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Slepian ML, Masicampo EJ, Ambady N.
J Pers Soc Psychol. 2015 Jan ;108(1):1-17.
PMID: 25603367
Across 7 studies, the authors examined the relationship between experiences of verticality and abstract versus concrete processing. Experiencing high, relative to low, verticality led to higher level identifications for actions (Study 1), greater willingness to delay short-term monetary gains for larger long-term monetary gains (Studies 2 and 5), and more frequent perceptions of meaningful relationships between objects and categories (Studies 3, 4, and 6), demonstrating that high verticality leads to more high-level construals. Mechanisms of these effects were explored, and the studies present evidence suggesting that mood (Studies 3 and 4), felt power (Study 4), arousal (Study 4), perceptual scope (Study 4), superficial semantic associations (Study 5), and movement (Study 5) do not mediate these effects. Instead, we found that even minimal experiences of verticality influence construal level (Study 6) and that verticality can influence construal level independent of the many plausible mediators. Furthermore, the relationship is reciprocal with abstract and concrete processing influencing the verticality of one's visual perspective (Study 7), suggesting an intimate link between construal level (abstract vs. concrete processing) and experiences of verticality. (PsycINFO Database Record (c) 2015 APA, all rights reserved).
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Hammon JW.
J Thorac Cardiovasc Surg. 2015 Jan ;149(1):180-1.
PMID: 25451490
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Liss MA, Chen H, Hemal S, Krane S, Kane CJ, Xu J, Kader AK.
J Urol. 2015 Jan ;193(1):75-9.
PMID: 25066872
We assessed whether prostate cancer screening would decrease prostate cancer mortality in white men with a family history of prostate cancer.
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Icenhour L.
JAAPA. 2015 Jan ;28(1)
PMID: 25522022
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Williamson JD, Launer LJ, Miller ME, .
JAMA Intern Med. 2015 Jan ;175(1):144-5.
PMID: 25560951
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Freedman BI, Langefeld CD, Lu L, Palmer ND, Smith SC, Bagwell BM, Hicks PJ, Xu J, Wagenknecht LE, Raffield LM, Register TC, Carr JJ, Bowden DW, Divers J.
Kidney Int. 2015 Jan ;87(1):176-81.
PMID: 25054777
Albuminuria and reduced estimated glomerular filtration rate (eGFR) associate with two apolipoprotein L1 gene (APOL1) variants in nondiabetic African Americans (AAs). Whether APOL1 associates with subclinical atherosclerosis and survival remains unclear. To determine this, 717 African American-Diabetes Heart Study participants underwent computed tomography to determine coronary artery-, carotid artery-, and aorta-calcified atherosclerotic plaque mass scores in addition to the urine albumin:creatinine ratio (UACR), eGFR, and C-reactive protein (CRP). Associations between mass scores and APOL1 were assessed adjusting for age, gender, African ancestry, body mass index (BMI), hemoglobin A1c, smoking, hypertension, use of statins and angiotensin-converting enzyme inhibitors, albuminuria, and eGFR. Participants were 58.9% female with mean age 56.5 years, eGFR 89.5 ml/min per 1.73 m(2), UACR 169.6 mg/g, and coronary artery-, carotid artery-, and aorta-calcified plaque mass scores of 610, 171, and 5378, respectively. In fully adjusted models, APOL1 risk variants were significantly associated with lower levels of carotid artery-calcified plaque (β=-0.42, s.e. 0.18; dominant model) and marginally lower coronary artery plaque (β=-0.36, s.e. 0.21; dominant model), but not with aorta-calcified plaque, CRP, UACR, or eGFR. By the end of a mean follow-up of 5.0 years, 89 participants had died. APOL1 nephropathy risk variants were significantly associated with improved survival (hazard ratio 0.67 for one copy; 0.44 for two copies). Thus, APOL1 nephropathy variants associate with lower levels of subclinical atherosclerosis and reduced risk of death in AAs with type 2 diabetes mellitus.
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Langefeld CD, Divers J, Pajewski NM, Hawfield AT, Reboussin DM, Bild DE, Kaysen GA, Kimmel PL, Raj DS, Ricardo AC, Wright JT, Sedor JR, Rocco MV, Freedman BI, .
Kidney Int. 2015 Jan ;87(1):169-75.
PMID: 25029429
Apolipoprotein L1 gene (APOL1) G1 and G2 coding variants are strongly associated with chronic kidney disease (CKD) in African Americans (AAs). Here APOL1 association was tested with baseline estimated glomerular filtration rate (eGFR), urine albumin:creatinine ratio (UACR), and prevalent cardiovascular disease (CVD) in 2571 AAs from the Systolic Blood Pressure Intervention Trial (SPRINT), a trial assessing effects of systolic blood pressure reduction on renal and CVD outcomes. Logistic regression models that adjusted for potentially important confounders tested for association between APOL1 risk variants and baseline clinical CVD (myocardial infarction, coronary, or carotid artery revascularization) and CKD (eGFR under 60 ml/min per 1.73 m(2) and/or UACR over 30 mg/g). AA SPRINT participants were 45.3% female with a mean (median) age of 64.3 (63) years, mean arterial pressure 100.7 (100) mm Hg, eGFR 76.3 (77.1) ml/min per 1.73 m(2), and UACR 49.9 (9.2) mg/g, and 8.2% had clinical CVD. APOL1 (recessive inheritance) was positively associated with CKD (odds ratio 1.37, 95% confidence interval 1.08-1.73) and log UACR estimated slope (β) 0.33) and negatively associated with eGFR (β -3.58), all significant. APOL1 risk variants were not significantly associated with prevalent CVD (1.02, 0.82-1.27). Thus, SPRINT data show that APOL1 risk variants are associated with mild CKD but not with prevalent CVD in AAs with a UACR under 1000 mg/g.
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Fadeyi EA, Simmons JH, Jones MR, Palavecino EL, Pomper GJ.
Lab Med. 2015 Winter ;46(1):55-9.
PMID: 25617394
Most cases of autoimmune hemolytic anemia (AIHA) are caused by the production of an autoantibody that targets determinants on red blood cells (RBCs). This autoantibody can be immunoglobulin (Ig) G, IgM, or IgA. Some autoantibodies react optimally at 0° to 4°C (ie, cold agglutinin) and usually are clinically insignificant. High-titer cold agglutinins are associated with IgM autoantibody and complement fixation induced by infectious agents, including the Epstein-Barr virus (EBV). This case report describes a 31-year-old man who had jaundice, a hemoglobin of 6.0 gdL, and was diagnosed with a hemolytic crisis of AIHA. He received a total of 11 RBC transfusions during a 15-hour period without sustained response and later died. The direct antiglobulin test results for this patient were positive, whereas the cold-agglutinin-testing results were negative. We detected EBV DNA in blood via polymerase chain reaction (PCR). We report a rare case of AIHA associated with an IgG autoantibody and exacerbated by EBV infection, causing a fatal hemolytic anemia.
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Orbai AM, Truedsson L, Sturfelt G, Nived O, Fang H, Alarcón GS, Gordon C, Merrill J, Fortin PR, Bruce IN, Isenberg DA, Wallace DJ, Ramsey-Goldman R, Bae SC, Hanly JG, Sanchez-Guerrero J, Clarke AE, Aranow CB, Manzi S, Urowitz MB, Gladman DD, Kalunian KC, Costner MI, Werth VP, Zoma A, Bernatsky S, Ruiz-Irastorza G, Khamashta MA, Jacobsen S, Buyon JP, Maddison P, Dooley MA, Van Vollenhoven RF, Ginzler E, Stoll T, Peschken C, Jorizzo JL, Callen JP, Lim SS, Fessler BJ, Inanc M, Kamen DL, Rahman A, Steinsson K, Franks AG, Sigler L, Hameed S, Pham N, Brey R, Weisman MH, McGwin G, Magder LS, Petri M.
Lupus. 2015 Jan ;24(1):42-9.
PMID: 25124676
Anti-C1q has been associated with systemic lupus erythematosus (SLE) and lupus nephritis in previous studies. We studied anti-C1q specificity for SLE (vs rheumatic disease controls) and the association with SLE manifestations in an international multicenter study.
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Carver KA, Smith TL, Gallagher PE, Tallant EA.
Microcirculation. 2015 Jan ;22(1):19-27.
PMID: 25079175
The effect of the heptapeptide hormone Ang-(1-7) on microvascular fibrosis in rats with Ang II-induced hypertension was investigated, since vascular fibrosis/remodeling plays a prominent role in hypertension-induced end-organ damage and Ang-(1-7) inhibits vascular growth and fibrosis.
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Larsen CP, Beggs ML, Saeed M, Ambruzs JM, Cossey LN, Messias NC, Walker PD, Freedman BI.
Mod Pathol. 2015 Jan ;28(1):95-102.
PMID: 25081748
The effects of nephropathy risk variants in the apolipoprotein L1 gene (APOL1) on renal histopathology in African Americans with arterionephrosclerosis or putative 'hypertension-associated' nephropathy are unknown. APOL1 genotype-phenotype correlations were performed in a blinded manner from renal biopsies in 196 self-reported African Americans with arterionephrosclerosis on kidney biopsy at a large national nephropathology practice. Subjects had chronic kidney disease without nephrotic syndrome. A discovery analysis compared histopathologic changes in the glomerular and tubulointerstitial compartments in 58 subjects with 2 versus 56 subjects with 0 APOL1 risk variants. Validation was performed in biopsies from 82 additional subjects with 0, 1, and 2 risk variants. Two risk variant versus zero risk variant group genotype associations and subphenotypes were assessed by χ(2) analyses. ANOVA compared means of continuous variables. In discovery analyses, significantly less obsolescent glomerulosclerosis, more (solidified and disappearing) glomerulosclerosis, more thyroidization-type tubular atrophy, and more microcystic tubular dilatation were seen in patients with two versus zero APOL1 risk alleles. Greater degrees of arteriosclerosis were present in those with zero risk alleles. Segmental glomerulosclerosis did not differ significantly between groups. Presence of two of the following discriminatory histopathologic findings from discovery, that is, <50% obsolescent glomerulosclerosis, thyroidization-type tubular atrophy, and microcystic tubular dilatation, was specific for the presence of two APOL1 risk alleles in the validation phase. African Americans with arterionephrosclerosis who possess two APOL1 risk variants more often lack obsolescent glomerulosclerosis and have greater degrees of (solidified and disappearing) glomerulosclerosis, thyroidization-type tubular atrophy, and microcystic tubular dilation than patients with fewer than two risk variants. These findings support involvement of multiple cell types in subnephrotic forms of APOL1-associated nephropathy, particularly renal tubule cells with resultant tubulointerstitial disease.
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Quarta CC, Buxbaum JN, Shah AM, Falk RH, Claggett B, Kitzman DW, Mosley TH, Butler KR, Boerwinkle E, Solomon SD.
N Engl J Med. 2015 Jan 1;372(1):21-9.
PMID: 25551524
Approximately 4% of black Americans carry a valine-to-isoleucine substitution (V122I) in the transthyretin protein, which has been associated with late-onset restrictive amyloid cardiomyopathy and increased risks of death and heart failure.
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McQuail JA, Nicolle MM.
Neurobiol Aging. 2015 Jan ;36(1):323-33.
PMID: 25086838
Fischer 344 × Brown Norway F1 (F344 × BN-F1) hybrid rats express greater longevity with improved health relative to aging rodents of other strains; however, few behavioral reports have thoroughly evaluated cognition across the F344 × BN-F1 lifespan. Consequently, this study evaluated spatial reference memory in F344 × BN-F1 rats at 6, 18, 24, or 28 months of age in the Morris water maze. Reference memory decrements were observed between 6 and 18 months and 18 and 24 months. At 28 months, spatial learning was not worse than 24 months, but swim speed was significantly slower. Reliable individual differences revealed that ∼50% of 24- to 28-month-old rats performed similarly to 6 months, whereas others were spatial learning impaired. Aged rats were impaired at learning within daily training sessions but not impaired at retaining information between days of training. Aged rats were also slower to learn to escape onto the platform, regardless of strategy. In summary, these data clarify the trajectory of cognitive decline in aging F344 × BN-F1 rats and elucidate relevant behavioral parameters.
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Christopoulos GI, King-Casas B.
Neuroimage. 2015 Jan 1;104():326-35.
PMID: 25224998
In social environments, it is crucial that decision-makers take account of the impact of their actions not only for oneself, but also on other social agents. Previous work has identified neural signals in the striatum encoding value-based prediction errors for outcomes to oneself; also, recent work suggests that neural activity in prefrontal cortex may similarly encode value-based prediction errors related to outcomes to others. However, prior work also indicates that social valuations are not isomorphic, with social value orientations of decision-makers ranging on a cooperative to competitive continuum; this variation has not been examined within social learning environments. Here, we combine a computational model of learning with functional neuroimaging to examine how individual differences in orientation impact neural mechanisms underlying 'other-value' learning. Across four experimental conditions, reinforcement learning signals for other-value were identified in medial prefrontal cortex, and were distinct from self-value learning signals identified in striatum. Critically, the magnitude and direction of the other-value learning signal depended strongly on an individual's cooperative or competitive orientation toward others. These data indicate that social decisions are guided by a social orientation-dependent learning system that is computationally similar but anatomically distinct from self-value learning. The sensitivity of the medial prefrontal learning signal to social preferences suggests a mechanism linking such preferences to biases in social actions and highlights the importance of incorporating heterogeneous social predispositions in neurocomputational models of social behavior.
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Houston DK, Leng X, Bray GA, Hergenroeder AL, Hill JO, Jakicic JM, Johnson KC, Neiberg RH, Marsh AP, Rejeski WJ, Kritchevsky SB, .
Obesity (Silver Spring). 2015 Jan ;23(1):77-84.
PMID: 25452229
To assess the long-term effects of an intensive lifestyle intervention on physical function using a randomized post-test design in the Look AHEAD trial.
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Rauck RL, North J, Eisenach JC.
Pain. 2015 Jan ;156(1):88-95.
PMID: 25599305
Chronic pain may be accompanied by hyperalgesia and allodynia, and analgesic interventions may reduce these hypersensitivity phenomena. Preclinical data suggest that intrathecal clonidine and adenosine reduce hypersensitivity, but only clonidine reduces pain; therefore, we tested the effects of these interventions in patients with chronic pain. Twenty-two subjects with pain and hyperalgesia in a lower extremity from complex regional pain syndrome were recruited in a double-blind crossover study to receive intrathecal clonidine, 100 μg, or adenosine, 2 mg. Primary outcome measure was proportion with ≥30% reduction in pain 2 hours after injection, and secondary measures were pain report, areas of hypersensitivity, and temporal summation to heat stimuli. Treatments did not differ in the primary outcome measure (10 met success criterion after clonidine administration and 5 after adenosine administration), although they did differ in pain scores over time, with clonidine having a 3-fold greater effect (P = 0.014). Both drugs similarly reduced areas of hyperalgesia and allodynia by approximately 30% and also inhibited temporal summation. The percentage change in pain report did not correlate with the percentage change in areas of hyperalgesia (P = 0.09, r = 0.08) or allodynia (P = 0.24, r = 0.24) after drug treatment. Both intrathecal clonidine and adenosine acutely inhibit experimentally induced and clinical hypersensitivity in patients with chronic regional pain syndrome. Although these drugs do not differ in analgesia by the primary outcome measure, their difference in effect on pain scores over time and lack of correlation between effect on pain and hypersensitivity suggest that analgesia does not parallel antihyperalgesia with these treatments.
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Eisenach JC, Tong C, Curry RS.
Pain. 2015 Jan ;156(1):81-7.
PMID: 25599304
In rodents, acute exposure to opioids results in transient antinociception followed by longer lasting hypersensitivity to tactile or thermal stimuli, a phenomenon termed opioid-induced hyperalgesia. This hypersensitivity can be blocked or reversed by intrathecally administered cyclooxygenase inhibitors, including ketorolac, suggesting a role for spinal prostaglandins. In surgical patients, the dose of intraoperative opioid, particularly the short-acting drug, remifentanil, is directly related to increased pain and opioid requirements for many hours postoperatively. In addition, experimentally induced tactile hypersensitivity in humans is exaggerated after cessation of remifentanil infusions. The degree of this experimental opioid-induced hyperalgesia is reduced by systemic treatment with cyclooxygenase inhibitors, and investigators have speculated that this reduction reflects the actions in the central nervous system, most likely in the spinal cord. To test this hypothesis, we measured cerebrospinal fluid prostaglandin E2 concentrations during and after remifentanil infusion in 30 volunteers. These volunteers received intrathecal ketorolac or saline in a random, blinded manner during intravenous remifentanil infusion after generation of hypersensitivity by topical capsaicin. Remifentanil reduced pain to noxious heat stimuli and reduced areas of capsaicin-induced hypersensitivity similarly in those receiving intrathecal ketorolac or saline. The primary outcome measure, area of capsaicin-induced hypersensitivity after stopping remifentanil, showed a similar increase in those receiving ketorolac as in those receiving saline. Cerebrospinal fluid prostaglandin E2 concentrations did not increase during postinfusion hyperalgesia compared with those during infusion, and they were not increased during infusion compared with those in historical controls. These data fail to support the hypothesis that acute opioid-induced hyperalgesia reflects spinal cyclooxygenase activation causing central sensitization.
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Coghill RC, Keefe FJ.
Pain. 2015 Jan ;156(1):4-5.
PMID: 25599294
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Kuban KC, O'Shea TM, Allred EN, Fichorova RN, Heeren T, Paneth N, Hirtz D, Dammann O, Leviton A, .
Pediatr Neurol. 2015 Jan ;52(1):42-8.
PMID: 25459361
We hypothesized that the risk of brain damage in extremely preterm neonates increases with the breadth and type of systemic inflammation, indexed by the number of elevated inflammation-related proteins and the number of functional categories of inflammation-related proteins exhibiting an elevated concentration.
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Jules A, Grijalva CG, Zhu Y, Talbot HK, Williams JV, Poehling KA, Chaves SS, Edwards KM, Schaffner W, Shay DK, Griffin MR.
Pediatrics. 2015 Jan ;135(1):e66-74.
PMID: 25489015
In the United States, recommendations for annual influenza vaccination gradually expanded from 2004 to 2008, to include all children aged ≥6 months. The effects of these policies on vaccine uptake and influenza-associated health care encounters are unclear. The objectives of the study were to examine the annual incidence of influenza-related health care encounters and vaccine uptake among children age 6 to 59 months from 2000-2001 through 2010-2011 in Davidson County, TN.
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