Efficacy of red and infrared lasers in treatment of temporomandibular disorders — a double-blind,randomized, parallel clinical trial

Aim:

Low-level laser therapy has still not been well established, and it is important to define a standardized protocol for the treatment of temporomandibular disorders (TMDs) using low level laser. There is no consensus on controlled clinical trials concerning the best option for laser therapy with regard to wavelength. The aim of this study was to evaluate the efficacy of red and infrared laser therapy in patients with TMD, using a randomized parallel-group double-blind trial.

Methodology:

Each hemiface of 19 subjects was randomized to receive intervention, in a total of 116 sensitive points. Pain was measured at baseline and time intervals of 24 hours, 30 days, 90 days, and 180 days after treatment. Irradiation of 4 J/cm² in the temporomandibular joints and 8 J/cm² in the muscles was used in three sessions.

Results:

Both treatments had statistically significant results (P<0·001); there was statistical difference between them at 180 days in favor of the infrared laser (P?=?0·039). There was improvement in 24 hours, which extended up to 180 days in both groups.

Conclusion:

Both lasers are effective in the treatment and remission of TMD symptoms.     

A clonally distinct recurrence of Burkitt's lymphoma at 15 years

A human immunodeficiency virus-negative male was successfully treated for two occurrences of Burkitt's lymphoma, 15 years apart. As consolidation of his second remission, he underwent high-dose chemotherapy with peripheral blood stem cell transplantation. In an effort to prove whether the second lymphoma was a relapse of the first or a second primary lymphoma, we obtained paraffin-embedded material from both lymphomas. DNA was extracted from this material and amplified by polymerase chain reaction (PCR) using consensus JH and VH region primers. Analysis of the PCR products, which mostly reflects VDJ joints, showed two sharp bands of different molecular size, proving the monoclonal nature of the lymphomas and suggesting that each had different Ig gene rearrangements. Sequencing of both PCR products showed a marked dissimilarity in nucleotide sequence in the clonally unique VDJ joint region, providing strong evidence for the separate cellular genesis of each lymphoma. These results suggest that late relapses of Burkitt's lymphoma should be examined for clonal distinctiveness. If the second lymphoma is distinct from the primary one, it might be treated as a primary lymphoma rather than as recurrent disease.     

Differential effects of trabecular meshwork stiffness on outflow facility in normal human and porcine eyes

Purpose. The study was designed to determine trabecular meshwork (TM) stiffness and its relationship to outflow facility (C) in perfused normal human and porcine eyes. Methods. Human and porcine eyes were perfused at pressures of 10, 20, 30, and 40 mm Hg to determine C and how outflow resistance (R = 1/C) varied with the pressure. Following perfusions, TM tissue segments were dissected and stretched uniaxially to determine the circumferential bulk Young's modulus (E). The statistical significance of difference between different groups was evaluated using a two-tailed Student's t-test or Mann-Whitney U test. Results. A larger E correlated with a higher C measured at 10 and 20 mm Hg (P < 0.05), and a similar trend was observed at 30 and 40 mm Hg in human eyes (n = 7). Additionally, a higher C correlated to a lower variance of R, and a stiffer TM correlated to a lower variance of R in human eyes (P < 0.05). For porcine TM, E was inversely correlated to a cross-sectional area (P < 0.003, n = 11), and its value (24.9 and 1.5 kPa; geometric mean and geometric SE) was lower than E of human TM (515 ± 136 kPa; mean ± SE) (P < 0.01). C and variance of R were not significantly different between the species. Conclusions. A higher circumferential stiffness of the TM correlated with a higher outflow facility and less IOP elevation-induced variation in outflow resistance in normal human eyes, but not in porcine eyes. For future studies, these correlations need to be evaluated in glaucomatous eyes to better understand normal and abnormal TM functions.     

Identification and characterization of a low-affinity granulocyte- macrophage colony-stimulating factor receptor on primary and cultured human melanoma cells

Hematopoietic growth factor receptors are present on cells of normal nonhematopoietic tissues such as endothelium and placenta. We previously demonstrated functional human granulocyte-macrophage colony- stimulating factor (GM-CSF) receptors on small cell carcinoma of the lung cell lines, and others have reported that certain solid tumor cell lines respond to GM-CSF in clonogenic assays. In the current study, we examine human melanoma cell lines and fresh specimens of melanoma to determine whether they have functional GM-CSF receptors. Scatchard analyses of 125I-GM-CSF equilibrium binding to melanoma cell lines showed a mean of 542 +/- 67 sites per cell with a kd of 0.72 +/- 0.14 nmol/L. Cross-linking studies in the melanoma cell line, M14, showed a major GM-CSF receptor species of 84,000 daltons. Under the conditions tested, the M14 cells did not have a proliferative response to GM-CSF in vitro, nor was any induction of primary response genes detected by Northern analysis in response to GM-CSF. Studies to determine internal translocation of the receptor-ligand complex indicated less than 10% of the 125I-GM-CSF internalized was specifically bound to receptors. Primary melanoma cells from five surgical specimens had GM-CSF receptors; Scatchard analysis was performed on one sample, showing 555 sites/cell with a kd of 0.23 nmol/L. These results indicate that human tumor cells may express a low-affinity GM-CSF receptor protein that localizes to the cell surface and binds ligand, but lacks functional components or accessory factors needed to transduce a signal.     

Hormonal effects on cell proliferation in a human erythroleukemia cell line (K562)

We have investigated the hormonal responsiveness of K562 cells using a serum-substituted in vitro clonogenic assay. Dexamethasone inhibited colony formation by the K562 cells, and the inhibitory effect could be reversed by progesterone (10(-6) M). Fluoxymesterone caused a prominent enhancement of K562 colony growth, whereas estriol had no effect. Stimulation by triiodothyronine was maximal at 10(-7) M, and the thyroid effect could be abrogated by the beta 2-adrenergic antagonist butoxamine in equimolar concentrations. Using standard tissue culture conditions, the beta-adrenergic agent isoproterenol, but not the alpha catecholamine phenylephrine, enhanced the proliferation of K562 cells. When K562 cells were grown under hormone-depleted conditions, they developed responsiveness to phenylephrine and were no longer stimulated by isoproterenol. DbcAMP and prostaglandins of the E series also caused K562 colony enhancement. Prostaglandin F2 alpha had no effect on cell proliferation. Insulin was an effective stimulant of colony formation of K562 cells, as were human growth hormone and ovine prolacin. Bovine growth hormone had no effect. Our results are consistent with the identificaiton of K562 as an erythroid line, and they indicate that K562 cells respond to endocrine hormones in a manner analogous to normal erythroid progenitors.     

Activation of the CPP32 protease in apoptosis induced by 1-beta-D- arabinofuranosylcytosine and other DNA-damaging agents

The response of human myeloid leukemia cells to treatment with 1-beta- arabinofuranosylcytosine (ara-C) includes the induction of apoptosis. Ara-C induced apoptosis is associated with proteolytic cleavage of poly(ADP-ribose) polymerase (PARP) and protein kinase C (PKC) delta. However, the signals involved in this response are unknown. The present studies show that ara-C treatment of U-937 cells is associated with induction of a protease activity that cleaves the tetrapeptides Ac-DEVD- pNA and Ac-DMOD-pNA found at the cleavage sites of PARP and PKC delta, respectively. The ara-C-induced protease activity was sensitive to overexpression of the anti-apoptotic protein Bcl-xL and the baculovirus protein p35. By contrast, overexpression of the cowpox virus protein CrmA blocked apoptosis induced by engagement of the Fas receptor but not that induced by ara-C. CrmA overexpression also had no detectable effect on ara-C-induced cleavage of PKC delta. The results further show that ara-C induces activation of the CPP32 protease by a CrmA- insensitive and p35-sensitive mechanism. Similar results were obtained with cisplatinum, etoposide, and camptothecin. These findings indicate that ara-C and other DNA-damaging agents activate a CrmA-insensitive apoptotic pathway involving CPP32 and that these signals differ from those associated with apoptosis induced by the Fas receptor.