In this task, you are given an abstract of article. Your task is to generate label "True" if abstract is structured, otherwise generate "False". A structured abstract is composed of a topic sentence (or key sentence), relevant supporting sentences, and a closing (or transition) sentence. This structure is key to keeping your abstract focused on the main idea and creating a clear and concise image.
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Question: OBJECTIVE Islet-reactive CD8(+) T-cells play a key role in the pathogenesis of type 1 diabetes in the NOD mouse. The predominant T-cell specificities change over time, but whether similar shifts also occur after clinical diagnosis and insulin treatment in type 1 diabetic patients is unknown. RESEARCH DESIGN AND METHODS We took advantage of a recently validated islet-specific CD8(+) T-cell gamma-interferon enzyme-linked immunospot (ISL8Spot) assay to follow responses against preproinsulin (PPI), GAD, insulinoma-associated protein 2 (IA-2), and islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) epitopes in 15 HLA-A2(+) adult type 1 diabetic patients close to diagnosis and at a second time point 7-16 months later.
RESULTS CD8(+) T-cell reactivities were less frequent at follow-up, as 28.6% of responses tested positive at type 1 diabetes diagnosis vs. 13.2% after a median of 11 months (P = 0.003). While GAD and IA-2 autoantibody (aAb) titers were unchanged in 75% of cases, the fraction of patients responding to PPI and/or GAD epitopes by ISL8Spot decreased from 60-67 to 20% (P < 0.02). The previously subdominant IA-2(206-214) and IGRP(265-273) peptides were newly targeted, thus becoming the immunodominant epitopes.
CONCLUSIONS Shifts both in frequency and in immunodominance of CD8(+) T-cell responses occur more rapidly than do changes in aAb titers. These different kinetics may suggest complementary clinical applications for T-cell and aAb measurements.

Answer: True

Question: OBJECTIVES To determine whether the ankle brachial index (ABI, a marker of generalized atherosclerosis) is associated with cognitive impairment after 10 years in older people.
DESIGN Cohort study (Edinburgh Artery Study).
SETTING Eleven general practices in Edinburgh, Scotland.
PARTICIPANTS Seven hundred seventeen men and women aged 55 to 74 from the general population, followed for 10 years.
MEASUREMENTS ABI measured at baseline and major cognitive functions (including premorbid function using the National Adult Reading Test, NART) tested after 10 years.
RESULTS After adjustment for age and sex, a low ABI was associated with lower scoring (bottom tertile vs top tertile) on Raven's Matrices (odds ratio (OR)=1.6, 95% confidence interval (CI) =1.0-2.6), Verbal Fluency (OR =1.8, 95% CI =1.1-3.0), and Digit Symbol Test (OR =2.3, 95% CI =1.3-4.2), suggesting that the ABI is predictive of poorer performance in nonverbal reasoning, verbal fluency, and information processing speed. The association between ABI and the Digit Symbol Test remained significant after further adjustment for premorbid cognitive function (tested using the NART), suggesting that the ABI is also predictive of decline in information processing speed (from premorbid ability to that measured here in older age).
CONCLUSION The ABI may be useful in identifying older individuals at higher risk of cognitive impairment. In the future, preventive measures developed to target individuals with a low ABI should consider measures to reduce vascular-related cognitive decline as well as cardiovascular events, in an effort to reduce the incidence and consequences of subsequent cognitive impairment and dementia.

Answer: True

Question: Developmental abnormalities, cancer, and premature aging each have been linked to defects in the DNA damage response (DDR). Mutations in the ATR checkpoint regulator cause developmental defects in mice (pregastrulation lethality) and humans (Seckel syndrome). Here we show that eliminating ATR in adult mice leads to defects in tissue homeostasis and the rapid appearance of age-related phenotypes, such as hair graying, alopecia, kyphosis, osteoporosis, thymic involution, fibrosis, and other abnormalities. Histological and genetic analyses indicate that ATR deletion causes acute cellular loss in tissues in which continuous cell proliferation is required for maintenance. Importantly, thymic involution, alopecia, and hair graying in ATR knockout mice were associated with dramatic reductions in tissue-specific stem and progenitor cells and exhaustion of tissue renewal and homeostatic capacity. In aggregate, these studies suggest that reduced regenerative capacity in adults via deletion of a developmentally essential DDR gene is sufficient to cause the premature appearance of age-related phenotypes.

Answer:
False