Publications by authors named "G T Porter"

Preterm infants exposed to supplemental oxygen (hyperoxia) are at risk for developing heart failure later in life. Exposing rodents in early postnatal life to hyperoxia causes heart failure that resembles cardiac disease seen in adult humans who were born preterm. Neonatal hyperoxia exposure affects the left atrium and left ventricle differently, inhibiting the proliferation and survival of atrial cardiomyocytes while enhancing cardiomyocyte differentiation in the ventricle.

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Variants with large effect contribute to congenital heart disease (CHD). To date, recessive genotypes (RGs) have commonly been implicated through anecdotal ascertainment of consanguineous families and candidate gene-based analysis; the recessive contribution to the broad range of CHD phenotypes has been limited. We analyzed whole exome sequences of 5,424 CHD probands.

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Abnormal tau modifications are one of the main contributors to neurodegenerative processes present during Alzheimer's disease (AD). In this context, truncated tau by caspase-3, a pathological tau form, affects mitochondrial function and antioxidant regulation, contributing to synaptic and cognitive impairment in AD mouse models. We previously showed that the presence of caspase-3 cleaved tau promotes mitochondrial impairment in neuronal cells, where Cyclophilin-D (CypD) protein could be a crucial element.

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Traumatic brain injury (TBI) is an established risk factor for accelerated cognitive decline and increased dementia risk. The specific characteristics of TBI (e.g.

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Hospitalized patients lacking the mental capacity to consent to treatment may demand to be discharged from the hospital against medical advice. Forced custody of these patients, including the use of restraints, may be required if the plan is to proceed with treatment. This raises ethical concerns with regard to depriving people of their liberty.

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