Carcinoma Verrucoso e Leucoplasia em um mesmo paciente: relato de caso clínico

The authors report a case of a 65 years-old female patient with two lesions that were present for 4 years. The patient did not smoke or drink alcohol. One of the lesions was proliferative, had verruciform and whiteness surface and was located in the buccal mucosa, at the right side; the other lesion was a plaque with irregular shape and white color and was located in tongue border, right side. The clinical vliagnosis was Oral Verrucous Carcinoma to the buccal mucosa and Leukoplakia to the border tongue lesion; both clinical diagnoses were confirmed by histopathologic exams. The patient was treated by surgery; after 6 months, she is well and recovering facial and tongue movement, with physiotherapy.Os autores descrevem o caso clínico de duas lesões presentes há mais de 4 anos, em uma paciente do sexo feminino, 65 anos de idade, que negou hábitos de tabagismo e etilismo. Uma das lesões encontrava-se em mucosa jugal, lado direito, exofítica, com superfície verrucóide e esbranquiçada; outra localizava-se na borda da língua, lado direito, em forma de placa branca. Os diagnósticos clínicos estabelecidos foram de Carcinoma Verrucoso para a lesão de mucosa jugal e de Leucoplasia para a lesão de língua, os quais foram confirmados no exame histopatológico. A paciente foi encaminhada para remoção cirúrgica de ambas as lesões. Decorridos 6 meses da cirurgia, a mesma encontra-se em bom estado de saúde geral, recuperando os movimentos faciais e linguais, através de fisioterapia

Cell carcinoma in a patient with Fanconi anemia

Fanconi anemia (FA) is an autosomal recessive disorder that might cause a variety of congenital and developmental abnormalities. The most important features of FA are progressive bone marrow failure and development of malignancies, particularly acute myeloid leukemia and solid tumors. This paper reports the case of a 12-year-old patient with FA assisted at the Stomatology and Bucomaxillofacial Cancer Prevention Service of São Lucas Hospital, Brazil, who had been submitted to bone marrow transplantation (BMT) at the age of 5 and exhibited oral lesions characteristic of chronic graft versus host disease (GVHD). The patient was treated and followed-up for the oral lesions. Eleven years after the BMT, he developed squamous cell carcinoma of the tongue with an aggressive behavior, which was considered an untreatable condition. The patient died few months later from asphyxia at the age of 16. The reasons for development of these malignant conditions are unknown. However, chromosomal instability typically observed in FA cases, BMT factors and GVHD have been considered. Systematic follow-up of these patients allows early and less invasive therapeutic approaches

A single pair of leucokinin neurons are modulated by feeding state and regulate sleep-metabolism interactions.

Dysregulation of sleep and feeding has widespread health consequences. Despite extensive epidemiological evidence for interactions between sleep and metabolic function, little is known about the neural or molecular basis underlying the integration of these processes. D. melanogaster potently suppress sleep in response to starvation, and powerful genetic tools allow for mechanistic investigation of sleep-metabolism interactions. We have previously identified neurons expressing the neuropeptide leucokinin (Lk) as being required for starvation-mediated changes in sleep. Here, we demonstrate an essential role for Lk neuropeptide in metabolic regulation of sleep. The activity of Lk neurons is modulated by feeding, with reduced activity in response to glucose and increased activity under starvation conditions. Both genetic silencing and laser-mediated microablation localize Lk-dependent sleep regulation to a single pair of Lk neurons within the Lateral Horn (LHLK neurons). A targeted screen identified a role for 5' adenosine monophosphate-activated protein kinase (AMPK) in starvation-modulated changes in sleep. Knockdown of AMPK in Lk neurons suppresses sleep and increases LHLK neuron activity in fed flies, phenocopying the starvation state. Further, we find a requirement for the Lk receptor in the insulin-producing cells (IPCs), suggesting LHLK-IPC connectivity is critical for sleep regulation under starved conditions. Taken together, these findings localize feeding-state-dependent regulation of sleep to a single pair of neurons within the fruit fly brain and provide a system for investigating the cellular basis of sleep-metabolism interactions

Sympathetic NPY controls glucose homeostasis, cold tolerance, and cardiovascular functions in mice

Summary: Neuropeptide Y (NPY) is best known for its effects in the brain as an orexigenic and anxiolytic agent and in reducing energy expenditure. NPY is also co-expressed with norepinephrine (NE) in sympathetic neurons. Although NPY is generally considered to modulate noradrenergic responses, its specific roles in autonomic physiology remain under-appreciated. Here, we show that sympathetic-derived NPY is essential for metabolic and cardiovascular regulation in mice. NPY and NE are co-expressed in 90% of prevertebral sympathetic neurons and only 43% of paravertebral neurons. NPY-expressing neurons primarily innervate blood vessels in peripheral organs. Sympathetic-specific NPY deletion elicits pronounced metabolic and cardiovascular defects in mice, including reductions in insulin secretion, glucose tolerance, cold tolerance, and pupil size and elevated heart rate, while notably, however, basal blood pressure was unchanged. These findings provide insight into target tissue-specific functions of NPY derived from sympathetic neurons and imply its potential involvement in metabolic and cardiovascular diseases