ABSTRACT
The aquaporins (AQP), a protein family, were first discovered in the early 1990s. The primary role of aquaporins is to facilitate water transport across multiple cell types. In the spinal cord and brain responsible for most of the water diffusion are AQP4 and AQP1. In this paper, we describe the structure, localization and role of this water channel family, especially AQP4 and AQP1. AQP4 is involved in various pathologies such as: stroke, brain tumors, Neuromyelitis optica (NMO), Alzheimer's Disease (AD), traumatic brain injury, Parkinson's Disease, hydrocephalus, schizophrenia, epilepsy, major depressive disorder, autism. Brain edema is the most important acute complication of the hypoxic-ischemic and it has no pathogenic treatment. Imaging and histopathology studies have shown that inhibition of AQP4 reduces brain edema.
ABSTRACT
Polycystic kidney disease represented by autosomal dominant polycystic kidney disease (ADPKD) and autosomal recessive polycystic kidney disease (ARPKD) have a major impact of mortality in children. We conducted a study of a premature infant with an estimated gestation date of 32 weeks with a presumptive prenatal diagnosis of right polycystic kidney. A 28-year-old primigravida with pre-eclampsia was admitted at the gynecology unit of Clinical Emergency County Hospital of Craiova. The clinical examination revealed a large abdominal distention due probably to the right polycystic kidney, suspected on prenatal ultrasound and radiography. The preterm neonate undergone right nephrectomy 5 days after birth. Histopathology of the kidney was performed in the Pathology Department of the Emergency County Hospital of Craiova and in the Center for Microscopic Morphology and Immunology of U.M.F. of Craiova. Microscopy revealed dilated cysts lined by simple cuboidal or flattened epithelium, and islets of remnant kidney parenchyma separated by edematous stroma. Immunohistochemistry for CD34 revealed incomplete blood arcades which did not seem to be in contact with all the tubular elements of the parenchyma, when compared to a control age-matched kidney. The patient had a favorable postoperative evolution, she was clinically stable on discharge from the hospital with a follow-up strategy including genetic testing.
ABSTRACT
Multiple sclerosis (MS) is a disease of the Central Nervous System (CNS) which alters over 2 million people, and involves an abnormal autoimmune response directed against the brain, nerves and spinal cord. The antigen or the autoimmune target still remains unknown, a fact for which MS is considered to be an immune mediated disease. The pathology involves mainly the white matter, but the gray matter demyelination plays an important role in its pathogenesis. In 80% of the cases with MS, the disease develops relapses. Experimental autoimmune encephalomyelitis (EAE) is the most used model to study MS and for assessing potential treatments. In the present study we report on the histopathological characterization of an EAE model in C57BL/6 mice immunized by injection with myelin oligodendrocyte glycoprotein, MOG35-55 in complete Freud's adjuvant supplemented with pertussis toxin. On a group of 10 immunized animals and on 5 control animals, we followed the development and grading signs of motor deficiency, and after a survival of 34 days, the study aimed to evaluate the histopathological changes in the telencephalon, brainstem, cervical spinal cord, the optic nerve and retina. We utilized histochemistry, immunohistochemistry, and densitometric image analysis methods to assess myelin loss [Luxol fast blue, immunohistochemistry for the presence of microglia (Iba1) and reactive astrocytes (GFAP)]. Moreover, the study includes a first analysis of the detailed histopathological changes of the optic nerve and retina on an EAE model, all of these as the background for testing drugs with potential therapeutic role in MS.
