Conus-like structure in the eye of the deep-sea teleost Radiicephalus elongatus (Pisces,Teleostei)

Summary A conus-like structure, the hyaloid conus, located on the optic nerve head of the mesopelagic deep-sea teleost Radiicephalus elongatus is described. The hyaloid conus consists of a tapering sheath of unpigmented, vascularized connective tissue enveloping the proximal part of the hyaloid artery which proceeds from the optic nerve head through the vitreous body to the ventrally located falciform process and lens muscles. The hyaloid artery passes through the hyaloid conus without giving off any branches. The conus vessels encircling the hyaloid artery receive arterial blood from the choroid via small arteries and are drained to the choroid by a single vein. The hyaloid conus is compared with the lacertilian conus papillaris. The function of the hyaloid conus is unknown. Because of its small dimensions relative to those of the eyeball and its few capillaries, it is unlikely that the hyaloid conus is a supplemental nutritive device for the retina.     

Hepatic reactions in erythropoietic protoporphyria (author's transl)

The main hepatic change in erythropoietic protoporphyria is the deposition of protoporphyrin. Brown deposits of this pigment occur in bile canaliculi and ductules, discretely in hepatocytes, and secondarily in macrophages and Kupffer cells. The pigment is deposited in a crystalline form. Under the fluorescence microscope with a mercury maximum pressure burner (HO 50) at a wave length of 380--500 nm, it shows a typical red fluorescence even after paraffin embedding. Its crystalline structure results in a characteristic double refraction under the polarising microscope. Light-microscopically, hepatocellular reactions are characterised mainly by discrete alterations in the ergastoplasm. However, cell damage is indicated by diffusely distributed, hyaline single cell necrosis and by cytolytic piecemeal necrosis at the peripheries of hepatic lobules. Numerous, often disturbed mitoses produce binuclear and multinuclear hepatocytes. The obligatory secretion of protoporphyrin into the bile ducts leads to an alteration in the canalicular and ductular excretion apparatus which involves distinct ductular proliferation and accompanying fibrosis. Piecemeal necrosis is a further consequence of this process. The resulting histological picture is similar to sclerosing cholangitis with which it also has in common the slowly progressive development of hepatic cirrhosis.     

Intracellular transport of endocytosed chylomicron [3H]retinyl ester in rat liver parenchymal cells. Evidence for translocation of a [3H]retinoid from endosomes to endoplasmic reticulum

The intracellular transport of chylomicron remnants labeled with [3H]retinyl ester was studied in rat liver parenchymal cells by means of subcellular fractionation in Nycodenz and sucrose density gradients. The data presented indicate that endocytosed chylomicron remnant [3H]retinyl ester initially is located in low density endosomes. Radioactivity is subsequently transferred to a denser vesicle. Equilibrium as well as rate zonal centrifugation suggest that this denser [3H] retinoid-containing vesicle may represent endoplasmic reticulum. We have compared the intracellular transport of chylomicron remnant [3H]retinyl ester and 125I-asialofetuin. The receptor-mediated endocytosis of asialoglycoproteins in rat liver parenchymal cells is a thoroughly studied system. Our results suggest that the [3H] retinoid and 125I-asialofetuin follow the same path initially to the endosomes. After transit in endosomes, the intracellular transport differs. While asialofetuin is transported to the lysosomes, the retinoid is probably transferred to the endoplasmic reticulum.     

Effect of bromocriptine on prostacyclin release and cyclic nucleotides on rat aortic and uterine tissues

The effect of bromocriptine mesylate on cyclic nucleotides and PGI₂ release by rat aortic and uterine tissues was investigated. Treatment of rats with bromocriptine (10 mg kg⁻¹ I.P. daily for 14 days) increased PGI₂ release by the thoracic aorta from 0.67 ± 0.02 to 1.4 ± 0.03 ng/mg wet tissue (P < 0.001; n = 6). This increase was antagonized by treatment with sulpiride (15 mg kg⁻¹). Incubation of the arterial tissue with bromocriptive (50 ug ml⁻) in vitro also stimulated PGI₂ release. Mepacrine (160 μg ml⁻) significantly decreased both basal and stimulated PGI₂ release. Incubation of myometrial tissue from pregnant rats with bromocriptine (50 μg ml⁻¹) in vitro significantly decreased PGI₂ release from 1.25 ± 0.07 to 0.60 ± 0.08 ng/mg wet tissue (P < 0.05, n = 6).It also elevated uterine cAMP from 40 ± 2 to 64 ± 3 pmoles/100 mg wet tissue. Both effects were antagonized by sulpiride. Bromocriptine did not affect uterine cGMP or the cyclic nucleotides in the aorta. It is concluded that the increase in aortic PGI₂ was mediated via activation of dopamine D-2 receptors that stimulate phospholipase A₂ enzyme. The decrease in myometrial PGI₂ release may be related to the increase in uterine cAMP resulting from activation of dopamine D-1 receptors. Previous studies suggested a role for PGI₂ in implantation in the rat. The results suggest that the inhibitory effèct on uterine PGI₂ may underlie the reported inhibition of bromocriptine on implantation. On broad basis, the decrease in uterine PGI₂ together with the reported luteolytic effect of bromocriptine point to a potential role for the compound in postcoital contraception.     

Modulation of ornithine decarboxylase activity in the normal and regenerating rat liver by different doses of hydra peptide morphogen

The authors studied the anabolic effect of peptide morphogen of the hydra undecapeptide on normal and regenerating rat liver. Ornithine decarboxylase (EC 4.1.1.17) activity served as a marker. Intraperitoneal injection of the peptide into intact animals stimulated ornithine decarboxylase activity in a dose-dependent manner. In partially hepatectomized rats the peptide stimulated ornithine decarboxylase activity in the dose of 20 micrograms/kg body weight while greater doses inhibited the enzyme activity.     

Immune deficiency in the X-linked lymphoproliferative syndrome. I. Epstein-Barr virus-specific defects

Eleven males with XLP were evaluated for EBV-specific antibodies during periods of 2 to 7 yr. Variable responses to EBV-specific antigens were found. All 11 patients had subnormal anti-EBNA titers, which probably reflected a T cell deficiency. The patients showed four different patterns in their anti-VCA response: 1) two boys who had experienced malignant lymphoma mounted no antibodies at all; 2) two patients showed intermittent anti-VCA titers; 3) four males had persistently elevated anti-VCA titers; and 4) three patients showed normal anti-VCA titers. ADCC against EBV-infected cells was abnormally low in six patients and was elevated in two patients given gamma-globulin. ADCC titers did not correlate with anti-VCA titers. However, most patients with XLP failed to effect regression of autologous EBV-infected lymphoblastoid cell lines, indicating a deficiency in long-lived T cell-mediated immunity to EBV.