Biomedical subjects

Emily P Tierney

Publications and source records attributed to Emily P Tierney.

4 recordsLinked to original sources

PubMed2006

Challenges facing academic dermatology: survey data on the faculty workforce.

BACKGROUND: There is a perception among many academic dermatologists that departments of dermatology face severe challenges with recruitment and retention of faculty. In an era when evidence points to a shortage of dermatologists and residency graduates have plentiful private practice offers in almost every geographic area, some fear that academic programs will face even steeper challenges attracting and keeping enough dermatologists on staff. METHODS: To compare the practice patterns of academic dermatologists with those of the dermatology workforce in other settings, data from the American Academy of Dermatology 2002 Practice Profile Survey were analyzed (1425 respondents, 35% response rate). RESULTS: The mean age of academic dermatologists (45.6 years) was younger than that of those in other practice settings (51.9 years solo practice, 49.0 years multispecialty group), and older age cohorts were significantly less likely to be working in academics (P < .001). Academic physicians were much more likely than those in solo practice or dermatology-only groups (62.2% vs 18.3%-39.4%) to report that their institution or practice was seeking new dermatologists. The average waiting time for new patient appointments varied from a low of 31.1 days in solo practices to a high of 55.9 days in academic practices. Academic dermatologists saw 32% to 41% fewer patients per week, but spent much more time (24.1 vs 5.5-8.6 h/wk) participating in research, hospital consults, medical writing, administrative activities, and teaching than dermatologists in any other setting. LIMITATIONS: Academic dermatologists reflected a relatively small proportion of survey respondents, and may not be representative of the nation's dermatology faculty (although the percentage of academics in the survey was similar to that in the overall workforce). Possible response biases could also have affected the survey results. CONCLUSIONS: The survey results identify a number of differences between the practice patterns of academic dermatologists and their colleagues in other settings, and suggest that academic departments of dermatology may be facing unique workforce challenges.

Adult↗

PubMed2004

Etiology and pathogenesis of necrolytic migratory erythema: review of the literature.

CONTEXT: Necrolytic migratory erythema (NME) is a characteristic skin condition seen in the presence of a pancreatic glucagonoma. The presence of NME in the absence of a pancreatic tumor has been termed the pseudoglucagonoma syndrome. In such cases, NME is commonly associated with conditions, such as liver disease, inflammatory bowel disease, pancreatitis, malabsorption disorders (ie, celiac sprue), and other malignancies. There are many theories on the pathogenesis of NME, which include the direct action of glucagon in inducing skin necrolysis, hypoaminoacidemia-inducing epidermal protein deficiency and necrolysis, a nutritional or metabolic deficiency of zinc or essential fatty acids, liver disease, glucagon induction of inflammatory mediators, a substance secreted from pancreatic and other visceral tumors associated with NME, and generalized malabsorption. OBJECTIVE: To present a review of the literature on the clinical presentation, etiology, pathogenesis, and treatment of NME. DESIGN: Review of the literature on NME occurring in patients both with and without a pancreatic glucagonoma. METHODS: We performed a PubMed review of the literature on the etiology and pathogenesis of NME to identify case reports and reviews published in both the internal medicine and dermatology literature. RESULTS: Our literature review encompassed 17 primary case reports and literature reviews published in the dermatologic and internal medicine literature on NME in patients both with and without a pancreatic glucagonoma. Although we found no clear consensus among the investigators of a universally accepted pathogenesis for NME, we did identify 4 main categories of etiologic/pathogenetic mechanisms for NME (glucagon excess, nutritional deficiencies, inflammatory mediators, and liver disease) that were discussed by many of the investigators and validated by both clinical and scientific evidence. CONCLUSION: The exact pathogenesis and treatment of NME remain ill-defined despite many case reports and studies on NME in the literature. The many systemic diseases and nutritional deficiencies that have been found to be associated with NME suggest a multifactorial model for the pathogenesis of the disease. The most comprehensive, postulated mechanism for NME involves a combination of zinc, amino acid, and fatty acid deficiencies (arising from a wide variety of causes, such as dietary insufficiency, malabsorption syndromes, liver disease, elevated glucagon levels, and disorders of metabolism) that contributes to increased inflammation in the epidermis in response to trauma and to the necrolysis observed in NME. The importance of gaining an understanding of the etiology and pathogenesis of NME lies in the fact that there is no universally accepted mechanism of pathogenesis for NME, and that the only treatment reported to resolve the rash in these patients is to adequately identify and treat the underlying associated systemic condition or nutritional deficiency.

Erythema↗

PubMed2004

Role of activin A as a mediator of in vitro endometrial stromal cell decidualization via the cyclic adenosine monophosphate pathway.

OBJECTIVE: To elucidate the regulation and role of activin A in endometrial stromal decidualization. DESIGN: In vitro model of human stromal cell decidualization with cyclic adenosine monophosphate (cAMP) used to evaluate expression of activin A and to evaluate the effect of the addition of follistatin, a known activin inhibitor, on expression of the decidualized phenotype (as measured by levels of insulin-like growth factor binding protein-1 [IGFBP-1]). SETTING: Academic research environment. PATIENT(S): Four premenopausal, normally cycling subjects (age range: 32-40 years). INTERVENTION(S): Endometrial samples were obtained from the subjects after informed consent was obtained. Endometrial stromal cells were treated with cAMP (decidualizing stimulus) and 50 ng/mL, 100 ng/mL, and 200 ng/mL of follistatin for 48 hours. MAIN OUTCOME MEASURE(S): Levels of IGFBP-1 secreted from cells decidualized in the absence and presence of three different concentrations of follistatin. RESULT(S): Addition of follistatin, a known binding protein inhibitor of activin A, resulted in a dose-dependent inhibition of IGFBP-1 secreted into conditioned medium, with the greatest decrease observed at 4 days of decidualization. Cells treated with cAMP and 50 ng/mL, 100 ng/mL, and 200 ng/mL of follistatin demonstrated 67.3%, 58.6%, and 35.5%, respectively, of the IGFBP-1 levels observed with cAMP but without follistatin. CONCLUSION(S): These data suggest that activin A is a necessary component of the cAMP pathway leading to endometrial stromal decidualization. The role of activin A in regulating endometrial stromal decidualization and its known promotion of the invasive phenotype of the trophoblast suggest unique autocrine and paracrine interactions at the maternal/fetal interface during implantation, which might have important clinical implications for the understanding and treatment of fertility and pregnancy disorders.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed2003

Activation of the protein kinase A pathway in human endometrial stromal cells reveals sequential categorical gene regulation.

Decidualization of endometrial stromal cells is a prerequisite for human implantation and occurs in vivo in response to progesterone and involves activation of the protein kinase A (PKA) pathway. The objective of this study was to determine the molecular signatures and patterns of gene expression during stimulation of this pathway with an analog of cAMP. Endometrial stromal cells from two subjects were treated with or without 8-Br-cAMP (1 mM) for 0, 2, 12, 24, 36, and 48 h and were processed for microarray analysis, screening for 12,686 genes and ESTs. Most abundantly upregulated genes included neuropeptides, immune genes, IGF family members, cell cycle regulators, extracellular matrix proteases, cholesterol trafficking, cell growth and differentiation, hormone signaling, and signal transduction. Most abundantly downregulated genes included activator of NF-kappaB, actin/tropomyosin/calmodulin binding protein, cyclin B, IGFBP-5, alpha1 type XVI collagen, lipocortin III, l-kynurenine hydrolase, frizzle-related protein, and cyclin E2. RT-PCR validated upregulation of IGFBP-1, preprosomatostatin, and IL-11, and Northern analysis validated their kinetic upregulation. RT-PCR confirmed downregulation of IGFBP-5, cyclin B, and TIL-4. K-means analysis revealed four major patterns of up- and downregulated genes, and genes within each ontological group were categorized into these four kinetic patterns. Within each ontological group different patterns of temporal gene expression were observed, indicating that even genes within one functional category are regulated differently during activation of the PKA pathway in human endometrial stromal cells. Overall, the data demonstrate kinetic reprogramming of genes within specific functional groups and changes in genes associated with nucleic acid binding, cell proliferation, decreased G protein signaling, increased STAT pathway signaling, structural proteins, cellular differentiation, and secretory processes. These changes are consistent with cAMP modulating early events (0-6 h) primarily involving cell cycle regulation, subsequent events (12-24 h) involving cellular differentiation (including changes in morphology and secretory phenotype), and late events (24-48 h) mediating more specialized function, including immune modulators, in the human endometrial stromal cell.

8-Bromo Cyclic Adenosine Monophosphate↗