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During the Covid-19 outbreak in northern Italy, the daily rate of admissions for acute coronary syndrome at 15 hospitals was significantly lower than the rate during two control intervals (13.3 admissions vs. 18.0 and 18.9 admissions for the two control periods).

In this paper, we aim at establishing a new existence result for the quasilinear elliptic equation - div ( a ( x , u , ∇ u ) ) + A t ( x , u , ∇ u ) + V ( x ) | u | p - 2 u = g ( x , u ) in R N with p > 1 , N ≥ 2 and V : R N → R suitable measurable positive function. Here, we suppose A : R N × R × R N → R is a given C 1 -Carathéodory function which grows as | ξ | p , with A t ( x , t , ξ ) = ∂ A ∂ t ( x , t , ξ ) , a ( x , t , ξ ) = ∇ ξ A ( x , t , ξ ) , V : R N → R is a suitable measurable function and g : R N × R → R is a given Carathéodory function which grows as | ξ | q with 1 < q < p . Since the coefficient of the principal part depends on the solution itself, under suitable assumptions on A ( x , t , ξ ) , V ( x ) and g ( x ,  t ), we study the interaction of two different norms in a suitable Banach space with the aim of obtaining a good variational approach. Thus, a minimization argument on bounded sets can be used to state the existence of a nontrivial weak bounded solution on an arbitrary bounded domain. Then, one nontrivial bounded solution of the given equation can be found by passing to the limit on a sequence of solutions on bounded domains. Finally, under slightly stronger hypotheses, we can able to find a positive solution of the problem.

Kidney damage represents a frequent event in the course of hypertension, ranging from a benign to a malignant form of nephropathy depending on several factors, that is, individual susceptibility, degree of hypertension, type of etiology and underlying kidney disease. Multiple mechanisms are involved in determination of kidney glomerular, tubular and interstitial injuries in hypertension. The present review article discusses relevant contributory molecular mechanisms underpinning the promotion of hypertensive renal damage, such as the renin–angiotensin–aldosterone system (RAAS), oxidative stress, endothelial dysfunction, and genetic and epigenetic determinants. We highlighted major pathways involved in the progression of inflammation and fibrosis leading to glomerular sclerosis, tubular atrophy and interstitial fibrosis, thus providing a state of the art review of the pathogenetic background useful for a better understanding of current and future therapeutic strategies toward hypertensive nephropathy. An adequate control of high blood pressure, obtained through an appropriate therapeutic intervention, still represents the key strategy to achieve a satisfactory control of renal damage in hypertension. In this regard, we reviewed the impact of currently available antihypertensive pharmacological treatment on kidney damage, with particular regard to RAAS inhibitors. Notably, recent findings underscored the ability of the kidneys to regenerate and to repair tissue injuries through the differentiation of resident embryonic stem cells. Pharmacological modulation of the renal endogenous reparative process (that is, with angiotensin-converting enzyme inhibitors and AT1 angiotensin II receptor blockers), as well as future therapeutic strategies targeted to the renopoietic system, offers interesting perspectives for the management of hypertensive nephropathy.

Somatic mitochondrial DNA (mtDNA) mutations are implicated as important drivers of ageing and age-related diseases. Their pathological effect can be counteracted by increasing the absolute amount of wild-type mtDNA via moderately upregulating TFAM, a protein important for mtDNA packaging and expression. However, strong TFAM overexpression can also have detrimental effects as it results in mtDNA hypercompaction and subsequent impairment of mtDNA gene expression. Here, we have experimentally addressed the propensity of moderate TFAM modulation to improve the premature ageing phenotypes of mtDNA mutator mice, carrying random mtDNA mutations. Surprisingly, we detect tissue-specific endogenous compensatory mechanisms acting in mtDNA mutator mice, which largely affect the outcome of TFAM modulation. Accordingly, moderate overexpression of TFAM can have negative and beneficial effects in different tissues of mtDNA mutator mice. We see a similar behavior for TFAM reduction, which improves brown adipocyte tissue homeostasis, while other tissues are unaffected. Our findings highlight that the regulation of mtDNA copy number and gene expression is complex and causes tissue-specific effects that should be considered when modulating TFAM levels. Additionally, we suggest that TFAM is not the sole determinant of mtDNA copy number in situations where oxidative phosphorylation (OXPHOS) is compromised, but other important players must be involved.

In this paper, we aim at establishing a new existence result for the quasilinear elliptic equation$$\\begin{aligned} - \\textrm{div} (a(x,u,\\nabla u)) + A_t(x,u,\\nabla u) + V(x) {\\vert u \\vert }^{p-2} u= g(x,u) \\quad \\quad \\hbox { in }{{\\mathbb {R}}}^{N} \\end{aligned}$$- div ( a ( x , u , ∇ u ) ) + A t ( x , u , ∇ u ) + V ( x ) | u | p - 2 u = g ( x , u ) in R N with$$p>1$$p > 1 ,$$N\\ge 2\\ $$N ≥ 2 and$$V:{\\mathbb {R}}^N\\rightarrow {\\mathbb {R}}$$V : R N → R suitable measurable positive function. Here, we suppose$$A: {\\mathbb {R}}^N \\times {\\mathbb {R}}\\times {\\mathbb {R}}^N \\rightarrow {\\mathbb {R}}$$A : R N × R × R N → R is a given$${C}^{1}$$C 1 -Carathéodory function which grows as$$|\\xi |^p$$| ξ | p , with$$A_t(x,t,\\xi ) = \\frac{\\partial A}{\\partial t}(x,t,\\xi )$$A t ( x , t , ξ ) = ∂ A ∂ t ( x , t , ξ ) ,$$a(x,t,\\xi ) = \\nabla _\\xi A(x,t,\\xi )$$a ( x , t , ξ ) = ∇ ξ A ( x , t , ξ ) ,$$V:{\\mathbb {R}}^N\\rightarrow {\\mathbb {R}}$$V : R N → R is a suitable measurable function and$$g:{\\mathbb {R}}^N \\times {\\mathbb {R}}\\rightarrow {\\mathbb {R}}$$g : R N × R → R is a given Carathéodory function which grows as$$|\\xi |^q$$| ξ | q with$$1

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