Recent Research Articles from UNTHSC

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NCBI: db=pubmed; Term="University of North Texas Health Science Center"[All Fields] OR "Univ. of North Texas Health Science Center"[All Fields] OR "UNT Health Science Center"[All Fields] OR "Osteopathic Research Center"[All Fields] OR "University of North Texas System College of Pharmacy"[All Fields] OR "UNT System College of Pharmacy"[All Fields] OR "College of Pharmacy, University of North Texas System"[All Fields]
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Comparison of Outcomes between Individuals with Pure and Mixed Lupus Nephritis: A Retrospective Study.

Thu, 06/16/2016 - 06:30

Comparison of Outcomes between Individuals with Pure and Mixed Lupus Nephritis: A Retrospective Study.

PLoS One. 2016;11(6):e0157485

Authors: Ilori TO, Enofe N, Oommen A, Cobb J, Navarrete J, Adedinsewo DA, Oshikoya O, Fevrier H, Farris AB, Plantinga L, Ojo AO

Abstract
INTRODUCTION: Lupus nephritis (LN) is a serious organ manifestation of systemic lupus erythematosus. Histologic overlap is relatively common in the six pathologic classes (I to VI) of LN. For example, mixed proliferative LN (MPLN) often includes features of classes III & V or classes IV & V combined. We performed a comparative evaluation of renal outcomes in patients with MPLN to patients with pure proliferative LN (PPLN) against pre-specified renal outcomes, and we also identified predictor of clinical outcomes among those with PPLN and MPLN.
HYPOTHESIS: Individuals with MPLN will have worse short-term renal outcomes compared to those with PPLN.
METHODS: We retrospectively reviewed 278 adult LN patients (≥18 years old) identified from an Emory University Hospital registry of native renal biopsies performed between January 2000 and December 2011. The final analytic sample consisted of individuals with a diagnosis of PPLN (n = 60) and MPLN (n = 96). We analyzed differences in clinical and laboratory characteristics at baseline. We also assessed associations between LN category and renal outcomes (complete remission and time to ESRD) with logistic and Cox proportional hazards models within two years of baseline.
RESULTS: The study population was predominantly female (83.97%) and African American (71.8%) with a mean age of 33.4 years at baseline. Over a median follow up of 1.02 years, we did not find any statistically significant associations between MPLN and the development of ESRD or remission when compared to patients with PPLN (adjusted HR = 0.30, 95% CI = 0.07, 1.26).
CONCLUSION: There was no association between mixed or pure histopathologic features of LN at presentation and rate of complete or partial remission but higher baseline eGFR was associated with a lower probability of complete remission among patients with lupus nephritis.

PMID: 27304068 [PubMed - as supplied by publisher]

Cerebral blood velocity regulation during progressive blood loss compared with lower body negative pressure in humans.

Thu, 06/16/2016 - 06:30
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Cerebral blood velocity regulation during progressive blood loss compared with lower body negative pressure in humans.

J Appl Physiol (1985). 2015 Sep 15;119(6):677-85

Authors: Rickards CA, Johnson BD, Harvey RE, Convertino VA, Joyner MJ, Barnes JN

Abstract
Lower body negative pressure (LBNP) is often used to simulate blood loss in humans. It is unknown if cerebral blood flow responses to actual blood loss are analogous to simulated blood loss during LBNP. Nine healthy men were studied at baseline, during three levels of LBNP (5 min at -15, -30, and -45 mmHg), and during three levels of blood loss (333, 667, and 1,000 ml). LBNP and blood loss conditions were randomized. Intra-arterial mean arterial pressure (MAP) during LBNP was similar to that during blood loss (P ≥ 0.42). Central venous pressure (2.8 ± 0.7 vs. 4.0 ± 0.8, 1.2 ± 0.6 vs. 3.5 ± 0.8, and 0.2 ± 0.9 vs. 2.1 ± 0.9 mmHg for levels 1, 2, and 3, respectively, P ≤ 0.003) and stroke volume (71 ± 4 vs. 80 ± 3, 60 ± 3 vs. 74 ± 3, and 51 ± 2 vs. 68 ± 4 ml for levels 1, 2, and 3, respectively, P ≤ 0.002) were lower during LBNP than blood loss. Despite differences in central venous pressure, middle cerebral artery velocity (MCAv) and cerebrovascular conductance were similar between LBNP and blood loss at each level (MCAv at level 3: 62 ± 6 vs. 66 ± 5 cm/s, P = 0.37; cerebrovascular conductance at level 3: 0.72 ± 0.05 vs. 0.73 ± 0.05 cm·s(-1)·mmHg(-1), P = 0.53). While the slope of the MAP-MCAv relationship was slightly different between LBNP and blood loss (0.41 ± 0.03 and 0.66 ± 0.04 cm·s(-1)·mmHg(-1), respectively, P = 0.05), time domain gain between MAP and MCAv at maximal LBNP/blood loss (P = 0.23) and low-frequency MAP-mean MCAv transfer function coherence, gain, and phase were similar (P ≥ 0.10). Our results suggest that cerebral hemodynamic responses to LBNP to -45 mmHg and blood loss up to 1,000 ml follow a similar trajectory, and the arterial pressure-cerebral blood velocity relationship is not altered from baseline under these conditions.

PMID: 26139213 [PubMed - indexed for MEDLINE]

The US Cancer Moonshot initiative.

Wed, 06/15/2016 - 06:33

The US Cancer Moonshot initiative.

Lancet Oncol. 2016 May;17(5):e178-e180

Authors: Aelion CM, Airhihenbuwa CO, Alemagno S, Amler RW, Arnett DK, Balas A, Bertozzi S, Blakely CH, Boerwinkle E, Brandt-Rauf P, Buekens PM, Chandler GT, Chang RW, Clark JE, Cleary PD, Curran JW, Curry SJ, Roux AV, Dittus R, Ellerbeck EF, El-Mohandes A, Eriksen MP, Erwin PC, Evans G, Finnegan JR, Fried LP, Frumkin H, Galea S, Goff DC, Goldman LR, Guilarte TR, Rivera-Gutiérrez R, Halverson PK, Hand GA, Harris CM, Healton CG, Hennig N, Heymann J, Hunter D, Hwang W, Jones RM, Klag MJ, Klesges LM, Lahey T, Lawlor EF, Maddock J, Martin WJ, Mazzaschi AJ, Michael M, Mohammed SD, Nasca PC, Nash D, Ogunseitan OA, Perez RA, Perri M, Petersen DJ, Peterson DV, Philbert M, Pinto-Martin J, Raczynski JM, Raskob GE, Rimer BK, Rohrbach LA, Rudkin LL, Siminoff L, Szapocznik J, Thombs D, Torabi MR, Weiler RM, Wetle TF, Williams PL, Wykoff R, Ying J

PMID: 27301041 [PubMed - as supplied by publisher]

Increased Global DNA Methylation and Decreased TGFβ1 Promoter Methylation in Glaucomatous Lamina Cribrosa Cells.

Wed, 06/15/2016 - 06:33

Increased Global DNA Methylation and Decreased TGFβ1 Promoter Methylation in Glaucomatous Lamina Cribrosa Cells.

J Glaucoma. 2016 Jun 13;

Authors: McDonnell FS, McNally SA, Clark AF, O'Brien CJ, Wallace DM

Abstract
BACKGROUND: Glaucoma is an optic neuropathy that affects 60 million people worldwide. There is an underlying fibrosis associated with the lamina cribrosa (LC) in glaucoma. DNA methylation is well established in regulating fibrosis and may be a therapeutic target for glaucoma. The purpose of this study was to compare global DNA methylation levels in primary human normal (NLC) and glaucomatous (GLC) cells, and to investigate DNA methylation in driving fibrosis through regulation of transforming growth factor β1 (TGFβ1).
MATERIALS AND METHODS: LC cells were cultured from normal and glaucomatous human donors. Global methylation was assessed by ELISA. qPCR was conducted for DNA methyltransferases (DNMTs), methyl-CpG-binding protein 2 (MeCP2), TGFβ 1 and 2, collagen 1α1 (COL1A1), and α-smooth muscle actin (αSMA). TGFβ1 and DNMT1 were examined by immunofluorescence. Methylation of the TGFβ1 promoter was determined by methylation-specific PCR (MSP).
RESULTS: Global DNA methylation demonstrated an increase in GLC compared with NLC cells (P<0.05). The previously mentioned methylation and matrix genes were increased in GLC compared with NLC cells (P<0.05). Immunofluorescence showed increased TGFβ1 and DNMT1 in GLC compared with NLC cells. MSP showed increased unmethylated DNA in the TGFβ1 promoter of GLC compared with NLC cells.
CONCLUSIONS: We found increased expression of fibrotic genes in GLC cells and demonstrated an increase in global DNA methylation and in associated enzymes in GLC cells. Furthermore, we showed decreased promoter methylation of TGFβ1 in GLC cells. Determining a role for methylation in glaucoma and in regulating TGFβ1 may provide a novel therapeutic approach.

PMID: 27300643 [PubMed - as supplied by publisher]

Resolving the etiology of atopic disorders by using genetic analysis of racial ancestry.

Wed, 06/15/2016 - 06:33

Resolving the etiology of atopic disorders by using genetic analysis of racial ancestry.

J Allergy Clin Immunol. 2016 Jun 10;

Authors: Gupta J, Johansson E, Bernstein JA, Chakraborty R, Khurana Hershey GK, Rothenberg ME, Mersha TB

Abstract
Atopic dermatitis (AD), food allergy, allergic rhinitis, and asthma are common atopic disorders of complex etiology. The frequently observed atopic march from early AD to asthma, allergic rhinitis, or both later in life and the extensive comorbidity of atopic disorders suggest common causal mechanisms in addition to distinct ones. Indeed, both disease-specific and shared genomic regions exist for atopic disorders. Their prevalence also varies among races; for example, AD and asthma have a higher prevalence in African Americans when compared with European Americans. Whether this disparity stems from true genetic or race-specific environmental risk factors or both is unknown. Thus far, the majority of the genetic studies on atopic diseases have used populations of European ancestry, limiting their generalizability. Large-cohort initiatives and new analytic methods, such as admixture mapping, are currently being used to address this knowledge gap. Here we discuss the unique and shared genetic risk factors for atopic disorders in the context of ancestry variations and the promise of high-throughput "-omics"-based systems biology approach in providing greater insight to deconstruct their genetic and nongenetic etiologies. Future research will also focus on deep phenotyping and genotyping of diverse racial ancestry, gene-environment, and gene-gene interactions.

PMID: 27297995 [PubMed - as supplied by publisher]

Involvement of AMPA Receptor and Its Flip and Flop Isoforms in Retinal Ganglion Cell Death Following Oxygen/Glucose Deprivation.

Wed, 06/15/2016 - 06:33
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Involvement of AMPA Receptor and Its Flip and Flop Isoforms in Retinal Ganglion Cell Death Following Oxygen/Glucose Deprivation.

Invest Ophthalmol Vis Sci. 2016 Feb;57(2):508-26

Authors: Park YH, Broyles HV, He S, McGrady NR, Li L, Yorio T

Abstract
PURPOSE: The α-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) receptors (AMPAR) subunits can be posttranscriptionally modified by alternative splicing forming flip and flop isoforms. We determined if an ischemia-like insult to retinal ganglion cells (RGCs) increases AMPAR susceptibility to s-AMPA-mediated excitotoxicity through changes in posttranscriptional modified isoforms.
METHODS: Purified neonatal rat RGCs were subjected to either glucose deprivation (GD) or oxygen/glucose deprivation (OGD) conditions followed by treatment with either 100 μM s-AMPA or Kainic acid. A live-dead assay and caspase 3 assay was used to assess cell viability and apoptotic changes, respectively. We used JC-1 dye and dihydroethidium to measure mitochondria depolarization and reactive oxygen species (ROS), respectively. Calcium imaging with fura-2AM was used to determine intracellular calcium, while the fluorescently-labeled probe, Nanoprobe1, was used to detect calcium-permeable AMPARs. Quantitative PCR (qPCR) analysis was done to determine RNA editing sites AMPAR isoforms.
RESULTS: Glucose deprivation, as well as an OGD insult followed by AMPAR stimulation, produced a significant increase in RGC death. Retinal ganglion cell death was independent of caspase 3/7 activity, but was accompanied by increased mitochondrial depolarization and increased ROS production. This was associated with an elevated intracellular Ca(2+) and calcium permeable-AMPARs. The mRNA expression of GLUA2 and GLUA3 flop isoform decreased significantly, while no appreciable changes were found in the corresponding flip isoforms. There were no changes in the Q/R editing of GLUA2, while R/G editing of GLUA2 flop declined under these conditions.
CONCLUSIONS: Following oxidative injury, RGCs become more susceptible to AMPAR-mediated excitotoxicity. RNA editing and changes in alternative spliced flip and flop isoforms of AMPAR subunits may contribute to increased RGC death.

PMID: 26868754 [PubMed - indexed for MEDLINE]

MicroRNA-124 Targets Tip110 Expression and Regulates Hematopoiesis.

Wed, 06/15/2016 - 06:33
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MicroRNA-124 Targets Tip110 Expression and Regulates Hematopoiesis.

Stem Cells Dev. 2015 Sep 1;24(17):2009-17

Authors: Liu Y, Huang X, Timani KA, Broxmeyer HE, He JJ

Abstract
MicroRNA (miR) regulates hematopoiesis through targeting different genes post-transcriptionally. We have recently shown that Tip110 expression is downregulated during hematopoietic stem cell differentiation. However, the underlying mechanisms are not known. In this study, we identified a conserved miR-124-binding site on the Tip110 3'-untranslated region (3'-UTR) and showed that Tip110 was downregulated by miR-124 through its 3'-UTR. We then examined the relationship among miR-124 and Tip110 expression and differentiation of human cord blood CD34(+) cells. We found that miR-124 was expressed in a low level in human cord blood CD34(+) cells, but it was considerably upregulated during culturing and differentiation of these cells. Moreover, we demonstrated that miR-124 expression decreased Tip110 expression and promoted differentiation of human cord blood CD34(+) cells, while miR-124 knockdown increased Tip110 expression, slowed down differentiation of human cord blood CD34(+) cells, and caused an expansion of hematopoietic progenitor cells in vitro. Finally, we used mouse embryonic fibroblasts derived from Tip110 transgenic mice, performed the exon array analysis, and found that Tip110 altered a number of genes in the hematopoiesis pathways. Dnmt3a as de novo methyltransferase was also significantly upregulated. That miR-124 was markedly upregulated during human cord blood CD34(+) cell differentiation could be the result of direct loss of its promoter methylation from Dnmt3a. Taken together, our study demonstrates that miR-124 regulates Tip110 expression and differentiation of human cord blood CD34(+) cells and suggests important roles of miR-124/Tip110 in hematopoiesis.

PMID: 25928721 [PubMed - indexed for MEDLINE]

Comparing the Knotless Tension Band and the Traditional Stainless Steel Wire Tension Band Fixation for Medial Malleolus Fractures: A Retrospective Clinical Study.

Tue, 06/14/2016 - 06:30
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Comparing the Knotless Tension Band and the Traditional Stainless Steel Wire Tension Band Fixation for Medial Malleolus Fractures: A Retrospective Clinical Study.

Scientifica (Cairo). 2016;2016:3201678

Authors: Downey MW, Duncan K, Kosmopoulos V, Motley TA, Carpenter BB, Ogunyankin F, Garrett A

Abstract
The traditional stainless steel wire tension band (WTB) has been popularized for small avulsion fractures at the medial malleolus. Despite the tension band principle creating a stable construct, complications continue to arise utilizing the traditional stainless steel WTB with patients experiencing hardware irritation at the tension band site and subsequent hardware removal. Coupled with hardware irritation is fatigue failure with the wire. The goal of this investigation was to retrospectively compare this traditional wire technique to an innovative knotless tension band (KTB) technique in order to decrease costly complications. A total of 107 patients were reviewed with a minimum follow-up of 1 year. Outcome measures include descriptive data, fracture classification, results through economic costs, and fixation results (including hardware status, healing status, pain status, and time to healing). The KTB group had a 13% lower true cost as compared to the WTB group while the fixation results were equivocal for the measured outcomes. Our results demonstrate that the innovative KTB is comparable to the traditional WTB while offering a lower true cost, an irritation free reduction all without the frustration of returning to the operating room for additional hardware removal, which averages approximately to $8,288.

PMID: 27293969 [PubMed]

Homelessness and ED use: myths and facts- the author's reply.

Tue, 06/14/2016 - 06:30
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Homelessness and ED use: myths and facts- the author's reply.

Am J Emerg Med. 2016 Feb;34(2):307-8

Authors: Wang H, Nejtek VA, Robinson RD

PMID: 26589465 [PubMed - indexed for MEDLINE]

Trileaflet Mitral Valve with Three Papillary Muscles Associated with Hypertrophic Cardiomyopathy: A Novel Case.

Tue, 06/14/2016 - 06:30
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Trileaflet Mitral Valve with Three Papillary Muscles Associated with Hypertrophic Cardiomyopathy: A Novel Case.

Echocardiography. 2015 Sep;32(9):1435-7

Authors: Rosanio S, Simonsen CJ, Starwalt J, Keylani AM, Vitarelli A

Abstract
Congenital mitral valve (MV) malformations are uncommon, except for MV prolapse. Despite their infrequency, most of them are well-known and defined entities, such as congenital MV stenosis with two papillary muscles, parachute MV, supravalvular mitral ring, hypoplastic MV, isolated cleft in the anterior and/or posterior leaflets, and double-orifice MV. A trileaflet MV with three separate papillary muscles with concordant atrioventricular and ventricle-arterial connections is exceptionally rare. To the best of the authors' knowledge, it has been reported only once in association with subaortic valvular stenosis. We hereby describe a novel case associated with hypertrophic cardiomyopathy.

PMID: 25809503 [PubMed - indexed for MEDLINE]

Exaggerated sympathoexcitatory reflexes develop with changes in the rostral ventrolateral medulla in obese Zucker rats.

Fri, 06/10/2016 - 06:36

Exaggerated sympathoexcitatory reflexes develop with changes in the rostral ventrolateral medulla in obese Zucker rats.

Am J Physiol Regul Integr Comp Physiol. 2016 Jun 8;:ajpregu.00085.2016

Authors: Huber DA, Schreihofer AM

Abstract
Obesity leads to altered autonomic reflexes that reduce stability of mean arterial pressure (MAP). Sympathoinhibitory reflexes such as baroreflexes are impaired, but reflexes that raise MAP appear to be augmented. In obese Zucker rats (OZR) sciatic nerve stimulation evokes larger increases in MAP by unknown mechanisms. We sought to determine the autonomic underpinnings of this enhanced somatic pressor reflex, and whether other sympathoexcitatory reflexes are augmented. We also determined whether their final common pathway, glutamatergic activation of the rostral ventrolateral medulla (RVLM), was enhanced in male OZR compared to lean Zucker rats (LZR). Sciatic nerve stimulation or activation of the nasopharyngeal reflex evoked larger rises in splanchnic SNA (79% and 45% larger in OZR respectively, P<0.05) and MAP in urethane-anesthetized, ventilated, paralyzed adult OZR compared to LZR. After elimination of baroreflex feedback by pharmacological prevention of changes in MAP and heart rate, these two sympathoexcitatory reflexes were still exaggerated in OZR (167% and 69% larger respectively, P<0.05). In adult OZR microinjections of glutamate, AMPA, or NMDA into the RVLM produced larger rises in SNA (~61% larger in OZR, P<0.05 for each drug) and MAP, but stimulation of axonal fibers in the upper thoracic spinal cord yielded equivalent responses in OZR and LZR. In juvenile OZR and LZR, sympathoexcitatory reflexes and physiological responses to RVLM activation were comparable. These data suggest the ability of glutamate to activate the RVLM becomes enhanced in adult OZR and may contribute to the development of exaggerated sympathoexcitatory responses independent of impaired baroreflexes.

PMID: 27280427 [PubMed - as supplied by publisher]

The Role of Presenilin-1 in the Excitatory Stress of Ethanol Withdrawal.

Fri, 06/10/2016 - 06:36

The Role of Presenilin-1 in the Excitatory Stress of Ethanol Withdrawal.

J Pharmacol Exp Ther. 2016 Jun 8;

Authors: Jung ME, Metzger DB, Das HK

Abstract
Presenilin-1 (PS1) is a core component of γ-secretase that is involved in neurodegeneration. We have previously shown that PS1 interacts with a MAPK (JNK), and another MAPK (p38) is activated by ethanol withdrawal (EW), abrupt termination from chronic ethanol-exposure. EW is excitotoxic in nature, induces glutamate upregulation, and provokes neuronal damage. Here, we explored a potential mechanistic pathway involving glutamate, p38 (p38α isozyme), and PS1 that may mediate EW-induced excitotoxic stress. We used the prefrontal cortex of male rats withdrawn from a chronic ethanol diet. Additionally, we used ethanol withdrawn HT22 cells (mouse hippocampal) treated with the inhibitor of glutamate receptors (MK-801), p38α (SB203580), or γ-secretase (DAPT) during EW. Separately, ethanol-free HT22 cells were exposed to glutamate with or without SB203580 or DAPT. Protein levels, mRNA levels, and cell viability were assessed using immunoblotting, q-PCR, and Calcein assay, respectively. The prefrontal cortex of ethanol withdrawn rats or HT22 cells showed an increase in PS1 and p38α, which was attenuated by MK-801 and SB203580, but mimicked by glutamate treatment to ethanol-free HT22 cells. DAPT attenuated the toxic effect of EW or glutamate on HT22 cells. These results suggest that PS1 expression is triggered by glutamate through p38α, contributing to the excitotoxic stimulus of EW.

PMID: 27278235 [PubMed - as supplied by publisher]

HIV-1 and alcohol abuse promote astrocyte inflammation: A mechanistic synergy via the cytosolic phospholipase A2 pathway.

Fri, 06/10/2016 - 06:36
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HIV-1 and alcohol abuse promote astrocyte inflammation: A mechanistic synergy via the cytosolic phospholipase A2 pathway.

Cell Death Dis. 2015;6:e2017

Authors: Pandey R, Ghorpade A

PMID: 26658191 [PubMed - indexed for MEDLINE]

Interaction of astrocytes and T cells in physiological and pathological conditions.

Fri, 06/10/2016 - 06:36
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Interaction of astrocytes and T cells in physiological and pathological conditions.

Brain Res. 2015 Oct 14;1623:63-73

Authors: Xie L, Yang SH

Abstract
The central nervous system (CNS) has long been recognized as a site of 'immune privilege' because of the existence of the blood brain barrier (BBB) which presumably isolates CNS from the peripheral immunosurveillance. Different from the peripheral organs, CNS is unique in response to all forms of CNS injury and disease which is mainly mediated by resident microglia and astrocyte. There is increasing evidence that immune cells are not only involved in neuroinflammation process but also the maintenance of CNS homeostasis. T cells, an important immune cell population, are involved in the pathogenesis of some neurological diseases by inducing either innate or adaptive immune responses. Astrocytes, which are the most abundant cell type in the CNS, maintain the integrity of BBB and actively participate in the initiation and progression of neurological diseases. Surprisingly, how astrocytes and T cells interact and the consequences of their interaction are not clear. In this review we briefly summarized T cells diversity and astrocyte function. Then, we examined the evidence for the astrocytes and T cells interaction under physiological and pathological conditions including ischemic stroke, multiple sclerosis, viral infection, and Alzheimer's disease. This article is part of a Special Issue entitled SI: Cell Interactions In Stroke.

PMID: 25813828 [PubMed - indexed for MEDLINE]

Coupling of neurogenesis and angiogenesis after ischemic stroke.

Fri, 06/10/2016 - 06:36
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Coupling of neurogenesis and angiogenesis after ischemic stroke.

Brain Res. 2015 Oct 14;1623:166-73

Authors: Ruan L, Wang B, ZhuGe Q, Jin K

Abstract
Stroke is a leading cause of mortality and severe long-term disability worldwide. Development of effective treatment or new therapeutic strategies for ischemic stroke patients is therefore crucial. Ischemic stroke promotes neurogenesis by several growth factors including FGF-2, IGF-1, BDNF, VEGF and chemokines including SDF-1, MCP-1. Stroke-induced angiogenesis is similarly regulated by many factors most notably, eNOS and CSE, VEGF/VEGFR2, and Ang-1/Tie2. Important findings in the last decade have revealed that neurogenesis is not the stand-alone consideration in the fight for full functional recovery from stroke. Angiogenesis has been also shown to be critical in improving post-stroke neurological functional recovery. More than that, recent evidence has shown a highly possible interplay or dependence between stroke-induced neurogenesis and angiogenesis. Moving forward, elucidating the underlying mechanisms of this coupling between stroke-induced neurogenesis and angiogenesis will be of great importance, which will provide the basis for neurorestorative therapy. This article is part of a Special Issue entitled SI: Cell Interactions In Stroke.

PMID: 25736182 [PubMed - indexed for MEDLINE]

Postmortem medicolegal genetic diagnostics also require reporting guidance.

Fri, 06/10/2016 - 06:36
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Postmortem medicolegal genetic diagnostics also require reporting guidance.

Eur J Hum Genet. 2016 Mar;24(3):329-30

Authors: Sajantila A, Budowle B

PMID: 25469540 [PubMed - indexed for MEDLINE]

Exfoliative Excrement.

Thu, 06/09/2016 - 14:33

Exfoliative Excrement.

JAMA Dermatol. 2016 Jun 1;152(6):701

Authors: Roman J, Reynolds SD

PMID: 27276354 [PubMed - as supplied by publisher]

Sources and implications of NADH/NAD(+) redox imbalance in diabetes and its complications.

Thu, 06/09/2016 - 14:33

Sources and implications of NADH/NAD(+) redox imbalance in diabetes and its complications.

Diabetes Metab Syndr Obes. 2016;9:145-153

Authors: Wu J, Jin Z, Zheng H, Yan LJ

Abstract
NAD(+) is a fundamental molecule in metabolism and redox signaling. In diabetes and its complications, the balance between NADH and NAD(+) can be severely perturbed. On one hand, NADH is overproduced due to influx of hyperglycemia to the glycolytic and Krebs cycle pathways and activation of the polyol pathway. On the other hand, NAD(+) can be diminished or depleted by overactivation of poly ADP ribose polymerase that uses NAD(+) as its substrate. Moreover, sirtuins, another class of enzymes that also use NAD(+) as their substrate for catalyzing protein deacetylation reactions, can also affect cellular content of NAD(+). Impairment of NAD(+) regeneration enzymes such as lactate dehydrogenase in erythrocytes and complex I in mitochondria can also contribute to NADH accumulation and NAD(+) deficiency. The consequence of NADH/NAD(+) redox imbalance is initially reductive stress that eventually leads to oxidative stress and oxidative damage to macromolecules, including DNA, lipids, and proteins. Accordingly, redox imbalance-triggered oxidative damage has been thought to be a major factor contributing to the development of diabetes and its complications. Future studies on restoring NADH/NAD(+) redox balance could provide further insights into design of novel antidiabetic strategies.

PMID: 27274295 [PubMed - as supplied by publisher]

Depressive symptoms as a cause and effect of job loss in men and women: evidence in the context of organisational downsizing from the Swedish Longitudinal Occupational Survey of Health.

Thu, 06/09/2016 - 14:33
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Depressive symptoms as a cause and effect of job loss in men and women: evidence in the context of organisational downsizing from the Swedish Longitudinal Occupational Survey of Health.

BMC Public Health. 2015;15:1045

Authors: Andreeva E, Magnusson Hanson LL, Westerlund H, Theorell T, Brenner MH

Abstract
BACKGROUND: Few studies have examined depression as both a cause and effect of unemployment, but no prior work investigated these relationships in the context of organisational downsizing. We explored whether the exposure to downsizing is associated with subsequent depression (social causation), and whether pre-existing depression increases the risk of being laid off when organisations downsize (health selection).
METHODS: Two successive waves of the nationally representative Swedish Longitudinal Occupational Survey of Health represented the baseline (2008) and follow-up (2010) of this study. Analyses included 196 workers who lost their jobs through downsizing, 1462 layoff survivors remaining in downsized organisations and 1845 employees of non-downsized workplaces. The main outcomes were: (1) Depressive symptoms at follow-up, assessed with a brief subscale from the Symptom Checklist 90, categorised by severity levels ("major depression", "less severe symptoms" and "no depression") and analysed in relation to earlier downsizing exposure; (2) Job loss in persons with downsizing in relation to earlier depressive symptoms. The associations were assessed by means of multinomial logistic regression.
RESULTS: Job loss consistently predicted subsequent major depression among men and women, with a somewhat greater effect size in men. Surviving a layoff was significantly associated with subsequent major depression in women but not in men. Women with major depression have increased risks of exclusion from employment when organisations downsize, whereas job loss in men was not significantly influenced by their health.
CONCLUSIONS: The evidence from this study suggests that the relative importance of social causation and health selection varies by gender in the context of organisational downsizing. Strategies for handling depression among employees should be sensitive to gender-specific risks during layoffs. Policies preventing social exclusion can be important for female workers at higher risk of depression.

PMID: 26458894 [PubMed - indexed for MEDLINE]

Universal cholesterol screening of children in community-based ambulatory pediatric clinics.

Thu, 06/09/2016 - 14:33
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Universal cholesterol screening of children in community-based ambulatory pediatric clinics.

J Clin Lipidol. 2015 Sep-Oct;9(5 Suppl):S88-92

Authors: Wilson DP, Davis S, Matches S, Shah D, Leung-Pineda V, Mou M, Hamilton L, McNeal CJ, Bowman WP

Abstract
BACKGROUND: Early identification and treatment of individuals with elevated levels of atherogenic cholesterol have been shown to be effective and safe in reducing morbidity and mortality, especially in familial hypercholesterolemia. To better inform providers and identify children and adolescents at risk of premature cardiovascular disease, in November 2011, the National Heart, Lung, and Blood Institute (NHLBI) published guidelines recommending cholesterol screening of all children aged between 9 to 11 and 17 to 21 years regardless of the child's general health or the presence or the absence of cardiovascular disease risk factors.
OBJECTIVE: To compare the number of 9- to 11-year-old children screened for hypercholesterolemia in 5 community-based ambulatory pediatric clinics before and after publication of the NHLBI's guidelines.
METHODS: Practice demographics, screening frequency, and test results for each clinic were collected before and after publication of the NHLBI's recommendation. Provider education was provided between measures.
RESULTS: Of all eligible 9- to 11-year-old children, 489 (17.1%) were screened before and 686 (20.1%) after the NHLBI's guidelines and provider education.
CONCLUSIONS: Baseline rates of lipid screening for the 5 community-based ambulatory pediatric clinics were higher than those previously reported and increased significantly after publication of the NHLBI's recommendations and provider education. However, overall screening rates remained low. Given the high prevalence of premature cardiovascular disease associated with atherogenic cholesterol, especially familial hypercholesterolemia, additional strategies are needed to improve screening rates.

PMID: 26343216 [PubMed - indexed for MEDLINE]

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