Recent Research Articles from UNTHSC

Recent research articles indexed in PubMed from authors affiliated with the UNT Health Science Center.

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Chronic intermittent hypoxia induces oxidative stress and inflammation in brain regions associated with early-stage neurodegeneration.

Sun, 05/07/2017 - 13:41
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Chronic intermittent hypoxia induces oxidative stress and inflammation in brain regions associated with early-stage neurodegeneration.

Physiol Rep. 2017 May;5(9):

Authors: Snyder B, Shell B, Cunningham JT, Cunningham RL

Abstract
Sleep apnea is a common comorbidity of neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD). Previous studies have shown an association between elevated oxidative stress and inflammation with severe sleep apnea. Elevated oxidative stress and inflammation are also hallmarks of neurodegenerative diseases. We show increased oxidative stress and inflammation in a manner consistent with early stages of neurodegenerative disease in an animal model of mild sleep apnea. Male rats were exposed to 7 days chronic intermittent hypoxia (CIH) for 8 h/day during the light period. Following CIH, plasma was collected and tested for circulating oxidative stress and inflammatory markers associated with proinflammatory M1 or anti-inflammatory M2 profiles. Tissue punches from brain regions associated with different stages of neurodegenerative diseases (early stage: substantia nigra and entorhinal cortex; intermediate: hippocampus; late stage: rostral ventrolateral medulla and solitary tract nucleus) were also assayed for inflammatory markers. A subset of the samples was examined for 8-hydroxydeoxyguanosine (8-OHdG) expression, a marker of oxidative stress-induced DNA damage. Our results showed increased circulating oxidative stress and inflammation. Furthermore, brain regions associated with early-stage (but not late-stage) AD and PD expressed oxidative stress and inflammatory profiles consistent with reported observations in preclinical neurodegenerative disease populations. These results suggest mild CIH induces key features that are characteristic of early-stage neurodegenerative diseases and may be an effective model to investigate mechanisms contributing to oxidative stress and inflammation in those brain regions.

PMID: 28473320 [PubMed - in process]

New Models of Pregnancy-Associated Hypertension.

Fri, 05/05/2017 - 07:35
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New Models of Pregnancy-Associated Hypertension.

Am J Hypertens. 2017 May 02;:

Authors: Cushen SC, Goulopoulou S

Abstract
Pregnancy-associated hypertensive disorders are leading causes of maternal and fetal mortality. These include: pre-pregnancy hypertension that persists throughout gestation (chronic/preexisting hypertension), de novo hypertension that is diagnosed after 20 weeks of gestation and resolves after birth (gestational hypertension), de novo hypertension that is diagnosed after 20 weeks of gestation with or without proteinuria and end-organ damage (preeclampsia and eclampsia), and chronic hypertension with superimposed preeclampsia during gestation. Preeclampsia is the most severe form of these disorders. Animal models have been developed by employing surgical, genetic, and pharmacological approaches in order to recapitulate the maternal symptoms of preeclampsia and other hypertensive disorders of pregnancy. The scope of this brief review is to present an up-to-date synthesis of our knowledge of experimental models of pregnancy-associated hypertensive disorders. Novel models, defined in this review as characterized within the last 5 years, will be described and critically discussed. In this review, we will also discuss established experimental models of pregnancy-associated hypertensive disorders in the context of their contribution to new advances in our knowledge about the pathophysiology of these disorders and potential therapeutics. Emphasis will be placed on animal models of preeclampsia; however, models of other hypertensive disorders in pregnancy will also be reviewed.

PMID: 28472224 [PubMed - as supplied by publisher]

Immune senescence: significance of the stromal microenvironment.

Thu, 05/04/2017 - 07:32
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Immune senescence: significance of the stromal microenvironment.

Clin Exp Immunol. 2017 Jan;187(1):6-15

Authors: Masters AR, Haynes L, Su DM, Palmer DB

Abstract
The immune system undergoes age-associated changes known as immunosenescence, resulting in increased susceptibility to infections, cancers and autoimmunity in the aged. The basis of our understanding of immunosenescence has been derived primarily from studies examining intrinsic defects within many of the cells of the immune system. While these studies have provided insight into the mechanisms of immunosenescence, a picture is now emerging that the stromal microenvironment within lymphoid organs also contributes significantly to the age-associated decline of immune function. These extrinsic defects appear to impact the functional activity of immune cells and may offer a potential target to recover immune activity. Indeed, rejuvenation studies which have targeted the stromal niche have restored immune function in aged successfully, highlighting the impact of the microenvironment towards the aetiology of immunosenescence.

PMID: 27529161 [PubMed - indexed for MEDLINE]

Mechanical Concepts Applied in Congenital Heart Disease and Cardiac Surgery.

Tue, 05/02/2017 - 07:33
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Mechanical Concepts Applied in Congenital Heart Disease and Cardiac Surgery.

Ann Thorac Surg. 2017 Apr 27;:

Authors: Gerrah R, Haller SJ, George I

Abstract
All biological processes are governed by principles of physics that dictate the pathophysiology and even the treatment of congenital heart diseases. In this review, basic concepts such as flow, pressure, resistance, and velocity are introduced, followed by more complex laws that describe the relationship between these variables and the disease processes. Finally, physical phenomena such as turbulence, steal and runoff phenomenon, and energy loss are discussed. By application of these principles, one can accurately quantify modifications undertaken to treat diseases, for example, the size of a patch that augments a vessel and the angle of an anastomosis to allow a certain flow.

PMID: 28457478 [PubMed - as supplied by publisher]

The dual modulatory effects of efavirenz on GABAA receptors are mediated via two distinct sites.

Mon, 05/01/2017 - 07:36
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The dual modulatory effects of efavirenz on GABAA receptors are mediated via two distinct sites.

Neuropharmacology. 2017 Apr 26;:

Authors: Huang R, Chen Z, Dolan S, Schetz JA, Dillon GH

Abstract
Efavirenz is a widely prescribed medicine used to treat type 1 human immunodeficiency virus (HIV-1), the most prevalent pathogenic strain of the virus responsible for the acquired immune deficiency syndrome (AIDS) pandemic. Under prescribed dosing conditions, either alone or in combination therapy, efavirenz-induced CNS disturbances are frequently reported. Efavirenz was recently reported to interact in a similar concentration range with a number of receptors, transporters and ion channels including recombinant rat α1β2γ2 GABAA receptors whose actions were potentiated (Gatch et al., 2013; Dalwadi et al., 2016). Now we report on the molecular mechanism of efavirenz on GABAA receptors as a function of concentration and subunit composition via whole-cell recordings of GABA-activated currents from HEK293 cells expressing varying subunit configurations of GABAA receptors. Efavirenz elicited dual effects on the GABA response; it allosterically potentiated currents at low concentrations, whereas it inhibited currents at higher concentrations. The allosteric potentiating action on GABAA receptors was pronounced in the α1β2γ2, α2β2γ2 and α4β2γ2 configurations, greatly diminished in the α6β2γ2 configuration, and completely absent in the α3β2γ2 or α5β2γ2 configuration. In stark contrast, the inhibitory modulation of efavirenz at higher concentrations was evident in all subunit configurations examined. Moreover, efavirenz-induced modulatory effects were dependent on GABA concentration ([GABA]), with a pronounced impact on currents activated by low [GABA] but little effect at saturating [GABA]. Mutation of a highly-conserved threonine to phenylalanine in transmembrane domain 2 of the α1 subunit abolished the inhibitory effect of efavirenz in α1β2 receptors. Finally, mutations of any of the three conserved extracellular residues in α1/2/4 subunits to the conserved residues at the corresponding positions in α3/5 subunits (i.e., R84P, M89L or I120L) completely eliminated he potentiating effect of efavirenz in α1β2γ2 configuration. These findings demonstrate that efavirenz's positive allosteric modulation of the GABAA receptor is mediated via a novel allosteric site associated with the extracellular domain of the receptor.

PMID: 28456686 [PubMed - as supplied by publisher]

Genome Sequence of a Providencia stuartii Strain Isolated from Luciliasericata Salivary Glands.

Sun, 04/30/2017 - 07:32
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Genome Sequence of a Providencia stuartii Strain Isolated from Luciliasericata Salivary Glands.

Genome Announc. 2017 Apr 27;5(17):

Authors: Yuan Y, Zhang Y, Fu S, Crippen TL, Visi DK, Benbow ME, Allen MS, Tomberlin JK, Sze SH, Tarone AM

Abstract
We present here the draft genome sequence of a Providencia stuartii strain, derived from the salivary glands of larval Lucilia sericata, a common blow fly important to forensic, medical, and veterinary science. The genome sequence will help dissect coinfections involving P. stuartii and Proteus mirabilis, as well as blow fly-bacteria interactions.

PMID: 28450516 [PubMed - in process]

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