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0 [0.71-1.4]). Also, locoregional failure was similar between the two groups (aHR 1.1 [CI 0.68 - 1.7]). Tumors were PD-L1+ in 76% of cases, significantly more among HPV p16+ tumors (82% vs. 70%, p = .01). Interestingly, higher prevalence of PD-L1+ expression was seen in HPV p16+ patients with less then 10 pack-years of tobacco-smoking (93%) compared to HPV p16+ smokers (76%) or HPV p16-negative patients (70%) (p = .003).Conclusion PD-L1 expression had no prognostic significance in OPSCC patients treated with primary radiotherapy alone. A substantial proportion of OPSCC tumors show PD-L1 overexpression, especially in HPV p16+ tumors in patients with little or no smoking history.Objective This study aims to investigate the protective effects and possible mechanism of methane-rich saline (MS) on lung ischemia-reperfusion injury (LIRI) in rats.Methods MS (2 ml/kg and 20 ml/kg) was injected intraperitoneally in rats after LIRI. Lung injury was assayed by Hematoxylin-eosin (HE) staining and wet-to-dry weight (W/D). The cells in the bronchoalveolar lavage fluid (BALF) and blood were counted. Oxidative stress was examined by the level of malondialdehyde (MDA) and superoxide dismutase (SOD). Inflammatory factors including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-10 (IL-10) were determined by ELISA. Lung tissue apoptosis was detected by TUNEL staining and western blotting of Bcl-2, Bax, and caspase-3. The expressions of IкBα, p38, PI3K, AKT, and NF-κB were analyzed with Western blotting.Results MS effectively decreased the lung W/D ratio as well as the lung pathological damage and reduced the localized infiltration of inflammatory cells. Methane suppressed the expression of the PI3K-AKT-NFκB signaling pathway during the lung IR injury, which inhibited the activation of NF-kB and decreased the level of inflammatory cytokines, such as TNF-α, IL-1β, and IL-10. Moreover, we found that MS treatment relieved reactive oxygen species (ROS) damage by downregulating MDA and upregulating SOD. MS treatment also regulated apoptosis-related proteins, such as Bcl-2, Bax, and caspase-3.Conclusions MS could repair LIRI and reduce the release of oxidative stress, inflammatory cytokines, and cell apoptosis via the PI3K-AKT-NFκB signaling pathway, which may provide a novel and promising strategy for the treatment of LIRI.It has been reported that male athletes face increased risk for low energy availability and resulting health consequences similar to female athletes. The present study aimed to reveal the energy status of Japanese male runners and to examine the association between energy deficiency and physiological characteristics such as energy metabolism, bone health, and hormonal status. Six male collegiate long-distance runners during a training season participated in this study. Energy intake (EI) was assessed using 3-day dietary records with food pictures. Exercise energy expenditure (EEE) was determined by the HR-VO2 method. Body composition and bone status were measured by dual-energy X-ray absorptiometry. Energy availability (EA) was calculated by subtraction of EEE from EI and normalized by fat-free mass (FFM). Energy balance (EB) was calculated EI minus estimated total energy expenditure (TEE). Resting energy expenditure (REE) was measured by indirect calorimetry using the Douglas bag technique, and blood sampling was conducted to assess hormonal status. The mean EA of the subjects was 18.9 ± 6.8 kcal/kg FFM/day, and severe negative EB (range -1444 ~ -722 kcal/d) was observed. REE of four runners was suppressed, and moreover, bone resorption was promoted in all subjects. The data in our study suggested that energy deficiency could promote bone resorption and energy metabolism suppression in Japanese male endurance runners. Additional short- and long-term studies are needed to clarify the health risks caused by energy deficiency in male athletes and explore strategies to prevent health problems related to energy deficiency in long-distance runners.Purpose We aimed at evaluating the feasibility of using MicroRNA (miR)-34a and miR-29b to detect inner ear damage in patients with mitochondrial disease (MD) and sensorineural hearing loss (SNHL).Material and Methods Three patients with MD and SNHL and seven healthy control subjects were included in this case series. MD patients underwent pure tone audiometry (PTA), distortion product otoacoustic emission (DPOAE) and auditory brain response tests to investigate the specific cochlear and retrocochlear functions; control patients underwent PTA. MiR-34a and miR-29b were extracted from blood in all subjects included in the study. The expression of miR-34a and miR-29b in MD patients and healthy controls were statistically compared, then the expression of these two miRs was compared with DPOAE values.Results In MD patients, miR-34a was significantly up-regulated compared to healthy controls; miR-34a and DPOAEs were negatively correlated. Conversely, miR-29b was up-regulated only in the youngest patient who suffered from the mildest forms of MD and SNHL, and negatively correlated with DPOAEs.Conclusion In MD patients, miR-34a and miR-29b might be a marker of inner ear damage and early damage, respectively. Additional studies on larger samples are necessary to confirm these preliminary results.Latest knowledge assigns the origins of autism spectrum disorder (ASD)-currently affecting 1% of children- to intrauterine life, when fetal brain develops. Orelabrutinib manufacturer Besides genetics, environmental factors, responsible for epigenetic changes contributed to its rising incidence. In vitro fertilization (IVF) and the most widely used intracytoplasmic sperm injection (ICSI) are implicated in epigenetic changes. A series of studies examined the impact of ICSI on ASD in the offspring. Results are usually conflicting, due to inherent problems of study design and power, mixed IVF/ICSI cases and not exclusively ASD diagnoses included. Furthermore, preterm birth, low birthweight infants, advanced parental age, hormonal disturbances, all associated with ICSI, are known factors affecting ASD. While solid data supporting ICSI contribution to currently alarming ASD increase are lacking, exploration of underlying molecular mechanisms would strengthen possible associations. In the meanwhile, ICSI use should be restricted to male-factor infertility cases.