•We build a sample of 75 EU banks using data from EBA Transparency Exercises.•We find that bank lending seems to be negatively affected by non-performing loans.•In terms of econometrics, we use panel ...least squares and quantile regressions.•Results are robust to three alternative methodological settings.
In the aftermath of the global financial crisis, considerable attention has been paid to the accumulation of non-performing loans in the balance sheet of European banks and to its potential negative effects on bank lending to the real economy. Using a dataset composed of bank-specific information and country aggregates, we study the impact of the stock and the flow of non-performing loans on the lending activities of a sample of 75 European banks between 2014 and 2018. In general, higher rates of non-performing loans, together with other variables, are associated with lower growth rates of performing loans. This effect persists across several econometric specifications and is more significant for those banks exhibiting lower growth rates of performing loans. Similarly, our econometric analysis suggests that banks with higher decreases in their rate of non-performing loans tend to lend more to the real economy, an effect which is particularly intense at the right tail of the distribution. The findings of our paper can be useful for policymakers when addressing the resolution of non-performing loans in banks.
Interleukin (IL)‐6 is a cytokine with pleiotropic functions in different tissues and organs. Skeletal muscle produces and releases significant levels of IL‐6 after prolonged exercise and is therefore ...considered as a myokine. Muscle is also an important target of the cytokine. IL‐6 signaling has been associated with stimulation of hypertrophic muscle growth and myogenesis through regulation of the proliferative capacity of muscle stem cells. Additional beneficial effects of IL‐6 include regulation of energy metabolism, which is related to the capacity of actively contracting muscle to synthesize and release IL‐6. Paradoxically, deleterious actions for IL‐6 have also been proposed, such as promotion of atrophy and muscle wasting. We review the current evidence for these apparently contradictory effects, the mechanisms involved and discuss their possible biological implications.
IL‐6 is a cytokine with pleiotropic functions. Skeletal muscle produces and releases IL‐6 after prolonged exercise and is considered a myokine. IL‐6 signaling stimulates hypertrophic muscle growth and de novo myogenesis. However, IL‐6 also promotes atrophy and muscle wasting. We review the current evidence for these apparently contradictory effects, the mechanisms involved and discuss their possible biological implications.
The repair process of damaged tissue involves the coordinated activities of several cell types in response to local and systemic signals. Following acute tissue injury, infiltrating inflammatory ...cells and resident stem cells orchestrate their activities to restore tissue homeostasis. However, during chronic tissue damage, such as in muscular dystrophies, the inflammatory-cell infiltration and fibroblast activation persists, while the reparative capacity of stem cells (satellite cells) is attenuated. Abnormal dystrophic muscle repair and its end stage, fibrosis, represent the final common pathway of virtually all chronic neurodegenerative muscular diseases. As our understanding of the pathogenesis of muscle fibrosis has progressed, it has become evident that the muscle provides a useful model for the regulation of tissue repair by the local microenvironment, showing interplay among muscle-specific stem cells, inflammatory cells, fibroblasts and extracellular matrix components of the mammalian wound-healing response. This article reviews the emerging findings of the mechanisms that underlie normal versus aberrant muscle-tissue repair.
Polishing after the removal of brackets is the final step in orthodontic treatment. It is simple to perform, though some studies have reported that polishing causes damage to the enamel surface. An ...in vitro study was made of the influence of the buccal surface convexity of the tooth upon possible enamel loss when the remaining resin and adhesive are removed after bracket decementing using two different polishing modes: a tungsten carbide bur at low and high speeds. The convexity of the buccal surface was quantified in 30 incisors and 30 premolars. A stereoscopic microscope was used to obtain photographs of the profile of the crown, and Image J software was used to calculate convexity by dividing the length of a line from the cementoenamel junction to the incisal margin by another line from the mentioned junction to the maximum convexity of the buccal surface. Brackets were cemented on all the teeth and were decemented 24 h later. In both groups, the residual composite was removed with a tungsten carbide bur at a low speed in one-half of the teeth and at a high speed in the other half. The buccal surface of each tooth was then photographed again, and the convexity was calculated and compared against the baseline value. The difference between the two values were taken to represent the enamel loss. The convexity of the premolars was significantly greater than that of the incisors, but this did not result in greater enamel loss when the same polishing mode was used. However, the tungsten carbide bur at a high speed proved more aggressive, causing significantly greater enamel loss than when used at a low speed.
Duchenne muscular dystrophy (DMD) is one of the most devastating neuromuscular genetic diseases caused by the absence of dystrophin. The continuous episodes of muscle degeneration and regeneration in ...dystrophic muscle are accompanied by chronic inflammation and fibrosis deposition, which exacerbate disease progression. Thus, in addition of investigating strategies to cure the primary defect by gene/cell therapeutic strategies, increasing efforts are being placed on identifying the causes of the substitution of muscle by non-functional fibrotic tissue in DMD, aiming to attenuate its severity. Congenital muscular dystrophies (CMDs) are early-onset diseases in which muscle fibrosis is also present. Here we review the emerging findings on the mechanisms that underlie fibrogenesis in muscular dystrophies, and potential anti-fibrotic treatments.
Mitochondrial dysfunction and accumulation of damaged mitochondria are considered major contributors to aging. However, the molecular mechanisms responsible for these mitochondrial alterations remain ...unknown. Here, we demonstrate that mitofusin 2 (Mfn2) plays a key role in the control of muscle mitochondrial damage. We show that aging is characterized by a progressive reduction in Mfn2 in mouse skeletal muscle and that skeletal muscle Mfn2 ablation in mice generates a gene signature linked to aging. Furthermore, analysis of muscle Mfn2‐deficient mice revealed that aging‐induced Mfn2 decrease underlies the age‐related alterations in metabolic homeostasis and sarcopenia. Mfn2 deficiency reduced autophagy and impaired mitochondrial quality, which contributed to an exacerbated age‐related mitochondrial dysfunction. Interestingly, aging‐induced Mfn2 deficiency triggers a ROS‐dependent adaptive signaling pathway through induction of HIF1α transcription factor and BNIP3. This pathway compensates for the loss of mitochondrial autophagy and minimizes mitochondrial damage. Our findings reveal that Mfn2 repression in muscle during aging is a determinant for the inhibition of mitophagy and accumulation of damaged mitochondria and triggers the induction of a mitochondrial quality control pathway.
Synopsis
Reduced muscle mitochondrial fusion protein Mfn2 is a determinant for age‐induced decay of mitochondrial function and quality, contributing to age‐associated metabolic alterations and sarcopenia.
Aging is characterized by a reduction of Mfn2 protein expression in skeletal muscle.
Reduction in Mfn2 impairs mitochondrial quality control and mitochondrial function in skeletal muscle.
Mfn2‐deficient mice show unhealthy aging characterized by impaired metabolic homeostasis and sarcopenia.
Reduction in Mfn2 triggers a mitochondrial retrograde signalling pathway in order to minimize mitochondrial damage.
Reduced muscle mitochondrial fusion protein Mfn2 is a determinant for age‐induced decay of mitochondrial function and quality, contributing to age‐associated metabolic alterations and sarcopenia.
Abstract
The COVID‐19 pandemic created an unprecedented demand and supply shock to the world economies. To understand its impact on corporate prices, we define a partial equilibrium model where ...non‐financial corporations operating in three sectors (suppliers, end‐producers and service providers) optimize their production under monopolistic competition and are subject to demand and supply shocks of different intensities. Our model confirms that when the demand shock dominates, prices tend to decrease. We then introduce data from the COVID‐19 pandemic in the European Union into our model and find that prices are expected to fall in the most acute phase of the pandemic, when lockdowns and similar health measures decrease demand, and to increase later as a result of tensions in the supply of intermediate goods and of the persistence of the supply shock. Inventories could play a decisive role in avoiding price increases in the moderate phase of the pandemic. In the post‐pandemic period, higher prices may continue for a time until the shock to suppliers vanishes. These are relevant insights on the macroeconomic impact of worldwide pandemics, also considering the current macroeconomic environment.
Regeneration of skeletal muscle is a highly synchronized process that requires muscle stem cells (satellite cells). We found that localized injuries, as experienced through exercise, activate a ...myofiber self-repair mechanism that is independent of satellite cells in mice and humans. Mouse muscle injury triggers a signaling cascade involving calcium, Cdc42, and phosphokinase C that attracts myonuclei to the damaged site via microtubules and dynein. These nuclear movements accelerate sarcomere repair and locally deliver messenger RNA (mRNA) for cellular reconstruction. Myofiber self-repair is a cell-autonomous protective mechanism and represents an alternative model for understanding the restoration of muscle architecture in health and disease.
During ageing, muscle stem-cell regenerative function declines. At advanced geriatric age, this decline is maximal owing to transition from a normal quiescence into an irreversible senescence state. ...How satellite cells maintain quiescence and avoid senescence until advanced age remains unknown. Here we report that basal autophagy is essential to maintain the stem-cell quiescent state in mice. Failure of autophagy in physiologically aged satellite cells or genetic impairment of autophagy in young cells causes entry into senescence by loss of proteostasis, increased mitochondrial dysfunction and oxidative stress, resulting in a decline in the function and number of satellite cells. Re-establishment of autophagy reverses senescence and restores regenerative functions in geriatric satellite cells. As autophagy also declines in human geriatric satellite cells, our findings reveal autophagy to be a decisive stem-cell-fate regulator, with implications for fostering muscle regeneration in sarcopenia.
The search for new materials that replace fossil fuel-based plastics has been focused on biopolymers with similar physicochemical properties to fossil fuel-based plastics, such as ...Polyhydroxyalkanoates (PHA). The present paper reviews the challenges of scaling-up PHA production from waste streams during the period from 2014 to 2016, focusing on the feasibility of the alternatives and the most promising alternatives to its scaling-up. The reviewed research studies mainly focus on reducing costs or obtaining more valuable polymers. In the future, the integration of PHA production into processes such as wastewater treatment plants, hydrogen production or biodiesel factories could enhance its implementation at industrial scale.
•The review focuses on the challenges of scaling-up PHA production from wastes.•Combination of two or more waste streams could avoid additional synthetic streams.•Pre-treatments to adjust the waste to an appropriate feed stream is highly proposed.•Integration of PHA production in existing processes enhances their implementation.•PHA production from waste should be adapted to different seasonal waste streams.
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