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This research work aims the development and optimization of an electrochemical biosensor based on molecularly-imprinted polymers [MIPs], for monitoring a melanoma biomarker, Galectin-3 (Gal-3). As it is a multifunctional protein that plays an important role in different types of tumors including melanoma, and has shown good results as a potential biomarker in several areas, the construction of a biosensor for the detection of this protein would be a simple and quick strategy to support the treatment of this type of pathology. The target molecule was recognized by a MIP material, created on the electrodes surface by electropolymerizing a mixture of analyte (Gal-3) and monomer (2-aminophenol). Then, the protein was removed from the polymeric material by oxalic acid treatment. This process formed a non-conductive polymer with recognition sites showing affinity for the Gal-3. The control of the surface modification was monitored by Raman spectroscopy and electroanalytical techniques, namely electrochemical impedance spectroscopy (EIS) and cyclic voltammetry (CV). The analytical performance of the sensor was evaluated by EIS, by following the analytical response of standard solutions ranging from 0.5 ng/mL to 5000 ng/mL Gal-3 in spyked serum. In general, the biosensor displayed good analytical features, considering limit of detection, response time and reproducibility. Overall, this study resulted from the need to create a new strategy for monitoring melanoma through the creation of a cheaper, faster and sensitive device, which can be commercialized and thus integrate the entire process associated with the treatment and follow-up of this pathology., MindGAP –, Bridging the gap between Mind, Brain and Body: exosome role and monitoring, FET-Open/H2020, European Commission (Brussels), Grant agreement 829040. 0624_2IQBIONEURO_6_E, , Impulso de una red de I + i en química biologica ´ para diagnostico ´ y tratamiento de enfermedades neurologicas ´ EP – INTERREG V A Espana ˜ Portugal (POCTEP)., info:eu-repo/semantics/publishedVersion

There is increasing attention on the complex interactions occurring between schistosome parasites and their hosts. However, little is known about the occurrence, epidemiology, and mechanisms of schistosomiasis-associated infertility. In this article, we argue that an in-depth understanding of the interplay between parasites and the host endocrine system may significantly enhance current knowledge of infertility in infected individuals. We discuss the basic hormonal mechanisms that may lead to the discovery of entirely novel anthelmintic interventions against schistosomiasis. Highlights: In spite of a plethora of epidemiological evidence supporting a key role for schistosome infection for infertility, little is known about the mechanisms of their association. To date, one of the few well characterized mechanisms by which schistosomes interact with their hosts is the estrogenic imbalance and downregulation of the estrogen receptor. Remarkably, our understanding of this mechanism has already been successfully studied in cancer-associated schistosomiasis. The relentless advancement in molecular studies, together with the discovery of novel biomarkers, provide unprecedented opportunities to investigate schistosomiasis and exploit parasite–host relationships for the development of novel strategies of disease control. There is increasing attention on the complex interactions occurring between schistosome parasites and their hosts. However, little is known about the occurrence, epidemiology, and mechanisms of schistosomiasis-associated infertility. In this article, we argue that an in-depth understanding of the interplay between parasites and the host endocrine system may significantly enhance current knowledge of infertility in infected individuals. We discuss the basic hormonal mechanisms that may lead to the discovery of entirely novel anthelmintic interventions against schistosomiasis. info:eu-repo/semantics/publishedVersion

Aims Obesity is a complex health disorder and a trigger to many diseases like Diabetes mellitus (DM) and breast cancer (BrCa), both leading causes of morbidity and mortality worldwide. Also evidence demonstrates that abnormal glucose metabolism termed ‘the Warburg effect’ in cancer cell is closely associated with malignant phenotypes and promote the aggressiveness of several types of cancer, including BrCa. In this study, we evaluated the breast cancer cell metabolism in normoglycemia, hyperglycemia and in an obesity condition in order to clarify the potential underlined mechanisms that link these disorders. Materials and methods MCF-7 cells were exposed to low and high glucose levels, the latter either in the presence of 3T3-L1 adipocyte conditioned medium (CM), thus mimicking the adiposity observed in obese patients. Cell viability, migration, proliferation, cytotoxicity and cell death assays were performed under the different culture conditions. Hormonal and lipid profile were also characterized by biochemical assays and primary metabolism was determined by Nuclear Magnetic Resonance (NMR)-based metabolomics. Results Our results show an increased aggressiveness in the condition mimicking diabetogenic obesity with an altered energy/lipid metabolism. Interestingly in the experimental obesity-mimicking status, lipids and amino acids were expended while glucose was produced by tumor cells from lactate. These findings reveal a shift on tumor cells metabolism that is opposite to ‘the Warburg effect’. Conclusions Overall, this experimentally obesity-mimicking condition not only revealed an increased tumor proliferation and aggressiveness but also disclosed a new mechanism of cancer metabolism, the ‘Warburg Effect Inversion’.

Submitted by Biblioteca Escola Superior de Saúde (biblioteca@ess.ipp.pt) on 2021-11-22T12:25:26Z No. of bitstreams: 1 ART_Joana A. Pereira.pdf: 1271845 bytes, checksum: decebb55e62b544b7c89c022205e1606 (MD5) Approved for entry into archive by Biblioteca Escola Superior de Saúde (biblioteca@ess.ipp.pt) on 2021-11-22T12:25:39Z (GMT) No. of bitstreams: 1 ART_Joana A. Pereira.pdf: 1271845 bytes, checksum: decebb55e62b544b7c89c022205e1606 (MD5) Approved for entry into archive by Biblioteca Escola Superior de Saúde (biblioteca@ess.ipp.pt) on 2021-11-22T12:25:56Z (GMT) No. of bitstreams: 1 ART_Joana A. Pereira.pdf: 1271845 bytes, checksum: decebb55e62b544b7c89c022205e1606 (MD5) Made available in DSpace on 2021-11-22T12:25:56Z (GMT). No. of bitstreams: 1 ART_Joana A. Pereira.pdf: 1271845 bytes, checksum: decebb55e62b544b7c89c022205e1606 (MD5) Previous issue date: 2015-06-05 info:eu-repo/semantics/publishedVersion

The increasing prevalence of antimicrobial resistances is now a worldwide problem. Investigating the mechanisms by which pets harboring resistant strains may receive and/or transfer resistance determinants is essential to better understanding how owners and pets can interact safely. Here, we characterized the genetic determinants conferring resistance to β-lactams and quinolones in 38 multidrug-resistant Escherichia coli isolated from fecal samples of dogs, through PCR and sequencing. The most frequent geno-type included the β-lactamase groups TEM (n = 5), and both TEM + CTX-M-1 (n = 5). Within the CTX-Mgroup, we identified the genes CTX-M-32, CTX-M-1, CTX-M-15, CTX-M-55/79, CTX-M-14 and CTX-M-2/44. Thirty isolates resistant to ciprofloxacin presented two mutations in the gyrA gene and one or two mutations in the par C gene. A mutation in gyr A (reported here for the first time), due to a transversion andtransition (TCG → GTG) originating a substitution of a serine by a valine in position 83 was also detected.The plasmid-encoded quinolone resistance gene, qnrs1, was detected in three isolates. Dogs can be a reservoir of genetic determinants conferring antimicrobial resistance and thus may play an important role in the spread of antimicrobial resistance to humans and other co-habitant animals.

Quinoxaline is a chemical compound that presents a structure that is similar to quinolone antibiotics. The present work reports the study of the antimicrobial activity of quinoxaline N,N-dioxide and some derivatives against bacterial and yeast strains. The compounds studied were quinoxaline-1,4-dioxide (QNX), 2-methylquinoxaline-1,4-dioxide (2MQNX), 2-methyl-3-benzoylquinoxaline-1,4-dioxide (2M3BenzoylQNX), 2-methyl-3-benzylquinoxaline-1,4-dioxide (2M3BQNX), 2-amino-3-cyanoquinoxaline-1,4-dioxide (2A3CQNX), 3-methyl-2-quinoxalinecarboxamide-1,4-dioxide (3M2QNXC), 2-hydroxyphenazine-N,N-dioxide (2HF) and 3-methyl-N-(2-methylphenyl)quinoxalinecarboxamide-1,4-dioxide (3MN(2MF)QNXC). The prokaryotic strains used were Staphylococcus aureus ATCC 6538, S. aureus ATCC 6538P, S. aureus ATCC 29213, Escherichia coli ATCC 25922, E. coli S3R9, E. coli S3R22, E. coli TEM-1 CTX-M9, E. coli TEM-1, E. coli AmpC Mox-2, E. coli CTX-M2 e E. coli CTX-M9. The Candida albicans ATCC 10231 and Saccharomyces cerevisiae PYCC 4072 were used as eukaryotic strains. For the compounds that presented activity using the disk diffusion method, the minimum inhibitory concentration (MIC) was determined. The alterations of cellular viability were evaluated in a time-course assay. Death curves for bacteria and growth curves for S. cerevisiae PYCC 4072 were also accessed. The results obtained suggest potential new drugs for antimicrobial activity chemotherapy since the MIC's determined present low values and cellular viability tests show the complete elimination of the bacterial strain. Also, the cellular viability tests for the eukaryotic model, S. cerevisiae, indicate low toxicity for the compounds tested.

Submitted by Rúben Fernandes (rpf@estsp.ipp.pt) on 2013-07-25T20:47:35Z No. of bitstreams: 1 1-s2-2.0-S0024320513003378-main.pdf: 1734444 bytes, checksum: b168be310bfefb33531f15de2a69d266 (MD5) Approved for entry into archive by Rúben Fernandes (rpf@estsp.ipp.pt) on 2013-07-26T18:52:50Z (GMT) No. of bitstreams: 2 9242197306595785.zip: 1578959 bytes, checksum: 9db6c67c1cbad4f3f4d684a99ce55dec (MD5) 1-s2-2.0-S0024320513003378-main.pdf: 1734444 bytes, checksum: b168be310bfefb33531f15de2a69d266 (MD5) Rejected by Manuel Brandão (msa@eu.ipp.pt), reason: Artigo já depositado anteriormente. on 2014-02-03T11:05:55Z (GMT) Submitted by Rúben Fernandes (rpf@estsp.ipp.pt) on 2014-07-31T07:44:07Z No. of bitstreams: 2 1-s2-2.0-S0024320513003378-main.pdf: 1734444 bytes, checksum: b168be310bfefb33531f15de2a69d266 (MD5) 9242197306595785.zip: 1578959 bytes, checksum: 9db6c67c1cbad4f3f4d684a99ce55dec (MD5) Approved for entry into archive by Rúben Fernandes (rpf@estsp.ipp.pt) on 2014-07-31T07:45:42Z (GMT) No. of bitstreams: 2 1-s2-2.0-S0024320513003378-main.pdf: 1734444 bytes, checksum: b168be310bfefb33531f15de2a69d266 (MD5) 9242197306595785.zip: 1578959 bytes, checksum: 9db6c67c1cbad4f3f4d684a99ce55dec (MD5) Rejected by Manuel Brandão (mbrandao@estsp.ipp.pt), reason: Artigo já se encontra depositado. Pode consultar em: http://recipp.ipp.pt/handle/10400.22/3559 on 2014-07-31T09:12:49Z (GMT) Submitted by Rúben Fernandes (rpf@estsp.ipp.pt) on 2015-12-01T04:56:46Z No. of bitstreams: 2 1-s2-2.0-S0024320513003378-main.pdf: 1734444 bytes, checksum: b168be310bfefb33531f15de2a69d266 (MD5) 9242197306595785.zip: 1578959 bytes, checksum: 9db6c67c1cbad4f3f4d684a99ce55dec (MD5) Approved for entry into archive by Rúben Fernandes (rpf@estsp.ipp.pt) on 2015-12-01T04:57:42Z (GMT) No. of bitstreams: 2 1-s2-2.0-S0024320513003378-main.pdf: 1734444 bytes, checksum: b168be310bfefb33531f15de2a69d266 (MD5) 9242197306595785.zip: 1578959 bytes, checksum: 9db6c67c1cbad4f3f4d684a99ce55dec (MD5) Approved for entry into archive by Manuel Brandão (mbrandao@estsp.ipp.pt) on 2015-12-01T15:16:40Z (GMT) No. of bitstreams: 2 1-s2-2.0-S0024320513003378-main.pdf: 1734444 bytes, checksum: b168be310bfefb33531f15de2a69d266 (MD5) 9242197306595785.zip: 1578959 bytes, checksum: 9db6c67c1cbad4f3f4d684a99ce55dec (MD5) Made available in DSpace on 2015-12-01T15:16:40Z (GMT). No. of bitstreams: 2 1-s2-2.0-S0024320513003378-main.pdf: 1734444 bytes, checksum: b168be310bfefb33531f15de2a69d266 (MD5) 9242197306595785.zip: 1578959 bytes, checksum: 9db6c67c1cbad4f3f4d684a99ce55dec (MD5) Previous issue date: 2013