¿Los supuestos de la mecánica cuántica contribuirían a entender ciertas desigualdades sistêmicas capitalistas? El asunto Piketty / Could the assumptions of quantum mechanics should contribute to understand certain systemic inequalities of capitalism? The Piketty s affair / Será que as hipóteses da mecânica quântica ajudariam a entender certas desigualdades sistêmicas capitalistas? O caso Piketty

RESUMEN El artículo busca probar la hipótesis de que ciertas desigualdades del crecimiento económico se podrían entender más allá de las características del sistema capitalista mismo. El artículo, primero expone algunos aspectos de las formas de pensar determinista newtoniana y mecánica cuántica Luego, utiliza herramientas cuánticas propuestas, entre otros, por Hawking y Otro (2010), Morin (1990), Prigogine (1990, 1993, 1997) y Russell (1986), probando su utilidad para comprender desigualdades capitalistas expuestas, entre otros, por Marx y Engels (2000), Marx (1970) y Keynes (1970). Y al final, intenta desvirtuar algunas propuestas de Piketty (2014) en relación con su crítica al crecimiento desigual. La metodología del artículo es descriptivo-comparada. A manera de hallazgo, el artículo propone que la ausencia de herramientas cuánticas en los análisis y terapias aplicadas para resolver problemas cada vez más complejos, explicaría cierto creciente desprestigio de los economistas contemporáneos en el entorno global. CLASIFICACIÓN JEL A12

ABSTRACT The article seeks to test the hypothesis that certain inequalities of economic growth could be understood beyond the characteristics of the capitalist system by itself. The article first exposes some aspects of Newtonian deterministic ways of thinking and also of quantum mechanics. Then, he uses quantum tools proposed, among others, by Hawking and Other (2010), Morin (1990), Prigogine (1990, 1993, 1997), and Russell (1986), proving their usefulness in understanding exposed capitalist inequalities, among others, by Marx and Engels (2000), Marx (1970) and Keynes (1970). And, in the end, he tries to distort some proposals of Piketty (2014) in relation to his criticism of unequal growth. The methodology of the article is descriptive comparative. By way of finding, the article proposes that the absence of quantum tools in the analyzes and therapies applied to solve increasingly complex problems, would explain some growing discredit of contemporary economists in the global environment. JEL CLASSIFICATION A12

RESUMO O artigo procura testar a hipótese de que certas desigualdades de crescimento econômico poderiam ser compreendidas além das características do próprio sistema capitalista. O artigo expõe primeiro alguns aspectos do pensamento determinista e da mecânica quântica newtoniana. Depois, utiliza ferramentas quânticas propostas, entre outras, por Hawking e Outro (2010), Morin (1990), Prigogine (1990, 1993, 1997), e Russell (1986), provando sua utilidade na compreensão das desigualdades capitalistas expostas, entre outros, por Marx e Engels (2000), Marx (1970) e Keynes (1970). E, no final, tenta distorcer algumas propostas de Piketty (2014) em relação à sua crítica ao crescimento desigual. A metodologia do artigo é descritivo-comparativa. Como conclusão, o artigo propõe que a ausência de ferramentas quânticas nas análises e terapias aplicadas para resolver problemas cada vez mais complexos, explicaria um certo descrédito crescente dos economistas contemporâneos no ambiente global. CLASSIFICAÇÃO JEL A12

Understanding the impacts of missense mutations on structures and functions of human cancer-related genes: A preliminary computational analysis of the COSMIC Cancer Gene Census.

Genomics and genome screening are proving central to the study of cancer. However, a good appreciation of the protein structures coded by cancer genes is also invaluable, especially for the understanding of functions, for assessing ligandability of potential targets, and for designing new drugs. To complement the wealth of information on the genetics of cancer in COSMIC, the most comprehensive database for cancer somatic mutations available, structural information obtained experimentally has been brought together recently in COSMIC-3D. Even where structural information is available for a gene in the Cancer Gene Census, a list of genes in COSMIC with substantial evidence supporting their impacts in cancer, this information is quite often for a single domain in a larger protein or for a single protomer in a multiprotein assembly. Here, we show that over 60% of the genes included in the Cancer Gene Census are predicted to possess multiple domains. Many are also multicomponent and membrane-associated molecular assemblies, with mutations recorded in COSMIC affecting such assemblies. However, only 469 of the gene products have a structure represented in the PDB, and of these only 87 structures have 90-100% coverage over the sequence and 69 have less than 10% coverage. As a first step to bridging gaps in our knowledge in the many cases where individual protein structures and domains are lacking, we discuss our attempts of protein structure modelling using our pipeline and investigating the effects of mutations using two of our in-house methods (SDM2 and mCSM) and identifying potential driver mutations. This allows us to begin to understand the effects of mutations not only on protein stability but also on protein-protein, protein-ligand and protein-nucleic acid interactions. In addition, we consider ways to combine the structural information with the wealth of mutation data available in COSMIC. We discuss the impacts of COSMIC missense mutations on protein structure in order to identify and assess the molecular consequences of cancer-driving mutations.

Innate immunity. A Spaetzle-like role for nerve growth factor ß in vertebrate immunity to Staphylococcus aureus.

Many key components of innate immunity to infection are shared between Drosophila and humans. However, the fly Toll ligand Spaetzle is not thought to have a vertebrate equivalent. We have found that the structurally related cystine-knot protein, nerve growth factor ß (NGFß), plays an unexpected Spaetzle-like role in immunity to Staphylococcus aureus infection in chordates. Deleterious mutations of either human NGFß or its high-affinity receptor tropomyosin-related kinase receptor A (TRKA) were associated with severe S. aureus infections. NGFß was released by macrophages in response to S. aureus exoproteins through activation of the NOD-like receptors NLRP3 and NLRP4 and enhanced phagocytosis and superoxide-dependent killing, stimulated proinflammatory cytokine production, and promoted calcium-dependent neutrophil recruitment. TrkA knockdown in zebrafish increased susceptibility to S. aureus infection, confirming an evolutionarily conserved role for NGFß-TRKA signaling in pathogen-specific host immunity.

Loss-of-function mutations in HPSE2 cause the autosomal recessive urofacial syndrome.

Previously, we localized the defective gene for the urofacial syndrome (UFS) to a region on chromosome 10q24 by homozygosity mapping. We now report evidence that Heparanse 2 (HPSE2) is the culprit gene for the syndrome. Mutations with a loss of function in the Heparanase 2 (HPSE2) gene were identified in all UFS patients originating from Colombia, the United States, and France. HPSE2 encodes a 592 aa protein that contains a domain showing sequence homology to the glycosyl hydrolase motif in the heparanase (HPSE) gene, but its exact biological function has not yet been characterized. Complete loss of HPSE2 function in UFS patients suggests that HPSE2 may be important for the synergic action of muscles implicated in facial expression and urine voiding.

S-Adenosyl-L-methionine increases serum BUN and creatinine in cisplatin-treated mice.

Cisplatin is an effective antineoplastic agent in the treatment of various solid tumors, although its full clinical utility is limited because of its renal toxicity. Several measures to protect the kidneys from cisplatin toxicity have been investigated and implemented in clinical trials; however, none of these were completely effective or without secondary effects. The aim of this study was to investigate S-adenosyl-L-methionine (SAM) as an agent that protects against cisplatin nephrotoxicity without affecting the antineoplastic activity of cisplatin. The cytotoxic effect was evaluated in cultured HeLa cells treated with cisplatin, SAM, and the combination cisplatin + SAM. No modification of the cytotoxic effect of cisplatin was induced by SAM. Similarly, SAM did not influence the antitumoral activity of cisplatin observed in HeLa cells implanted in nude mice. However, a significant increase in renal dysfunction was induced by SAM in animals treated with cisplatin. To our knowledge, this is the first report of a potential severe adverse effect of SAM administration, which should be considered for further evaluation due to the wide use of SAM as a nutritional supplement in humans.

Can a congenital dysfunctional bladder be diagnosed from a smile? The Ochoa syndrome updated.

During the last 40 years over 100 patients have been reported with a dysfunctional lower urinary tract associated with a peculiar distortion of the facial expression. This most unusual disorder was initially considered a local observation. Time, however, has proven otherwise, since patients with this syndrome have now been reported from various countries throughout the world. This association of lower urinary tract and bowel dysfunction with an abnormal facial expression was named the urofacial (Ochoa) syndrome. Genetic studies have demonstrated that this condition is inherited as an autosomal recessive trait, and a potential gene has been mapped to chromosome 10q23-q24. There is also enough evidence to suggest that patients with this syndrome as well as those with subclinical neurological bladder, occult neuropathic bladder, non-neurogenic neurogenic bladder or Hinman syndrome, dysfunctional voiding, or dysfunctional elimination may be affected by the same congenital disorder of neurological origin.

High resolution mapping and mutation analyses of candidate genes in the urofacial syndrome (UFS) critical region.

The urofacial (Ochoa) syndrome (UFS) characterized by congenital obstructive uropathy and abnormal facial expression is a rare disorder caused by a single recessive disease gene. Our previous studies using homozygosity mapping have located the UFS gene to a genomic interval of approximately 360 kb on chromosome 10q23-10q24. In this study, we have constructed a genomic sequence map covering the entire UFS interval and narrowed the disease interval to a genomic region of 220 kb that harbor the newly identified ACDP1 gene in addition to part of the GOT1 gene which has already been excluded as a candidate for UFS. Extensive search for mutations in the coding region, the 5' and 3' untranslated regions, the promoter region, and the exon/intron junctions failed to identify a pathogenic mutation in UFS patients. Furthermore, our analyses indicated that the same gene on chromosome 10q is responsible for all UFS patients from multiple ethnic groups.