Quality of life after total laryngectomy: impact of different vocal rehabilitation methods in a middle income country.

INTRODUCTION: The impact of advanced laryngeal cancer and its extensive surgical treatments cause significant morbidity for these patients. Total laryngectomy impacts essential functions such as breathing, communication and swallowing, and may influence the quality of life as well as affecting the social life of laryngeal cancer patients. OBJECTIVE: Describe the quality of life and analyze the factors associated with the reduced quality of life in patients who have undergone total laryngectomy. METHOD: Observational cross-sectional study was carried out to evaluate the quality of life of patients who had undergone total laryngectomy due to laryngeal cancer. The fourth version of the UW-QOL Quality of Life Assessment Questionnaire from Washington University, validated for Portuguese, was used. RESULTS: The study population was 95 patients, and the mean composite score of the QOL was 80.4. In the subjective domains the majority of the patients (38.9%) reported they felt much better at present compared to the month before being diagnosed with cancer. When questioned about how they evaluated their health-related quality of life, there was a predominance of those who considered it good (43.2%), and most considered they had a good quality of life (46.3%) considering personal well-being. The overall quality of life was considered good to excellent by 83.2% of the patients. Patients with tracheoesophageal prosthesis reported a better quality of life, compared to patients using an electrolarynx or esophageal voice. CONCLUSION: The high mean value of the composite score for quality of life revealed that the patients assessed their quality of life positively. The absence of vocal emission was the only variable associated with a lower quality of life within the composite score according to the UW-QOL questionnaire.

Existence of a tricritical point in the antiferromagnet KFe3(OH)6(SO4)2 on a kagome lattice.

We study the phase diagram in the H-T plane of the potassium jarosite compound KFe(3)(OH)(6)(SO(4))(2) for the antiferromagnetic XY model with Dzyaloshinskii-Moriya (DM) interaction using the mean-field theory for different value of DM. In our approach, we obtain the tricritical point in the H-T plane and the adjustment has a strong correlation with experimental data.

Distribution pattern of histone H3 phosphorylation at serine 10 during mitosis and meiosis in Brachiaria species.

Histones are the major eukaryotic DNA-binding proteins. Posttranslational modifications on N-terminal tails of histones that form nucleosomes are often associated with distinct biological functions. Some theories suggest that one of these modifications, the phosphorylation of histone H3 at serine 10 (H3S10ph) plays a role in both chromosome condensation and sister chromatid cohesion. Although histones and some of their modifications are highly conserved, studies have shown that role and distribution of H3S10ph may differ between species. We evaluated the pattern of H3 phosphorylation using immunodetection during mitosis and meiosis in both diploid and tetraploid genotypes of Brachiaria species. Results revealed differences in chromosome distribution of H3S10ph when mitosis and meiosis were compared. Whole chromosomes were phosphorylated during meiosis I, whereas phosphorylation was restricted to the pericentromeric region in both meiosis II and mitosis. There was no variation in phosphorylation patterns between Brachiaria species and diploid and tetraploid genotypes. Regarding spatiotemporal coordination in the Brachiaria species evaluated, H3S10ph is related to maintenance of sister chromatid cohesion during cell divisions.

Urinary transforming growth factor-beta (TGF-beta) excretion and renal production of TGF-beta in rats with subtotal renal ablation: effect of enalapril and nifedipine.

The aim of the present study was to investigate the effect of enalapril and nifedipine on renal transforming growth factor-beta (TGF-beta) production and on the rate of urinary TGF-beta excretion in rats with subtotal renal ablation. After subtotal nephrectomy some animals were treated with enalapril or nifedipine. Renal cortical TGF-beta mRNA levels were 68% higher in untreated nephrectomized rats (p < 0.05) and 39% higher in rats treated with nifedipine (p < 0.05) compared with controls. There was no difference in renal cortical TGF-beta mRNA content between the nephrectomized rats treated with enalapril and sham animals, showing that enalapril treatment prevented the increase of TGF-beta mRNA in nephrectomized rats. The rate of urinary TGF-beta excretion was 2.2 +/- 0.8 pg/min in sham animals, 61.5 +/- 40.1 pg/min in untreated nephrectomized rats, 9.6 +/- 4.2 pg/min in nephrectomized rats treated with enalapril, and 55.2 +/- 24.46 pg/min in rats treated with nifedipine. The immunohistochemical reaction for TGF-beta in the renal cortex was less intense in the nephrectomized rats treated with enalapril than in the other groups of rats with subtotal renal ablation. These data show that enalapril induces a decrease in renal TGF-beta production and in urinary TGF-beta excretion in rats with subtotal renal ablation, an effect associated with the protective action of this treatment on renal structure and function and suggest that the determination of the rate of urinary TGF-beta could be a useful procedure for the evaluation of disease progression and therapeutic efficacy in the remnant kidney model.

Controlled production of cirrhosis in the rat liver.

In the present study we propose a standardization of the method for the induction of fibrosis of the liver in rats by weekly administration of CCl4 by the intragastric route. The present method is a variation of that described by Proctor and Chatamra. The initial CCl4 dose is 0.04 ml (X dose) but the subsequent doses are calibrated using a 5% variation in animal weight as a reference point. For a weight gain of 5% or more, the successive doses are progressively increased by 50 to 150% (1.5X, 2X, 2.5X). When there is no variation in weight or loss in less than 5%, the previous dose is maintained. For a weight loss of more than 5%, the CCl4 dose is decreased by 50%. Consistent fibrosis if obtained as early as during the 8th week. Collagen content increases progressively from the 8th to the 12th week, reaching on average a level eight-fold higher than that observed in the control.

Chemistry, biology, and toxicology of domoic acid and its isomers.

The causative agent of toxicity in cultured mussels from a localized area of eastern Prince Edward Island has been identified as domoic acid, a neuroexcitatory amino acid. The toxin was isolated by a number of different bioassay-directed separation techniques including high-performance liquid chromatography (HPLC), high-voltage paper electrophoresis (HVPE), and ion-exchange chromatography, and characterized by a number of spectroscopic techniques including ultraviolet, infrared, mass spectrometry, and nuclear magnetic resonance. The isolation and purification methods are described in detail and some new analytical data for domoic acid are reported. A plankton bloom at the time of the outbreak gave positive mouse bioassays and consisted almost entirely of the pennate diatom, Nitzschia pungens f. multiseries. A positive correlation was found between the number of N. pungens cells and the concentration of domoic acid in the plankton. N. pungens f. multiseries isolated from Cardigan Bay produced domoic acid de novo during stationary phase culture at levels (1 to 10 pg/cell) comparable to values estimated for N. pungens in the plankton samples. We conclude that N. pungens was the major source of the domoic acid in toxic mussels in eastern Prince Edward Island. The recurrence, in November 1988, of a monospecific bloom of N. pungens and the presence of domoic acid in plankton and mussels reinforces this conclusion.

Zinc from oyster tissue as causative factor in mouse deaths in official bioassay for paralytic shellfish poison.

Toxicity (extreme weakness, body temperature drop, cyanosis, some slow deaths) in test mice, upon intraperitoneal injection of standard-method paralytic shellfish poison (PSP) extracts of some PSP-free oysters, is consistent with the relatively high levels of zinc in these extracts. As a rough guideline, the threshold for a toxic response corresponds to a drained tissue zinc level of over 900 micrograms/g. The identification of zinc as the substance responsible has been supported by inducing toxicity in control extracts by spiking with nontoxic levels of zinc, and by eliminating toxicity from toxic extracts by chemical removal (precipitation, ion exchange) of metals.