Næstved, Denmark
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Jodi L. Flynn, MSCS, PA-C, Physician Assistant at the Center for Health Improvement, and affiliated with Cox Hospital South, has been named a 2017 Top Doctor in Springfield, Missouri. Top Doctor Awards is dedicated to selecting and honoring those healthcare practitioners who have demonstrated clinical excellence while delivering the highest standards of patient care. Jodi L. Flynn is a highly experienced and respected physician assistant, who has been in practice for more than 15 years. She graduated with her Bachelor of Science Degree in Biology and Pre-Medicine in 2000 from Drury University in Springfield, Missouri. In 2002, Jodi earned a Master of Science Degree from Southwest Missouri State University, and became a nationally certified Physician Assistant. With a wealth of high level experience to call upon, Jodi provides expert medical care treating a wide range of conditions, and for patients of all ages over 18. She is particularly renowned as an expert in adult cardiology and cardiac electrophysiology, helping to treat conditions including heart arrhythmia, hypertension, familial hypercholesterolemia and cardiovascular disease. She  has opened 2 lipid clinics with a strong emphasis in preventative medicine and integrative therapies to optimize health.  Jodi also has extensive experience as a physician assistant in the field of neurology with specialization in Multiple Sclerosis.  She became nationally certified in Multiple Sclerosis in 2016 by the Consortium of Multiple Sclerosis Center.  She currently combines these past areas of expertise in the Cox Specialty Medication Clinic which provides care for those with the most severe chronic health conditions like Rheumatoid Arthritis, Multiple Sclerosis, Crohn’s Disease, Psoriasis, Diabetes, Oncology, and Cardiovascular Disease/Stroke. Jodi is committed to continual learning and education, and alongside her work as a Physician Assistant she has served as an Assistant Professor at Springfield’s Missouri State University. She was honored by the Springfield Business Journal in 2010 as a “Champion in Healthcare” within the Physician Assistant community. Her dedication and commitment makes Jodi L. Flynn a very worthy winner of a 2017 Top Doctor Award. Top Doctor Awards specializes in recognizing and commemorating the achievements of today’s most influential and respected doctors in medicine. Our selection process considers education, research contributions, patient reviews, and other quality measures to identify top doctors.


Gravgaard K.H.,University of Southern Denmark | Lyng M.B.,University of Southern Denmark | Laenkholm A.-V.,Hospital South | Sokilde R.,Exiqon A S | And 3 more authors.
Breast Cancer Research and Treatment | Year: 2012

Metastases are the major cause of cancer-related deaths, but the mechanisms of the metastatic process remain poorly understood. In recent years, the involvement of microRNAs (miRNAs) in cancer has become apparent, and the objective of this study was to identify miRNAs associated with breast cancer progression. Global miRNA expression profiling was performed on 47 tumor samples from 14 patients with paired samples from primary breast tumors and corresponding lymph node and distant metastases using LNA-enhanced miRNA microarrays. The identified miRNA expression alterations were validated by real-time PCR, and tissue distribution of the miRNAs was visualized by in situ hybridization. The patients, in which the miRNA profile of the primary tumor and corresponding distant metastasis clustered in the unsupervised cluster analysis, showed significantly shorter intervals between the diagnosis of the primary tumor and distant metastasis (median 1.6 years) compared to those that did not cluster (median 11.3 years) (p < 0.003). Fifteen miRNAs were identified that were significantly differentially expressed between primary tumors and corresponding distant metastases, including miR-9, miR-219-5p and four of the five members of the miR-200 family involved in epithelial- mesenchymal transition. Tumor expression of miR-9 and miR-200b were confirmed using in situ hybridization, which also verified higher expression of these miRNAs in the distant metastases versus corresponding primary tumors. Our results demonstrate alterations in miRNA expression at different stages of disease progression in breast cancer, and suggest a direct involvement of the miR-200 family and miR-9 in the metastatic process. © 2012 Springer Science+Business Media, LLC.


Coskun M.,Copenhagen University | Olsen A.K.,Copenhagen University | Olsen A.K.,Hospital South | Holm T.L.,Novo Nordisk AS | And 5 more authors.
Biochimica et Biophysica Acta - Molecular Basis of Disease | Year: 2012

Background/aims: High levels of pro-inflammatory cytokines are linked to inflammatory bowel disease (IBD). The transcription factor Caudal-related homeobox transcription factor 2 (CDX2) plays a crucial role in differentiation of intestinal epithelium and regulates IBD-susceptibility genes, including meprin 1A (MEP1A). The aim was to investigate the expression of CDX2 and MEP1A in colitis; to assess if they are regulated by tumor necrosis factor-α (TNF-α), and finally to reveal if CDX2 is involved in a TNF-α-induced down-regulation of MEP1A. Methods: Expression of CDX2 and MEP1A was investigated in colonic biopsies of ulcerative colitis (UC) patients and in dextran sodium sulfate (DSS)-induced colitis. CDX2 protein expression was investigated by immunoblotting and immunohistochemical procedures. CDX2 and MEP1A regulation was examined in TNF-α-treated Caco-2 cells by reverse transcription-polymerase chain reaction and with reporter gene assays, and the effect of anti-TNF-α treatment was assessed using infliximab. Finally, in vivo CDX2-DNA interactions were investigated by chromatin immunoprecipitation. Results: The CDX2 and MEP1A mRNA expression was significantly decreased in active UC patients and in DSS-colitis. Colonic biopsy specimens from active UC showed markedly decreased CDX2 staining. TNF-α treatment diminished the CDX2 and MEP1A mRNA levels, a decrease which, was counteracted by infliximab treatment. Reporter gene assays showed significantly reduced CDX2 and MEP1A activity upon TNF-α stimulation. Finally, TNF-α impaired the ability of CDX2 to interact and activate its own, as well as the MEP1A expression. Conclusions: The present results indicate that a TNF-α-mediated down-regulation of CDX2 can be related to suppressed expression of MEP1A during intestinal inflammation. © 2012 Elsevier B.V.


Olsen A.K.,Copenhagen University | Olsen A.K.,Hospital South | Boyd M.,Copenhagen University | Danielsen E.T.,Copenhagen University | Troelsen J.T.,Roskilde University
American Journal of Physiology - Gastrointestinal and Liver Physiology | Year: 2012

Upon developmental or environmental cues, the composition of transcription factors in a transcriptional regulatory network is deeply implicated in controlling the signature of the gene expression and thereby specifies the cell or tissue type. Novel methods including ChIP-chip and ChIP-Seq have been applied to analyze known transcription factors and their interacting regulatory DNA elements in the intestine. The intestine is an example of a dynamic tissue where stem cells in the crypt proliferate and undergo a differentiation process toward the villus. During this differentiation process, specific regulatory networks of transcription factors are activated to target specific genes, which determine the intestinal cell fate. The expanding genomewide mapping of transcription factor binding sites and construction of transcriptional regulatory networks provide new insight into how intestinal differentiation occurs. This review summarizes the current overview of the transcriptional regulatory networks driving epithelial differentiation in adult intestine. The novel technologies that have been implied to study these networks are presented and their prospects for implications in future research are also addressed. © 2012 the American Physiological Society.


Jones B.L.,University College London | Raga T.O.,Addis Ababa Institute of Technology | Liebert A.,University College London | Zmarz P.,University College London | And 8 more authors.
American Journal of Human Genetics | Year: 2013

The persistent expression of lactase into adulthood in humans is a recent genetic adaptation that allows the consumption of milk from other mammals after weaning. In Europe, a single allele (-13910*T, rs4988235) in an upstream region that acts as an enhancer to the expression of the lactase gene LCT is responsible for lactase persistence and appears to have been under strong directional selection in the last 5,000 years, evidenced by the widespread occurrence of this allele on an extended haplotype. In Africa and the Middle East, the situation is more complicated and at least three other alleles (-13907*G, rs41525747; -13915*G, rs41380347; -14010*C, rs145946881) in the same LCT enhancer region can cause continued lactase expression. Here we examine the LCT enhancer sequence in a large lactose-tolerance-tested Ethiopian cohort of more than 350 individuals. We show that a further SNP, -14009T>G (ss 820486563), is significantly associated with lactose-digester status, and in vitro functional tests confirm that the -14009*G allele also increases expression of an LCT promoter construct. The derived alleles in the LCT enhancer region are spread through several ethnic groups, and we report a greater genetic diversity in lactose digesters than in nondigesters. By examining flanking markers to control for the effects of mutation and demography, we further describe, from empirical evidence, the signature of a soft selective sweep. © 2013 The Authors.


Mohammadi M.,Hospital South | Garbyal R.S.,Hospital South | Kristensen M.H.,Hospital South | Madsen P.M.,Hospital South | And 2 more authors.
Pathology Research and Practice | Year: 2011

Sessile serrated lesion (SSL), belonging to non-dysplastic serrated polyps (SP), has lately received much focus. Its role in the serrated neoplasia pathway(s) seems well established. Data on prevalence rate, demography, and some polyp characteristics remain, however, to be firmly established. Nor has its relation to SPs with subtle aberrant features, falling short of definite SSL-histology, been sufficiently addressed.The aim of this study was to highlight variables that may influence recorded data on SSL and to further discuss the appropriate place of SPs that possess histological attributes intermediate between traditional hyperplastic polyp (HP) and SSL, termed borderline SSL (BSSL).Upon review of 8.324 consecutive colorectal polyps signed-out as HP, 219 SSLs and 206 BSSLs were segregated, using strict predetermined criteria.Predominant left-sidedness and equal gender distribution characterized the present series, though right-sided SSLs occurred significantly more often in older subjects with a trend toward more females. The lower age of patients with SSL/BSSL in the last part of the study reflects the increased focus on hereditary neoplasm. BSSL differed from SSL only by a smaller polyp size.Discordant SSL-data can be ascribed primarily to diversities in endoscopic procedure, though tissue handling, the criteria used, and study design may contribute. A precursor status of BSSL to SSL is an attractive, though still unsubstantiated thesis. © 2011 Elsevier GmbH.


Mohammadi M.,Hospital South | Kristensen M.H.,Hospital South | Nielsen H.J.,Copenhagen University | Bonde J.H.,Copenhagen University | Holck S.,Copenhagen University
Journal of Clinical Pathology | Year: 2012

Aims: Although much data have accumulated on sessile serrated adenoma/polyp/lesion (SSA/P/L) in general, its characteristics in specified contexts are less well elucidated. This lack of knowledge is even more conspicuous concerning its borderline counterpart, referred to as BSSA/P/L. The previous histological observations of the authors on SSA/P/L and BSSA/P/L in general are here extended to encompass attributes of these polyps in the context of synchronous colorectal carcinoma (SCRC), with a focus on the place of BSSA/P/L in the spectrum of non-dysplastic serrated polyps. Methods: 219 SSA/P/Ls, 206 BSSA/P/Ls and 170 hyperplastic polyps (HPs) were examined for SCRC. Demographics, polyp details (size, site, BRAF (V600E)) and advanced synchronous conventional adenomas were recorded. Results SCRC was present in 12.3% of SSA/P/Ls, 7.1% of HPs (p=0.09) and 8.3% of BSSA/P/Ls. Patients' ages were comparable. Gender distribution of SSA/P/L and BSSA/P/L was equal, which differed, albeit insignificantly, from a male predominance of HPs. More SSA/P/Ls and BSSA/P/Ls than HPs exceeded 4 mm (p≤0.0001). A proximal site characterised SSA/P/L compared with BBSA/P/L and HP (p<0.0001). BRAF mutation was more prevalent in SSA/P/Ls and BSSA/P/Ls, which further coexisted with advanced synchronous conventional adenomas less commonly than HPs. Conclusions: BSSA/P/L was like SSA/P/L in most respects. The lower SCRC prevalence of BSSA/P/L could fit the idea of BSSA/P/L as a precursor to SSA/P/L, a notion that deserves attention when formulating guidelines for CRC screening.


PubMed | VU University Amsterdam and Hospital South
Type: Journal Article | Journal: Nucleosides, nucleotides & nucleic acids | Year: 2016

Antimetabolites are incorporated into DNA and RNA, affecting their function. Liquid-chromatography-mass-spectrometry (LC-MS-MS) permits the sensitive, selective analysis of normal nucleosides. The method was adapted to measure the incorporation of deoxyuridine, gemcitabine (difluorodeoxycytidine), its metabolite difluorodeoxyuridine (dFdU), and the novel compound fluorocyclopentenylcytosine (RX3117). DNA was degraded to its deoxynucleotides for quantification by LC-MS-MS, gradient chromatography on a Phenomenex prodigy-3-ODS with positive ionization. The range of deoxyuridine DNA-mis-incorporation varied nine-fold in 27 cell lines (leukemia, colon, ovarian, lung cancer). At low-folate conditions a 2.1-fold increase in deoxyuridine was observed. Global methylation (given as % 5-methyl-deoxycytidine) was comparable between the cell lines (4.6-6.5%). Exposure of A2780 cells to 1M gemcitabine (4hours) resulted in 3.6pmol gemcitabine/g DNA, but in AG6000 cells (deoxycytidine-kinase-deficient) no incorporation was found. However, when A2780, AG6000, or CCRF-CEM cells were exposed to 100M dFdU we found it as gemcitabine, 20.5, 19.6, and 0.51pmol gemcitabine/g DNA, respectively. Preincubation of CCRF-CEM cells with cyclopentenyl-cytosine (a CTP-synthetase inhibitor) increased dFdU incorporation four-fold. Apparently dFdU is activated independently of deoxycytidine-kinase and possibly converted in-situ to dFdCMP. RX3117 was incorporated into both DNA and RNA (0.0037 and 0.00515pmol/g, respectively). In summary, a sensitive method to quantify the incorporation of gemcitabine, deoxyuridine, and RX-3117 was developed, which revealed that dFdU was incorporated into DNA as the parent compound gemcitabine.


Kristensen M.H.,Hospital South | Pedersen P.L.,Hospital South | Melsen G.V.,Hospital South | Ellehauge J.,Hospital South | Mejer J.,Hospital South
Journal of International Medical Research | Year: 2010

Adverse drug reactions to 5-fluorouracil (5-FU)-based chemotherapy have been reported to be due, in part, to genetic variants of the genes for the drug-related enzymes thymidylate synthase (TS; TYMS gene), methylenetetrahydrofolate reductase (MTHFR gene) and dihydropyrimidine dehydrogenase (DPD;DPYD gene). This study investigated whether selected genetic variants of the TYMS, MTHFR and DPYD genes predict 5-FU-related early toxicity. The prevalence of the genetic variants was determined in 122 colorectal cancer patients and in a reference population of 320 blood donors. Subgroup analysis of 68 of the colorectal cancer patients was carried out to determine the relationship between selected gene variants detected in peripheral mononuclear cells and tolerability during the first or second cycle of 5-FU based treatment. Toxicity was linked to the TYMS 2R/2R variant (relative risk [RR] 1.66; sensitivity 0.37; specificity 0.77) and to the MTHFR c1298 C/C genetic variant (RR 1.77; sensitivity 0.17; specificity 0.91). Patients with the genetic variant IVS14+1 G/A or c1896 C/T in the DPYD gene had a statistically significant increased risk of experiencing toxicity (RR 2 and 6, respectively), both having a high specificity (0.97 and 0.98, respectively) and low sensitivity (0.04 and 0.13, respectively). It is concluded that pre-treatment detection of genetic variants can help to predict early toxicity experienced by patients receiving 5-FU-based chemotherapy. © 2010 Field House Publishing LLP.


Kristensen M.H.,Hospital South | Pedersen P.,Hospital South | Mejer J.,Hospital South
Journal of International Medical Research | Year: 2010

This study investigated the relationship between the dihydrouracil/uracil (UH2/U) plasma ratio, a surrogate marker of dihydropyrimidine dehydrogenase (DPD) activity, and 5-fluorouracil (5-FU)-related early toxicity. Plasma UH2/U ratios were determined in 68 colorectal cancer patients and 100 healthy controls. A cutoff value indicative of DPD deficiency was calculated using receiver operator characteristics. Patients experiencing toxicity were screened for the DPD G-to-A point mutation within the 5′-splicing donor site of intron 14 (IVS14+1G>A). Overall, 24/68 patients (35%) experienced toxicity (all grades) and abnormal UH2/U ratios were demonstrated in 21/24 (87.5%) patients. Drug concentrations up to 130 times the recommended level were found in 13/24 (54%) patients experiencing toxicity. One patient experiencing toxicity was a heterozygous carrier of the IVS14+1G>A mutation. A low UH2/U plasma ratio had a sensitivity of 0.87 and specificity of 0.93 for predicting 5-FUinduced toxicity. Systematic detection of DPD-deficient patients using the UH2/U ratio could optimize 5-FU-based chemotherapy and minimize lifethreatening toxicity. © 2010 Field House Publishing LLP.

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