Mesenchymal stromal cells (MSCs) may provide crucial support in the regeneration of destructed alveolar tissue (emphysema) in chronic obstructive pulmonary disease (COPD). We hypothesized that lung-derived MSCs (LMSCs) from patients with emphysema are hampered in their repair capacity, either intrinsically or due to their interaction with the damaged microenvironment. LMSCs were isolated from the lung tissue of controls and patients with severe emphysema and characterized at baseline. In addition, LMSCs were seeded onto control and emphysematous decellularized lung tissue scaffolds and assessed for deposition of extracellular matrix (ECM). We observed no differences in surface markers, differentiation/proliferation potential, and expression of ECM genes between control- and COPD-derived LMSCs. Notably, COPD-derived LMSCs displayed lower expression of FGF10 and HGF messenger RNA (mRNA) and hepatocyte growth factor (HGF) and decorin protein. When seeded on control decellularized lung tissue scaffolds, control- and COPD-derived LMSCs showed no differences in engraftment, proliferation, or survival within 2  wk, with similar ability to deposit new matrix on the scaffolds. Moreover, LMSC numbers and the ability to deposit new matrix were not compromised on emphysematous scaffolds. Collectively, our data show that LMSCs from patients with COPD compared with controls show less expression of FGF10 mRNA, HGF mRNA and protein, and decorin protein, whereas other features including the mRNA expression of various ECM molecules are unaffected. Furthermore, COPD-derived LMSCs are capable of engraftment, proliferation, and functioning on native lung tissue scaffolds. The damaged, emphysematous microenvironment as such does not hamper the potential of LMSCs. Thus, specific intrinsic deficiencies in growth factor production by diseased LMSCs may contribute to impaired alveolar repair in emphysema.The degree to which executive function (EF) abilities (including working memory [WM], inhibitory control [IC], and cognitive flexibility [CF]) can be enhanced through training is an important question; however, research in this area is inconsistent. Saracatinib nmr Previous cognitive training studies largely agree that training leads to improvements in the trained task, but the generalisability of this improvement to other related tasks remains controversial. In this article, we present a pre-registered experiment that used an adaptive training procedure to examine whether EFs can be enhanced through cognitive training, and directly compared the efficacy and generalisability across sub-components of EF using training programmes that target WM, IC, or CF versus an active control group. Participants (n = 160) first completed a battery of tasks that assessed EFs, then were randomly assigned to one of the four training groups, and completed an adaptive procedure over 21 days (10 training sessions) that targeted a specific sub-component of EF (or was comparatively engaging and challenging, but did not train a specific EF). At post-test, participants returned to the lab to repeat the battery of EF tasks. Results revealed robust direct training effects (i.e., on trained task), but limited evidence to support near (i.e., same EF, different task) and far (i.e., different EF and task) transfer effects. Where indirect training benefits emerged, the effects were more readily attributable to the overlapping training/assessment task routines, rather than more general enhancements to the underlying cognitive processes or neural circuits. In spite of supposedly successful surgery, slight residual knee laxity may be found at follow-up evaluations after anterior cruciate ligament reconstruction (ACLR), and its clinical effect is undetermined. To investigate whether a 3- to 5-mm increase in anterior translation 6 months after ACLR affects the risk of graft failure, rate of return to sports, and long-term outcome. Cohort study; Level of evidence, 2. From a cohort of 234 soccer, team handball, and basketball players undergoing ACLR using bone-patellar tendon-bone graft, 151 athletes were included who attended 6-month follow-up that included KT-1000 arthrometer measures. A graft was defined as <3-mm side-to-side difference between knees (n = 129), a graft as 3 to 5 mm (n = 20), and a graft as >5 mm (n = 2). Graft failure was defined as ACL revision surgery, >5-mm side-to-side difference, or anterolateral rotational instability 2+ or 3+ at 2-year follow-up. Finally, a 25-year evaluation was performed, including a clinical ex respectively, among patients with slightly loose grafts. A slightly loose graft at 6 months after ACLR increased the risk of later ACL revision surgery and/or graft failure, reduced the length of the athlete's sports career, caused permanent increased anterior laxity, and led to an inferior Lysholm score.A slightly loose graft at 6 months after ACLR increased the risk of later ACL revision surgery and/or graft failure, reduced the length of the athlete's sports career, caused permanent increased anterior laxity, and led to an inferior Lysholm score.Although the prevalence of pancreatic cancer is increasing, treatment strategies remain limited, and success is rare. A growing body of evidence links pancreatic cancer to pre-existing metabolic disorders, including, but not limited to, type 2 diabetes mellitus and obesity. An infrequently described finding, fatty pancreas, initially described in the context of obesity in the early 20th century, appears to be at the crossroads of type 2 diabetes and obesity on the one hand, and the development of pancreatic cancer on the other. Similarly, other conditions of the pancreas, such as intrapancreatic mucinous neoplasms, also seem to be related to diabetes while increasing the subsequent risk of pancreatic cancer. In this review, the author explores the diagnostic criteria for, and prevalence of, fatty pancreas and the potential link to other pancreatic conditions, including pancreatic cancer. Diagnostic limitations, and areas of controversy are also addressed, as are potential therapeutic approaches to fatty pancreas intended to reduce the subsequent risk of pancreatic cancer.