Fournier gangrene - would you KISS it?

Fournier gangrene is a disease characterized by necrotizing fasciitis of the perineal and genital region, resulting from synergistic polymicrobiotic infection. Most infections can be localized to a cutaneous, urethral, or rectal source and can culminate in a fulminant sepsis. Current state of the art is systemic broad-spectrum antibiotics and serial aggressive debridement which result in superficial perineal defect of wide dimensions.

A Model for Cognitive Personalization of Microtask Design.

The study of data quality in crowdsourcing campaigns is currently a prominent research topic, given the diverse range of participants involved. A potential solution to enhancing data quality processes in crowdsourcing is cognitive personalization, which involves appropriately adapting or assigning tasks based on a crowd worker's cognitive profile. There are two common methods for assessing a crowd worker's cognitive profile: administering online cognitive tests, and inferring behavior from task fingerprinting based on user interaction log events.

Ulcerating stasis dermatitis of the forearm associated with arteriovenous graft and central vein stenosis.

Introduction: Stasis dermatitis is a pathologic condition of the skin that most commonly occurs in the lower limb, where it is caused by chronic venous insufficiency. Stasis dermatitis of the upper limb is rare.

Case Report: A 45-year-old male, resident in Angola, presented to the emergency department with an ulcer encompassing the entire left forearm.

Neuronal cholinergic signaling constrains norepinephrine activity in the heart.

It is well known that cholinergic hypofunction contributes to cardiac pathology, yet, the mechanisms involved remain unclear. Our previous study has shown that genetically engineered model of cholinergic deficit, the vesicular acetylcholine transporter knockdown homozygous (VAChT KD) mice, exhibit pathological cardiac remodeling and a gradual increase in cardiac mass with aging. Given that an increase in cardiac mass is often caused by adrenergic hyperactivity, we hypothesized that VAChT KD mice might have an increase in cardiac norepinephrine (NE) levels.

Streptococcus anginosus and Phalangeal Osteomyelitis: An Unusual Presentation.

Introduction: Osteomyelitis of the hand is a rare entity and almost always occurs after catastrophic injuries. Streptococcus anginosus is a part of the normal microbial flora of the oral cavity and the gastrointestinal tract. It is frequently associated with purulent infections in several anatomic locations but rarely harms bony structures.

Necrotizing Fasciitis Caused by Photobacterium damselae: The First Case in Portugal.

Necrotizing fasciitis is a severe soft tissue infection with a high mortality rate and therefore requires emergent surgical treatment. Several microorganisms can cause this infection, Photobacterium damselae being one of them, with only eight cases previously published in the literature. We report the first ever case of necrotizing fasciitis, caused by this microorganism, in Portugal.

Fast and slow-twitching muscles are differentially affected by reduced cholinergic transmission in mice deficient for VAChT: A mouse model for congenital myasthenia.

Congenital myasthenic syndromes (CMS) result from reduced cholinergic transmission at neuromuscular junctions (NMJs). While the etiology of CMS varies, the disease is characterized by muscle weakness. To date, it remains unknown if CMS causes long-term and irreversible changes to skeletal muscles.

Brain-derived neurotrophic factor mediates neuroprotection against Aβ-induced toxicity through a mechanism independent on adenosine 2A receptor activation.

Brain-derived neurotrophic factor (BDNF) promotes neuronal survival through TrkB-FL activation. The activation of adenosine A2A receptors (A2AR) is essential for most of BDNF-mediated synaptic actions, such as synaptic plasticity, transmission and neurotransmitter release. We now aimed at evaluating the A2AR influence upon BDNF-mediated neuroprotection against Aβ25-35 toxicity in cultured neurons.

An analysis of the myocardial transcriptome in a mouse model of cardiac dysfunction with decreased cholinergic neurotransmission.

Autonomic dysfunction is observed in many cardiovascular diseases and contributes to cardiac remodeling and heart disease. We previously reported that a decrease in the expression levels of the vesicular acetylcholine transporter (VAChT) in genetically-modified homozygous mice (VAChT KD(HOM)) leads to decreased cholinergic tone, autonomic imbalance and a phenotype resembling cardiac dysfunction. In order to further understand the molecular changes resulting from chronic long-term decrease in parasympathetic tone, we undertook a transcriptome-based, microarray-driven approach to analyze gene expression changes in ventricular tissue from VAChT KD(HOM) mice.

Dysautonomia due to reduced cholinergic neurotransmission causes cardiac remodeling and heart failure.

Overwhelming evidence supports the importance of the sympathetic nervous system in heart failure. In contrast, much less is known about the role of failing cholinergic neurotransmission in cardiac disease. By using a unique genetically modified mouse line with reduced expression of the vesicular acetylcholine transporter (VAChT) and consequently decreased release of acetylcholine, we investigated the consequences of altered cholinergic tone for cardiac function.

Angiotensin-(1-7) prevents cardiomyocyte pathological remodeling through a nitric oxide/guanosine 3',5'-cyclic monophosphate-dependent pathway.

The renin-angiotensin (Ang) system plays a pivotal role in the pathogenesis of cardiovascular disease, with Ang II being the major effector of this system. Multiple lines of evidence have shown that Ang-(1-7) exerts cardioprotective effects in the heart by counterregulating Ang II actions. The questions that remain are how and where Ang-(1-7) exerts its effects.