Schiff bases: A short review of their antimicrobial activities

AbstractSchiff bases are aldehyde- or ketone-like compounds in which the carbonyl group is replaced by an imine or azomethine group. They are widely used for industrial purposes and also exhibit a broad range of biological activities. This short review compiles examples of the most promising antimalarial, antibacterial, antifungal, and antiviral Schiff bases. An overview of synthetic methodologies used for the preparation of Schiff bases is also described

Correlation Between Audiometric Data And The 35delg Mutation In Ten Patients

Mutations in the connexin 26 gene seem to be extremely common in non-syndromic hereditary deafness genesis, especially the 35delG, but there are still only a few studies that describe the audiometric characteristics of patients with these mutations. Aim: to analyze the audiometric characteristics of patients with mutations in the connexin 26 gene in order to outline genotype-phenotype correlation. Materials and Methods: Tonal audiometries of 33 index cases of non-syndromic sensorineural hearing loss were evaluated and eight affected relatives. Specific molecular tests were carried out to analyze mutations in the connexin 26 gene. Experiment Design: Retrospective, cross-sectional study. Results: A 27.3% prevalence of mutation 35delG was found in the index cases and 12.5% among the relatives affected. In relation to hearing loss degree, 41.5% of the patients were found with profound hearing loss, 39% with severe HL and 19.5% with moderate HL with homozygote and heterozygote patients for the 35delG predominating in the severe-moderate hearing losses. Conclusion: Our results suggest that the audiometric data associated with the molecular diagnose of hearing loss helped us to outline a genotype-phenotype correlation in ten patients with 35delG mutation. However, it is still necessary to run multicentric studies to verify the real phenotypic expression in the Brazilian population, as far as the 35delG mutation is concerned. © Revista Brasileira de Otorrinolaringologia. All Rights reserved.736777783Morton, N.E., Genetic epidemiology of hearing impairment (1991) Ann N Y Acad Sci, 630, pp. 16-31Mustafa, T., Arnos, K.S., Pandya, A., Advances in hereditary deafness (2001) Lancet, 358, pp. 1082-1090Skvorak Giersch, A.B., Morton, C.C., Genetic causes of nonsyndromic hearing loss (1999) Curr Opin Pediatr, 11 (6), pp. 551-557Petit, C., Genes responsible for human hereditary deafness: Symphony of a thousand (1996) Nature Genet, 14, pp. 385-391Van Camp, G., Willems, P.J., Smith, R.J.H., Nonsyndromic hearing impairment: Unparalleled heterogeneity (1997) Am J Hum Genet, 60, pp. 758-764Kelsell, D.P., Dunlop, J., Stevens, H.P., Lench, N.J., Liang, J.N., Parry, G., Mueller, R.F., Leigh, I.M., Connexin 26 mutations in hereditary non-syndromic sensorineural deafness (1997) Nature, 387, pp. 80-83Kelley, P.M., Harris, D.J., Comer, B.C., Askew, J.W., Fowler, T., Smith, S.D., Kimberling, W.J., Novel mutations in the connexin 26 gene (GJB2) that cause autossomal recessive (DFNB1) hearing loss (1998) Am J Hum Genet, 62, pp. 792-799Scott, D.A., Kraft, M.L., Carmi, R., Ramesh, A., Elbedour, K., Yari, Y., Srisailapathy, C.R.S., Identification of mutation on the connexin 26 gene that cause autossomal recessive nonsyndromic hearing loss (1998) Hum Mutat, 11, pp. 387-394Gabriel H, Kupsch P, Sudendey Jr, Winterhager E, Jahnke K, et al. Mutations in the connexin 26/GJB2 gene are the most common event in non-syndromic hearing loss among the German population. Hum Mutat 2001;17:521-2Van Camp G, Smith RJH. Na Hereditary Hearing Loss Homepage [Site na Internet]. Disponível em: http://webhost.ua.ac.be/hhh/. Acessado em 2006Zelante, L., Gasparini, P., Estivill, X., Melchionda, S., D'Agruma, L., Govea, N., Mila, M., Della Monica, M., Connexin 26 mutations associated with the most common form of non-syndromic neurosensory autossomal recessive deafness (DFNB1) in Mediterraneans (1997) Hum Molec Genet, 6, pp. 1605-1609Estivill, X., Fortina, P., Surrey, S., Rabionet, R., Melchionda, S., D'Agruma, L., Mansfield, E., Rappaport, E., Connexin 26 mutations in sporadic and inherited sensorineural deafness (1998) Lancet, 351, pp. 394-398Antoniadi, T., Gronskov, K., Sand, A., Pampanos, A., Brondum-Nielsen, K., Petersen, M.B., Mutation analysis of the GJB2 (connexin 26) gene by DGGE in greek patients with sensorineural deafness (2000) Hum Mutat, 16, pp. 7-12Oliveira, C.A., Maciel-Guerra, A.T., Sartorato, E.L., Deafness resulting from mutations in the GJB2 (connexin 26) gene on Brazilian patients (2002) Clin Genet, 61, pp. 354-358Kammen-Jolly, K., Ichiki, H., Scholtz, A.W., Gsenger, M., Kreczy, A., Schrott-Fischer, A., Connexin 26 in human fetal development of the inner ear (2001) Hear Res, 160 (1-2), pp. 15-21Denoyelle, F., Marlin, S., Weil, D., Moatti, L., Chauvin, P., Garabedian, E.N., Petit, C., Clinical features of the prevalent form of childhood deafness, DFNB1, due to a connexin 26 gene defect: Implications for genetic counselling (1999) Lancet, 17 (9161), pp. 1298-1303Cryns, K., Orzan, E., Murgia, A., Huygen, P.L.M., Moreno, F., del Castilo, I., A genotype-phenotype correlation for GJB2 (connexin 26) deafness) (2004) J Med Genet, 41, pp. 147-154(1991) Report of the informal working group on prevention of deafness and hearing impairment programme planning, , World Health Organization, Geneva: WHO, 22pAntoniadi, T., Gronskov, K., Sand, A., Pampanos, A., Brondum-Nielsen, K., Petersen, M.B., Mutation analysis of the GJB2 (connexin 26) gene by DGGE in Greek patients with sensorineural deafness (2000) Hum Mutat, 16, pp. 7-12del Castillo, I., Villamar, M., Moreno-Pelayo, M.A., del Castillo, F.J., Alvarez, A., Telleria, D., A deletion involving the connexin 30 gene in nonsyndromic hearing impairment (2002) N Engl J Med, 346, pp. 243-249Kelley, P.M., Harris, D.J., Comer, B.C., Askew, J.W., Fowler, T., Smith, S.D., Kimberling, W.J., Novel mutations in the connexin 26 gene (GJB2) that cause autossomal recessive (DFNB1) hearing loss (1998) Am J Hum Genet, 62, pp. 792-799Sobe, T., Vreugde, S., Shahin, H., Berlin, M., Davis, N., The prevalence and expression of inherited connexin 26 mutations associated with non-syndromic hearing loss in the Israeli population (2000) Hum Genet, 106, pp. 50-57Wilcox, S.A., Saunders, K., Osborn, A.H., Arnold, A., Wunderlich, J., High frequency hearing loss correlated with mutations in the GJB2 gene (2000) Hum Genet, 106, pp. 399-405del Castillo, I., Villamar, M., Moreno-Pelayo, M.A., del Castillo, F.J., Alvarez, A., Telleria, D., A deletion involving the connexin 30 gene in nonsyndromic hearing impairment (2002) N Engl J Med, 346, pp. 243-249Frei, K., Szuhai, K., Lucas, T., Weipoltshammer, K., Schofer, C., Ramsebner, R., Connexin 26 mutations in cases of sensorineural deafness in eastern Austria (2002) Eur J Hum Genet, 10, pp. 427-432Pampanos, A., Economides, J., Iliadou, V., Neou, P., Leotsakos, P., Voyiatzis, Prevalence of GJB2 mutations in prelingual deafness in the Greek population (2002) Int J Pediatr Otorhinolaryngol, 65, pp. 101-108Gasparini, P., Estivill, X., Volpini, V., Totaro, A., Castellvi-Bel, S., Linkage of DFNB1 to non-syndromic neurosensory autosomal-recessive deafness in Mediterranean families (1997) Eur J Hum Genet, 5, pp. 83-88Estivill, X., Fortina, P., Surrey, S., Rabionet, R., Melchionda, S., D'Agruma, L., Mansfield, E., Rappaport, E., Connexin 26 mutations in sporadic and inherited sensorineural deafness (1998) Lancet, 351, pp. 394-398Kenna, M.A., Wu, B.-L., Cotanche, D.A., Korf, B.R., Rehm, H.L., Connexin 26 studies in patientes with sensorineural hearing loss (2001) Arch Otolaryngol Head Neck Surg, 127, pp. 1037-1042Simsek, M., Al-Wardy, N., Al-Khayat, A., Shanmugakonar, M., Al-Bulushi, T., Al-Khabory, M., Absence of deafness associated connexin 26 (GJB2) gene mutations in the Omani population (2001) Hum Mutat, 18, pp. 545-546Nance, W.E., The genetics of deafness (2003) Ment Retard Disabil Res Rev, 9, pp. 109-119del Castillo, I., Moreno-Pelayo, M.A., del Castillo, F.J., Brownstein, Z., Marlin, S., Adina, Q., Prevalence and Evolutionary Origins of the del(GJB6-D13S1830) Mutation in the DFNB1 Locus in Hearing Impaired Subjects: A Multicenter Study (2003) Am J Hum Genet, 73, pp. 1452-1458Piatto, V.B., Oliveira, C.A., Alexandrino, F., Pimpinati, C.J., Sartorato, E.L., Perspectivas para triagem auditiva genética: Rastreamento da mutação 35delG em neonatos. (2005) J Pediatr, 81, pp. 139-142Sartorato, E.L., Gottardi, E., Oliveira, C.A., Magna, L.A., Annichio-Bizzacchi, J.M., Seixas, C.A., Maciel-Guerra, A.T., Determination of the frequency of the 35delG in Brazilian neonates (2000) Clin Genet, 58, pp. 339-340Oliveira, C.A., Alexandrino, F., Abe-Sandes, K., Silva Jr, W.A., Maciel-Guerra, A.T., Magna, L.A., Sartorato, E.L., Frequency of 35delG in the GJB2 gene in samples of Caucasians, Asians and African Brazilians (2004) Hum Biol, 76, pp. 313-316Pandya, A., Arnos, K.S., Xia, X.J., Welch, K.O., Blanton, S.H., Friedman, T.B., Frequency and distribution of GJB2 (connexin 26) and GJB6 (connexin 30) mutations in a large North American repository of deaf probands (2003) Genet Med, 5, pp. 295-303Stevenson, V.A., Ito, M., Milunsky, J.M., Connexin-30 deletion analysis in connexin-26 heterozygotes (2003) Genet Test, 7, pp. 151-154Cohn, E.S., Kelley, P.M., Fowler, T.W., Gorga, M.P., Lefkowitz, Clinical studies of families with hearing loss attributable to mutations in the connexin 26 gene (GJB2/DFNB1) (1999) Pediatrics, 103, pp. 546-550Murgia, A., Orzan, E., Polli, R., Martella, M., Vinazi, C., Leonardi, E., Arslan, E., Zacchello, F., Cx26 deafness: Mutation analysis and clinical variability (1999) J Med Genet, 36, pp. 829-832Marlin, S., Garabedian, E.-N., Roger, G., Moatti, L., Matha, N., Lewin, P., Petit, C., Denoyelle, F., Connexin 26 gene mutations in congenitally deaf children (2001) Arch Otolaryngol Head Neck Surg, 127, pp. 927-933Rabionet, R., Zelante, L., Lopez-Bigas, N., DAgruma, L., Melchionda, S., Restagno, G., Molecular basis of childhood deafness resulting from mutations in the GJB2 (connexin 26) gene (2000) Hum Genet, 106, pp. 40-44Cohn, E.S., Kelley, P.M., Clinical phenotype and mutations in connexin 26 (DFNB1/GJB2), the most commom cause of childhood hearing loss (1999) Am J Med Genet, 89, pp. 130-136Denoyelle, F., Marlin, S., Weil, D., Moatti, L., Chauvin, P., Garabedian, E.N., Petit, C., Clinical features of the prevalent form of childhood deafness, DFNB1, due to a connexin 26 gene defect: Implications for genetic counselling (1999) Lancet, 17, pp. 1298-1303Engel-Yeger, B., Zaaroura, S., Zlotogora, J., Shalev, S., Hujeirat, Y., Carrasquilo, M., Barges, S., Pratt, H., The effects of a connexin 26 mutation - 35delG - an oto-acoustic emissions and brainstem evoked potentials: Homozygotes and carriers (2002) Hear Res, 163, pp. 93-100Mustapha, M., Salem, N., Delague, V., Chouery, E., Ghassibeh, M., Rai, M., Loiselet, J., Megarbane, A., Autosomal recessive non-syndromic hearing loss in the Libanese population: Prevalence of the 30delG mutation and report of two novel mutations in the connexin 26 (GJB2) gene (2001) J Med Genet, 38, pp. e36Yoshinaga-Itano, C., Sedey, A.L., Coulter, D.K., Mehl, A.L., Language of early-and later-identified children with hearing loss (1998) Pediatrics, 102, pp. 1161-117

Cholesterol-functionalized carvedilol-loaded PLGA nanoparticles: anti-inflammatory, antioxidant, and antitumor effects

The inflammation has been identified as factor of tumor progression, which has increased the interest and use of molecules with anti-inflammatory and antioxidant activities in the cancer treatment. In this study, the antioxidant, anti-inflammatory, and antitumor potentials of carvedilol was explored in a different approach. The cholesterol (CHO) was investigated as facilitated agent in the action of carvedilol-loaded nanoparticles. Different formulations exhibited spherical and stable nanoparticle with mean diameter size < 250 nm. The cholesterol changed the copolymer-drug interactions and the encapsulation efficiency. The in vitro cancer study was performed using murine colorectal cancer cell line (CT-26) to observe the cell viability and apoptosis on MTS assay and flow cytometry, respectively. The experiments have demonstrated that cholesterol improved the performance of drug-loaded nanoparticles, which was much better than free drug. The in vivo inflammation peritonitis model revealed that carvedilol-loaded nanoparticles increased the level of glutathione and leukocyte migration mainly when the functionalized drug-loaded nanoparticles were tested, in a lower dose than the free drug. As hypothesized, the experimental data suggest that cholesterol-functionalized carvedilol-loaded PLGA nanoparticles can be a novel and promising approach in the inflammation-induced cancer therapy since showed anti-inflammatory, antioxidant, and antitumor effects.Graphical abstractRadiolog

Zero-inflated Poisson regression models for QTL mapping applied to tick-resistance in a Gyr × Holstein F2 population

Now a days, an important and interesting alternative in the control of tick-infestation in cattle is to select resistant animals, and identify the respective quantitative trait loci (QTLs) and DNA markers, for posterior use in breeding programs. The number of ticks/animal is characterized as a discrete-counting trait, which could potentially follow Poisson distribution. However, in the case of an excess of zeros, due to the occurrence of several noninfected animals, zero-inflated Poisson and generalized zero-inflated distribution (GZIP) may provide a better description of the data. Thus, the objective here was to compare through simulation, Poisson and ZIP models (simple and generalized) with classical approaches, for QTL mapping with counting phenotypes under different scenarios, and to apply these approaches to a QTL study of tick resistance in an F2 cattle (Gyr × Holstein) population. It was concluded that, when working with zero-inflated data, it is recommendable to use the generalized and simple ZIP model for analysis. On the other hand, when working with data with zeros, but not zero-inflated, the Poisson model or a data-transformation-approach, such as square-root or Box-Cox transformation, are applicable

Recent advances in neutrinoless double beta decay search

Even after the discovery of neutrino flavour oscillations, based on data from atmospheric, solar, reactor, and accelerator experiments, many characteristics of the neutrino remain unknown. Only the neutrino square-mass differences and the mixing angle values have been estimated, while the value of each mass eigenstate still hasn't. Its nature (massive Majorana or Dirac particle) is still escaping. Neutrinoless double beta decay ($0\nu$-DBD) experimental discovery could be the ultimate answer to some delicate questions of elementary particle and nuclear physics. The Majorana description of neutrinos allows the $0\nu$-DBD process, and consequently either a mass value could be measured or the existence of physics beyond the standard should be confirmed without any doubt. As expected, the $0\nu$-DBD measurement is a very difficult field of application for experimentalists. In this paper, after a short summary of the latest results in neutrino physics, the experimental status, the R&D projects, and perspectives in $0\nu$-DBD sector are reviewed.Comment: 36 pages, 7 figures, To be publish in Czech Journal of Physic

Sensor Surface Design with NanoMaterials: A New Platform in the Diagnosis of COVID-19

Mass testing for COVID-19 is essential to defining patient management strategies, choosing the best clinical management, and dimensioning strategies for controlling viral dissemination and immunization strategies. Thus, it is of utmost importance to search for devices that allow a quick and reliable diagnosis of low cost that can be transposed from the bench to the bedside, such as biosensors. These devices can help choose the correct clinical management to minimize factors that lead to infected patients developing more severe diseases. The use of nanomaterials to modify biosensors’ surfaces to increase these devices’ sensitivity and their biofunctionality enables high-quality nanotechnological platforms. In addition to the diagnostic benefits, nanotechnological platforms that facilitate the monitoring of anti-SARS-CoV-2 antibodies may be the key to determining loss of protective immune response after an episode of COVID-19, which leads to a possible chance of reinfection, as well as how they can be used to assess and monitor the success of immunization strategies, which are beginning to be administered on a large scale and that the extent and duration of their protection will need to be determined. Therefore, in this chapter, we will cover nanomaterials’ use and their functionalities in the surface design of sensors, thus generating nanotechnological platforms in the various facets of the diagnosis of COVID-19