Verruciform xanthoma of the penis in a young male masquerading as squamous cell carcinoma: Case Report

Verruciform xanthoma (VX) is a relatively rare benign lesion of unknown etiology with a predilection for oral mucosa. Penis is an uncommon location and to date only 17 cases of VX of penis have been reported. The lesion assumes importance as it can be easily mistaken for verrucous carcinoma or squamous cell carcinoma. We present herein a case of penile VX in a 25-year-old man who was referred to our institute with a histopathologic diagnosis of squamous cell carcinoma reported elsewhere. On microscopy the lesion demonstrated florid verruciform hyperplasia of the epidermis with hyperkeratosis, parakeratosis and acanthosis. There was a dense infiltrate of foam cells in the papillary dermis (a hallmark of VX), which were positive for CD68 and negative for S-100 protein. We present this case to highlight the significance of recognizing VX in extra oral location. An awareness of this entity is crucial to prevent misdiagnosis and halt inappropriate therapeutic intervention. Keywords: penis, squamous cell carcinoma, verruciform xanthoma, verrucous carcinoma.     

Virtual cystoscopy: reality in imaging of bladder tuberculosis

We present a case of urinary tuberculosis investigated initially by ultrasound and multidetector computed tomography (MDCT). The MDCT-derived volumetric data were used to generate virtual cystoscopy (VC) images, which revealed a bladder ulcer. The presence of this ulcer was confirmed by conventional cystoscopy-guided biopsy and there was good agreement regarding various features of the ulcer, such as the site, size and shape, as detected by virtual and conventional cystoscopies. VC, a result of simple postprocessing of preacquired MDCT data, proved valuable in the characterization of the bladder lesion in conjunction with CT and ultrasound images. Although a larger study is warranted, in our case these en face VC representations of the ulcer served as useful precursors to conventional cystoscopic biopsy.     

α-synuclein fission yeast model

Despite fission yeast's history of modeling salient cellular processes, it has not yet been used to model human neurodegeneration-linked protein misfolding. Because alpha-synuclein misfolding and aggregation are linked to Parkinson's disease (PD), here, we report a fission yeast (Schizosaccharomyces pombe) model that evaluates alpha-synuclein misfolding, aggregation, and toxicity and compare these properties with those recently characterized in budding yeast (Saccharomyces cerevisiae). Wild-type alpha-synuclein and three mutants (A30P, A53T, and A30P/A53T) were expressed with thiamine-repressible promoters (using vectors of increasing promoter strength: pNMT81, pNMT41, and pNMT1) to test directly in living cells the nucleation polymerization hypothesis for alpha-synuclein misfolding and aggregation. In support of the hypothesis, wild-type and A53T alpha-synuclein formed prominent intracellular cytoplasmic inclusions within fission yeast cells in a concentration- and time-dependent manner, whereas A30P and A30P/A53T remained diffuse throughout the cytoplasm. A53T alpha-synuclein formed aggregates faster than wild-type alpha-synuclein and at a lower alpha-synuclein concentration. Unexpectedly, unlike in budding yeast, wild-type and A53T alpha-synuclein did not target to the plasma membrane in fission yeast, not even at low alpha-synuclein concentrations or as a precursor step to forming aggregates. Despite alpha-synuclein's extensive aggregation, it was surprisingly nontoxic to fission yeast. Future genetic dissection might yield molecular insight into this protection against toxicity. We speculate that alpha-synuclein toxicity might be linked to its membrane binding capacity. To conclude, S. pombe and S. cerevisiae model similar yet distinct aspects of alpha-synuclein biology, and both organisms shed insight into alpha-synuclein's role in PD pathogenesis.     

Whole body hyperthermia and preconditioning of the heart: basic concepts,complexity, and potential mechanisms

Whole body hyperthermia (WBH) is a distinctive pathophysiological condition with significant impact on tissue metabolism and organ functions. WBH has been investigated as a promising adjunct therapy to the conventional chemo- or radiotherapy for treating certain types of cancer. Numerous studies have shown that WBH is associated with induction of heat shock proteins (HSPs), which in turn modulate cellular survival or death. A brief period of WBH (40-42°C; 15-20min) can induce delayed protection against lethal endotoxemia as well as various forms of injury in brain, heart, liver, lungs, small intestine, and skeletal muscle. This review article focuses on discussing the WBH-induced myocardial protection against ischemia/reperfusion injury. Most recently, possible involvement of protein kinase C, mitogen-activated protein kinases, nitric oxide, ATP-sensitive potassium channels, and neural peptides in the signal transduction pathways has been demonstrated. On the other hand, whether HSPs or antioxidant enzymes are the primary end-effector of the cardioprotection continues to be a matter of ongoing debates. It has also been recognized that the complex nature of WBH may be the responsible factor for the discordant results among various studies, especially across different animal species or strains, in terms of the time course and potency of WBH-induced cardioprotection. Nevertheless, a better understanding of the WBH-elicited myocardial ischemic resistance may have a wide spectrum of clinical implications as well as insightful inputs into the hyperthermic biology.