Publications by authors named "Marcus Zaayman"

5 Publications

  • Page 1 of 1

Penile calciphylaxis with extragenital gangrene.

Proc (Bayl Univ Med Cent) 2021 Jan 28;34(3):416-418. Epub 2021 Jan 28.

Division of Dermatology, Baylor University Medical Center, Dallas, Texas.

Penile calciphylaxis is a rare cause of penile gangrene and is typically associated with multiple comorbidities, most commonly diabetes mellitus and hyperparathyroidism. It demonstrates a high mortality rate of 64% and is seen almost exclusively in patients with end-stage renal disease on hemodialysis. Underreporting of this disease likely occurs, contributing to a paucity of data and lack of formal therapeutic guidelines and approved treatments. Conflicting guidance exists regarding effective treatment strategies, with most formal literature existing in the form of case reports. Herein, we describe a 44-year-old man with end-stage renal disease on hemodialysis who presented with a 2-month history of nonhealing wounds on his penis and lower extremities.
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http://dx.doi.org/10.1080/08998280.2020.1868280DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8059885PMC
January 2021

Comparative profile of refractory status epilepticus models following exposure of cholinergic agents pilocarpine, DFP, and soman.

Neuropharmacology 2021 Apr 17:108571. Epub 2021 Apr 17.

Department of Neuroscience and Experimental Therapeutics, Texas A&M University Health Science Center College of Medicine, Bryan, TX 77807.

Status epilepticus (SE) is a medical emergency with continuous seizure activity that causes profound neuronal damage, morbidity, or death. SE incidents can arise spontaneously, but mostly are elicited by seizurogenic triggers. Chemoconvulsants such as the muscarinic agonist pilocarpine and organophosphates (OP), such as the pesticide diisopropylfluorophosphate (DFP) and the nerve agent soman, can induce SE. Pilocarpine, DFP, and soman share a common feature of cholinergic crisis that transitions into a state of refractory SE, but their comparative profiles remain unclear. Here, we evaluated the comparative convulsant profile of pilocarpine, DFP, and soman to produce refractory SE and brain damage in rats. Behavioral and electrographic seizures were monitored for 24 h after exposure and the extent of brain injury was determined by histological markers of neuronal injury and degeneration. Seizures were elicited rather slowly after pilocarpine as compared to DFP or soman, which caused rapid onset of spiking that swiftly developed into persistent SE. Time-course of SE activity after DFP was comparable to that after soman, a potent nerve agent. Diazepam controlled pilocarpine-induced SE, but it was ineffective in reducing OP-induced SE. All three agents produced modestly different degrees of neuronal injury and neurodegeneration in the brain. These results reveal distinct convulsant and neuronal injury patterns following exposure to cholinergic agonists, OP pesticides, and nerve agents. A battery of SE models, especially SE induced by cholinergic agents and other etiologies including epilepsy and brain tumors, is essential to identify novel anticonvulsant therapies for the management of refractory SE.
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http://dx.doi.org/10.1016/j.neuropharm.2021.108571DOI Listing
April 2021

Ixekizumab in the treatment of moderate-to-severe plaque psoriasis: Patient adherence, satisfaction, and preferences.

Dermatol Ther 2021 Jan 10;34(1):e14486. Epub 2020 Nov 10.

College of Medicine, Texas A&M University, Dallas, Texas, USA.

Ixekizumab is a humanized monoclonal antibody that exhibits its immunomodulatory effects by binding to interleukin 17A (IL-17A), a proinflammatory cytokine. It was approved for the treatment of plaque psoriasis by the Food and Drug Administration in 2016. Ixekizumab has demonstrated superiority in clinical trials against etanercept, with no significant difference in the side effect profile. The chronicity of psoriasis requires continual treatment to achieve disease clearance. Many factors may affect adherence to treatment including patient satisfaction, patient preferences, medication cost, and medication side effects. Limited data on patient adherence, satisfaction, and preference exists in formal literature. Often, surrogate measures must be used to extrapolate information regarding these measures. In this narrative review, we describe patient adherence, satisfaction, and preferences via both direct and surrogate measures as they relate to ixekizumab treatment for moderate-to-severe plaque psoriasis.
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http://dx.doi.org/10.1111/dth.14486DOI Listing
January 2021

Diffuse dermal angiomatosis of the breast.

Proc (Bayl Univ Med Cent) 2020 Apr 6;33(2):273-275. Epub 2020 Feb 6.

Division of Dermatology, Baylor Scott & WhiteDallasTexas.

Diffuse dermal angiomatosis of the breast can be a painful, irritating, and persistent inflammatory condition. It tends to present in middle age and is associated with a number of risk factors, mainly relating to tissue hypoxia. There are no standard treatment guidelines, and current treatment focuses on mitigating tissue hypoxia by addressing atherosclerosis through lifestyle changes and medical and/or surgical intervention. Herein, we present a case of diffuse dermal angiomatosis of the breast, describing the condition and current treatment approaches and the likelihood that this diagnosis is more common than previously believed.
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http://dx.doi.org/10.1080/08998280.2020.1722052DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7155956PMC
April 2020

Histone deacetylase-1 (HDAC1) is a molecular switch between neuronal survival and death.

J Biol Chem 2012 Oct 23;287(42):35444-35453. Epub 2012 Aug 23.

Department of Molecular and Cell Biology, University of Texas at Dallas, Richardson, Texas 75080; School of Behavioral and Brain Sciences, University of Texas at Dallas, Richardson, Texas 75080. Electronic address:

Both neuroprotective and neurotoxic roles have previously been described for histone deacetylase-1 (HDAC1). Here we report that HDAC1 expression is elevated in vulnerable brain regions of two mouse models of neurodegeneration, the R6/2 model of Huntington disease and the Ca(2+)/calmodulin-dependent protein kinase (CaMK)/p25 double-transgenic model of tauopathic degeneration, suggesting a role in promoting neuronal death. Indeed, elevating HDAC1 expression by ectopic expression promotes the death of otherwise healthy cerebellar granule neurons and cortical neurons in culture. The neurotoxic effect of HDAC1 requires interaction and cooperation with HDAC3, which has previously been shown to selectively induce the death of neurons. HDAC1-HDAC3 interaction is greatly elevated under conditions of neurodegeneration both in vitro and in vivo. Furthermore, the knockdown of HDAC3 suppresses HDAC1-induced neurotoxicity, and the knockdown of HDAC1 suppresses HDAC3 neurotoxicity. As described previously for HDAC3, the neurotoxic effect of HDAC1 is inhibited by treatment with IGF-1, the expression of Akt, or the inhibition of glycogen synthase kinase 3β (GSK3β). In addition to HDAC3, HDAC1 has been shown to interact with histone deacetylase-related protein (HDRP), a truncated form of HDAC9, whose expression is down-regulated during neuronal death. In contrast to HDAC3, the interaction between HDRP and HDAC1 protects neurons from death, an effect involving acquisition of the deacetylase activity of HDAC1 by HDRP. We find that elevated HDRP inhibits HDAC1-HDAC3 interaction and prevents the neurotoxic effect of either of these two proteins. Together, our results suggest that HDAC1 is a molecular switch between neuronal survival and death. Its interaction with HDRP promotes neuronal survival, whereas interaction with HDAC3 results in neuronal death.
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http://dx.doi.org/10.1074/jbc.M112.394544DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3471765PMC
October 2012