LSUHSC Shreveport

Shreveport, LA, United States

LSUHSC Shreveport

Shreveport, LA, United States
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McCarty D.E.,LSUHSC Shreveport | Reddy A.,LSUHSC Shreveport | Keigley Q.,Louisiana State University in Shreveport | Kim P.Y.,LSUHSC Shreveport | And 2 more authors.
Nature and Science of Sleep | Year: 2013

Background: The purpose of this cross-sectional study was to test the hypothesis that serum vitamin D levels are abnormally low in sleep clinic patients admitting to chronic nonspecific musculoskeletal pain and to assess the associated risk factors. A secondary purpose was to identify a clinical biomarker for vitamin D deficiency. Methods: We enrolled 153 consecutive patients who admitted to the presence of chronic nonspecific musculoskeletal pain during a comprehensive sleep evaluation at a specialist sleep medicine clinic within an academic center. Venous blood sampling was performed for determination of serum 25-hydroxyvitamin D. Risk factors for vitamin D deficiency (25-hydroxyvitamin D , 20 ng/mL) were identified by odds ratios. Receiver-operating characteristic curve analysis was performed with 10-fold cross-validation to identify a biomarker for vitamin D deficiency calculated by linear discriminant analysis. Results: The mean serum 25-hydroxyvitamin D level was 19.8 ± 11.1, with 54% of the study population having vitamin D deficiency. This mean 25-hydroxyvitamin D level was lower than that observed historically in healthy controls, and was either similar or lower than in all but one representative historical cohort formed on the basis of chronic nonspecific musculoskeletal pain. Risk factors for vitamin D deficiency were black ethnicity, age , 60 years, and obesity. These risk factors were identified both in the entire cohort and separately in subgroups with and without obstructive sleep apnea. The biomarker (based on race, age, and body mass index) had a sensitivity and specificity for predicting vitamin D deficiency of 0.73 and 0.74, respectively. Conclusion: Vitamin D deficiency was prevalent in patients with sleep disorders and chronic nonspecific musculoskeletal pain on evaluation in a sleep medicine clinic. Vitamin D deficiency was reliably estimated in the study population using a biomarker derived from common demographic characteristics. © 2013 McCarty et al, publisher and licensee Dove Medical Press Ltd.


Ambekar S.,LSUHSC S | Amene C.,LSUHSC Shreveport | Sonig A.,Louisiana State University Health Sciences Center | Guthikonda B.,LSUHSC S | Nanda A.,Louisiana State University Health Sciences Center
Journal of Neurological Surgery, Part B: Skull Base | Year: 2013

Background Retrosigmoid transtentorial (RTT) and retrosigmoid intradural suprameatal (RISA) approaches have been used in the treatment of petroclival tumors. Objective To compare the area of exposure of brainstem and petroclival region obtained through RTT and RISA in cadaveric specimens. Methods Five cadaveric specimens with a total of 10 sides were analyzed. RTT and RISA were performed on five sides each. Brainstem and petroclival surface exposure were measured using both the approaches. These values were compared between the two approaches. Results Brainstem area exposure with RTT was 441 ± 63 mm 2 and that with RISA was 311 ± 61 mm2. Student's t-test revealed that the difference was significant (p = 0.01). The area of petroclival exposure medial to the Meckel cave through RTT was 696 ± 57 mm2, and that through RISA was 716 ± 51 mm2 (p = 0.69). The area of brainstem exposure between V and VII-VII complex through RTT and RISA was 387 ± 86 mm2 and 378 ± 76 mm2 (p = 0.87). Conclusion The RTT approach is an excellent approach to ventrolateral brainstem and petroclival region. It provides greater superoventral exposure of the ventrolateral brainstem than RISA and provides similar petroclival exposure. © 2013 Georg Thieme Verlag KG Stuttgart - New York.


Maxwell J.H.,University of Pittsburgh | Mehta V.,LSUHSC Shreveport | Wang H.,University of Pittsburgh | Cunningham D.,University of Pittsburgh | And 4 more authors.
Laryngoscope | Year: 2014

Objectives/Hypothesis To determine posttreatment quality of life (QOL) in head and neck cancer patients, stratifying by human papillomavirus (HPV)/p16 status and primary treatment modality. Study Design Retrospective study. Methods One hundred and seventy-seven patients (N=177) with head and neck squamous cell carcinoma and known HPV/p16 status were included. All patients completed at least one baseline or posttreatment University of Washington QOL survey. QOL scores were averaged and compared across patients, stratifying by HPV/p16 status and primary treatment modality (surgical vs. nonsurgical). In the analysis, p16 was used as a surrogate marker for HPV. Results Of the 177 patients, 80 (45.2%) were p16-positive and 49.7% of subsites were oropharyngeal. Nearly 60% (105/177) of patients underwent primary surgery, 26.7% (28/105) of patients with transoral robotic or laser techniques. The remainder 40.7% of patients underwent primary radiation and/or chemotherapy. Overall, QOL scores were better for p16-positive patients compared to p16-negative patients at baseline (P=0.008), at 6 months posttreatment (P=0.034), and at greater than 1 year posttreatment (P=0.013). P16-positive patients had better QOL scores in speech (P=0.0009), chewing (P=0.0004), and swallowing (P=0.021) after 1 year posttreatment compared to p16-negative patients. Primary treatment modality did not affect overall QOL or any of the 12 QOL categories in p16-positive patients at any time point. At over 1 year posttreatment, QOL was at or above baseline in both p16-positive treatment groups. Conclusion The p16-positive patients had better baseline and posttreatment overall QOL compared to p16-negative patients. The overall and category specific QOL scores for p16-positive patients were not affected by primary treatment modality. Level of Evidence 4. Laryngoscope, 124:1592-1597, 2014 © 2013 The American Laryngological, Rhinological and Otological Society, Inc.


Wang Y.,LSUHSC Shreveport | Wang Y.,Louisiana State University Health Sciences Center | Lewis D.F.,University of Cincinnati | Gu Y.,LSUHSC Shreveport | And 2 more authors.
Hypertension | Year: 2011

Increased inflammatory response plays a significant role in the vascular pathophysiology in preeclampsia. However, the mechanism for increased inflammatory response in preeclampsia is largely unknown. Interleukin (IL)-6 levels are elevated in women with preeclampsia. IL-6 and its receptors, IL-6R and glycoprotein (gp)130, play a critical role in mediating antiinflammatory response via induction of SOCS-3 (suppressor of cytokine signaling-3). However, IL-6 receptor levels and expressions have not been studied in preeclampsia. In this study, we measured IL-6 and its 2 soluble receptors, soluble IL-6R and soluble gp130, in maternal plasma from normal and preeclamptic pregnant women and found that not only IL-6 but also soluble gp130 levels were significantly higher in preeclamptic women than in normotensive pregnant controls. We further examined IL-6R, gp130, and SOCS-3 expressions in maternal vessels and leukocytes and found that gp130 and SOCS-3 expressions were downregulated in both vessel endothelium and leukocytes from preeclampsia. Different patterns for IL-6R and gp130 expressions were found. IL-6R expression was also downregulated in leukocytes from preeclampsia. Our results suggest that increased plasma soluble gp130/soluble IL-6R/IL-6 ratio and reduced membrane transsignaling gp130 expression could contribute to decreased SOCS-3 expression and subsequent reduction in SOCS-3 antiinflammatory activity in women with preeclampsia. Thus, reduced gp130 and SOCS-3 expressions may offer, at least in part, a plausible explanation of reduced antiinflammatory protection in the maternal vascular system in preeclampsia. © 2011 American Heart Association. All rights reserved.


Zhong W.,Harbin Medical University | Gu B.,LSUHSC Shreveport | Gu Y.,LSUHSC Shreveport | Groome L.J.,LSUHSC Shreveport | And 2 more authors.
Journal of Steroid Biochemistry and Molecular Biology | Year: 2014

Endothelial dysfunction associated with vitamin D deficiency has been linked to many chronic vascular diseases. Vitamin D elicits its bioactive actions by binding to its receptor, vitamin D receptor (VDR), on target cells and organs. In the present study, we investigated the role of VDR in response to 1,25(OH)2D3 stimulation and oxidative stress challenge in endothelial cells. We found that 1,25(OH)2D3 not only induced a dose- and time-dependent increase in VDR expression, but also induced up-regulation of vascular endothelial growth factor (VEGF) and its receptors (Flt-1 and KDR), as well as antioxidant CuZn-superoxide dismutase (CuZn-SOD) expression in endothelial cells. We demonstrated that inhibition of VDR by VDR siRNA blocked 1,25(OH)2D3 induced increased VEGF and KDR expression and prevented 1,25(OH)2D3 induced endothelial proliferation/migration. Using CoCl2, a hypoxic mimicking agent, we found that hypoxia/oxidative stress not only reduced CuZn-SOD expression, but also down-regulated VDR expression in endothelial cells, which could be prevented by addition of 1,25(OH)2D3 in culture. These findings are important indicating that VDR expression is inducible in endothelial cells and oxidative stress down-regulates VDR expression in endothelial cells. We conclude that sufficient vitamin D levels and proper VDR expression are fundamental for angiogenic and oxidative defense function in endothelial cells. © 2013 Elsevier Ltd.


Chittiboina P.,LSUHSC Shreveport | Ganta V.,LSUHSC Shreveport | Monceaux C.P.,LSUHSC Shreveport | Scott L.K.,LSUHSC Shreveport | And 2 more authors.
Pathophysiology | Year: 2013

Traumatic brain injury (TBI) and sub-arachnoid hemorrhage (SAH) are major causes of long-term disability, mortality, and enormous economic costs to society. The full spectrum of neurological damage created by TBI or SAH is not usually manifested at the time of injury, but evolves gradually over the course of hours to days (or weeks) following these injuries. Angiopoietins, important regulators of vascular structure and function, are hallmark indicators of vascular injury and may therefore represent promising targets in the treatment of SAH and TBI. In animal models and human tissues, normal intracerebral and pial vessels show strong expression of Angiopoietin-1 (Ang-1), but only minimal expression or presentation of Angiopoietin-2 (Ang-2). After several types of neurotrauma, the ratios of Ang-1 and Ang-2 expression in brain microvessel are disturbed and appear to contribute to the remarkable loss of blood-brain barrier (BBB) in these injuries. Angiopoietins levels, and perhaps more importantly, Angiopoietin ratios (1:2) may have novel and important diagnostic and prognostic uses in TBI and SAH brain injury. Ang-1/2 evaluation in plasma, serum and cerebrospinal fluid may provide new therapeutic modalities which can modify 'secondary' forms of brain injury after TBI and SAH. © 2012.


Bacha F.,Childrens Hospital of Pittsburgh of UPMC | Bacha F.,Mellitus | Bacha F.,Baylor College of Medicine | Gungor N.,LSUHSC Shreveport | And 4 more authors.
Pediatric Diabetes | Year: 2013

Objective: In adults, type 2 diabetes (T2DM) is characterized with progressive deterioration in insulin secretion. Data are scanty in youth. We investigated prospectively the change in β-cell function and in insulin sensitivity in youth with T2DM. Research Design and Methods: Six adolescents with T2DM [hemoglobin A1c (HbA1c) 6.6±1.0%] underwent evaluation of hepatic glucose production (HGP; [6,6-2H2] glucose), insulin-stimulated glucose disposal (Rd; hyperinsulinemic-euglycemic clamp), first- and second-phase insulin/C-peptide secretion (hyperglycemic clamp), body composition dual energy X-ray absorptiometry (DEXA), and abdominal adiposity (computed tomography) within 3 yr of the diagnosis of diabetes and after 12-16 months of follow-up. Results: Weight, body mass index (37.1±6.9), HbA1c (6.3±0.7%), HGP (2.8±1.2 mg/kg/min), and Rd (4.9±3.4 mg/kg/min) did not change significantly from baseline. However, first-phase insulin and C-peptide declined (152.6±261.2 vs. 75.9±108.5 μU/mL, p=0.028; 8.0±6.3 vs. 5.9±4.4 ng/mL, p=0.048, respectively) with no significant change in second-phase insulin/C-peptide. The rate of decline in β-cell function was ∼20% per year. Conclusions: After a median duration of 20 months of diabetes, youth with T2DM manifest a rapid decline in β-cell function with no significant changes in peripheral or hepatic insulin sensitivity. Interventions to retard this deterioration in β-cell function should be investigated. © 2012 John Wiley & Sons A/S.


Venkatesh P.K.,LSUHSC Shreveport | Pattillo C.B.,LSUHSC Shreveport | Branch B.,LSUHSC Shreveport | Hood J.,LSUHSC Shreveport | And 6 more authors.
Cardiovascular Research | Year: 2010

AimsAnti-platelet agents, such as dipyridamole, have several clinical benefits for peripheral artery disease with the speculation of angiogenic potential that could preserve ischaemic tissue viability, yet the effect of dipyridamole on ischaemic arteriogenesis or angiogenesis is unknown. Here we test the hypothesis that dipyridamole therapy augments arteriolar vessel development and function during chronic ischaemia.Methods and resultsMice were treated with 200 mg/kg dipyridamole twice daily to achieve therapeutic plasma levels (0.8-1.2 μg/mL). Chronic hindlimb ischaemia was induced by permanent femoral artery ligation followed by measurement of tissue perfusion using laser Doppler blood flow along with quantification of vascular density, cell proliferation, and activation of nitric oxide (NO) metabolism. Dipyridamole treatment quickly restored ischaemic hindlimb blood flow, increased vascular density and cell proliferation, and enhanced collateral artery perfusion compared with control treatments. The beneficial effects of dipyridamole on blood flow and vascular density were dependent on NO production as dipyridamole did not augment ischaemic tissue reperfusion, vascular density, or endothelial cell proliferation in endothelial NO synthase (eNOS)-deficient mice. Blood and tissue nitrite levels were significantly higher in dipyridamole-treated mice compared with controls and eNOS-/- mice, verifying increased NO production that was regulated in a PKA-dependent manner.ConclusionDipyridamole augments nitrite/NO production, leading to enhanced arteriogenesis activity and blood perfusion in ischaemic limbs. Together, these data suggest that dipyridamole can augment ischaemic vessel function and restore blood flow, which may be beneficial in peripheral artery disease.


Wadhwa R.,LSUHSC Shreveport | Toms J.,LSUHSC Shreveport | Nanda A.,LSUHSC Shreveport | Abreo K.,LSUHSC Shreveport | Cuellar H.,LSUHSC Shreveport
Seminars in Dialysis | Year: 2012

Hemodialysis catheterization through the right internal jugular vein (IJV) is widely used for mid- to long-term hemodialysis for patients with renal failure. The purpose of this report is to address a serious complication in conjunction with this procedure. This is a case report of an iatrogenic jugular-carotid fistula (JCF) and a method for rectifying such a vascular conundrum, using endovascular techniques. We describe the technique used to achieve closure of the fistula as well a review of the literature. An 82-year-old woman with history of congestive heart failure, chronic renal failure, and diabetes mellitus developed an iatrogenic arteriovenous fistula, following an attempt of canalizing the right IJV. The patient was treated using three different stents, which achieved closure of the fistula. Venous catheter misplacement into an artery is a serious complication. Early endovascular treatment should be considered for a JCF. © 2011 Wiley Periodicals, Inc.


Ponce L.L.,Baylor College of Medicine | Navarro J.C.,Baylor College of Medicine | Ahmed O.,LSUHSC Shreveport | Robertson C.S.,Baylor College of Medicine
Pathophysiology | Year: 2013

Numerous experimental studies in recent years have suggested that erythropoietin (EPO) is an endogenous mediator of neuroprotection in various central nervous system disorders, including TBI. Many characteristics of EPO neuroprotection that have been defined in TBI experimental models suggest that it is an attractive candidate for a new treatment of TBI. EPO targets multiple mechanisms known to cause secondary injury after TBI, including anti-excitotoxic, antioxidant, anti-edematous, and anti-inflammatory mechanisms. EPO crosses the blood-brain barrier. EPO has a known dose response and time window for neuroprotection and neurorestoration that would be practical in the clinical setting. However, EPO also stimulates erythropoiesis, which can result in thromboembolic complications. Derivatives of EPO which do not bind to the classical EPO receptor (carbamylated EPO) or that have such a brief half-life in the circulation that they do not stimulate erythropoiesis (asialo EPO and neuro EPO) have the neuroprotective activities of EPO without these potential thromboembolic adverse effects associated with EPO administration. Likewise, a peptide based on the structure of the Helix B segment of the EPO molecule that does not bind to the EPO receptor (pyroglutamate Helix B surface peptide) has promise as another alternative to EPO that may provide neuroprotection without stimulating erythropoiesis. © 2012 Elsevier Ireland Ltd.

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