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1.
J Consult Clin Psychol ; 89(6): 537-550, 2021 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-34264701

RESUMO

OBJECTIVE: To determine if the Transdiagnostic Intervention for Sleep and Circadian Dysfunction (TranS-C) improves functional impairment, psychiatric symptoms, and sleep and circadian functioning. METHOD: Adults diagnosed with serious mental illness (SMI) and sleep and circadian dysfunction (N = 121) were randomly allocated to TranS-C plus usual care (TranS-C + UC; n = 61; 8 individual weekly sessions) or 6 months of Usual Care followed by Delayed Treatment with TranS-C (UC-DT; n = 60). Schizophrenia (45%) and anxiety disorders (47%) were common. Blind assessments were conducted pre-treatment, post-treatment, and 6 months later (6FU). The latter two were the post-randomization points of interest. The location was Alameda County Behavioral Health Care Services (ACBHCS), a Community Mental Health Center (CMHC) in California. RESULTS: For the primary outcomes, relative to UC-DT, TranS-C + UC was associated with reduction in functional impairment (b = -3.18, p = 0.025, d = -0.58), general psychiatric symptoms (b = -5.88, p = 0.001, d = -0.64), sleep disturbance (b = -5.55, p < .0001, d = -0.96), and sleep-related impairment (b = -9.14, p < .0001, d = -0.81) from pre-treatment to post-treatment. These effects were maintained to 6-month follow-up (6FU; d = -0.42 to -0.82), except functional impairment (d = -0.37). For the secondary outcomes, relative to UC-DT, TranS-C + UC was associated with improvement in sleep efficiency and on the Sleep Health Composite score from pre-treatment to 6FU. TranS-C + UC was also associated with reduced total wake time and wake time variability from pre-treatment to post-treatment, as well as reduced hallucinations and delusions, bedtime variability, and actigraphy measured waking activity count variability from pre-treatment to 6FU. CONCLUSIONS: A novel transdiagnostic treatment, delivered within a CMHC setting, improves selected measures of functioning, symptoms of comorbid disorders, and sleep and circadian outcomes. (PsycInfo Database Record (c) 2021 APA, all rights reserved).


Assuntos
Centros Comunitários de Saúde Mental , Transtornos Mentais/terapia , Psicoterapia/métodos , Transtornos do Sono do Ritmo Circadiano/terapia , Transtornos do Sono-Vigília/terapia , Adulto , Ansiedade/terapia , Transtornos de Ansiedade/terapia , California , Feminino , Humanos , Masculino , Transtornos Mentais/complicações , Pessoa de Meia-Idade , Esquizofrenia/terapia , Sono , Transtornos do Sono do Ritmo Circadiano/complicações , Transtornos do Sono-Vigília/complicações , Resultado do Tratamento
2.
NPJ Breast Cancer ; 3: 50, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-29238750

RESUMO

Radiation and chemotherapy are effective treatments for cancer, but are also toxic to healthy cells. Little is known about whether prior exposure to these treatments is related to markers of cellular aging years later in breast cancer survivors. We examined whether past exposure to chemotherapy and/or radiation treatment was associated with DNA damage, telomerase activity, and telomere length 3-6 years after completion of primary treatments in breast cancer survivors (stage 0-IIIA breast cancer at diagnosis). We also examined the relationship of these cellular aging markers with plasma levels of Interleukin (IL)-6, soluble TNF-receptor-II (sTNF-RII), and C-reactive protein (CRP). Ninety-four women (36.4-69.5 years; 80% white) were evaluated. Analyses adjusting for age, race, BMI, and years from last treatment found that women who had prior exposure to chemotherapy and/or radiation compared to women who had previously received surgery alone were more likely to have higher levels of DNA damage (P = .02) and lower telomerase activity (P = .02), but did not have differences in telomere length. More DNA damage and lower telomerase were each associated with higher levels of sTNF-RII (P's < .05). We found that exposure to chemotherapy and/or radiation 3-6 years prior was associated with markers of cellular aging, including higher DNA damage and lower telomerase activity, in post-treatment breast cancer survivors. Furthermore, these measures were associated with elevated inflammatory activation, as indexed by sTNF-RII. Given that these differences were observed many years after the treatment, the findings suggest a long lasting effect of chemotherapy and/or radiation exposure.

3.
Inhal Toxicol ; 29(12-14): 555-566, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-29336178

RESUMO

Although industrial uses of asbestos have declined since the 1970s, in recent years there has been a renewed interest in para-occupational ("take-home") exposure to these fibers. The aim of this study was to quantify the release of asbestos fibers, if any, during the shaking out of crocidolite- and chrysotile-contaminated clothing in a simulated at-home setting. An exposure study was conducted in which personal and area air samples were collected during the handling (i.e. shake-out) of work clothing (shirt and pants) previously worn by an operator who had cut asbestos-containing cement pipe. During eight "loading" events, the operator cut a historically representative asbestos-containing cement pipe (10% crocidolite and 25% chrysotile) using a powered abrasive saw. Subsequently, 30-minute air samples were collected during four "shake-out" events, each of which consisted of the handling of two complete sets of contaminated work clothes. Samples were analyzed in accordance with NIOSH methods 7400 and 7402. The mean phase contrast microscopy equivalent (PCME) airborne concentrations were 0.52 f/cc (SD = 0.34 f/cc) for total asbestos fibers, 0.36 f/cc (SD = 0.26 f/cc) for chrysotile and 0.17 f/cc (SD = 0.096 f/cc) for crocidolite. Based on likely estimates of the frequency of laundering activities, and assuming that the dusty clothing (1) is not blown off in the occupational setting using compressed air and (2) is not shaken out before entering the home, a family member handling the clothing could potentially have a lifetime cumulative exposure to chrysotile and crocidolite of approximately 0.20 f/cc-year and 0.096 f/cc-year, respectively.


Assuntos
Poluentes Ocupacionais do Ar/análise , Asbestos/análise , Vestuário , Materiais de Construção/análise , Exposição por Inalação/análise , Exposição Ocupacional/análise , Poluentes Ocupacionais do Ar/efeitos adversos , Asbestos/efeitos adversos , Vestuário/efeitos adversos , Materiais de Construção/efeitos adversos , Humanos , Exposição por Inalação/efeitos adversos , Exposição por Inalação/prevenção & controle , Exposição Ocupacional/efeitos adversos , Exposição Ocupacional/prevenção & controle
4.
Lung Cancer ; 102: 122-134, 2016 12.
Artigo em Inglês | MEDLINE | ID: mdl-27987580

RESUMO

Lung cancer is the leading cause of cancer-related mortality. While the majority of lung cancers are associated with tobacco smoke, approximately 10-15% of U.S. lung cancers occur in never smokers. Evidence suggests that lung cancer in never smokers appears to be a distinct disease caused by driver mutations which are different than the genetic pathways observed with lung cancer in smokers. A meta-analysis of human epidemiologic data was conducted to evaluate the profile of common or therapy-targetable mutations in lung cancers of never and ever smokers. Epidemiologic studies (N=167) representing over 63,000 lung cancer cases were identified and used to calculate summary odds ratios for lung cancer in never and ever smokers containing gene mutations: EGFR, chromosomal rearrangements and fusion of EML4 and ALK, and KRAS. This analysis also considered the effect of histopathology, smoking status, sex, and ethnicity. There were significantly increased odds of presenting the EGFR and ALK-EML4 mutations in 1) adenocarcinomas compared to non-small cell lung cancer and 2) never smokers compared to ever smokers. The prevalence of EGFR mutations was higher in Asian women as compared to women of Caucasian/Mixed ethnicity. As the smoking history increased, there was a decreased odds for exhibiting the EGFR mutation, particularly for cases >30 pack-years. Compared to ever smokers, never smokers had a decreased odds of KRAS mutations among those of Caucasian/Mixed ethnicity (OR=0.22, 95% CI: 0.17-0.29) and those of Asian ethnicity (OR=0.39, 95% CI: 0.30-0.50). Our findings show that key driver mutations and several patient features are highly prevalent in lung cancers of never smokers. These associations may be helpful as patient demographic models are developed to predict successful outcomes of targeted therapeutic interventions NSCLC.


Assuntos
Receptores ErbB/genética , Neoplasias Pulmonares/genética , Proteínas Proto-Oncogênicas p21(ras)/genética , Receptores Proteína Tirosina Quinases/genética , Fumar/genética , Quinase do Linfoma Anaplásico , Humanos , Neoplasias Pulmonares/enzimologia , Neoplasias Pulmonares/epidemiologia , Mutação , Prevalência , Fumar/epidemiologia , Fumar/metabolismo
5.
Mutat Res ; 749(1-2): 58-65, 2013 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-23748015

RESUMO

Cigarette smoke causes direct oxidative DNA damage as well as indirect damage through inflammation. Epidemiological studies show a strong relationship between secondhand smoke and cancer; however, the mechanisms of secondhand smoke-induced cancer are not well understood. Animal models with either (i) deficient oxidative DNA damage repair, or (ii) a decreased capacity to combat oxidative stress may help determine the pathways important in mitigating damage caused by smoke. In this study, we used mice lacking Ogg1 and Myh, both of which are involved in base excision repair by removing oxidatively damaged DNA bases. Gclm-deficient mice, which have decreased levels of glutathione (GSH), were used to look at the role of smoke-induced oxidative damage. Ex vivo experiments show significantly elevated levels of DNA single-strand breaks and chromosomal aberrations in peripheral blood lymphocytes from Ogg1(-/-)Myh(-/-) double knockout mice compared to wild type (WT) mice after 24h of exposure to cigarette smoke extract (CSE). The average γH2AX foci per cell was significantly elevated 3h after exposure to CSE in cells from Ogg1(-/-)Myh(-/-) double knockout mice compared to wildtype mice. In vivo we found that all mice had increased markers of DNA damage after exposure to side-stream tobacco smoke (SSTS). Ogg1(-/-)Myh(-/-) and Gclm(-/-) mice had altered levels of peripheral blood glutathione after SSTS exposure whereas wild type mice did not. This may be due to differential regulation of glutathione synthesis in the lung. We also found that Ogg1(-/-)Myh(-/-) mice had a decreased lifespan after oral gavage with benzo[a]pyrene compared to wildtype mice and sham-exposed Ogg1(-/-)Myh(-/-) mice. Our results are important in investigating the roles of oxidative stress and oxidative DNA damage repair in cigarette smoke-induced cancers and characterizing the role of genetic polymorphisms in smoke-related disease susceptibility.


Assuntos
Células Sanguíneas/efeitos dos fármacos , Distúrbios no Reparo do DNA/genética , Glutationa/deficiência , Estresse Oxidativo/genética , Poluição por Fumaça de Tabaco/efeitos adversos , Animais , Células Sanguíneas/metabolismo , Dano ao DNA/efeitos dos fármacos , Dano ao DNA/genética , DNA Glicosilases/genética , Distúrbios no Reparo do DNA/sangue , Distúrbios no Reparo do DNA/patologia , Feminino , Glutamato-Cisteína Ligase/genética , Glutationa/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Estresse Oxidativo/efeitos dos fármacos
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