Mistras Group (Greece)

Bladder dysfunction is a common clinical problem in stroke patients and a strong prognostic factor of disability and exerts an enormous impact on health and economy. The aim of this narrative review was tο examine the pathophysiological mechanisms of lower urinary tract symptoms after stroke, as well as the relevant clinical anatomy. Normal micturition is achieved through complex coordination between brain regions, spinal cord, and peripheral nerves, and anatomic brain connectivity is crucial to lower urinary tract physiology. The most important neurotransmitters involved in bladder control include γ-aminobutyric acid, opioids, glutamate, dopamine, norepinephrine, acetylcholine, and nitric oxide. The precise correspondence between brain damage and relevant urinary symptoms is not well understood. Urodynamic changes after stroke include detrusor overactivity, dyssynergia, and uninhibited sphincter relaxation. Several brain regions could be implicated in post-stroke urinary dysfunction. Brainstem lesions can cause various urinary symptoms. A lesion superiorly to the pontine micturition center (PMC) results in an uninhibited bladder, whereas a lesion between the sacral spinal cord and PMC leads to either a spastic bladder or sphincter-detrusor dyssynergia. Supra-pontine lesions usually cause bladder storage dysfunction. Frontoparietal lesions have been associated with urinary incontinence and insular lesions with urinary retention. Understanding the mechanisms underlying the dysfunction of the lower urinary tract following stroke can aid in the development of new therapeutic strategies for these patients.

Anais do IV Simpósio Brasileiro de Desenvolvimento Territorial Sustentável - SBDTS e do IV Seminário Internacional da Rede Ibero-americana de Estudos sobre Desenvolvimento Territorial e Governança – SIDETEG (978-85-5722-700-2) - A Meliponicultura Como Patrimônio Territorial: Primeiros Acúmulos

It has been clear that at least 1 billion adults worldwide are smokers and at least 700 million children are passive smokers at home. Smoking exerts a detrimental effect to many organ systems and is responsible for illnesses such as lung cancer, pneumonia, chronic obstructive pulmonary disease, cancer of head and neck, cancer of the urinary and gastrointestinal tract, periodontal disease, cataract and arthritis. Additionally, smoking is an important modifiable risk factor for the development of cardiovascular disease such as coronary artery disease, stable angina, acute coronary syndromes, sudden death, stroke, peripheral vascular disease, congestive heart failure, erectile dysfunction and aortic aneurysms via initiation and progression of atherosclerosis. A variety of studies has proved that cigarette smoking induces oxidative stress, vascular inflammation, platelet coagulation, vascular dysfunction and impairs serum lipid pro-file in both current and chronic smokers, active and passive smokers and results in detrimental effects on the cardiovascular system. The aim of this review is to depict the physical and biochemical properties of cigarette smoke and, furthermore, elucidate the main pathophysiological mechanisms of cigarette-induced atherosclerosis and overview the new therapeutic approaches for smoking cessation and augmentation of cardiovascular health.