Distribution of Collagen I, III, and IV and Laminin in the Human Liver during Prenatal Development.

In the absence of systematized data on the extracellular matrix components during prenatal liver development, the present study aimed to investigate the time of appearance and distribution of collagen types I, III, and IV and laminin. The study material included embryonic and fetal livers, aged 7-37 weeks, categorized into 3 trimesters. The material was stained using hematoxylin-eosin and immunohistochemistry methods for the identification of collagen I, III, and IV and laminin. Collagen I was detected near the end of the first trimester in the capsules and walls of interlobular veins. As the liver matures, collagen I is increasingly abundant in the capsules, portal area connective tissues, arterial walls, interlobular veins, sinusoids, and central veins. Collagen III and collagen IV appear in the middle of the first trimester in the capsules, portal areas, and walls of central veins, as well as the sinusoids particularly. In trimesters 2 and 3, these collagens are increasingly present in all the structures, but collagen IV is also present in nerve fibers. Laminin is sporadically present adjacent to the sinusoids in trimester 1, while in trimesters 2 and 3 this protein commonly appears in the walls of arteries and interlobular veins, in the basal membrane of bile ducts, and in nerve fibers. The contents of collagen I, III, and IV increase during prenatal development in the liver capsule, arterial and vein walls, sinusoids, and portal area. Laminin expression is consistent with that of the collagens with the exception that, within lobules, laminin disappears with liver maturation.

Peutz-Jeghers syndrome: quantitative study on enterochromaffin cells in hamartomatous intestine polyps.

INTRODUCTION: Peutz-Jeghers (PJ) syndrome is a rare familial disorder with the autosomal transmission characterized by multiple intestinal polyps, mucocutaneous pigmentation and increased incidence of various malignancies. Some clinical manifestations of PJ syndrome may be associated with the serotonin secretion from the enterochromaffin cells (EC). OBJECTIVE: Since no data have been reported so far regarding EC cells in PJ polyps, the aim of our study was to quantitatively investigate EC population in hamartomatous intestinal polyps in patients with the PJ syndrome. METHODS: The samples of surgically removed PJ polyps from family members with the PJ syndrome were collected during 34-year follow-up period. Formalin-fixed paraffin-embedded specimens of twenty-one PJ polyps were stained with HE, AB-PAS, Van Gieson, Fontana-Masson, FIF and Grimelius. For immunohistochemical analysis, the following antibodies were used: chromogranin A, serotonin, Ki-67, desmin, vimentin and cytokeratin in order to eliminate differential diagnostic possibilities and to confirm diagnosis of PJ polyps. RESULTS: Strong EC cell hyperplasia was observed within the tissue of the investigated polyps. Statistical analysis demonstrated significantly higher content of EC cells in PJ polyps than in the normal ileal mucosa. CONCLUSION: Marked hyperplasia of EC cells within the PJ polyps may be the most important contributor to functional disorders in patients with the PJ syndrome.

Proatlantal intersegmental artery: a review of normal and pathological features.

OBJECTS: Primitive carotid-vertebral and carotid-basilar anastomoses are formed early during human embryogenesis at approximately 24 days. From cephalic to caudal direction, these anastomoses are cranial extensions of the primitive internal carotid, trigeminal, otic, hypoglossal and proatlantal intersegmental arteries. MATERIALS AND METHODS: Normal and/or abnormal morphofunctional aspects of prenatal and postnatal forms of the proatlantal intersegmental artery, from the 24th day of gestation to postnatal eight decades, are described according to personal and literature data. Many (ab) normal carotid-vertebral anastomoses are also marked in differential diagnosis of the proatlantal intersegmental artery. CONCLUSIONS: The proatlantal intersegmental artery maintains the posterior circulation until the vertebral arteries are fully developed between the seventh and eighth gestational weeks. When this artery fails to obliterate, it becomes persistent one. The proatlantal intersegmental artery, most commonly, is an incidental finding or it may be of clinical significance in some patients.