Greater behavioral effects of stress in immature as compared to mature male mice

The effect of sexual maturity on behavioral effects of stress was examined in male mice. Immature (4-week-old) or mature (8-week-old) animals were subjected to either social stress (exposure to an isolated adult male) or restraint stress for 5 days and examined for body weight, food intake, or plus-maze behavior. Social stress reduced food intake, body weight, and open-arm entries in 4-week-old but not 8-week-old mice. Restraint reduced body weight in 4-week-old but not 8-week-old mice. It is concluded that immature male mice show greater behavioral disturbances after stress than their mature counterparts. The findings are in agreement with much anecdotal evidence that children are more vulnerable to stress than adults.     

The COMMIT dental model: tobacco control practices and attitudes

The National Cancer Institute's program to help dentists reduce tobacco use among their patients is part of the Community Intervention Trial for Smoking Cessation, a 22-community, randomly controlled trial of an intervention program for smoking cessation. Results of COMMIT baseline surveys of dentists in the 11 intervention communities are presented.     

Thrombolytic and endovascular treatment of peripartum iliac vein thrombosis: a case report

This case report details the multidisciplinary treatment of peripartum left iliac vein thrombosis using percutaneous catheter-directed urokinase thrombolysis and balloon thromboplasty. Enhanced chances for long-term patency and the normalization of venous function make these minimally invasive procedures accepted options for the treatment of iliofemoral deep venous thrombosis in selected peripartum patients.     

Insulin-like growth factor I activates the invasion suppressor function of E-cadherin in MCF-7 human mammary carcinoma cells in vitro

The calcium-dependent cell-cell adhesion molecule E-cadherin has been shown to counteract invasion of epithelial neoplastic cells. Using three monoclonal antibodies, we have demonstrated the presence of E-cadherin at the surface of human MCF-7/6 mammary carcinoma cells by indirect immunofluorescence coupled to flow cytometry and by immunocytochemistry. Nevertheless, MCF-7/6 cells failed to aggregate in a medium containing 1.25 mM CaCl2, and they were invasive after confrontation with embryonic chick heart fragments in organ culture. Treatment of MCF-7/6 cells with 0.5 microgram ml-1 insulin-like growth factor I (IGF-I) led to homotypic aggregation within 5 to 10 min and inhibited invasion in vitro during at least 8 days. The effect of IGF-I on cellular aggregation was insensitive to cycloheximide. However, monoclonal antibodies that interfered with the function of either the IGF-I receptor (alpha IR3) or E-cadherin (HECD-1, MB2) blocked the effect of IGF-I on aggregation. The effects of IGF-I on aggregation and on invasion could be mimicked by 1 microgram ml-1 insulin, but not by 0.5 microgram ml-1 IGF-II. The insulin effects were presumably not mediated by the IGF-I receptor, since they could not be blocked by an antibody against this receptor (alpha IR3). Our results indicate that IGF-I activates the invasion suppressor role of E-cadherin in MCF-7/6 cells.     

The effects of guided tissue regeneration and fixation technique on osseous wound healing in rabbit zygomatic arch osteotomies

So called lethal midline granuloma is of great clinical and theoretical interest. Recent evidence has shown that most lethal midline granulomas are associated with a T-cell phenotype and they are therefore referred to as nasal T-cell lymphomas (NTCL). Immunohistochemical studies, however, have shown peculiar phenotypic features such as expression of natural killer (NK)-cell-related markers and extensive T-cell antigen loss including absence of expression of alpha beta T-cell receptor (TCR). In this study, we reported genotypic and immunohistochemical features in two cases of lethal midline granuloma. The histopathological diagnosis of the biopsy specimens was polymorphic reticulosis/midline malignant reticulosis. Both cases displayed a CD2+, CD3-, CD3 epsilon+, CD4-, CD8-, CD16-, CD56+ phenotype, suggesting that these tumors may be peripheral T-cell lymphomas with extensive loss of T-cell antigens and expression of NK cell antigen (CD56), or, alternatively, NK cell neoplasias. No TCR beta gene rearrangement was detected in these cases. Monoclonal Epstein-Barr virus (EBV) genome was detected in each specimen by Southern blot hybridization. The tumor cells in one of the two cases expressed latent membrane protein (LMP). These findings support the concept that lethal midline granuloma constitutes a distinct group of lymphomas that, in addition to their peculiar clinical features, exhibits the phenotype of extensive loss of T-cell antigens and expression of the NK cell antigen, as well as harbors the EBV. In view of the LMP-transforming potential, these data suggest that EBV may play a role in the pathogenesis of lethal midline granuloma.     

Plasma viral RNA load predicts disease progression in accelerated feline immunodeficiency virus infection

Viral RNA load has been shown to indicate disease stage and predict the rapidity of disease progression in human immunodeficiency virus type 1 (HIV-1)-infected individuals. We had previously demonstrated that feline immunodeficiency virus (FIV) RNA levels in plasma correlate with disease stage in infected cats. Here we expand upon those observations by demonstrating that plasma virus load is 1 to 2 logs higher in cats with rapidly progressive FIV disease than in long-term survivors. Differences in plasma FIV RNA levels are evident by 1 to 2 weeks after infection and are consistent throughout infection. We also evaluated humoral immune responses in FIV-infected cats for correlation with survival times. Total anti-FIV antibody titers did not differ between cats with rapidly progressive FIV disease and long-term survivors. These findings indicate that virus replication plays an important role in FIV disease progression, as it does in HIV-1 disease progression. The parallels in virus loads and disease progressions between HIV-1 and FIV support the idea that the accelerated disease model is well suited for the study of therapeutic agents directed at reducing lentiviral replication.     

Spinal cord regeneration: a phenomenon unique to urodeles?

To study the triggering mechanism(s) of the induction of apoptosis following exposure to u.v. light, we used a genetic approach involving cell strains derived from patients with inherited deficiencies in nucleotide excision repair. It was found that cells from patients with Cockayne's syndrome, which are deficient in the processing of u.v.-induced pyrimidine dimers from the transcribed DNA strand, are induced to undergo apoptosis at much lower doses of u.v. light than cells with proficient strand-specific repair. The induction of apoptosis correlated to the induction of p53 and to the inhibition of total RNA and poly(A) mRNA synthesis. We also show that active p53 proteins accumulate following u.v.-irradiation without any apparent requirement for DNA strand breaks or excision repair intermediates. We propose that the blockage of RNA polymerases at DNA lesions in the transcribed strand triggers the induction of a pathway leading to apoptosis. These findings may help explain a long standing enigma of why, despite the DNA repair deficiency, patients with Cockayne's syndrome do not experience an elevated risk for skin cancer since potentially pre-mutagenic cells are eliminated by an easily triggered apoptotic pathway.