Photic evoked responses during induced epileptic seizures.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to S Gonzalez.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In this randomized, open-label, 8-week comparative study, the efficacy and safety of venlafaxine and fluoxetine were assessed in outpatients with major depression. One hundred forty-five patients were assigned to receive venlafaxine 37.5 mg twice daily or fluoxetine 20 mg once daily. On day 15, if clinically indicated to improve patient response, the dosage could be increased at the investigator's discretion to venlafaxine 75 mg twice daily or fluoxetine 40 mg once daily. One hundred forty-five patients were evaluated for safety and 110, for efficacy. The mean age was 37 years, and 70% of the patients were female. In both treatment groups, mean scores on the Hamilton Depression Rating Scale decreased significantly between baseline (27.8, venlafaxine; 29.2, fluoxetine) and the end of the study (8.7, venlafaxine; 8.2, fluoxetine). Similarly, mean scores on the Montgomery-Asberg Depression Rating Scale decreased significantly between baseline (31.4, venlafaxine; 31.6, fluoxetine) and the end of the study (8.3, venlafaxine; 7.6, fluoxetine). In venlafaxine patients, the most common adverse events were nausea (44.3%), headache (40.0%), insomnia (31.4%), dizziness (30.0%), and dry mouth (22.9%); in fluoxetine patients, they were headache (32.0%), nausea (28.0%), insomnia (24.0%), anxiety (21.3%), sleepiness (20.0%), and generalized tremor (20.0%). The results of this study indicate that venlafaxine is effective and well tolerated for the treatment of major depression at doses of 37.5 or 75 mg twice daily and not significantly different from fluoxetine 20 or 40 mg once daily.
Rats genetically selected for their different ethanol voluntary consumption, UChA (low consumer) and UChB (high consumer) were used. Naive UChA and UChB rats or submitted to ethanol chronic exposure, received an i.p. dose of ethanol (2.76 g/kg) alone or 30 min after an oral dose of diltiazem (10 mg/kg), a calcium channel blocker. A significant potentiation of the narcosis and hypothermia induced by the dose of ethanol was observed in UChA diltiazem-pretreated rats not previously exposed to ethanol, while no potentiation in narcosis time appears in UChA rats chronically exposed to ethanol that acquire tolerance. In the UChB line of rats, diltiazem did not potentiate ethanol depressant actions in naive or chronic ethanol-exposed rats. Diltiazem did not modify ethanol blood levels. These results indicate that the inhibition of voltage-dependent calcium channels can exaggerate ethanol-induced effects in naive rats but not when tolerance was developed. Results suggest that UChB rats may have some innate tolerance that may be due to genetic difference in calcium channel function.
The skin is exposed to benzene and its derivatives, prevalent environmental chemicals. They may impair the structural integrity of the skin by increased expression of matrix metalloproteinase 1 (MMP-1; degrades structural collagen) and elastin, synthesized primarily by the dermal fibroblasts. We examined the metabolism of benzene in dermal fibroblasts and identified the benzene metabolites as toluene, benzaldehyde, aniline and benzoic acid. These metabolites were not toxic to the cells with regard to cell viability, apoptosis and lipid peroxidation, unlike the phenolic benzene metabolites (hydroquinone, t-butyl hydroquinone and phenol) or hydrogen peroxide. Toluene and phenol, which compose cigarette smoke, and benzaldehyde stimulated MMP-1 and/or elastin expression. In summary, the dermal fibroblasts metabolize benzene to nonphenolic metabolites that are less toxic to the cellular components than the phenolic benzene derivatives. Toluene, benzaldehyde and phenol can directly cause facial wrinkling and impaired structural integrity by upregulating MMP-1 and/or elastin.
Substance P (SP) is one of several neuropeptides found in nasal mucosa. It exists primarily in sensory afferent neurons, which are best demonstrated by immunohistochemical staining. These substance P-like immunoreactive (SPLI) nerve fibers are unmyelinated C fibers, which connect to the trigeminal ganglion and the spinal trigeminal nucleus. They are found around vessels and seromucinous glands in the submucosa. When the nasal mucosa receives a noxious stimulus, SP is released and acts orthodromically as a comediator of nasal pain, while antidromically it induces vasodilatation, plasma extravasation, mucosal edema, and rhinorrhea. Its antidromic effects have been implicated in vasomotor rhinitis and can be blocked by topical intranasal capsaicin application. Wolf and others have demonstrated in human subjects that vasomotor rhinitis can be blocked up to 1 year by a series of intranasal capsaicin applications. It has not yet been demonstrated that nasal mucous SP levels following noxious nasal stimulus change after intranasal capsaicin pretreatment. Consequently a project was designed to determine whether intranasal capsaicin pretreatment would affect nasal substance P release measured in nasal secretion. Nasal secretion SP levels were measured before and after noxious nasal stimulus in controls and in capsaicin pretreated rats. The difference in measured nasal secretion SP levels were significant (p < 0.05).
In the present study we show the capacity of an extract of the fern Polypodium leucotomos (PLE) to partially inhibit the production of cytokines showing a Th1 pattern (IL-2, IFN-gamma and TNF-alpha) in human PHA-stimulated peripheral blood mononuclear cells. The percentage of inhibition was 24% for IL-2, 72% for INF-gamma and 53% for TNF-alpha. With regard to Th2 cytokines, the addition of PLE resulted in a significant increase (33%) in IL-10 production. Surprisingly, the production of the inflammatory cytokine IL-6 was completely abolished (100% inhibition) by PLE at all doses tested. In a second experiment in vivo we show that, the topical application of PLE to the skin of hairless albino mice (Skh-1) significantly diminished the mast cell infiltrate as well as the number of blood vessels triggered by chronic ultraviolet B (UVB) irradiation. These data show that PLE moderately inhibits the immunological Th1 responses, thus explaining the immunosuppressive as well as the anti-inflammatory and antioxidant activities reported in other studies carried out with PLE. The clear inhibitory effect on TFN-alpha and IL-6 production strongly suggest that this may be the mechanism by which PLE: (a) inhibits angiogenesis in vivo in the mouse model described here, and (b) prevents Langerhans' cells depletion caused by solar irradiation in humans. Taken together, these data suggest that PLE works through the induction of suppressive/anti-inflammatory cytokines such as IL-10 and/or TGF-beta which in turn appear to allow the partial deactivation of macrophages or other accessory cells. These features suggest that PLE could be useful in the treatment of autoaggressive/inflammatory conditions due to an exacerbation of Th1 responses.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Although a high percentage of smokers attempt to quit each year, success rates are low. Thus, public health strategies must not only convince some smokers to attempt cessation, but also improve the success rate among other smokers already motivated to quit. Specific cessation strategies may be required for smokers in these two groups. This study compares sociodemographic and health behavior characteristics of smokers who have and have not attempted to quit and of those who recently succeeded. To determine whether these characteristics vary for men and women, we stratified analyses on gender. Data were obtained from random sample health surveys conducted 1981-1982 and 1983-1984 in two New England communities. Analyses include data on 2,086 respondents who reported smoking cigarettes in the previous year. Men and women were equally likely both to attempt cessation and to quit. Except for an inverse association with age, attempting to quit was not associated with sociodemographic variables. In men and women, attempts were associated with encouraging others to quit and attempting to increase exercise. Successful cessation attempts were associated with not living with a smoker in women; marital status, attempted weight loss, and increased age in men; and with efforts to increase exercise in both men and women. These characteristics could be useful in targeting smokers who attempt to quit, but fail. Improving the success rate in this group could greatly reduce smoking prevalence in the community.
Some individuals remain uninfected by human immunodeficiency virus type 1 (HIV-1), despite multiple sexual contacts with subjects with confirmed HIV-1 infection. Several studies have confirmed that individuals who are homozygous for a 32 base pair (bp) deletion mutation in the chemokine receptor gene CCR5, designated as delta 32/ delta 32, are protected against HIV-1 infection. Heterozygotes of the same chemokine receptor deletion mutation are, however, not protected from acquiring HIV-1 infection but seemingly have slower progression to acquired immunodeficiency syndromes (AIDS). Genotype frequencies of the delta 32 CCR5 mutation vary markedly among different ethnic groups; heterozygosity is found in approximately 15% of Caucasians, about 5-7% of Hispanics and African Americans and 1% or less of Asians. The ethnic background of Puerto Ricans is highly complex and usually includes admixture of Caucasian, Caribbean Indian and African traits to a varying extent. This study was conducted to examine the frequencies of the delta 32 CCR5 mutation among Puerto Ricans who are infected with HIV-1. Samples were received from different geographical regions of the island. Of 377 samples tested, 94.2% were wild type (non-deletion mutant) homozygotes, 5.8% were delta 32 CCR5 heterozygotes, and none were delta 32 CCR5 homozygotes. The incidence of CCR5 delta 32/w heterozygous mutation among Puerto Ricans seems to be somewhat lower than what was reported with US Hispanics. Some age and gender associated bias of the mutation frequency were observed with the study population, the reason for which is unclear at present.