MASSETERIC ELECTROMYOGRAPHIC SILENT PERIOD DURATION IN PATIENTS WITH TEMPOROMANDIBULAR-JOINT DYSFUNCTION

1. The present study compared the duration of the electromyographic silent period (SP) of the masseter muscles elicited by chin-tapping in normal asymptomatic adults (N = 39) and in a group with symptoms of temporomandibular joint dysfunction (TMJD) (N = 31).2. EMG activity was recorded from right (RM) and left (LM) masseter muscles using bipolar surface electrodes coupled to a DISA 1500 EMG-System. During maximal clenching, ten taps were applied downwards to the chin with a reflex hammer.3. The mean SP durations obtained for the normal group were 25.45 +/- 4.20 ms (RM) and 25.33 +/- 4.18 ms (LM), whereas the TMJD group presented significantly greater values (P < 0.01, Student t-test) of 41.89 +/- 12.94 ms (RM) and 42.40 +/- 12.99 ms (LM). The upper limits of normality calculated for RM and LM were 32.36 ms and 31.21 ms, respectively. Eighty-four percent of patients with TMJD showed SP durations above these limits.4. The results indicate that the measurement of masseteric SP duration may be used as an objective diagnostic method of TMJ disorders, provided that borderline values are interpreted with caution along with clinical impressions.

Multidisciplinary approach to chronic pain from myofascial pain dysfunction syndrome: A four-year experience at a Brazilian center

Chronic pain is the major complaint of myofascial pain dysfunction syndrome (MPDS) and is a complex problem which involves physical, psychological and social aspects, the etiology of MPDS is multifactorial and the multidisciplinary approach is essential for differential diagnosis and for comprehensive treatment planning, In 1993, the Dental School of Piracicaba-UNICAMP, Brazil, opened a Center for Pain Studies (CPS), staffed by health care providers including, dentists, psychologists, physicians, physiotherapists and phonoaudiologists. The major aims of the CPS are to provide clinical care and to develop basic and applied research, Sixty-two MPDS patients had been admitted to the CPS by 1997, There were 60 females and 2 males, mean age -32.5 years, the mean duration of chronic pain was 48 months. Pain intensity and unpleasantness were measured employing the Visual Analogue Scale, the tendency to develop stress-related diseases was assessed by the Social Readjustment de Scale, There was a mean reduction of chronic pain of 69.89% and 71.78% relative to intensity and unpleasantness, respectively, the experience of clinical attendance at a multidisciplinary center showed the relevance of a team consisting of health care providers from different specialties with well-established aims, completely integrated and sensitive enough to understand the painful complaints of MPDS patients.

Endothelial dysfunction in DOCA-salt hypertension - Possible involvement of prostaglandin endoperoxides

The effects of the arachidonic acid metabolism inhibitors on the acetylcholine responses of aortae from control (CR) and deoxycorticosterone acetate (DOCA)-salt hypertensive (HR) rats were investigated. The acetylcholine decreased response observed in HR [relaxation (%): CR 95.5 +/- 2.7, n = 4; HR 52.0 +/- 6.3, n = 5, p < 0.05] was restored by the cyclooxygenase inhibitor piroxicam [relaxation (%): CR 99.8 +/- 0.2, n = 4; HR 86.0 +/- 4.0, n = 5] and by the thromboxane synthetase inhibitor and the thrombox ane A(2)/prostaglandin H-2 receptor antagonist ridogrel [relaxation (%): CR 92.1 +/- 4.4, n = 7; HR 93.1 +/- 2.0, n = 7] but not by the inhibitors of thromboxane synthetase, prostacyclin synthetase, cytochrome P-450 monooxygenase, and lipoxygenase. So, endoperoxide intermediates seem to be involved in the decreased endothelium-dependent relaxation to acetylcholine in DOCA-salt hypertension. (C) 1999 Elsevier B.V. All rights reserved.

Effects of cardiomyopathic mutations on the biochemical and biophysical properties of the human alpha-tropomyosin

Mutations in the protein alpha-tropomyosin (Tm) can cause a disease known as familial hypertrophic cardiomyopathy. In order to understand how such mutations lead to protein dysfunction, three point mutations were introduced into cDNA encoding the human skeletal tropomyosin, and the recombinant Tms were produced at high levels in the yeast Pichia pastoris. Two mutations (A63V and K70T) were located in the N-terminal region of Tm and one (E180G) was located close to the calcium-dependent troponin T binding domain. The functional and structural properties of the mutant Tms were compared to those of the wild type protein. None of the mutations altered the head-to-tail polymerization, although slightly higher actin binding was observed in the mutant Tm K70T, as demonstrated in a cosedimentation assay. The mutations also did not change the cooperativity of the thin filament activation by increasing the concentrations of Ca2+. However, in the absence of troponin, all mutant Tms were less effective than the wild type in regulating the actomyosin subfragment 1 Mg2+ ATPase activity. Circular dichroism spectroscopy revealed no differences in the secondary structure of the Tms. However, the thermally induced unfolding, as monitored by circular dichroism or differential scanning calorimetry, demonstrated that the mutants were less stable than the wild type. These results indicate that the main effect of the mutations is related to the overall stability of Tm as a whole, and that the mutations have only minor effects on the cooperative interactions among proteins that constitute the thin filament.

Detection of immunoglobulin G antibodies to Neospora caninum in humans: High seropositivity rates in patients who are infected by human immunodeficiency virus or have neurological disorders

Considering that little is known about the epidemiology of Neospora caninum infection in humans, particularly in populations with high Toxoplasma gondii infection rates, the present study aimed to investigate the presence of antibodies to N. caninum in T. gondii-seropositive and -seronegative individuals. A total of 256 serum samples divided into four groups (61 samples from human immunodeficiency virus [HIV]-positive patients, 50 samples from patients with neurological disorders, 91 samples from newborns, and 54 samples from healthy subjects) were assessed for N. caninum and T. gondii serologies by indirect fluorescent-antibody test, enzyme-linked immunosorbent assay, and immunoblotting (IB). Immunoglobulin G antibodies to N. caninum were predominantly detected in HIV-infected patients (38%) and patients with neurological disorders (18%), while newborns and healthy subjects showed lower seropositivity rates (5% and 6%, respectively). Seropositivity to N. caninum was significantly associated with seropositivity to T. gondii in both HIV-infected patients and patients with neurological disorders. Seroreactivity to N. caninum was confirmed by IB, with positive sera predominantly recognizing the 29-kDa antigen of N. caninum. The results of this study indicate the presence of N. caninum infection or exposure in humans, particularly in HIV-infected patients or patients with neurological disorders, who could have opportunistic and concurrent infections with T. gondii. These findings may bring a new concern for the unstable clinical health of HIV-infected patients and the actual role of N. caninum infection in immunocompromised patients.

Canine cerebral leishmaniasis: Potential role of matrix metalloproteinase-2 in the development of neurological disease

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Vitamin E responsive neurological signs in ostriches (Struthio camelus).

Encephalomalacia in birds is commonly related to vitamin E deficiency. To the best of our knowledge, in ostriches there are no reports of neurological signs associated to nutritional deficiencies. Fourteen ostriches aged from 1 day to 3 weeks old were sent to necropsy and showed apathy, progressive weight loss, twisting or S-shaped flexure of the neck and mortality. Gross changes were mild and consisted of congested blood vessels besides edematous aspect of the cerebrum and cerebellum. Microscopic examination revealed congested meningeal vessels. Capillaries were evident in cortex and white matter of the encephalon. Focal spongy vacuolation and reactive gliosis were observed within the white matter of cerebellum. Four birds that presented neurological signs were inoculated by the subcutaneous route in the neck with 50 mg of vitamin E (alfatocoferol acetate), followed by clinical evaluation. These birds were fully recovered in a period of 24 h. Macroscopic and microscopic lesions associated to the clinical signs and to the therapeutic improvement provided by vitamin E administration are strong evidences of nutritional encephalomalacia (vitamin E deficiency).

Upregulation of gp91(phox) Subunit of NAD(P)H Oxidase Contributes to Erectile Dysfunction Caused by Long-term Nitric Oxide Inhibition in Rats: Reversion by Regular Physical Training

OBJECTIVES To test the hypothesis that glyco protein 91phox (gp91(phox)) subunit of nicotinamide adenine dinucleotide phosphate [NAD(P) H] oxidase is a fundamental target for physical activity to ameliorate erectile dysfunction (ED). Vascular risk factors are reported to contribute to ED. Regular physical exercise prevents cardiovascular diseases by increasing nitric oxide (NO) production and/or decreasing NO inactivation.METHODS Male Wistar rats received the NO synthesis inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) for 4 weeks, after which animals were submitted to a run training program for another 4 weeks. Erectile functions were evaluated by in vitro cavernosal relaxations and intracavernous pressure measurements. Expressions of gp91(phox) subunit and neuronal nitric oxidase synthase in erectile tissue, as well as superoxide dismutase activity and nitrite/nitrate (NO(x)) levels were determined.RESULTS The in vitro acetylcholine-and electrical field stimulation-induced cavernosal relaxations, as well as the increases in intracavernous pressure were markedly reduced in sedentary rats treated with L-NAME. Run training significantly restored the impaired cavernosal relaxations. No alterations in the neuronal nitric oxidase synthase protein expression (and its variant penile neuronal nitric oxidase synthase) were detected. A reduction of NO(x) levels and superoxide dismutase activity was observed in L-NAME-treated animals, which was significantly reversed by physical training. Gene expression of subunit gp91(phox) was enhanced by approximately 2-fold in erectile tissue of L-NAME-treated rats, and that was restored to basal levels by run training.CONCLUSIONS Our study shows that ED seen after long-term L-NAME treatment is associated with gp91(phox) subunit upregulation and decreased NO bioavailability. Exercise training reverses the increased oxidative stress in NO-deficient rats, ameliorating the ED. UROLOGY 75: 961-967, 2010. (C) 2009 Elsevier B.V.

Effects of olive oil and its minor phenolic constituents on obesity-induced cardiac metabolic changes

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Food restriction-induced myocardial dysfunction demonstrated by the combination of in vivo and in vitro studies

The aim of this study was to test the hypothesis that protein-calorie undernutrition decreases myocardial contractility jeopardizing ventricular function, and that ventricular dysfunction can be detected noninvasively. Five-month-old male Wistar-Kyoto rats were fed with regular rat chow ad libitum for 90 days (Control group, n = 14). A second group of rats received 50% of the amount of diet consumed by de control group (Food restricted group, n = 14). Global LV systolic function was evaluated in vivo, noninvasively, by transthoracic echocardiogram. After echocardiographic study, myocardial contractility was assessed in vitro in the isovolumetrically beating isolated heart in eight animals from each group (Langendorff preparation). The in vivo LV fractional shortening showed that food restriction depressed LV systolic function (p < 0.05). Myocardial contractility was impaired as assessed by the maximal rate of rise of LV pressure (+dP/dt), and developed pressure at diastolic pressure of 25 mmHg (p < 0.05). Furthermore, food restriction induced eccentric ventricular remodeling, and reduced myocardial elasticity and LV compliance (p < 0.05). In conclusion, food restriction causes systolic dysfunction probably due to myocardial contractility impairment and reduction of myocardial elasticity. © 2002 Elsevier B.V. All rights reserved.