ASSESSMENT OF THE PREVALENCE INDEX ON SIGNS OF COMBINATION SYNDROME IN PATIENTS TREATED AT BAURU SCHOOL OF DENTISTRY,UNIVERSITY OF SAO PAULO

A group of destructive changes occurring in jaws in patients with maxillary complete dentures and mandibular removable partial dentures (bilaterally) has been described in the literature as the combination syndrome. However, this condition is not clinically observed in all patients. The aim of this study was to establish the prevalence index on signs of combination syndrome and to verify whether these changes also occurred in patients rehabilitated with a mandibular removable partial denture (unilaterally). Sample was composed of 44 patients, completely edentulous in the maxilla. Thirty-two patients had a Kennedy Class I removable partial denture and 12 a Kennedy Class II. Three major alterations were observed in 20.5% of the studied population. Nevertheless, these changes were present only in 25% of patients with Kennedy Class I removable partial denture. Based on the findings of this study, it can be concluded that patients with Kennedy Class II removable partial denture do not have similar signs that lead to the combination syndrome’s condition.     

Randomised prospective study on renal effects of two different contrast media in humans: protective role of a calcium channel blocker

Contrast media affect renal hemodynamics. Hyperosmolality is regarded as the major factor responsible for renal hemodynamic changes. In this study, the role of osmolality was evaluated in 30 hospitalized patients without risk factors during intravenous pyelography. Contrast media with low and high osmolality were used. In addition, nifedipine was administered before infusion of high-osmolality contrast to evaluate the role of calcium ions in radiocontrast-induced changes of renal hemodynamics. Hyperosmolar contrast reduced renal plasma flow and glomerular filtration rate. Calcium channel blocker prevented changes of renal hemodynamics. Hyperosmolality appears the most likely factor affecting renal hemodynamics during hyperosmolar radiocontrast infusion. Calcium channel blocker may prevent renal changes due to hyperosmolar medium.     

Lymphocyte proliferation assays as potential biomarkers for toxicant exposures

Recently there has been interest in developing assays that can be used as indicators (biomarkers) of exposure to toxic agents. We have been exploring the potential utility of three lymphocyte proliferation assays [the responses of B lymphocytes to the mitogen lipopolysaccharide (LPS), the responses of T lymphocytes to the mitogen concanavalin A (ConA), and the responses of T lymphocytes to antigenic stimuli in a mixed lymphocyte culture (MLC) assay] as biomarkers of toxicant exposure. Studies were initiated to assess the applicability and specificity of these assays and to investigate the mechanisms by which toxicants alter lymphocyte proliferation. All studies were performed using cells isolated from Fischer 344 rats. To assess applicability, mitogen assays were performed using in vitro exposures to eight different toxicants: hydroquinone, benzoquinone, Aroclor 1254, styrene oxide, and the salts of mercury, cadmium, chromate, and nickel. In vitro concentrations spanned five orders of magnitude (100 to 0.01 mg/l). At the lowest concentration tested, all eight compounds induced changes in at least one mitogen assay, indicating that these assays may be applicable to a wide range of toxicants. Variations of the ConA and MLC assays were used to test for specificity. In both assays, splenocytes taken from rats exposed in vivo to either chromate or to cadmium responded differently when the cells were cocultured with exogenously added chromate or cadmium ions, indicating that it may be possible to detect exposure to a specific toxicant by performing modified lymphocyte proliferation assays. In the mechanistic studies, splenocytes from cadmium and chromate-treated rats altered the ConA-induced proliferation of cocultured syngeneic cells. In addition, the antigenicity of splenocytes isolated from cadmium-treated rats was enhanced when these cells were used as stimulators for allogeneic splenocytes. The results of these studies indicate that lymphocyte proliferation assays may be useful for detecting exposure to a wide range of toxicants and that variations of these assays may be useful for implementing immunologically based tests for detecting exposures to specific chemicals.     

Inhaled corticosteroids reduce neutrophilic bronchial inflammation in patients with chronic obstructive pulmonary disease

BACKGROUND—Airwaysinflammation is a feature of chronic obstructive pulmonary disease(COPD), but the role of corticosteroids in the management ofclinically stable patients has yet to be established. A randomisedcontrolled study was carried out to investigate the effect of high doseinhaled beclomethasone dipropionate (BDP) administered for two monthsto patients with stable, smoking related COPD. Sputum induction wasused to evaluate bronchial inflammation response.
METHODS—34 patients(20 men and 14 women) were examined on three separate occasions. At theinitial clinical assessment (visit 0), spirometry and blood gasanalysis were performed. On visit 1 (within one week of visit 0) sputuminduction was performed and each patient was randomised to receiveeither BDP 500 µg three times daily (treated group) or nothing(control group). After two months (visit 2), all patients underwentrepeat clinical assessment, spirometry, and sputum induction.
RESULTS—There were nodifferences in sputum cell counts between the groups at baseline. Aftertwo months of treatment, induced sputum samples from patients in thetreated group showed a reduction in both neutrophils (−27%) andtotal cells (−42%) with respect to baseline, while the control groupdid not (neutrophils +9%, total cells +7%). Macrophages increased inthe treated group but not in the control group. The mean final value ofsputum neutrophils was 52% in the treated group and 73.3% in thecontrol group (95% confidence interval (CI) −27.2 to −15.4). Themean final value of sputum macrophages was 35.8% in treated group and19.3% in control group (95% CI 10.3 to 22.8). The differences betweenthe treated and control groups for neutrophils (−21.3%), macrophages (+16.5%), and total cells (−65%) were significant. Spirometry andblood gas data did not change from baseline in either patient group.
CONCLUSIONS—A twomonth course of treatment with high dose inhaled BDP reducessignificantly neutrophil cell counts in patients with clinically stable, smoking related COPD. Further studies on the effectiveness ofinhaled steroids in COPD are needed to confirm the clinical importanceof this observation.

     

Coronary occlusion secondary to blunt chest trauma: a first attempt at balloon angioplasty

There have been only 58 angiographically documented reports of transmural myocardial infarction due to closed-chest trauma. None of these cases has been treated by percutaneous transluminal coronary angioplasty. We report the case of a 40-year-old man who developed an anterior-wall myocardial infarction secondary to blunt chest trauma suffered in an automobile accident. Angiographic study performed 2 months after the injury revealed an isolated total obstruction of the left anterior descending coronary artery. The patient was judged a good candidate for balloon angioplasty, but total reocclusion occurred within 24 hours of the procedure and a 2nd attempt did not restore patency. Surgical revascularization was performed a week later. A year after his injury, the patient remains asymptomatic and is back at work. Despite the failure of percutaneous transluminal coronary angioplasty in its 1st application to coronary artery repair after blunt chest trauma, we believe it to be the treatment of choice in young patients and in single-vessel disease.     

Onco-suppressor genes in human cancer

The analysis of the molecular mechanisms governing multistep carcinogenesis became experimentally approachable since the identification and characterization in tumor cells of altered or activated versions of cellular genes (oncogenes) that normally control cell growth and differentiation. The activating mutations confer new properties to the oncogene products and should therefore be considered as gain of function mutations. In addition, the oncogenes appear to act as dominant genetic traits since they act also in the presence of the homologous wild-type allele. However, the concept of a dominance of the transformed phenotype has been challenged by early experiments with somatic cell hybrids which showed that the fusion of normal and malignant cells may suppress the tumorigenic phenotype. The suppression or reversion of the malignant phenotype by the introduction of a normal chromosome into a tumor cell line has lent support to the idea that a family of cellular genes are coding for factors capable to interact with the cell-growth control machinery. These genes seem to reconstitute the normal control of cell growth even in the presence of an activated oncogene. In addition, a two-mutation model has been proposed to explain the epidemiological and clinical features of childhood cancers. According to the model, the development of these malignancies can be caused by the loss or inactivation of both alleles of cellular genes, as suggested by the somatic cell hybrid experiments where the function of the inactivated genes is restored by the contribution of those derived from the normal parental cells. This family of genes is designated as onco-suppressor genes since their product is necessary for the normal regulated cell growth and is lacking or inactivated in malignant cells. At gene level they should be considered as recessive genetic traits, since the tumor phenotype appears when both alleles of an onco-suppressor gene are inactivated. The mutations affecting their normal functions belong to the type "loss of function". The molecular analysis of retinoblastoma has led to the cloning and sequencing of the related onco-suppressor gene (RB gene) whose product displays the features of a gene-regulatory protein. In addition, a binding between the RB product and various viral onco-proteins (E1A, large T, E7) has been demonstrated, thus suggesting a mechanism of RB inactivation by which some DNA viruses can transform the host cell.(ABSTRACT TRUNCATED AT 400 WORDS)