with the view that insulin resistance in NIDDM also involves the ability of insulin to regulate FFA metabolism.
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Carbohydrate Metabolism
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