Interlaminar endoscopic uniportal approach for implantation of a paddle lead larger than 10 mm for spinal cord stimulation: illustrative case.

BACKGROUND: The authors aim to describe a new technique for implantation of a spinal cord stimulation paddle lead sized over 10 mm through an endoscopic uniportal approach. A new endoscopic cannula was developed for the passage of a paddle lead width between 10 and 13 mm. The distal portion of the cannula was designed with a larger opening, providing better visibility of the anterior portion of the adjacent structures, thus allowing a panoramic view of the electrode passage. An electrode was implanted in an 11-mm paddle. OBSERVATIONS: After searching PubMed, Cochrane, and Lilacs databases, the authors found no mention of the implantation of a paddle electrode with a width greater than 10 mm. The implantation of a paddle electrode less than 10 mm wide is possible via endoscopic access using 10-mm working channels. However, for electrodes with a width greater than 10 mm, access via endoscopy is impossible, since the working channel is only 10 mm. LESSONS: The authors concluded that it is possible to pass electrodes safely and effectively with a paddle width between 10 and 13 mm using spinal endoscopy via uniportal interlaminar access. However, it is necessary to expand studies to elucidate this technique of endoscopic implantation of electrodes for neurostimulation.

MageC2 protein is upregulated by oncogenic activation of MAPK pathway and causes impairment of the p53 transactivation function.

Normal-to-tumor cell transition is accompanied by changes in gene expression and signal transduction that turns the balance toward cancer-cell phenotype, eluding by different mechanisms, the response of tumor-suppressor genes. Here, we observed that MageC2, a MAGE-I protein able to regulate the p53 tumor-suppressor, is accumulated upon MEK/ERK MAPK activation. Overexpression of H-RasV12 oncogene causes an increase in MageC2 protein that is prevented by pharmacologic inhibition of MEK. Similarly, decrease in MageC2 protein levels is shown in A375 melanoma cells (which harbor B-RafV600E oncogenic mutation) treated with MEK inhibitors. MageC2 protein levels decrease when p14ARF is expressed, causing an Mdm2-independent upregulation of p53 transactivation. However, MageC2 is refractory to p14ARF-driven downregulation when H-RasV12 is co-expressed. Using MageC2 knockout A375 cells generated by CRISPR/CAS9 technology, we demonstrated the relevance of MageC2 protein in reducing p53 transcriptional activity in cells containing hyperactive MEK/ERK signaling. Furthermore, gene expression analysis performed in cancer-genomic databases, supports the correlation of reduced p53 transcriptional activity and high MageC2 expression, in melanoma cells containing Ras or B-Raf driver mutations. Data presented here suggest that MageC2 can be a functional target of the oncogenic MEK/ERK pathway to regulate p53.

Generation of patient-specific pluripotent induced stem cell line UFRJi007-A from a Brazilian familial amyotrophic lateral sclerosis patient.

Induced pluripotent stem cell (iPSC) line were generated from erythroblasts of a Brazilian patient with familiar form of amyotrophic lateral sclerosis (ALS). NGS analysis demonstrated that patient carried a mutation in SOD1 gene, as well as a deletion in FUS gene. CytoTune™-iPS 2.0 Sendai Reprogramming Kit (containing the reprogramming factors OCT3/4, KLF4, SOX2 and cMYC) was used to generate the cell lines. The iPSCs express pluripotency markers, have normal karyotype and differentiated spontaneously in the three germ layers. The expression of Sendai virus was lost in all iPSC lines after 15 passages.

Generation of four patient-specific pluripotent induced stem cell lines from two Brazilian patients with amyotrophic lateral sclerosis and two healthy subjects.

Induced pluripotent stem cell (iPSC) lines were generated from erythroblasts of two patients with amyotrophic lateral sclerosis (ALS) and two healthy individuals. One familial and one sporadic ALS patients were used, both with genetic alterations in VAPB gene. CytoTune™-iPS 2.0 Sendai Reprogramming Kit (containing the reprogramming factors OCT3/4, KLF4, SOX2 and cMYC) was used to generate the iPSC cell lines. The four iPSCs express pluripotency markers, have normal karyotype and differentiated spontaneously in the three germ layers. The expression of Sendai virus was lost in all iPSC lines after 15 passages.

Thickness and marking quality of different occlusal contact registration strips

Objectives Evaluate the thickness and the marking quality of different occlusal contact registration strips (OCRS) and a possible correlation between them. Material and Methods The following OCRS were selected: Accufilm II, BK20, BK21, BK22, BK23, BK28, and BK31. The thickness was measured in three points of the OCRS with an electronic measuring device (TESA), and the mean was calculated. To produce the marks on the strips, composite resin specimens were adapted to a universal testing machine (Versat 2000) with 40 kgf load cell at a speed of 1.0 mm/min. The mark images were photographed with a stereoscopic microscope (Stemi SV11) and processed and analyzed by the 550-Leica Qwin® analyzer. Results Values (μm) found in the 1st and 2nd thickness measurements were: Accufilm II - 16.4 and 14.2; BK20 - 10.0 and 8.1; BK21 - 9.5 and 8.0; BK22 - 9.7 and 8.7; BK23 - 9.8 and 7.9; BK28 - 12.8 and 10.0; and BK31 - 8.4 and 8.0, respectively. The mean (mm2) values found in the mark areas were: Accufilm II - 0.078; BK20 - 0.035; BK21 - 0.045; BK22 - 0.012; BK23 - 0.022; BK28 - 0.024; and BK31 - 0.024. The results were submitted to the Kruskal-Wallis (p<0.05) and Pearson’s correlation tests. Conclusions Only in the 2nd measurement, the OCRS thickness observed was similar to the value indicated by the manufacturers; the Accufilm II and the BK28 strips showed the better marks; and no correlation was found between the thickness and the marking area. .

Thickness and marking quality of different occlusal contact registration strips.

OBJECTIVES: Evaluate the thickness and the marking quality of different occlusal contact registration strips (OCRS) and a possible correlation between them. MATERIAL AND METHODS: The following OCRS were selected: Accufilm II, BK20, BK21, BK22, BK23, BK28, and BK31. The thickness was measured in three points of the OCRS with an electronic measuring device (TESA), and the mean was calculated. To produce the marks on the strips, composite resin specimens were adapted to a universal testing machine (Versat 2000) with 40 kgf load cell at a speed of 1.0 mm/min. The mark images were photographed with a stereoscopic microscope (Stemi SV11) and processed and analyzed by the 550-Leica Qwin analyzer. RESULTS: Values (µm) found in the 1st and 2nd thickness measurements were: Accufilm II - 16.4 and 14.2; BK20 - 10.0 and 8.1; BK21 - 9.5 and 8.0; BK22 - 9.7 and 8.7; BK23 - 9.8 and 7.9; BK28 - 12.8 and 10.0; and BK31 - 8.4 and 8.0, respectively. The mean (mm2) values found in the mark areas were: Accufilm II - 0.078; BK20 - 0.035; BK21 - 0.045; BK22 - 0.012; BK23 - 0.022; BK28 - 0.024; and BK31 - 0.024. The results were submitted to the Kruskal-Wallis (p<0.05) and Pearson's correlation tests. CONCLUSIONS: Only in the 2nd measurement, the OCRS thickness observed was similar to the value indicated by the manufacturers; the Accufilm II and the BK28 strips showed the better marks; and no correlation was found between the thickness and the marking area.

Tumor-specific MAGE proteins as regulators of p53 function.

Since its discovery in 1991, the knowledge about the tumor specific melanoma antigen gene (MAGE-I) family has been continuously increasing. Initially, MAGE-I proteins were considered as selective targets for immunotherapy. More recently, emerging data obtained from different cellular mechanisms controlled by MAGE-I proteins suggest a key role in the regulation of important pathways linked to cell proliferation. This is in part due to the ability of some MAGE-I proteins to control the p53 tumor suppressor. In this review, we focus on the mechanisms proposed to explain how MAGE-I proteins affect p53 functions.

Avaliação in vitro da resistência ao cisalhamento de três materiais adesivos na colagem de braquetes ortodônticos / In vitro evaluation of strength to shear of three adhesive materials in the collage of orthodontic brackets

Objetivo: Este estudo objetivou avaliar a resistência ao cisalhamento da união esmalte/resina/braquete de três materiais adesivos: Transbond XT (3M Unitek) de uso específico em ortodontia, RelyX ARC (3M) e Enforce (Dentsply). Metodologia: Foram utilizados 60 dentes bovinos incluídos em resina acrílica em tubos de PVC. Os espécimes foram divididos em três grupos de 20, de acordo com o material de cimentação utilizado. Os braquetes foram cimentados aos dentes e, após 24 horas, aferida a resistência ao cisalhamento em uma máquina universal de ensaios Versat 2000, com velocidade de 1 mm/min. e célula de carga de 50 kgf. Os resultados obtidos foram submetidos a análise estatística (ANOVA e teste de Tukey). Resultados: Não foi verificada diferença significativa entre os materiais avaliados (P<0,05). Conclusão: Todas as resinas testadas apresentaram adesividade suficiente para resistir às forças durante o tratamento ortodôntico, constituindo alternativa viável para a cimentação de braquetes ortodônticos

Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production.

p53 is a crucial transcription factor with tumor suppressive properties that elicits its function through specific target genes. It constitutes a pivotal system that integrates information received by many signaling pathways and subsequently orchestrates cell fate decisions, namely, growth-arrest, senescence, or apoptosis. Reactive oxygen species (ROS) production in cells can play a key role in signal transduction, being able to trigger different processes as cell death or cell proliferation. Sustained oxidative stress can induce genomic instability and collaborates with cancer development, whereas acute enhancement of high ROS levels leads to toxic oxidative cell damage and cell death. Here, it has been considered p53 broad potential contribution through its ability to regulate selected key cancer signaling pathways, where ROS participate as inductors or effectors of the final biological outcome. Further, we have discussed how p53 could play a role in preventing potentially harmful oxidative state and cell proliferation by pro-oncogenic pathways such as PI3K/AKT/mTOR and WNT/ß-catenin or under hypoxia state. In addition, we have considered potential mechanisms by which p53 could collaborate with signal transduction pathways such as transforming growth factor-ß (TGF-ß) and stress-activated protein kinases (SAPK) that produce ROS, to stop or eliminate uncontrolled proliferating cells.

Manifestações clínicas intrabucais da doença de Crohn – Relato de caso clínico / Oral manifestation in Crohn’s Disease − Case report

A doença de Crohn é uma doença inflamatória granulomatosa, de etiologia desconhecida, mas de natureza imunológica relacionada a uma suscetibilidade genética. A doença foi descrita pela primeira vez por Crohn e colaboradores em 1932, usando o termo inflamação regional do íleo. Atualmente está claro, que qualquer nível do trato gastrintestinal pode ser acometido. A doença afeta pacientes jovens e pode se apresentar da forma aguda ou crônica podendo ocorrer diversas manifestações sistêmicas, inclusive na cavidade bucal. O tratamento médico varia em função do quadro clínico e muitas vezes se baseia apenas no controle dos sintomas. A prevalência na cavidade bucal varia conforme a faixa etária atinge ambos os sexos e é mais prevalente em leucodermas. Essa doença apresenta um polimorfismo de lesões bucais, muitas vezes de maneira inespecífica. Em aproximadamente 30por cento dos casos as lesões bucais precedem as manifestações sistêmicas O relato de caso explorou a literatura atual e enfatizou os aspectos clínicos odontológicos, os diagnósticos diferenciais e o papel do cirurgião-dentista no diagnóstico precoce dessa doença.