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Despite an increasing number of reports on the associations between chronic occupational stress and structural and functional changes of the brain, the underlying neural correlates of perceived occupational stress is still not clear. Perceived stress reflects the extents to which situations are appraised as stressful at a given point in one’s life. Using near-infrared spectroscopy, we investigated the associations between perceived occupational stress and cortical activity over the bilateral frontotemporal regions during a verbal fluency test. Sixty-eight participants (17 men, 51 women), 20-62 years of age were recruited. Perceived occupational stress was measured using the Chinese version of Job Content Questionnaire, and the Chinese version of the Copenhagen Burnout Inventory. We found statistically significant negative associations between occupational burnout and brain cortical activity over the fronto-polar and dorsolateral prefrontal cortex during the VFT (r = −0.343 to −0.464). In conclusion, our research demonstrated a possible neural basis of perceived occupational stress that are distributed across the prefrontal cortex.
Perceived Occupational Stress is associated with Decreased Cortical Activity of the Prefrontal Cortex: A Multichannel Near-infrared Spectroscopy Study
Po-Han Chou,a,1,2,3,4 Wei-Hao Lin,1 Chao-An Hung,5,6 Chiung-Chih Chang,7 Wan-Rung Li,1 Tsuo-Hung Lan,1,2 and Min-Wei Huangb,8
Low-grade squamous intraepithelial lesions (LSIL) are the earliest lesions of the uterine cervix, the persistence and integration of high-risk human papillomavirus (HR-HPV) as type 16, which promotes the development of more aggressive lesions.
To select more aggressive lesions with tendency to progress to invasive cervical cancer.
Materials and Methods:
A total of 75 cytological specimens in liquid base (Liqui-PREP) were analyzed: 25 specimens were with no signs of SIL (NSIL) and without HPV; 25 NSIL with HPV-16, and 25 with both LSIL and HPV-16. The expression of Ki-67, telomerase, and viral E6 was evaluated by immunocytochemistry; and the detection of viral DNA was done by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLPs) for genotyping or sequencing of HPV-16. The physical state of HPV-16 was evaluated by in situ hybridization with amplification with tyramide.
Of the total group, 58.6% had LSIL associated with persistence and of these 59.3% was associated with integrated state of HPV as intense expression of E6, Ki-67 (P = 0.013, P = 0.055) has except for the expression of telomerase present a non-significant association (P<0.341). Conclusions: Overexpression of E6 and Ki-67 is associated with the integration of HPV-16, favoring viral persistence, and increasing the risk of progression in women with NSIL and LSIL.
Cervical lesions, E6, HPV-16, integration, Ki-67, telomerase
Risk of progression of early cervical lesions is associated with integration and persistence of HPV-16 and expression of E6, Ki-67, and telomerase
Arianna Vega-PeNa, Berenice Illades-Aguiar,1 Eugenia Flores-Alfaro,2 Esther Lopez-Bayghen,3 Marco Antonio Leyva-Vazquez,1 Eduardo CastaNeda-Saucedo,4 and Luz Del Carmen Alarcon-Romero
Prolonged breathing of nitric oxide reduces myocardial ischemia-reperfusion injury but the precise mechanisms responsible for the cardioprotective effects of inhaled nitric oxide are incompletely understood.
We investigated the fate of inhaled nitric oxide (80 parts per million) in mice, and quantified the formation of nitric oxide metabolites (NO-metabolites) in blood and tissues. We tested whether the accumulation of NO-metabolites correlated with the ability of inhaled nitric oxide to protect against cardiac ischemia-reperfusion injury.
Mice absorbed nitric oxide in a nearly linear fashion (0.19±0.02 μmol/g·h). Breathing nitric oxide rapidly increased a broad spectrum of NO-metabolites. Levels of erythrocytic S-nitrosothiols, N-nitrosamines and nitrosyl-hemes exceeded nitrite within 30 sec of commencing nitric oxide inhalation. Marked increases of lung S-nitrosothiols and liver N-nitrosamines levels were measured, as well as elevated cardiac and brain NO-metabolite levels. Breathing hypoxic concentrations potentiated the ability of inhaled nitric oxide to increase cardiac NO-metabolite levels. Concentrations of each NO-metabolite, except nitrate, rapidly reached a plateau and were similar after 5 and 60 minutes. Studying a murine cardiac ischemia-reperfusion injury model, breathing nitric oxide for either 5 or 60 min before reperfusion decreased MI/AAR by 31 and 32%, respectively.
Breathing nitric oxide leads to the rapid accumulation of a variety of NO-metabolites in blood and tissues, contributing to the ability of brief periods of nitric oxide inhalation to provide cardioprotection against ischemia-reperfusion injury. The NO-metabolite concentrations achieved in a target tissue may be more important than the absolute amounts of nitric oxide absorbed.
Brief Periods of Nitric Oxide Inhalation Protect Against Myocardial Ischemia-Reperfusion Injury
Yasuko Nagasaka, M.D.,1,¤* Bernadette O. Fernandez, Ph.D.,2,¥* Maria F. Garcia-Saura, Ph.D.,2,¥ Bodil Petersen, M.D.,1,¥ Fumito Ichinose, M.D.,1,‡ Kenneth D. Bloch, M.D.,1,** Martin Feelisch, Ph.D.,2,#† and Warren M. Zapol, M.D.1,§†
2009 Oct 1.