Biomedical subjects

M A Vazquez

Publications and source records attributed to M A Vazquez.

23 records · Page 2Linked to original sources

PubMed1993

Prevention and treatment of renal allograft rejection: new therapeutic approaches and new insights into established therapies.

Renal transplantation is the preferred treatment modality for patients with ESRD who are good surgical risks and able to comply with chronic immunosuppressive medications. Clinical transplantation has advanced significantly, with most transplant centers reporting 1-yr renal allograft survival rates of better than 80%. Nevertheless, rejection and a progressive loss of allografts over time continue to occur. The immunosuppressive agents currently used may lead to the development of life-threatening infections, malignancies, and advanced atherosclerosis as a consequence of some of their side effects. This review examines the mechanisms involved in allograft rejection as currently understood. The recent knowledge into the mechanism of action of cyclosporine, FK506, and rapamycin on T cell activation is presented. Information recently available on some of the established therapies such as steroids, antimetabolites and monoclonal antibodies as well as the newer agents is also discussed. The interaction between clinical transplantation and basic research in immunology continues to result in exciting advances in both fields.

Animals↗

PubMed1992

Macrophage functions are regulated by murine decidual and tumor extracellular matrices.

Because of their paternal antigens, the fetus and placenta may be considered an allograft in the maternal host. Understanding the mechanisms which prevent maternal immunological rejection of the fetus remains a fundamental unsolved problem in immunology. We have previously reported that macrophages are inhibited by maternal decidual stromal cells residing at the maternal-fetal interface. In view of the central role of macrophages in cell-mediated immunity, this inhibition may contribute to preventing maternal antifetal responses. We now report that it was the solid phase signals embedded in the extracellular matrix (ECM) made by decidual cells which are responsible for inhibiting macrophage-mediated lysis of TNF-alpha-resistant P815 mastocytoma cells. The latter macrophage function is acquired after stimulation by interferon gamma and endotoxin. All these macrophage functions were also inhibited by ECM isolated from the Engelberth-Holm-Swarme (EHS) tumor. This tumor ECM has a similar biochemical composition to decidual ECM. This ECM inhibited the effector, as opposed to the stimulator, phase of macrophage-mediated tumor lysis. Laminin, type IV collagen, and heparan sulfate proteoglycans, the major known components of decidual and EHS ECMs, did not inhibit the above macrophage functions. Altogether these data indicate that macrophages were inhibited by solid phase signals embedded in decidual and EHS ECMs. Whether the solid phase signals in these two ECMs are biochemically identical remains to be determined. To our knowledge, such signals are a novel pathway of inhibiting macrophage functions which may be important in understanding the maternal-fetal immunologic relationship, and the pathogenesis of perinatal infections. Furthermore, the ability of EHS tumor ECM to inhibit macrophage functions may indicate that some tumors may defend themselves against host macrophage responses using solid phase signals. This may be important in understanding some host-tumor relationships.

Animals↗

PubMed1990

Macrophage functions are regulated by the substratum of murine decidual stromal cells.

Because of their paternal antigens, the fetus and placenta may be considered an allograft in the maternal host. Local properties of the maternal-fetal interface, the placenta and decidua basalis, are important in preventing maternal immunologic rejection of the fetoplacental allograft. However, the exact nature of these local properties remains a fundamental unsolved problem in immunology. We now report that three macrophage functions were inhibited by the substratum formed by monolayers of decidual stromal cells via a novel pathway. Solid-phase inhibitors blocked macrophage adhesion, spreading, and lysis of tumor necrosis factor-alpha-resistant P815 mastocytoma tumor cells. Inhibition was not solely attributable to an inability of macrophages to adhere to decidual substratum because there were differences in macrophage functions on this surface versus polyhema where no adherence occurred. Because macrophages play a central role in cell-mediated immunity, including allograft rejection, inhibiting their function in the decidua basalis may help prevent maternal antifetal responses.

Animals↗

PubMed1989

ADFR therapy in the prevention of bone loss after menopause.

Estrogens retard bone loss after menopause and constitute the most logical therapy for the prevention of postmenopausal osteoporosis. Estrogens are contraindicated in some circumstances and some postmenopausal women are unwilling to accept them. We have used ADFR therapy as an alternative in the prevention of postmenopausal bone loss. One hundred women in the early postmenopausal period (6-24 months since the last menses) were introduced into the study. 50 were treated with placebo and 50 were treated with ADFR therapy (phosphorus 1.5 gr/day during 3 days, followed by SCT 100 UI/day during 10 days and calcium 1 gr/day). After 77 days without any therapy we repeated the cycles every 3 months. Bone mass was evaluated at the beginning and at 3, 6, 12 and 18 months by dualphoton absorptionmetry lumbar spine. In the control group, the mean spinal BMD decreased 7.31% after 12 months and 6.16% after 18 months (p greater than 0.05). The ADFR group only had a mean spinal BMD decrease of 3.79% and 1.1% after 12 and 18 months respectively (NS). Bone loss was greater in control than in ADFR group after 12 and 18 months (p less than 0.05 at both times). We conclude that phosphorus and calcitonin like ADFR therapy may be a useful alternative to estrogen for the prevention of accelerated bone loss after menopause.

Aged↗

PubMedDate not supplied

13C-urea breath test for the diagnosis of Helicobacter pylori infection before treatment: is citric acid necessary?

AIM: 13C-urea breath test is one of the best methods for the diagnosis of Helicobacter pylori infection. Although a citric acid solution is generally used prior to urea intake, the superiority of this strategy has not been sufficiently demonstrated. Thus, our aim was to compare 13C-urea breath test with and without citric acid solution, to evaluate whether 13C-urea breath test can also achieve favourable results when the test meal is omitted. METHODS: 13C-urea breath test with and without citric acid were compared prospectively in 53 subjects without prior Helicobacter pylori eradication therapy prescription. Basal samples and at 15', 30', and 45' after taking 100 mg of 13C-urea were obtained. The gold standard for Helicobacter pylori diagnosis was the 13C-urea breath test result with citric acid at 30', and "Delta Over Baseline" values >5 at that time were considered positive. RESULTS: The prevalence of Helicobacter pylori infection was 68%. Mean Delta Over Baseline values with citric acid at 15', 30' and 45' were: 29.6+/-39, 30.8+/-37 and 24.6+/-27; whereas respective values without citric acid were lower: 14.9+/-22, 12.2+/-17 and 10D+/-13 (p<O. 001 for all comparisons, Wilcoxon test for paired data). Thus, the area under the curve (constructed with Delta Over Baseline values at different times) with citric acid was 85+/- 102, and 37+/-50 without citric acid [p<0.001). Correlation coefficient between Delta Over Baseline values with and without citric acid at 30' was 0.73 (p<0.0001). The percentage of subjects achieving the highest Delta Over Baseline value at 15', 30' and 45' with citric acid was 51%, 30% and 19%, whereas without citric acid it was 51%, 26% and 23% (non-significant differences). The area under receiver operating characteristic curve for 13C-urea breath test without citric acid was: 0.98 at 15', 1 at 30' and 0.97 at 45'. The best cut-off point for 13C-urea breath test without citric acid at 30' was anywhere between 3. 3 and 3.9 (that is, a lower value than that usually considered with citric acid), with 100% (95% confidence interval, 90-100%) sensitivity and 100% [82-100%) specificity CONCLUSIONS: 13C-urea breath test values with citric acid are higher than those obtained without citric acid, although this difference does not imply a diagnostic superiority in untreated patients when considering 13C-urea breath test without citric acid at 30'. Therefore, for the diagnosis of Helicobacter pylori infection in untreated patients, citric acid solution in 13C-urea breath test protocol can be omitted.

Adult↗