Ameliorative effect of NAP on laser‐induced retinal damage

Purpose: NAP is the smallest active element of activity‐dependent neuroprotective protein (ADNP) in the non‐myelinated neural tissue. This study evaluated the neuroprotective effect of NAP in reducing the spread of laser‐induced retinal damage in rat. Methods: Laser lesions were created in 72 DA pigmented rats. Two groups were treated by one intravenous or intravitreal injection of NAP immediately after exposure to laser. Two control groups were similarly administered saline injection. Histological and morphometrical evaluations of the lesions were preformed 3, 20 and 60 days after photocoagulation. Results: After intravitreal treatment with NAP, a significant reduction in the diameter of the laser‐induced lesions was found 3 days after photocoagulation (p < 0.001) but not after 20 and 60 days while the systemic treatment significantly reduced lesion diameter 20 and 60 days after photocoagulation (p = 0.001). Significant difference in photoreceptor cell loss was found in eyes treated intravitreally only 3 days after photocoagulation (p = 0.002). In the systemically treated animals such effect was found only after 20 and 60 days (p < 0.001). Conclusions:  Treatment with NAP ameliorates laser‐induced retinal lesions. Intravitreal treatment had an early short‐term effect while the effect of systemic administration was delayed and prolonged. This treatment may be of clinical significance in reducing laser‐induced retinal injuries in humans.     

A case of breast cancer associated with juvenile papillomatosis of the male breast.

Juvenile papillomatosis of the breast (JPB) was first described in 1980 and is occasionally associated with breast cancer. The literature reports only four cases of JPB in males; none of them associated simultaneously with breast cancer. We present a case of a male with JPB associated with a ductal carcinoma in the same gland.     

Inhibition of murine embryonic growth by human immunodeficiency virus envelope protein and its prevention by vasoactive intestinal peptide and activity-dependent neurotrophic factor.

Intrauterine growth retardation and neurodevelopmental handicaps are common among infants born to HIV-positive mothers and may be due to the actions of virions and/or maternally derived viral products. The viral envelope protein, gp120, is toxic to neurons, induces neuronal dystrophy, and retards behavioral development in neonatal rats. Vasoactive intestinal peptide, a neuropeptide regulator of early postimplantation embryonic growth, and the neuroprotective protein, activity-dependent neurotrophic factor, prevent gp120-induced neurotoxicity. Whole embryo culture of gestational day 9.5 mouse embryos was used to assess the effect of gp120 on growth. Embryos treated with gp120 exhibited a dose-dependent inhibition of growth. gp120-treated embryos (10(-8) M) grew 1.2 somites in the 6-h incubation period, compared with 3.9 somites by control embryos. Embryos treated with gp120 were significantly smaller in cross-sectional area and had significantly less DNA and protein than controls. Growth inhibition induced by gp120 was prevented by cotreatment with vasoactive intestinal peptide or activity-dependent neurotrophic factor. gp120 may play a role in the growth retardation and developmental delays experienced by infants born to HIV-positive mothers. Vasoactive intestinal peptide and related factors may provide a therapeutic strategy in preventing developmental deficits.     

Sodium dodecylsulphate induces a breach in the blood-brain barrier and enables a West Nile virus variant to penetrate into mouse brain

A novel and convenient assay was used to determine the effect of recombinant Interleukin-2 (IL-2) on the function of the blood-brain barrier (BBB). The assay is based on a variant of the West Nile virus, WN-25, which had lost its neuroinvasiveness but not its neurovirulence. WN-25, when injected intravenously, can cause the death of mice only if the function of the BBB is impaired. Sodium dodecylsulphate (SDS), a component in IL-2 excipient, was found to cause a short term breach in the BBB, enabling the penetration of viruses into the brain. Minimal amounts (30 ng/mouse) can induce a breach of about 10 min, which allows 0.1% of the injected virus to enter the brain. These findings demonstrate the possible use of SDS as a mean for intentional introduction of drugs into the brain, however they also call attention to the danger of using detergents as additives for drugs given intravenously.     

Neuropeptides: brain messengers of many faces

Neuropeptides 2001, 2nd Joint Meeting of the European Neuropeptide Club and the American Summer Neuropeptide Conference (11th Annual Meeting). 6–11 May 2001 with Satellite Symposium, Israeli–French Symposium, Israel Ministry of Science, Culture and Sport, 6 May 2001, held at Maale Hachmicha and Tel Aviv University, Israel.     

Monoclonal antibodies that recognize discrete forms of tubulin.

Anti-tubulin antibodies secreted by plasmacytoma NSI-spleen cell hybrids were detected by an indirect binding assay. Different antibodies bound to different combinations of the tubulins as resolved by isoelectric focusing. Two monoclonal antibodies (TUB 2.1 and TUB 2.5) labeled only (i) the tubulin band on a polyacrylamide electropherogram and (ii) beta-tubulins as resolved by isoelectric focusing. The fraction that was specifically bound and eluted from antibody affinity columns was enriched in beta-tubulins as compared with alpha-tubulins, suggesting the possibility of some soluble tubulin homodimers and alpha,beta-heterodimers. Double labeling experiments were used to show that all detectable microtubules contained beta-tubulin.