NASSP Bulletin最新文献

Background: Incidence of small-intestine neuroendocrine tumors (SINT) has been increasing in the United States over the past 40 years, with higher incidence in Utah than elsewhere. As information about how these tumors arise is limited, elucidating lifestyle factors associated with SINT in a statewide cohort could potentially identify those at risk to help mitigate their effects.

Methods: Cases of SINT with a carcinoid histology (8240 or 8241) diagnosed in Utah from 1996 to 2014 with no prior history of cancer within 5 years (n = 433) were matched to population controls (1:10 ratio). Tobacco and alcohol exposures before case diagnosis were identified from International Classification of Diseases codes in statewide medical records and from self-reported data captured at patient encounters beginning in 1996. Multivariate logistic regression was used to estimate risk of SINT associated with tobacco and alcohol in cases compared with controls.

Results: An increased risk of SINT was observed in tobacco-exposed individuals compared with unexposed [OR, 1.44; 95% confidence interval (CI), 1.11-1.86; P = 0.006]. Those who were exposed to alcohol exhibited an increased risk of SINT (OR, 1.62; 95% CI, 1.05-2.49; P = 0.03).

Conclusions: This study supports tobacco and alcohol use as risk factors for SINT, independent of family history. However, low rates of smoking and alcohol use in Utah coupled with higher rates of SINT suggest other factors may contribute to development of these tumors.

Impact: Although tobacco and alcohol modestly contribute to risk, our study suggests in addition to greater detection of tumors, other as-of-yet undefined exposures may drive rising SINT incidence.

Purpose Reorganization of language networks in aphasia takes advantage of the facts that (a) the brain is an organ of plasticity, with neuronal changes occurring throughout the life span, including following brain damage; (b) plasticity is highly experience dependent; and (c) as with any learning system, language reorganization involves a synergistic interplay between organism-intrinsic (i.e., cognitive and brain) and organism-extrinsic (i.e., environmental) variables. A major goal for clinical treatment of aphasia is to be able to prescribe treatment and predict its outcome based on the neurocognitive deficit profiles of individual patients. This review article summarizes the results of research examining the neurocognitive effects of psycholinguistically based treatment (i.e., Treatment of Underlying Forms; Thompson & Shapiro, 2005) for sentence processing impairments in individuals with chronic agrammatic aphasia resulting from stroke and primary progressive aphasia and addresses both behavioral and brain variables related to successful treatment outcomes. The influences of lesion volume and location, perfusion (blood flow), and resting-state neural activity on language recovery are also discussed as related to recovery of agrammatism and other language impairments. Based on these and other data, principles for promoting neuroplasticity of language networks are presented. Conclusions Sentence processing treatment results in improved comprehension and production of complex syntactic structures in chronic agrammatism and generalization to less complex, linguistically related structures in chronic agrammatism. Patients also show treatment-induced shifts toward normal-like online sentence processing routines (based on eye movement data) and changes in neural recruitment patterns (based on functional neuroimaging), with posttreatment activation of regions overlapping with those within sentence processing and dorsal attention networks engaged by neurotypical adults performing the same task. These findings provide compelling evidence that treatment focused on principles of neuroplasticity promotes neurocognitive recovery in chronic agrammatic aphasia. Presentation Videohttps://doi.org/10.23641/asha.10257587.

Carbonic acid H₂CO₃ (CA) is a key constituent of the universal CA/bicarbonate/CO₂ buffer maintaining the pH of both blood and the oceans. Here we demonstrate the ability of intact CA to quantitatively protonate bases with biologically-relevant pK_as and argue that CA has a previously unappreciated function as a major source of protons in blood plasma. We determine with high precision the temperature dependence of pK_a(CA), pK_a(T) = -373.604 + 16,500/T + 56.478 ln T. At physiological-like conditions pK_a(CA) = 3.45 (I = 0.15 M, 37 °C), making CA stronger than lactic acid. We further demonstrate experimentally that CA decomposition to H₂O and CO₂ does not impair its ability to act as an ordinary carboxylic acid and to efficiently protonate physiological-like bases. The consequences of this conclusion are far reaching for human physiology and marine biology. While CA is somewhat less reactive than (H⁺)_aq, it is more than 1 order of magnitude more abundant than (H⁺)_aq in the blood plasma and in the oceans. In particular, CA is about 70× more abundant than (H⁺)_aq in the blood plasma, where we argue that its overall protonation efficiency is 10 to 20× greater than that of (H⁺)_aq, often considered to be the major protonating agent there. CA should thus function as a major source for fast in vivo acid-base reactivity in the blood plasma, possibly penetrating intact into membranes and significantly helping to compensate for (H⁺)_aq's kinetic deficiency in sustaining the large proton fluxes that are vital for metabolic processes and rapid enzymatic reactions.