44 research outputs found
Anti-ganglioside antibodies in patients with Zika virus infection-associated Guillain-Barré Syndrome in Brazil.
Zika virus infection is associated with the development of Guillain-Barré syndrome (GBS), a neurological autoimmune disorder caused by immune recognition of gangliosides and other components at nerve membranes. Using a high-throughput ELISA, we have analyzed the anti-glycolipid antibody profile, including gangliosides, of plasma samples from patients with Zika infections associated or not with GBS in Salvador, Brazil. We have observed that Zika patients that develop GBS present higher levels of anti-ganglioside antibodies when compared to Zika patients without GBS. We also observed that a broad repertoire of gangliosides was targeted by both IgM and IgG anti-self antibodies in these patients. Since Zika virus infects neurons, which contain membrane gangliosides, antigen presentation of these infected cells may trigger the observed autoimmune anti-ganglioside antibodies suggesting direct infection-induced autoantibodies as a cause leading to GBS development. Collectively, our results establish a link between anti-ganglioside antibodies and Zika-associated GBS in patients
Magnon delocalization in ferromagnetic chains with long-range correlated disorder
We study one-magnon excitations in a random ferromagnetic Heisenberg chain
with long-range correlations in the coupling constant distribution. By
employing an exact diagonalization procedure, we compute the localization
length of all one-magnon states within the band of allowed energies . The
random distribution of coupling constants was assumed to have a power spectrum
decaying as . We found that for ,
one-magnon excitations remain exponentially localized with the localization
length diverging as 1/E. For a faster divergence of is
obtained. For any , a phase of delocalized magnons emerges at the
bottom of the band. We characterize the scaling behavior of the localization
length on all regimes and relate it with the scaling properties of the
long-range correlated exchange coupling distribution.Comment: 7 Pages, 5 figures, to appear in Phys. Rev.
Polypodium leucotomos targets multiple aspects of oral carcinogenesis and it is a potential antitumor phytotherapy against tongue cancer growth
Introduction: Oral cancer refers to malignant tumors, of which 90% are squamous cell carcinomas (OSCCs). These malignancies exhibit rapid progression, poor prognosis, and often mutilating therapeutical approaches. The determination of a prophylactic and/or therapeutic antitumor role of the polyphenolic extract Polypodium leucotomos(PL) would be relevant in developing new tools for prevention and treatment.Methods: We aimed to determine the antitumor effect of PL by treating OSCC cell lines with PL metabolites and evaluating its action during OSCC progression in vivo.Results: PL treatment successfully impaired cell cycling and proliferation, migration, and invasion, enhanced apoptosis, and modulated macrophage polarization associated with the tumoral immune-inflammatory response of tongue cancer cell lines (TSCC). PL treatment significantly decreased the expression of MMP1 (p < 0.01) and MMP2 (p < 0.001), and increased the expression of TIMP1 (p < 0.001) and TIMP2 (p < 0.0001) in these cells. The mesenchymal-epithelial transition phenotype was promoted in cells treated with PL, through upregulation of E-CAD (p < 0.001) and reduction of N-CAD (p < 0.05). PL restrained OSCC progression in vivo by inhibiting tumor volume growth and decreasing the number of severe dysplasia lesions and squamous cell carcinomas. Ki-67 was significantly higher expressed in tongue tissues of animals not treated with PL(p < 0.05), and a notable reduction in Bcl2 (p < 0.05) and Pcna (p < 0.05) cell proliferation-associated genes was found in dysplastic lesions and TSCCs of PL-treated mice. Finally, N-cad(Cdh2), Vim, and Twist were significantly reduced in tongue tissues treated with PL.Conclusion: PL significantly decreased OSCC carcinogenic processes in vitro and inhibited tumor progression in vivo. PL also appears to contribute to the modulation of immune-inflammatory oral tumor-associated responses. Taken together, these results suggest that PL plays an important antitumor role in processes associated with oral carcinogenesis and may be a potential phytotherapeutic target for the prevention and/or adjuvant treatment of TSCC
Dysregulation of Transcription Factor Networks Unveils Different Pathways in Human Papillomavirus 16-Positive Squamous Cell Carcinoma and Adenocarcinoma of the Uterine Cervix
Squamous cell carcinoma (SCC) and adenocarcinoma (ADC) are the most common
histological types of cervical cancer (CC). The worse prognosis of ADC cases highlights
the need for better molecular characterization regarding differences between these
CC types. RNA-Seq analysis of seven SCC and three ADC human papillomavirus
16-positive samples and the comparison with public data from non-tumoral human
papillomavirus-negative cervical tissue samples revealed pathways exclusive to each
histological type, such as the epithelial maintenance in SCC and the maturity-onset
diabetes of the young (MODY) pathway in ADC. The transcriptional regulatory network
analysis of cervical SCC samples unveiled a set of six transcription factor (TF) genes
with the potential to positively regulate long non-coding RNA genes DSG1-AS1,
CALML3-AS1, IGFL2-AS1, and TINCR. Additional analysis revealed a set of MODY TFs
regulated in the sequence predicted to be repressed bymiR-96-5p ormiR-28-3p in ADC.
These microRNAs were previously described to target LINC02381, which was predicted
to be positively regulated by two MODY TFs upregulated in cervical ADC. Therefore, we
hypothesize LINC02381might act by decreasing the levels ofmiR-96-5p andmiR-28-3p,
promoting the MODY activation in cervical ADC. The novel TF networks here described
should be explored for the development of more efficient diagnostic tools
Pb and Cd on growth, leaf ultrastructure and essential oil yield mint (Mentha arvensis L.)
Estimativa dos impactos econÎmicos decorrentes de eventual introdução do huanglongbing (HLB) no estado da Bahia
PrevalĂȘncia do papilomavĂrus humano (HPV) em BelĂ©m, ParĂĄ, Brasil, na cavidade oral de indivĂduos sem lesĂ”es clinicamente diagnosticĂĄveis
Increasing the compressive strength of Portland cement concrete using flat glass powder
Aspectos ultra-estruturais das vilosidades intestinais apĂłs o clampeamento do pedĂculo hepĂĄtico de ratos
Canagliflozin and renal outcomes in type 2 diabetes and nephropathy
BACKGROUND Type 2 diabetes mellitus is the leading cause of kidney failure worldwide, but few effective long-term treatments are available. In cardiovascular trials of inhibitors of sodiumâglucose cotransporter 2 (SGLT2), exploratory results have suggested that such drugs may improve renal outcomes in patients with type 2 diabetes. METHODS In this double-blind, randomized trial, we assigned patients with type 2 diabetes and albuminuric chronic kidney disease to receive canagliflozin, an oral SGLT2 inhibitor, at a dose of 100 mg daily or placebo. All the patients had an estimated glomerular filtration rate (GFR) of 30 to <90 ml per minute per 1.73 m2 of body-surface area and albuminuria (ratio of albumin [mg] to creatinine [g], >300 to 5000) and were treated with reninâangiotensin system blockade. The primary outcome was a composite of end-stage kidney disease (dialysis, transplantation, or a sustained estimated GFR of <15 ml per minute per 1.73 m2), a doubling of the serum creatinine level, or death from renal or cardiovascular causes. Prespecified secondary outcomes were tested hierarchically. RESULTS The trial was stopped early after a planned interim analysis on the recommendation of the data and safety monitoring committee. At that time, 4401 patients had undergone randomization, with a median follow-up of 2.62 years. The relative risk of the primary outcome was 30% lower in the canagliflozin group than in the placebo group, with event rates of 43.2 and 61.2 per 1000 patient-years, respectively (hazard ratio, 0.70; 95% confidence interval [CI], 0.59 to 0.82; P=0.00001). The relative risk of the renal-specific composite of end-stage kidney disease, a doubling of the creatinine level, or death from renal causes was lower by 34% (hazard ratio, 0.66; 95% CI, 0.53 to 0.81; P<0.001), and the relative risk of end-stage kidney disease was lower by 32% (hazard ratio, 0.68; 95% CI, 0.54 to 0.86; P=0.002). The canagliflozin group also had a lower risk of cardiovascular death, myocardial infarction, or stroke (hazard ratio, 0.80; 95% CI, 0.67 to 0.95; P=0.01) and hospitalization for heart failure (hazard ratio, 0.61; 95% CI, 0.47 to 0.80; P<0.001). There were no significant differences in rates of amputation or fracture. CONCLUSIONS In patients with type 2 diabetes and kidney disease, the risk of kidney failure and cardiovascular events was lower in the canagliflozin group than in the placebo group at a median follow-up of 2.62 years