Increasing disparities in the proportions of active treatment and 5-year overall survival over time by age groups among older patients with gastric cancer in Korea.

Purpose: As older patients with gastric cancer increase in Korea, no consensus indicative of anti-cancer treatment exists for the oldest old (age 85+). We investigated potential disparities in the proportion of surgery-including active treatment and the degree of survival improvement over time by age groups, and whether heterogeneity exists in the protective effect of time period on overall survival (OS) by age at diagnosis clusters. Materials and methods: A nationwide cohort (N = 63,975) of older patients with gastric cancer (age at diagnosis 70+) in 2005-2012 were followed until the end of 2018. Patients were categorized into four time period groups by their year of diagnosis. Cancer treatment patterns and 5-year OS were analyzed accordingly, and a random coefficients Cox model with random intercepts and random slopes of time period by age at diagnosis clusters was employed. Results: The mean age of patients was 76.4, and 60.4% were males. Most patients had 0-1 comorbidities (73.3%) and low-risk frailty scores (74.2%). Roughly two-thirds of patients received some form of anti-cancer treatment (62.4%), and while the number of comorbidities and the proportion of high-risk frailty scores trended toward an increase, the proportion of patients receiving anti-cancer treatment increased from 58% in 2005-2006 to 69.6% in 2011-2012. The proportion of surgery-including active treatment increased to over 70% in the 70-74 years old group, while stagnating at 10% in the 90+ years old group. Differences in the slope of 5-year OS improvement resulted in a widening survival gap between the old (age 70-84) and the oldest old. The protective effect of time period on OS hazard in the oldest old was not monotonically reduced with increasing "chronological" age but varied quite randomly, especially among female patients. Conclusion: Our study showed no upper age limit in terms of benefiting from the advances in the detection and treatment of gastric cancer over time. Thus, "functional" age rather than "chronological" age should be the criterion for anti-cancer screening and treatment, and actual implementation of proven treatments in the oldest old patients to reduce their non-compliance with treatment in clinical practice is needed to improve gastric cancer survival for all.

Long-Term Cognitive Performance of Retired Athletes with Sport-Related Concussion: A Systematic Review and Meta-Analysis.

Objective: The purpose of this systematic review is to quantitatively estimate (or invest) the impacts of sports-related concussions (SRCs) on cognitive performance among retired athletes more than 10 years after retirement. Methods: Six databases including (MEDLINE, Scopus, Web of Science, SPORTDiscus, CINAHL, and PsycArtilces) were employed to retrieve the related studies. Studies that evaluate the association between cognitive function and the SRC of retired athletes sustaining more than 10 years were included. Results: A total of 11 studies that included 792 participants (534 retired athletes with SRC) were identified. The results indicated that the retired athletes with SRCs, compared to the non-concussion group, had significant cognitive deficits in verbal memory (SMD = -0.29, 95% CI -0.59 to -0.02, I2 = 52.8%), delayed recall (SMD = -0.30, 95% CI -0.46 to 0.07, I2 = 27.9%), and attention (SMD = -0.33, 95% CI -0.59 to -0.06, I2 = 0%). Additionally, meta-regression demonstrated that the period of time between testing and the last concussion is significantly associated with reduced verbal memory (ß = -0.03681, p = 0.03), and increasing age is significantly associated with the verbal memory (ß = -0.03767, p = 0.01), immediate recall (ß = -0.08684, p = 0.02), and delay recall (ß = -0.07432, p = 0.02). Conclusion: The retired athletes who suffered from SRCs during their playing career had declined cognitive performance in partial domains (immediate recall, visuospatial ability, and reaction time) later in life.

Identifying the specific nanostructures responsible for the high thermoelectric performance of (Bi,Sb)2Te3 nanocomposites.

Herein, we report the synthesis of multiscale nanostructured p-type (Bi,Sb)(2)Te(3) bulk materials by melt-spinning single elements of Bi, Sb, and Te followed by a spark plasma sintering process. The samples that were most optimized with the resulting composition (Bi(0.48)Sb(1.52)Te(3)) and specific nanostructures showed an increase of approximately 50% or more in the figure of merit, ZT, over that of the commercial bulk material between 280 and 475 K, making it suitable for commercial applications related to both power generation and refrigeration. The results of high-resolution electron microscopy and small angle and inelastic neutron scattering along with corresponding thermoelectric property measurements corroborate that the 10-20 nm nanocrystalline domains with coherent boundaries are the key constituent that accounts for the resulting exceptionally low lattice thermal conductivity and significant improvement of ZT.

Microscopic annealing process and its impact on superconductivity in T'-structure electron-doped copper oxides.

High-transition-temperature superconductivity arises in copper oxides when holes or electrons are doped into the CuO(2) planes of their insulating parent compounds. Whereas hole doping quickly induces metallic behaviour and superconductivity in many cuprates, electron doping alone is insufficient in materials such as R(2)CuO(4) (R is Nd, Pr, La, Ce and so on), where it is necessary to anneal an as-grown sample in a low-oxygen environment to remove a tiny amount of oxygen in order to induce superconductivity. Here we show that the microscopic process of oxygen reduction repairs Cu deficiencies in the as-grown materials and creates oxygen vacancies in the stoichiometric CuO(2) planes, effectively reducing disorder and providing itinerant carriers for superconductivity. The resolution of this long-standing materials issue suggests that the fundamental mechanism for superconductivity is the same for electron- and hole-doped copper oxides.

Roles of JNK-1 and p38 in selective induction of apoptosis by capsaicin in ras-transformed human breast epithelial cells.

Efforts have been made to develop a chemoprevention strategy that selectively triggers apoptosis in malignant cancer cells. Previous studies showed that capsaicin, the major pungent ingredient of red pepper, had differential effect between normal and transformed cells. As an approach to unveil the molecular mechanism by which capsaicin selectively induces apoptosis in transformed cells, we investigated the effect of capsaicin in nontransformed and ras-transformed cells of a common origin: parental (MCF10A) and H-ras-transformed (H-ras MCF10A) human breast epithelial cells. Here, we show that capsaicin selectively induces apoptosis in H-ras-transformed cells but not in their normal cell counterparts. The capsaicin-induced apoptosis, which is dependent on ras transformation, involves the activity of DEVDase (caspase-3 like). In H-ras MCF10A cells, capsaicin treatment markedly activated c-Jun N-terminal protein kinase (JNK)-1 and p38 matigen-activated protein kinase (MAPK) while it deactivated extracellular signal-regulated protein kinases (ERKs). The use of kinase inhibitors and overexpression of dominant-negative forms of MAPKs demonstrated a role of JNK-1 and p38, but not that of ERKs, in apoptosis induced by capsaicin in H-ras-transformed MCF10A cells. Based on the present study, we propose that capsaicin selectively induces apoptosis through modulation of ras-downstream signaling molecules in ras-activated MCF10A cells. Taken in conjunction with the fact that uncontrolled ras activation is probably the most common genetic defect in human cancer cells, our finding may be critical to the chemopreventive potential of capsaicin and for developing a strategy to induce tumor cell-specific apoptosis.