Search

Leflunomide can be used in management of psoriatic disease. Leflunomide's active metabolite, teriflunomide, is used in the treatment of multiple sclerosis and has unexpectedly been rarely reported to induce pustular psoriasis. In this report, we present a patient with multiple sclerosis who developed inverse psoriasis after starting teriflunomide.

This article discusses a case of a patient with metastatic renal cell carcinoma who developed nivolumab-induced lichenoid dermatitis (LD), which initially presented as a penile ulcer. The patient later developed extensive mucocutaneous re-emergent LD, which was successfully treated with hydroxychloroquine. The article highlights the diverse clinical presentations and variable time of onset of cutaneous immune-related adverse events (cirAEs) associated with immune checkpoint inhibitor (ICI) treatment. It also suggests that hydroxychloroquine may be a safe and effective option for managing severe lichenoid cirAEs. [Extracted from the article]

Mucinous nevus (MN) is a rare, benign, cutaneous hamartoma that may be congenital or acquired. There are admixed CD34-positive fibroblasts and a few factor XIIIa-positive dendritic cells.3 Many cases show an acanthotic epidermis with elongation of the rete ridges and hyperkeratosis, similar to an epidermal nevus. 4 Oiso N, Kimura M, Kawada A. Follicular mucinous nevus: a possible new variant of mucinous nevus. [Extracted from the article]

The use of light and laser in the treatment of acne is increasing as these modalities are safe, effective, and associated with no or minimal complications when used appropriately. These light and laser sources are also being used in combination with pharmacological and/or physical measures to synergize their effects and optimize the therapeutic outcome. This review focuses on optical devices used in treating acne and serves to delineate the current application of various methods, including their utility and efficacy. [ABSTRACT FROM AUTHOR]

The molecular clones pSPeiav19 and p19/wenv17 of equine infectious anemia virus (EIAV) differ in env and long terminal repeats (LTRs) and produce viruses (EIAV19 and EIAV17, respectively) of dramatically different virulence phenotypes. These constructs were used to generate a series of chimeric clones to test the individual contributions of LTR, surface (SU), and transmembrane (TM)/Rev regions to the disease potential of the highly virulent EIAV17. The LTRs of EIAV19 and EIAV17 differ by 16 nucleotides in the transcriptional enhancer region. The two viruses differ by 30 amino acids in SU, by 17 amino acids in TM, and by 8 amino acids in Rev. Results from in vivo infections with chimeric clones indicate that both LTR and env of EIAV17 are required for the development of severe acute disease. In the context of the EIAV17 LTR, SU appears to have a greater impact on virulence than does TM. EIAV17SU, containing only the TM/Rev region from the avirulent parent, induced acute disease in two animals, while a similar infectious dose of EIAV17TM (which derives SU from the avirulent parent) did not. Neither EIAV17SU nor EIAV17FM produced lethal disease when administered at infectious doses that were 6- to 30-fold higher than a lethal dose of the parental EIAV17. All chimeric clones replicated in primary equine monocyte-derived macrophages, and there was no apparent correlation between macrophage tropism and virulence phenotype. [ABSTRACT FROM AUTHOR]

A 46-year-old African American man presented with a 3- to 4-day history of a new painful lesion on his left lower extremity. Other reported symptoms included a productive cough and chest pain; the patient denied fever and chills. His medical history was significant for a heart transplant 4 months prior to presentation followed by transplant rejection 2 weeks after the transplant. Medications included an antirejection/immunosuppressive regimen consisting of prednisone, tacrolimus, mycophenolate mofetil, and prophylaxis treatment with valganciclovir and trimethoprim-sulfamethoxazole.

Sequential cleavage of amyloid precursor protein by β- and γ-secretases generates β-amyloid peptides (Aβ), which accumulate in the brains of patients with Alzheimer's disease. We recently identified S-palmitoylation of two γ-secretase subunits, APH1 and nicastrin. S-Palmitoylation is an essential posttranslational modification for the proper trafficking and function of many neuronal proteins. In cultured cell lines, lack of S-palmitoylation causes instability of nascent APH1 and nicastrin but does not affect γ-secretase processing of amyloid precursor protein. To determine the importance of γ-secretase S-palmitoylation for Aβ deposition in the brain, we generated transgenic mice coexpressing human wild-type or S-palmitoylation-deficient APH1aL and nicastrin in neurons in the forebrain. We found that lack of S-palmitoylation did not impair the ability of APH1aL and nicastrin to form enzymatically active protein complexes with endogenous presenilin 1 and PEN2 or affect the localization of γ-secretase subunits in dendrites and axons of cortical neurons. When we crossed these mice with 85Dbo transgenic mice, which coexpress familial Alzheimer's disease-causing amyloid precursor protein and presenilin 1 variants, we found that coexpression of wild-type or mutant APH1aL and nicastrin led to marked stabilization of transgenic presenilin 1 in the brains of double-transgenic mice. Interestingly, we observed a moderate, but significant, reduction in amyloid deposits in the forebrain of mice expressing S-palmitoylation-deficient γ-secretase subunits compared with mice overexpressing wild-type subunits, as well as a reduction in the levels of insoluble Aβ(40-42). These results indicate that γ-secretase S-palmitoylation modulates Aβ deposition in the brain.