Anthocyanins, phenolics, and color of Cabernet Franc, Merlot, and Pinot Noir wines from British Columbia.

Changes in phenolics (anthocyanins, flavonols, tartaric esters, and total phenolics) during ripening of grapes and in phenolics and color during vinification and aging of Cabernet Franc, Merlot, and Pinot Noir wines were studied. Anthocyanins in grape skins showed variations in accumulation pattern, concentration, and distribution depending on variety and to a lesser extent on season. During vinification, colorless phenolics increased during alcoholic fermentation, reached maximum values at pressing, and remained stable during malolactic fermentation and subsequent storage. Anthocyanins and color density, on the other hand, increased during the early stages of alcoholic fermentation, reached maximum values 2-3 days after the start of fermentation, decreased during malolactic fermentation, and slowly declined during subsequent storage. Viticultural practices that increased cluster sun exposure generally led to higher phenolics and color density of wines, whereas changing yeasts used for fermentation had minimal effects.

Sexuality after laparoscopic-assisted vaginal hysterectomy.

STUDY OBJECTIVE: The aim of the study is to assess the degree of satisfaction of patients with their operation comparing laparoscopic-assisted vaginal hysterectomies (LAVH) with the data available in the literature. DESIGN: A questionnaire was sent to the patients approximately eight months after their operation (a minimum of six and a maximum of 24 months). The questionnaire was conceived to assess conflicting statements and to obtain objective data. SETTING: All the operations were performed at the Jan Palfijin General Hospital, Antwerp, Belgium. INTERVENTIONS: Between January 1991 and December 1993, 116 LAVHs were performed. MEASUREMENTS AND MAIN RESULTS: Fifty-three questionnaires were returned. From the patients returning their questionnaires, 98% prefer LAVH over abdominal hysterectomy because of the cosmetic results. CONCLUSIONS: The psychological and sexual reactions are determined solely by the patients' individual enlightenment.

Antimyeloperoxidase antibodies induce neutrophil adherence to cultured human endothelial cells.

Antimyeloperoxidase autoantibodies are found in the sera of some patients with glomerulonephritis and systemic vasculitis. Previously, we demonstrated that they were able to stimulate neutrophils to damage cultured human endothelial cells. We now report that antimyeloperoxidase antibodies are able to stimulate neutrophils to adhere to cultured human endothelial cells. Immunoglobulin G purified from myeloperoxidase-antineutrophil cytoplasmic autoantibody positive sera increased adherence to 331 +/- 60% of unstimulated controls. In a similar manner, rabbit antimyeloperoxidase enhanced neutrophil adherence. Stimulating the endothelial cells with 10 micrograms/mL endotoxin enhanced antimyeloperoxidase stimulated adherence. In the presence of a CD18 blocking antibody (MoAb 60.3), antimyeloperoxidase-stimulated adherence was significantly decreased. These results add further understanding to the antimyeloperoxidase-stimulated neutrophil-endothelial cell interaction and further support the hypothesis that antimyeloperoxidase autoantibodies are of pathogenic import in glomerulonephritis and vasculitis.

Do antineutrophil cytoplasmic autoantibodies cause Wegener's granulomatosis and other forms of necrotizing vasculitis?

The in vitro experimental observations support the theoretical pathogenic scenario depicted in Figure 14. A similar scenario could be portrayed for monocytes. ANCA in the circulation are unable to interact with unprimed neutrophils because the target antigens are within the cytoplasm (Fig. 14A). Synergistic priming of neutrophils, e.g., by an infection, causes small amounts of target antigens to be released at the cell surface (Fig. 14B) where they can interact with ANCA (Fig. 14C). ANCA-activated neutrophils then adhere to endothelial cells via adhesion molecule interactions that may require prior priming of the endothelial cells (Fig. 14C). These activated and adherent neutrophils then injure endothelial cells (and eventually underlying vessel wall structures) by releasing granule enzymes and toxic oxygen metabolites (Fig. 14D). Although many research groups throughout the world have been attempting to create an animal model of ANCA-induced disease based on the theoretical paradigm proposed in Figure 14, as well as on other paradigms, no one has reported complete success. Until this is accomplished, the role of ANCA in the pathogenesis of Wegener's granulomatosis and other forms of ANCA-associated vasculitides will remain conjectural.

Anti-myeloperoxidase antibodies stimulate neutrophils to damage human endothelial cells.

Anti-myeloperoxidase autoantibodies are found in association with idiopathic necrotizing glomerulonephritis and systemic vasculitis. It is not known if their presence is an epiphenomen or an integral part of the pathogenic process. To further delineate their hypothesized pathogenicity, we studied their ability to stimulate neutrophils to damage human umbilical vein endothelial cells in vitro. Anti-myeloperoxidase antibodies from human, rabbit and mouse sources were utilized. These antibodies stimulated neutrophils to damage endothelial cells as determined by 51Cr release. The effect was dependent on priming the neutrophils with tumor necrosis factor-alpha, and further enhanced with the addition of endotoxin. The amount of endothelial cell damage was dependent on the dose of anti-myeloperoxidase, the source of the neutrophils, the concentration of TNF, and the presence of endotoxin. Under identical conditions, control antibodies did not stimulate neutrophils to damage endothelial cells. The effect was confirmed by labeling the endothelial cells with 3H-adenine which yielded the same results. These results provide further in vitro evidence that anti-myeloperoxidase autoantibodies may play a significant role in the pathogenesis of idiopathic pauci-immune glomerulonephritis and vasculitis.

The pathogenic role of antineutrophil cytoplasmic autoantibodies.

Antineutrophil cytoplasmic autoantibodies (ANCA) are found in the sera of patients with systemic necrotizing vasculitis and glomerulonephritis. Their role in the pathogenesis of these diseases is not clearly understood; however, there is a growing body of data that supports a pathogenic function for these antibodies. In vitro they can activate neutrophils and monocytes to produce reactive oxygen species (ROS), degranulate, and damage target cells. The antigens to which they are directed stimulate T lymphocytes from patients with these diseases. The ANCA directed against proteinase 3 (PR3) may also play a role in growth regulation of monocytes by inactivating the enzymatic function of its antigen. The proposed model of ANCA-induced disease takes into account both the in vitro data and the natural history of these diseases.

Young children's conversations with their mothers and fathers: differences in breakdown and repair.

In this study we compared the conversations of mothers and fathers with their children at 1; 3 and 1; 9, with special attention to breakdown-repair sequences. We found that, overall, children and secondary caregiver fathers experienced more communicative breakdowns than did children and primary caregiver mothers. More specifically, fathers requested clarification of their children more often than did mothers, and they most often used a non-specific query (e.g. What?). Mothers used more specific queries (e.g. Put it where?) and were involved in more 'looped' sequences involving multiple requests for clarification. Fathers also failed to acknowledge child utterances more often than did mothers. After a father non-acknowledgement, children tended not to persist and when they did they often received further non-acknowledgements; the dyad did not often return to the child's original topic. After a maternal non-acknowledgement, on the other hand, children persisted and the dyad more often returned to its previous topic. The results are interpreted as support for the Bridge Hypothesis which claims that fathers present children with communicative challenges that help prepare them for communication with less familiar adults.

Ibuprofen-associated meningitis in a woman with only serologic evidence of a rheumatologic disorder.

A case of ibuprofen-associated meningitis is reported in a previously healthy 26-year-old woman. The association was substantiated with a rechallenge. She had no symptoms of rheumatoid factor and a positive antibody to the intranuclear antigen SS-A.