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Photodynamic therapy provides the formation of reactive oxygen species that are capable of inducing cell death. Human laryngeal carcinoma (HEp-2) cells have been evaluated in this study under PDT treatment. Cells were treated with photosensitizer aluminum phthalocyanine tetrasulfonate (AlPcS4) and irradiated with a Biopdi/Irrad-Led5 660 LED with 660 nm wavelength, intensity of delivered light of 25 mW/cm2, power of 70 mW, fluence of 5 J/cm2 for 24 h and 48 h, and then evaluated. Cell population was not increased by PDT treatment after the tested period. The apoptosis assay demonstrated that control groups exhibit approximately 60% of living cells in the 24 h and 48 h periods, however. A significant increase in apoptotic cells was observed after the photodynamic therapy treatments, for both 24 and 48 h groups. Over 50% of cells were under apoptosis after photodynamic therapy, evidencing a death process generated from the oxidative damage of the treatment. Comet assay and micronucleus assessments, both of which evaluate genotoxicity, demonstrated favorable results to damages caused by the photodynamic therapy treatment. Thus, photodynamic therapy is proposed to damage nuclear cells and the subcellular structure of carcinogenic cells. Impact statement Recently, the use of photodynamic therapy grows as an alternative treatment for cancer, since it has a noninvasive characteristic and affinity to the tumor tissue. Accordingly, understanding the therapy’s foci of action is important for the technique improvement. This work aims to understand the genotoxic effect triggered by the therapy action, thus evidencing the permanent changes caused to the genetic material of the tumor cell after the treatment. Therefore, to increase the knowledge in this study field, the methodology of the comet assay and count of micronucleus formed after the therapy was adopted in order to understand if the damage caused to the DNA of tumor cell makes its replication process unfeasible in future generations. The study allows a better therapeutic approach to the cancer treatment, making the process of association between therapies a more effective option during the disease treatment.

While nursing leaders play an important role in supporting new nurse graduates during their transition period, few studies have explored the perceptions of nursing leaders involved in transition support programs. A study was undertaken to explore the nursing leadership teams' perceptions of their role and the benefits and challenges of the Genesis Transition Support Program for New Nurse Graduates at McGill University Healthcare Centre, Quebec, Canada.A qualitative descriptive study design was used. Semistructured individual interviews were conducted with 12 nursing leaders from September to October 2013. Data analysis revealed 3 main themes regarding nursing leaders' role within the program: planning for the seminar, providing active learning opportunities and supporting new nurse graduates by listening, understanding, helping, and building stronger relationships. The program is largely associated with an enhanced experience of new nurse graduates transitioning into their professional role and has a positive impact on new nurse graduates, nursing leaders, and their individual nursing units.

Background High concentrations of hydrocortisone is known to cause oxidative stress in neural cell, impairing damage repair and, consequently, triggering cell death. This represents one of the mechanisms of Alzheimer's Disease (AD). To prevent oxidative stress, novel studies have demonstrated neuroprotective effects of taurine in specific concentrations, regulating brain activity, maintaining the integrity of neural membrane and controlling calcium homeostasis, thus preventing cell death by preventing oxidative stress. Method First, SH‐SY5Y (human neuroblastoma) cells were incubated with different concentrations of taurine (0.25 to 1 mg/mL), then, after 24h, cells were exposed to 200 µM of hydrocortisone for another 24h (a stablished concentration that reduces SH‐SY5Y viability and induces oxidative stress). Cell viability was evaluated by crystal violet technique. Cells not exposed to hydrocortisone or taurine were used as control. Result A concentration curve of taurine was performed (0.25 to 1 mg/mL), demonstrating that the compound stimulates SH‐SY5Y cell growth at 0.5 mg/mL (p = 0.0457) (Figure 1A). This concentration was stablished as protective. To verify the neuroprotective potential, cells were pre‐treated with 0.5 mg/mL of taurine and then exposed to 200 µM of hydrocortisone. Importantly, cytoviability was not only preserved but also statistically improved, compared to the control group (p < 0.0001) (Figure 1B). Conclusion In high concentration (200 µM), hydrocortisone induces oxidative stress in SH‐SY5Y, an important pathway observed in AD. Once cells are pre‐incubated with 0.5 mg/mL of taurine followed by 200 µM of hydrocortisone exposure, cytoviability is preserved and stimulated, representing a considerable step to further evaluate taurine as a significant neuroprotective tool for AD. (1) Moraes, C.D.G.O. et al. Genotoxic effects of photodynamic therapy in laryngeal cancer cells–An in vitro study. Experimental Biology and Medicine, v. 244, n. 3, p. 262‐271, 2019. (2) Salles, G.N. et al. Prolonged Drug‐Releasing Fibers Attenuate Alzheimer’s Disease‐like Pathogenesis. ACS applied materials & interfaces, v.10, n.43, p.36693‐36702, 2018. (3) Sergeeva, O.A. et al. Taurine‐induced long‐lasting enhancement of synaptic transmission in mice: Role oftransporters. The Journal of physiology, v.550, n.3, p.911‐919, 2003. (4) ROSSATO, R.C. et al. Hydrocortisone cytorestores oxidative stress‐induced neuroblastoma. Alzheimer's & Dementia: The Journal of the Alzheimer's Association, 15(7), p.642, 2019.

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A Doença de Alzheimer é um tipo de demência que acomete milhões de pessoas, sendo responsável por 60% de todos os casos de doenças neurodegenerativas. Embora não tenha cura, diversas estratégias de estudo vêm sendo desenvolvidas a fim de elucidar os mecanismos da doença. Estudos recentes abordam os benefícios do cortisol em aspectos imunológicos, musculares, renais, respostas inflamatórias e até mesmo em patologias neurodegenerativas.  A hidrocortisona é um medicamento sintético utilizado para simular o cortisol. Deste modo, o estudo explora os efeitos da hidrocortisona na senescência neural, objetivando analisar seu efeito neuroprotetor. Assim, desenvolveu-se um modelo experimental in vitro de estresse oxidativo, induzido por peróxido de hidrogênio na linhagem celular Neuro-2a (Neuroblastoma de Murino) a fim de simular aspectos característicos da Doença de Alzheimer. Foram então realizados experimentos de viabilidade e morfologia celular. A hidrocortisona em baixa concentração promoveu aumento na viabilidade celular, enquanto que o peróxido de hidrogênio diminuiu a viabilidade celular, ocorrendo o efeito de estresse oxidativo. No aspecto morfológico, a hidrocortisona preservou os prolongamentos das células, já o peróxido de hidrogênio fez com que os prolongamentos retraíssem, assim perdendo as sinapses. Com os resultados obtidos, pode-se concluir que a hidrocortisona preservou a célula neural do efeito do estresse oxidativo.