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Introduction Dysphonia and lower pitch after surgery of Reinke edema are common. They are caused especially due to chronic smoking but, probably, other factors should be associated. Objectives To evaluate the results of laryngeal microsurgery in patients with Reinke edema, following a standardized postoperative guidance protocol in our service. Methods Retrospective study. Thirty patients (3 males; 27 females) were included, 70% between 41 and 60 years old. The parameters analyzed in the pre- and postoperative (between 4 and 6 months) of patients undergoing laryngeal microsurgery for Reinke edema were: smoking, vocal symptoms, videolaryngostroboscopy, voice therapy, perceptual and acoustic vocal evaluation, histopathological report. Results Smoking was reported by 100% of the patients and maintained in the postoperative period by 80%. Complete improvement of symptoms in the postoperative period was reported by 43% of them, partial improvement by 40%, and maintenance by 17%.There was low adherence to voice therapy in the pre- and postsurgery.Postoperative videolaryngoscopy indicated congestion (19), atrophy and bowed vocal fold (1), subepithelial edema (2), and normal findings (8). The histological findings were subepithelial edema, enlargement of vessels, inflammation, epithelial hyperplasia, and thickening of the basement membrane. The perceptual and acoustic vocal analyzes indicated improvement of the analyzed parameters. Conclusions The maintenance of some vocal symptoms and laryngeal alterations in videolaryngoscopy after microsurgery of Reinke edema is frequent, even in patients who follow the recommendations of vocal rest and control of gastroesophageal reflux. Vocal symptoms are attributed to changes in the laryngeal mucosa caused by chronic smoking, aggravated by the maintenance of addiction in the postoperative period.
OBJECTIVES: To investigate the effect of frailty on 1-year mortality in long term-care facility (LTCF) residents. METHODS: This was a prospective cohort study with survival analysis of 209 participants living in 15 Brazilian LTCFs. Data on chronic diseases, age, sex, medication use, dependence in activities of daily living (ADLs; Katz index), and frailty (FRAIL scale) were collected at baseline, and death after 1 year was the outcome measure. Kaplan-Meier estimate and log-rank test were used to analyze the survival of residents. RESULTS: In the initial assessment, 65.07 of the residents were women, and the median age was 82 (interquartile range, 71–88) years, with 55% being over 80 years old. Overall, 88% had 2 or more diseases, 59.81% were using 5 or more medications, 42.11% were considered frail, 34.92% pre-frail, and 22.97% robust, and 69.94% were dependent in 3 or more ADLs. During the 12-month follow-up, 19.61% of the residents (n=41) died. In the survival analysis for death, there was a statistically significant association with frailty (p=0.03) and dependence in ADLs (p=0.04). CONCLUSIONS: In this population of LTCF residents, frailty and functional dependence were associated with death.
Studies have shown that maternal malnutrition, especially a low-protein diet (LPD), plays a key role in the developmental mechanisms underlying mammary cancer programming in female offspring. However, the molecular pathways associated with this higher susceptibility are still poorly understood. Thus, this study investigated the adverse effects of gestational and lactational low protein intake on gene expression of key pathways involved in mammary tumor initiation after a single dose of N-methyl-N-nitrosourea (MNU) in female offspring rats. Pregnant Sprague–Dawley rats were fed a normal-protein diet (NPD) (17% protein) or LPD (6% protein) from gestational day 1 to postnatal day (PND) 21. After weaning (PND 21), female offspring (n = 5, each diet) were euthanized for histological analysis or received NPD (n = 56 each diet). At PND 28 or 35, female offspring received a single dose of MNU (25 mg/kg body weight) (n = 28 each diet/timepoint). After 24 h, some females (n = 10 each diet/timepoint) were euthanized for histological, immunohistochemical, and molecular analyses at PDN 29 or 36. The remaining animals (n = 18 each diet/timepoint) were euthanized when tumors reached ≥2 cm or at PND 250. Besides the mammary gland development delay observed in LPD 21 and 28 groups, the gene expression profile demonstrated that maternal LPD deregulated 21 genes related to DNA repair and DNA replication pathways in the mammary gland of LPD 35 group after MNU. We further confirmed an increased γ-H2AX (DNA damage biomarker) and in ER-α immunoreactivity in mammary epithelial cells in the LPD group at PND 36. Furthermore, these early postnatal events were followed by significantly higher mammary carcinogenesis susceptibility in offspring at adulthood. Thus, the results indicate that maternal LPD influenced the programming of chemically induced mammary carcinogenesis in female offspring through increase in DNA damage and deregulation of DNA repair and DNA replication pathways. Also, Cidea upregulation gene in the LPD 35 group may suggest that maternal LPD could deregulate genes possibly leading to increased risk of mammary cancer development and/or poor prognosis. These findings increase the body of evidence of early-transcriptional mammary gland changes influenced by maternal LPD, resulting in differential response to breast tumor initiation and susceptibility and may raise discussions about lifelong prevention of breast cancer risk.
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