15 research outputs found
New Mechanics of Traumatic Brain Injury
The prediction and prevention of traumatic brain injury is a very important
aspect of preventive medical science. This paper proposes a new coupled
loading-rate hypothesis for the traumatic brain injury (TBI), which states that
the main cause of the TBI is an external Euclidean jolt, or SE(3)-jolt, an
impulsive loading that strikes the head in several coupled degrees-of-freedom
simultaneously. To show this, based on the previously defined covariant force
law, we formulate the coupled Newton-Euler dynamics of brain's micro-motions
within the cerebrospinal fluid and derive from it the coupled SE(3)-jolt
dynamics. The SE(3)-jolt is a cause of the TBI in two forms of brain's rapid
discontinuous deformations: translational dislocations and rotational
disclinations. Brain's dislocations and disclinations, caused by the
SE(3)-jolt, are described using the Cosserat multipolar viscoelastic continuum
brain model.
Keywords: Traumatic brain injuries, coupled loading-rate hypothesis,
Euclidean jolt, coupled Newton-Euler dynamics, brain's dislocations and
disclinationsComment: 18 pages, 1 figure, Late
Consensus statement for diagnosis of subcortical small vessel disease
Vascular cognitive impairment (VCI) is the diagnostic term used to describe a heterogeneous group of sporadic and hereditary diseases of the large and small blood vessels. Subcortical small vessel disease (SVD) leads to lacunar infarcts and progressive damage to the white matter. Patients with progressive damage to the white matter, referred to as Binswangerâs disease (BD), constitute a spectrum from pure vascular disease to a mixture with neurodegenerative changes. Binswangerâs disease patients are a relatively homogeneous subgroup with hypoxic hypoperfusion, lacunar infarcts, and inflammation that act synergistically to disrupt the bloodâbrain barrier (BBB) and break down myelin. Identification of this subgroup can be facilitated by multimodal disease markers obtained from clinical, cerebrospinal fluid, neuropsychological, and imaging studies. This consensus statement identifies a potential set of biomarkers based on underlying pathologic changes that could facilitate diagnosis and aid patient selection for future collaborative treatment trials
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Why are well-educated Muscovites more likely to survive? Understanding the biological pathways
There are large socioeconomic disparities in adult mortality in Russia, although the biological mechanisms are not well understood. With data from the study of Stress, Aging, and Health in Russia (SAHR), we use Gompertz hazard models to assess the relationship between educational attainment and mortality among older adults in Moscow and to evaluate biomarkers associated with inflammation, neuroendocrine function, heart rate variability, and clinical cardiovascular and metabolic risk as potential mediators of that relationship. We do this by assessing the extent to which the addition of biomarker variables into hazard models of mortality attenuates the association between educational attainment and mortality. We find that an additional year of education is associated with about 5% lower risk of age-specific all-cause and cardiovascular mortality. Inflammation biomarkers are best able to account for this relationship, explaining 25% of the education-all-cause mortality association, and 35% of the education-cardiovascular mortality association. Clinical markers perform next best, accounting for 13% and 23% of the relationship between education and all-cause and cardiovascular mortality, respectively. Although heart rate biomarkers are strongly associated with subsequent mortality, they explain very little of the education-mortality link. Neuroendocrine biomarkers fail to account for any portion of the link. These findings suggest that inflammation may be important for understanding mortality disparities by socioeconomic status