ABSTRACT
The liver is one of the major organs that is indirectly affected by cigarette smoke. The aim of this project is to define the histologic and ultrastructural changes in normal liver cells after exposing animals to cigarette smoke. Thirty albino rats were exposed to cigarette smoke for 90 days, followed by morphologic examination of their livers under light microscope and electron microscope. The liver cells of cigarette smoke exposed rats showed mild swelling with increased eosinophilia. Ultrastructural examination of these cells demonstrated cytoplasm with highly proliferated and crowded mitochondria. There were many electron dense mitochondria. These mitochondria were pleomorphic in shape compared to mitochondrias of control rats. Also, loss of mitochondrial cristae and widening of the intermembranous space was noticed. It is concluded that smoking exerts cellular damage and oxidative stress on normal liver cells resulting in ultrastructural changes.
El hígado es uno de los principales órganos indirectamente afectado por el humo del cigarrillo. El objetivo de este trabajo fue definir los cambios histológicos y ultraestructurales de las células normales del hígado después de exponer a los animales al humo del cigarrillo. Treinta ratas albinas fueron expuestas al humo de cigarrillo durante 90 días, seguido de un examen morfológico de los hígados bajo microscopio de luz y microscopio electrónico. Las células hepáticas de las ratas expuestas al humo de cigarrillo mostraron una leve inflamación con un aumento de la eosinofilia. En el examen ultraestructural de estas células se observó el citoplasma mitocondrial altamente proliferado y saturado. Se observó gran cantidad de mitocondrias electrón-densas y éstas presentaban forma pleomórfica en comparación con las mitocondrias del grupo control. Además, se observó pérdida de las crestas mitocondriales y ensanchamiento del espacio intermembranoso. Se concluye que el tabaquismo ejerce daño celular y estrés oxidativo en las células hepáticas normales, lo que resulta en la aparición de cambios ultraestructurales.
Subject(s)
Humans , Male , Rats , Hepatocytes/drug effects , Hepatocytes/pathology , Liver/drug effects , Liver/pathology , Tobacco Products/adverse effects , Hepatocytes/ultrastructure , Liver/ultrastructure , Microscopy, Electron, TransmissionABSTRACT
OBJECTIVE: The management of antenatally diagnosed ureteropelvic junction obstruction (PUJO) is controversial. Here, we present our experience over a period of 13 years and discuss our management protocol. MATERIALS AND METHODS: We reviewed the files of 234 patients with antenatally diagnosed congenital hydronephrosis due to PUJO. Management was tailored to each patient, based on a combination of diethylenetetraminepentacetic acid renogram outcome, pelvic diameter, as well as the patient's symptoms. RESULTS: Pyeloplasty was carried out early in 52 kidneys. Of the total, 182 patients were managed expectantly. Out of these, 45 underwent delayed pyeloplasty. The remaining 137 patients (189 units) were managed non-operatively. In patients who underwent early pyeloplasty, the mean split differential renal function was 37% before and 40.05% after surgery. In those with delayed intervention, the mean renal function was 37.8% before and 42.2% after surgery. In patients who did not have surgery, the mean differential renal function was 45.7% initially and 48.2% at the last accepted follow up. The overall operative success rate was 97.9%. CONCLUSION: We believe that pyeloplasty is the proper treatment for babies with congenital PUJO and <40% split differential function and/or pelvic diameter >35 mm at the initial visit. In other patients a period of observation is warranted, and pyeloplasty should be carried out only if their kidney function deteriorates or the renogram curve does not show improvement. With the excellent results of pyeloplasty we believe that a safer approach is to operate on more kidneys rather than risk of losing valuable kidney function.
