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1.
J Endod ; 50(5): 619-626, 2024 May.
Article in English | MEDLINE | ID: mdl-38311114

ABSTRACT

INTRODUCTION: Determination of the glide path is recommended before using rotary instruments. This study aimed to evaluate the dynamic cyclic fatigue resistance of new and used glider rotary instruments in up to 6 root canals. METHODS: Seventy-two TruNatomy Glider files were used for the preparation of root canals of extracted lower molars, which were then submitted to the dynamic cyclic fatigue test carried out in a curved metallic artificial canal. The instruments were divided into 4 groups (n = 18): Control group, new instruments without any use in the root canal; Group 2U, instruments used in 2 mesial canals; Group 4U, instruments used in 4 mesial canals; Group 6U, instruments used in 6 mesial canals. The time to failure (TF) of the instrument was recorded, and the number of cycles to failure (NCF) was calculated. The data were submitted to 1-way analysis of variance and to the Games-Howell test for multiple comparisons, adopting a significance level of 5%. RESULTS: TF and NCF were significantly affected by the number of file uses. The Games-Howell test revealed that TF and NCF were significantly greater in the control group than in Group 4U. In Group 2U, TF and NCF were intermediate and not significantly different from the control group. Group 6U had significantly lower TF and NCF than all other groups. CONCLUSION: The TruNatomy Glider can be used as a glide path for up to 2 mesial canals of mandibular molars, whereas its use on 4 or 6 root canals is not suggested.


Subject(s)
Equipment Failure , Root Canal Preparation , Root Canal Preparation/instrumentation , Root Canal Preparation/methods , Humans , Dental Instruments , Equipment Design , In Vitro Techniques , Molar , Dental Stress Analysis , Dental Pulp Cavity , Materials Testing
2.
Infect Immun ; 72(5): 2628-34, 2004 May.
Article in English | MEDLINE | ID: mdl-15102771

ABSTRACT

Immune factors influencing progression to active tuberculosis (TB) remain poorly defined. In this study, we investigated the expression of immunoregulatory cytokines and receptors by using lung bronchoalveolar lavage cells obtained from patients with pulmonary TB, patients with other lung diseases (OLD patients), and healthy volunteers (VOL) by using reverse transcriptase PCR, a transforming growth factor beta (TGF-beta) bioactivity assay, and an enzyme immunoassay. TB patients were significantly more likely than OLD patients to coexpress TGF-beta receptor I (RI) and RII mRNA, as well as interleukin-10 (IL-10) mRNA (thereby indicating the state of active gene transcription in the alveolar cells at harvest). In contrast, gamma interferon (IFN-gamma) and IL-2 mRNA was seen in both TB and OLD patients. Likewise, significantly elevated pulmonary steady-state protein levels of IL-10, IFN-gamma, and bioactive TGF-beta were found in TB patients versus those in OLD patients and VOL. These data suggest that the combined production of the immunosuppressants IL-10 and TGF-beta, as well as coexpression of TGF-beta RI and RII (required for cellular response to TGF-beta), may act to down-modulate host anti-Mycobacterium tuberculosis immunity and thereby allow uncontrolled bacterial replication and overt disease. Delineating the underlying mechanisms of M. tuberculosis-triggered expression of these immune elements may provide a molecular-level understanding of TB immunopathogenesis.


Subject(s)
Activin Receptors, Type I/genetics , Interleukin-10/biosynthesis , Receptors, Transforming Growth Factor beta/genetics , Transforming Growth Factor beta/biosynthesis , Tuberculosis, Pulmonary/genetics , Tuberculosis, Pulmonary/immunology , Adult , Base Sequence , Bronchoalveolar Lavage Fluid/immunology , Case-Control Studies , DNA, Complementary/genetics , Female , Gene Expression , Humans , Immune Tolerance , Interleukin-10/genetics , Lung Diseases/genetics , Lung Diseases/immunology , Male , Middle Aged , Protein Serine-Threonine Kinases , RNA, Messenger/genetics , RNA, Messenger/metabolism , Receptor, Transforming Growth Factor-beta Type I , Receptor, Transforming Growth Factor-beta Type II , Transforming Growth Factor beta/genetics
3.
Mem. Inst. Oswaldo Cruz ; 91(3): 389-394, May-Jun. 1996.
Article in English | LILACS | ID: lil-319857

ABSTRACT

Mycobacterium tuberculosis preferentially resides in mononuclear phagocytes. The mechanisms by which mononuclear phagocytes keep M. tuberculosis in check or by which the microbe evades control to cause disease remain poorly understood. As an initial effort to delineate these mechanisms, we examined by immunostaining the phenotype of mononuclear phagocytes obtained from lungs of patients with active tuberculosis. From August 1994 to March 1995, consecutive patients who had an abnormal chest X-ray, no demonstrable acid-fast bacilli in sputum specimens and required a diagnostic bronchoalveolar lavage (BAL) were enrolled. Of the 39 patients enrolled, 21 had microbiologically diagnosed tuberculosis. Thirteen of the 21 tuberculosis patients were either HIV seronegative (n = 12) or had no risk factor for HIV and constituted the tuberculosis group. For comparison, M. tuberculosis negative patients who had BAL samples taken during this time (n = 9) or normal healthy volunteers (n = 3) served as control group. Compared to the control group, the tuberculosis group had significantly higher proportion of cells expressing markers of young monocytes (UCHM1) and RFD7, a marker for phagocytic cells, and increased expression of HLA-DR, a marker of cell activation. In addition, tuberculosis group had significantly higher proportion of cells expressing dendritic cell marker (RFD1) and epithelioid cell marker (RFD9). These data suggest that despite recruitment of monocytes probably from the peripheral blood and local cell activation, host defense of the resident lung cells is insufficient to control M. tuberculosis.


Subject(s)
Humans , Male , Female , Adult , HIV Seronegativity , Phagocytes , Lung/pathology , Tuberculosis, Pulmonary , Antibodies, Monoclonal , Bronchoalveolar Lavage , Cell Count , Macrophage Activation , Macrophages, Alveolar , Monocytes , Phagocytes , Phenotype , Tuberculosis, Pulmonary
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