Dr. Joseph  White   image

Dr. Joseph White

233 Magnolia St
Hazlehurst MS 39083
800 914-4020
Medical School: Other - Unknown
Accepts Medicare: No
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: No
License #: 12269
NPI: 1144261793
Taxonomy Codes:

Request Appointment Information

Awards & Recognitions

About Us

Practice Philosophy


Medical Malpractice Cases

None Found

Medical Board Sanctions

None Found


None Found


Critical Limb Ischemia Secondary to Antiphospholipid Syndrome in a Pediatric Patient: Case Report and Review. - Annals of vascular surgery
Antiphospholipid syndrome (APS) is a condition that manifests as venous or arterial thrombosis, as well as complications of pregnancy. APS affecting primarily the arteries is less common when compared to venous complications. We present a case of arterial occlusion resulting in critical limb ischemia (CLI) in a pediatric patient.A 14-year old boy presented with worsening right lower extremity pain and ulcerative lesions of his foot. Laboratory analysis revealed a diagnosis of APS. This case report and review of the literature expands our understanding of arterial manifestations of APS in the pediatric patient.The patient was discovered to have proximal occlusion of the superficial femoral artery (SFA), the distal popliteal artery, the anterior tibial artery at the mid-calf, and the posterior tibial artery at the ankle. He underwent a common femoral artery to above-knee-popliteal artery bypass with reversed greater saphenous graft. Follow up after over one-year demonstrated an ABI of 1.0 and no evidence of stenosis in the bypass graft on duplex ultrasound (DUS).APS is a complex syndrome with a variety of clinical presentations. This case highlights arterial manifestations of APS and reviews the expanding literature to guide improved patient outcomes.Published by Elsevier Inc.
The Tax Exclusion for Employer-Sponsored Insurance Is Not Regressive-But What Is It? - Journal of health politics, policy and law
Conventional wisdom says that the tax exclusion for employer-sponsored health insurance (ESI) is "regressive and therefore unfair." Yet, by the standard definition of regressive tax policy, the conventional view is almost certainly false. It confuses the absolute size of the tax exclusion with its proportional effect on income. The error results from paying attention only to the marginal tax rate applied to ESI benefits as a portion of income and ignoring the fact that benefits are normally a much larger share of income for people with lower wages. This article explains the difference and then considers other distributional effects of ESI. It suggests that ESI-for those who receive it-further redistributes toward those with lesser means or greater need. The most evident effect is by need, favoring employees with families over those without. Yet there is good reason to believe there is also a redistribution by income, with the package of wages plus benefits being less unequal than wages alone would be. Therefore reformers should be much more careful before criticizing either ESI or its subsidy through the tax code as "unfair," especially as the likelihood of enacting something better in the United States seems quite low.Copyright © 2017 by Duke University Press.
Venous Compression Syndromes. - Vascular and endovascular surgery
Venous compression syndromes occur due to extrinsic compression causing complications of venous hypertension or venous thrombosis. This review focuses on 4 venous compression syndromes involving the left common iliac vein, subclavian vein, left renal vein, and popliteal vein. Clinical presentation, diagnostic methods, and management options are reviewed. When properly diagnosed and treated, long-term consequences can be avoided.
A quality improvement project to improve inferior vena cava filter retrieval. - Journal of vascular surgery. Venous and lymphatic disorders
Poor retrieval rates for retrievable inferior vena cava filters (R-IVCFs) have been reported throughout the literature, with poor follow-up a common cause. In 2009, we reported a retrieval rate of 18% despite an initial follow-up rate of 85%. Use of a registry has been shown to improve retrieval rates. As a quality improvement project, in May 2012, the vascular surgery fellowship implemented a reiterative registry to track R-IVCFs placed at Walter Reed National Military Medical Center to improve retrieval rates. We report the results in 125 patients after 38 months.Patients receiving an R-IVCF were entered into a registry. All patients were reviewed monthly using an electronic health record. When there was no longer an indication for the R-IVCF, the patient was scheduled for an outpatient appointment with a vascular surgeon followed by retrieval. Rates of retrieval, technical success, dwell time, indication, complications, and demographics were collected.There were 125 R-IVCFs placed between May 2012 and June 2015; 52 filters were placed for therapeutic and 73 for prophylactic indications. Our follow-up rate improved to 94%. A total of 79 filters were retrieved (63% absolute retrieval rate). Excluding patients who died before retrieval and patients with a permanent indication, 77% of filters were retrieved. The average dwell time was 101.5 days (7-460 days), and 63% of successful R-IVCF retrievals were within 3 months of placement. Technical success for retrieval was 92%. There were two major complications from retrievals (1.5% of retrievals).The creation of an R-IVCF registry promoted ongoing follow-up with patients. In our earlier experience, retrieval rates were poor despite a high follow-up rate. The use of a reiterative registry improved our retrieval rate by 45% and increased our follow-up rate to 94%. These results emphasize the importance of repetitive follow-up for R-IVCFs. Despite a follow-up rate >90%, around a third of R-IVCFs were not retrieved.Published by Elsevier Inc.
Microvascular Endothelial Dysfunction in Sedentary, Obese Humans Is Mediated by NADPH Oxidase: Influence of Exercise Training. - Arteriosclerosis, thrombosis, and vascular biology
The objectives of this study were to determine the impact of in vivo reactive oxygen species (ROS) on microvascular endothelial function in obese human subjects and the efficacy of an aerobic exercise intervention on alleviating obesity-associated dysfunctionality.Young, sedentary men and women were divided into lean (body mass index 18-25; n=14), intermediate (body mass index 28-32.5; n=13), and obese (body mass index 33-40; n=15) groups. A novel microdialysis technique was utilized to detect elevated interstitial hydrogen peroxide (H2O2) and superoxide levels in the vastus lateralis of obese compared with both lean and intermediate subjects. Nutritive blood flow was monitored in the vastus lateralis via the microdialysis-ethanol technique. A decrement in acetylcholine-stimulated blood flow revealed impaired microvascular endothelial function in the obese subjects. Perfusion of apocynin, an NADPH oxidase inhibitor, lowered (normalized) H2O2 and superoxide levels, and reversed microvascular endothelial dysfunction in obese subjects. After 8 weeks of exercise, H2O2 levels were decreased in the obese subjects and microvascular endothelial function in these subjects was restored to levels similar to lean subjects. Skeletal muscle protein expression of the NADPH oxidase subunits p22(phox), p47(phox), and p67(phox) was increased in obese relative to lean subjects, where p22(phox) and p67(phox) expression was attenuated by exercise training in obese subjects.This study implicates NADPH oxidase as a source of excessive ROS production in skeletal muscle of obese individuals and links excessive NADPH oxidase-derived ROS to microvascular endothelial dysfunction in obesity. Furthermore, aerobic exercise training proved to be an effective strategy for alleviating these maladies.© 2016 American Heart Association, Inc.
Copy-number variation is an important contributor to the genetic causality of inherited retinal degenerations. - Genetics in medicine : official journal of the American College of Medical Genetics
Despite substantial progress in sequencing, current strategies can genetically solve only approximately 55-60% of inherited retinal degeneration (IRD) cases. This can be partially attributed to elusive mutations in the known IRD genes, which are not easily identified by the targeted next-generation sequencing (NGS) or Sanger sequencing approaches. We hypothesized that copy-number variations (CNVs) are a major contributor to the elusive genetic causality of IRDs.Twenty-eight cases previously unsolved with a targeted NGS were investigated with whole-genome single-nucleotide polymorphism (SNP) and comparative genomic hybridization (CGH) arrays.Deletions in the IRD genes were detected in 5 of 28 families, including a de novo deletion. We suggest that the de novo deletion occurred through nonallelic homologous recombination (NAHR) and we constructed a genomic map of NAHR-prone regions with overlapping IRD genes. In this article, we also report an unusual case of recessive retinitis pigmentosa due to compound heterozygous mutations in SNRNP200, a gene that is typically associated with the dominant form of this disease.CNV mapping substantially increased the genetic diagnostic rate of IRDs, detecting genetic causality in 18% of previously unsolved cases. Extending the search to other structural variations will probably demonstrate an even higher contribution to genetic causality of IRDs.Genet Med advance online publication 13 October 2016.
Response to Comment on "Long-term climate forcing by atmospheric oxygen concentrations". - Science (New York, N.Y.)
Goldblatt argues that a decrease in pressure broadening of absorption lines in an atmosphere with low oxygen leads to an increase in outgoing longwave radiation and atmospheric cooling. We demonstrate that cloud and water vapor feedbacks in a global climate model compensate for these decreases and lead to atmospheric warming.Copyright © 2016, American Association for the Advancement of Science.
Axonal Transport and Neurodegeneration: How Marine Drugs Can Be Used for the Development of Therapeutics. - Marine drugs
Unlike virtually any other cells in the human body, neurons are tasked with the unique problem of transporting important factors from sites of synthesis at the cell bodies, across enormous distances, along narrow-caliber projections, to distally located nerve terminals in order to maintain cell viability. As a result, axonal transport is a highly regulated process whereby necessary cargoes of all types are packaged and shipped from one end of the neuron to the other. Interruptions in this finely tuned transport have been linked to many neurodegenerative disorders including Alzheimer's (AD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS) suggesting that this pathway is likely perturbed early in disease progression. Therefore, developing therapeutics targeted at modifying transport defects could potentially avert disease progression. In this review, we examine a variety of potential compounds identified from marine aquatic species that affect the axonal transport pathway. These compounds have been shown to function in microtubule (MT) assembly and maintenance, motor protein control, and in the regulation of protein degradation pathways, such as the autophagy-lysosome processes, which are defective in many degenerative diseases. Therefore, marine compounds have great potential in developing effective treatment strategies aimed at early defects which, over time, will restore transport and prevent cell death.
Amyloid precursor protein-mediated endocytic pathway disruption induces axonal dysfunction and neurodegeneration. - The Journal of clinical investigation
The endosome/lysosome pathway is disrupted early in the course of both Alzheimer's disease (AD) and Down syndrome (DS); however, it is not clear how dysfunction in this pathway influences the development of these diseases. Herein, we explored the cellular and molecular mechanisms by which endosomal dysfunction contributes to the pathogenesis of AD and DS. We determined that full-length amyloid precursor protein (APP) and its β-C-terminal fragment (β-CTF) act though increased activation of Rab5 to cause enlargement of early endosomes and to disrupt retrograde axonal trafficking of nerve growth factor (NGF) signals. The functional impacts of APP and its various products were investigated in PC12 cells, cultured rat basal forebrain cholinergic neurons (BFCNs), and BFCNs from a mouse model of DS. We found that the full-length wild-type APP (APPWT) and β-CTF both induced endosomal enlargement and disrupted NGF signaling and axonal trafficking. β-CTF alone induced atrophy of BFCNs that was rescued by the dominant-negative Rab5 mutant, Rab5S34N. Moreover, expression of a dominant-negative Rab5 construct markedly reduced APP-induced axonal blockage in Drosophila. Therefore, increased APP and/or β-CTF impact the endocytic pathway to disrupt NGF trafficking and signaling, resulting in trophic deficits in BFCNs. Our data strongly support the emerging concept that dysregulation of Rab5 activity contributes importantly to early pathogenesis of AD and DS.
Efficient In Silico Identification of a Common Insertion in the MAK Gene which Causes Retinitis Pigmentosa. - PloS one
Next generation sequencing (NGS) offers a rapid and comprehensive method of screening for mutations associated with retinitis pigmentosa and related disorders. However, certain sequence alterations such as large insertions or deletions may remain undetected using standard NGS pipelines. One such mutation is a recently-identified Alu insertion into the Male Germ Cell-Associated Kinase (MAK) gene, which is missed by standard NGS-based variant callers. Here, we developed an in silico method of searching NGS raw sequence reads to detect this mutation, without the need to recalculate sequence alignments or to screen every sample by PCR.The Linux program grep was used to search for a 23 bp "probe" sequence containing the known junction sequence of the insert. A corresponding search was performed with the wildtype sequence. The matching reads were counted and further compared to the known sequences of the full wildtype and mutant genomic loci. (See a test sample set consisting of eleven previously published homozygous mutants, detection of the MAK-Alu insertion was validated with 100% sensitivity and specificity. As a discovery cohort, raw NGS reads from 1,847 samples (including custom and whole exome selective capture) were searched in ~1 hour on a local computer cluster, yielding an additional five samples with MAK-Alu insertions and solving two previously unsolved pedigrees. Of these, one patient was homozygous for the insertion, one compound heterozygous with a missense change on the other allele (c. 46G>A; p.Gly16Arg), and three were heterozygous carriers.Using the MAK-Alu grep program proved to be a rapid and effective method of finding a known, disease-causing Alu insertion in a large cohort of patients with NGS data. This simple approach avoids wet-lab assays or computationally expensive algorithms, and could also be used for other known disease-causing insertions and deletions.

Map & Directions

233 Magnolia St Hazlehurst, MS 39083
View Directions In Google Maps

Nearby Doctors

240 Caldwell Dr
Hazlehurst, MS 39083
601 944-4732
217 S Extension St
Hazlehurst, MS 39083
601 128-8686
108 Trade Ctr Ln
Hazlehurst, MS 39083
601 944-4016
1001 Sandifer St
Hazlehurst, MS 39083
601 542-2669
213 Caldwell Dr
Hazlehurst, MS 39083
601 944-4661
640 Georgetown St
Hazlehurst, MS 39083
601 942-2271
331 W Gallatin St
Hazlehurst, MS 39083
601 941-1634
233 Magnolia St
Hazlehurst, MS 39083
800 914-4020
1047 W Gallman Rd
Hazlehurst, MS 39083
601 557-7844