The Permissible Scope of Texas Automobile Inventory Searches in the Aftermath of Colorado v. Bertine: A Talisman is Created

The fourth amendment to the United States Constitution guarantees freedom from unreasonable searches and seizures. The warrant and probable cause requirements advance this constitutionally implied privacy right. However, with respect to automobile searches, strict adherence to these safeguards has been eschewed in favor of more flexible, and arguably less protective, versions of reasonableness. In 1981, in Gill v. State, the Texas court addressed the permissible scope of inventory searches, holding that the police may not search the locked trunk of an automobile while conducting an inventory search. Despite the simplicity of the Gill rule, a number of recent cases, while not expressly overruling Gill, significantly expanded the scope of inventory permitted by a fair reading of Gill. These cases mean much more than the expansion of inventory scope, though. They mean that any expectation of privacy is meaningless in this context. Were that expectation replaced by another suitable safeguard, the result might have been less alarming, but, when one measure is removed from the balance without a corresponding adjustment, balancing becomes formalistic; the outcome is predetermined. Texas law should not uncritically follow this development of fourth amendment jurisprudence. No impediment exists, under either a fourth amendment analysis or an interpretation of the Texas Constitution, to reaffirmation of the balancing undertaken in Gill. Noble motivations cannot and should not protect illogic from criticism. Indeed, illogic undermines the persuasiveness of legal precedent while, at the same time, often imperiling fundamental and well-developed safeguards against improper governmental intrusion. If the United States Supreme Court has indulged the government’s desire to facilitate the finding of criminal evidence at the expense of personal liberty, the court of criminal appeals need not follow, nor set, the example

The Vehicle, Fall 1981

Vol. 23, No. 1 Table of Contents Maples At My HomeGary Ervinpage 4 I Remember (after Anne Sexton)Susan Mehlpage 5 Where Do They Put Their ArmsKathleen Alakspage 6 Sweet AdversityAlissa Finleypage 7 Love At Baskin-RobbinsCindy Fritzpage 9 What IfJohn Stockmanpage 10 Shaking HandsScott Fishelpage 12 The SouvenirKathleen Alakspage 13 Kelowna City Park At NightJerry McAnultypage 14 Canadian EuphoriaB.L. Davidsonpage 14 Water PaintingIsabel M. Parrotpage 15 Clearwater BeachSusan Mehlpage 16 SeaprintsJerry McAnultypage 17 Elegy For An Illinois TownJohn Stockmanpage 17 DepreciatingLaura Sharppage 18 U.S. Steel South WorksDiane Bartuspage 19 Blue BeadsB.L. Davidsonpage 20 Top HatVicki Ewingpage 21 29 Cent PoemSusan Mehlpage 24 Morning In OctoberCindy Fritzpage 26 PrerequisiteDevon Flesorpage 26 InvalidLynn Sronkoskipage 27 Nushagak Bay HarvestB.L. Davidsonpage 28 August, 1967Cathy Georgepage 29 The ParkSusan Burkpage 30 Summer of \u2778: With LoveDonna L. Lewispage 32 RhubarbScott Fishelpage 33 I\u27ll get it... Cathy Georgepage 34 The Night PeopleLenore Howardpage 35 Falling AsleepKaren Smithpage 38 Getting Life Off Your ShouldersStacey Flanniganpage 38 Thirst, and the anticipation of a week\u27s vacation in late summerCathy Georgepage 39 Art Cover Michelle Howe Pen and Ink DrawingIrene Brownpage 3 PhotographGregory A. Molchanpage 11 PhotographRuth Zurerzyckipage 15 PhotographGregory A. Molchanpage 25 Pen and Ink DrawingChristi Fullerpage 31 Pen and Ink DrawingChristi Fullerpage 40https://thekeep.eiu.edu/vehicle/1038/thumbnail.jp

The Vehicle, Fall 1981

Vol. 23, No. 1 Table of Contents Maples At My HomeGary Ervinpage 4 I Remember (after Anne Sexton)Susan Mehlpage 5 Where Do They Put Their ArmsKathleen Alakspage 6 Sweet AdversityAlissa Finleypage 7 Love At Baskin-RobbinsCindy Fritzpage 9 What IfJohn Stockmanpage 10 Shaking HandsScott Fishelpage 12 The SouvenirKathleen Alakspage 13 Kelowna City Park At NightJerry McAnultypage 14 Canadian EuphoriaB.L. Davidsonpage 14 Water PaintingIsabel M. Parrotpage 15 Clearwater BeachSusan Mehlpage 16 SeaprintsJerry McAnultypage 17 Elegy For An Illinois TownJohn Stockmanpage 17 DepreciatingLaura Sharppage 18 U.S. Steel South WorksDiane Bartuspage 19 Blue BeadsB.L. Davidsonpage 20 Top HatVicki Ewingpage 21 29 Cent PoemSusan Mehlpage 24 Morning In OctoberCindy Fritzpage 26 PrerequisiteDevon Flesorpage 26 InvalidLynn Sronkoskipage 27 Nushagak Bay HarvestB.L. Davidsonpage 28 August, 1967Cathy Georgepage 29 The ParkSusan Burkpage 30 Summer of \u2778: With LoveDonna L. Lewispage 32 RhubarbScott Fishelpage 33 I\u27ll get it... Cathy Georgepage 34 The Night PeopleLenore Howardpage 35 Falling AsleepKaren Smithpage 38 Getting Life Off Your ShouldersStacey Flanniganpage 38 Thirst, and the anticipation of a week\u27s vacation in late summerCathy Georgepage 39 Art Cover Michelle Howe Pen and Ink DrawingIrene Brownpage 3 PhotographGregory A. Molchanpage 11 PhotographRuth Zurerzyckipage 15 PhotographGregory A. Molchanpage 25 Pen and Ink DrawingChristi Fullerpage 31 Pen and Ink DrawingChristi Fullerpage 40https://thekeep.eiu.edu/vehicle/1038/thumbnail.jp

Periventricular hyperintensities are associated with elevated cerebral amyloid

ObjectiveTo investigate the association between periventricular white mater hyperintensities (PVWMH) and biomarkers of elevated cerebral β-amyloid (Aβ) in the Alzheimer's Disease Neuroimaging Initiative, a large prospective multicenter observational study.MethodsThe burden of frontal, parietal, and occipital PVWMH on 3T fluid-attenuated inversion recovery MRI was evaluated in 698 cognitively normal participants and participants with mild cognitive impairment (MCI) using a novel semiquantitative visual rating scale. Results were correlated with CSF-Aβ, florbetapir-PET, and fluorodeoxyglucose (FDG)-PET.ResultsIncreased burden of parietal, occipital, and frontal PVWMH was associated with elevated cerebral amyloid evidenced by high florbetapir-PET signal (p < 0.01) and low CSF-Aβ (p < 0.01). In logistic regression models, including PVWMH, age, sex, APOE status, vascular risk factors, pulse pressure, vascular secondary prevention medications, education, ethnicity, and race, parietal, occipital, and frontal PVWMH burden was independently associated with high florbetapir-PET uptake (p < 0.05). In a similar logistic regression model, parietal and occipital (p < 0.05) but not frontal (p = 0.05) PVWMH were independently associated with CSF-Aβ. Weaker associations were found between parieto-occipital PVWMH and elevated CSF-tau (p < 0.05) and occipital PVWMH and elevated CSF-phospho-tau (p < 0.05). PVWMH were associated with cerebral hypometabolism on FDG-PET independent of CSF-Aβ levels (p < 0.05). Absolute and consistency of agreement intraclass correlation coefficients were, respectively, 0.83 and 0.83 for frontal, 0.78 and 0.8 for parietal, and 0.45 and 0.75 for occipital PVWMH measurements.ConclusionsIncreased PVWMH were associated with elevated cerebral amyloid independent of potential confounders such as age, APOE genotype, and vascular risk factors. The mechanisms underlying the association between PVWMH and cerebral amyloid remain to be clarified

Association of common genetic variants in GPCPD1 with scaling of visual cortical surface area in humans.

Visual cortical surface area varies two- to threefold between human individuals, is highly heritable, and has been correlated with visual acuity and visual perception. However, it is still largely unknown what specific genetic and environmental factors contribute to normal variation in the area of visual cortex. To identify SNPs associated with the proportional surface area of visual cortex, we performed a genome-wide association study followed by replication in two independent cohorts. We identified one SNP (rs6116869) that replicated in both cohorts and had genome-wide significant association (P(combined) = 3.2 × 10(-8)). Furthermore, a metaanalysis of imputed SNPs in this genomic region identified a more significantly associated SNP (rs238295; P = 6.5 × 10(-9)) that was in strong linkage disequilibrium with rs6116869. These SNPs are located within 4 kb of the 5' UTR of GPCPD1, glycerophosphocholine phosphodiesterase GDE1 homolog (Saccharomyces cerevisiae), which in humans, is more highly expressed in occipital cortex compared with the remainder of cortex than 99.9% of genes genome-wide. Based on these findings, we conclude that this common genetic variation contributes to the proportional area of human visual cortex. We suggest that identifying genes that contribute to normal cortical architecture provides a first step to understanding genetic mechanisms that underlie visual perception

Association of common genetic variants in GPCPD1 with scaling of visual cortical surface area in humans.

Visual cortical surface area varies two- to threefold between human individuals, is highly heritable, and has been correlated with visual acuity and visual perception. However, it is still largely unknown what specific genetic and environmental factors contribute to normal variation in the area of visual cortex. To identify SNPs associated with the proportional surface area of visual cortex, we performed a genome-wide association study followed by replication in two independent cohorts. We identified one SNP (rs6116869) that replicated in both cohorts and had genome-wide significant association (P(combined) = 3.2 × 10(-8)). Furthermore, a metaanalysis of imputed SNPs in this genomic region identified a more significantly associated SNP (rs238295; P = 6.5 × 10(-9)) that was in strong linkage disequilibrium with rs6116869. These SNPs are located within 4 kb of the 5' UTR of GPCPD1, glycerophosphocholine phosphodiesterase GDE1 homolog (Saccharomyces cerevisiae), which in humans, is more highly expressed in occipital cortex compared with the remainder of cortex than 99.9% of genes genome-wide. Based on these findings, we conclude that this common genetic variation contributes to the proportional area of human visual cortex. We suggest that identifying genes that contribute to normal cortical architecture provides a first step to understanding genetic mechanisms that underlie visual perception

A data‐driven examination of apathy and depressive symptoms in dementia with independent replication

Apathy is one of the most common neuropsychiatric symptoms (NPS) and is associated with poor clinical outcomes. Research that helps define the apathy phenotype is urgently needed, particularly for clinical and biomarker studies. We used latent class analysis (LCA) with two independent cohorts to understand how apathy and depression symptoms co-occur statistically. We further explored the relationship between latent class membership, demographics, and the presence of other NPS. The LCA identified a four-class solution (no symptoms, apathy, depression, and combined apathy/depression), reproducible over both cohorts, providing robust support for an apathy syndrome distinct from depression and confirming that an apathy/depression syndrome exists, supported by the model fit test with the four-class solution scores evidencing better fitting (Bayesian information criterion adjusted and entropy R 2). Using a data-driven method, we show distinct and statistically meaningful co-occurrence of apathy and depressive symptoms. There was evidence that these classes have different clinical associations, which may help inform diagnostic categories for research studies and clinical practice.HighlightsWe found four classes: no symptoms, apathy, depression and apathy/depression.Apathy conferred a higher probability for agitation.Apathy diagnostic criteria should include accompanying neuropsychiatric symptoms

Higher CSF sTREM2 attenuates ApoE4-related risk for cognitive decline and neurodegeneration

Background!#!The Apolipoprotein E ε4 allele (i.e. ApoE4) is the strongest genetic risk factor for sporadic Alzheimer's disease (AD). TREM2 (i.e. Triggering receptor expressed on myeloid cells 2) is a microglial transmembrane protein brain that plays a central role in microglia activation in response to AD brain pathologies. Whether higher TREM2-related microglia activity modulates the risk to develop clinical AD is an open question. Thus, the aim of the current study was to assess whether higher sTREM2 attenuates the effects of ApoE4-effects on future cognitive decline and neurodegeneration.!##!Methods!#!We included 708 subjects ranging from cognitively normal (CN, n = 221) to mild cognitive impairment (MCI, n = 414) and AD dementia (n = 73) from the Alzheimer's disease Neuroimaging Initiative. We used linear regression to test the interaction between ApoE4-carriage by CSF-assessed sTREM2 levels as a predictor of longitudinally assessed cognitive decline and MRI-assessed changes in hippocampal volume changes (mean follow-up of 4 years, range of 1.7-7 years).!##!Results!#!Across the entire sample, we found that higher CSF sTREM2 at baseline was associated with attenuated effects of ApoE4-carriage (i.e. sTREM2 x ApoE4 interaction) on longitudinal global cognitive (p = 0.001, Cohen's f!##!Conclusion!#!Our results suggest that a higher CSF sTREM2 levels are associated with attenuated ApoE4-related risk for future cognitive decline and AD-typical neurodegeneration. These findings provide further evidence that TREM2 may be protective against the development of AD