- Kikuchi-Fujimoto disease diagnosed by correlating skin and lymph node biopsies. [Case Reports]
- JCJAAD Case Rep 2019; 5(5):416-418
- The Effect of Hookah Use on Buccal Mucosa: Evaluation of Repair Index [Journal Article]
- APAsian Pac J Cancer Prev 2019 Apr 29; 20(4):1109-1112
- CONCLUSIONS: The percentages of cells with micronucleus, karyorrhexis, karyolysis, and broken egg in the buccal mucosa of hookah users were significantly higher than those in control group; in addition, the repair index of the buccal mucosa cells in hookah users was significantly lower than that in the control group.
- Curcuma longa extracts suppress pathophysiology of experimental hepatic parenchymal cell necrosis. [Journal Article]
- PPathophysiology 2019; 26(2):153-162
- The study sought to investigate the protective potentials of Curcuma longa rhizome following potassium bromate-induced liver injury in Wistar rats. Thirty-five male Wistar rats were divided into 7 gr…
The study sought to investigate the protective potentials of Curcuma longa rhizome following potassium bromate-induced liver injury in Wistar rats. Thirty-five male Wistar rats were divided into 7 groups of 5 rats each (n = 5). Control group received normal saline while the other groups received oral administration of 100 mg/kg potassium bromate daily for two weeks to induce hepatic injury. Negative control I rats were sacrificed immediately after induction of hepatic injury, while the test groups were given oral dose of ethanol extract of Curcuma longa rhizome (EECLOR) at 100, 200 and 400 mg/kg for two weeks. Positive control group was treated with Silymarin for two weeks, while negative control II group was observed for the two-week period. At the end of the study, serum biochemical parameters of liver function enzymes, malondialdehyde and histopathological changes were investigated. Necrotic hepatocytes were quantified in H&E-stained liver sections using the morphologic criteria of typical necrotic tissue. Hepatocytes that remained intact were identified as those with round euchromatic nuclei with prominent nucleoli. Histological examination and morphological grading of the stained sections showed massive necrosis across the zones. EECLOR improved liver functions evidenced by reduced activity of serum amino transferases. It also reduced lipid peroxidation. In addition, there was significant reduction of hepatocytes showing morphological criteria of necrosis in EECLOR-treated rats across the zones, with appreciable radial sinusoidal arrangement. In conclusion, the protective actions of EECLOR against potassium bromate liver toxicity in rats, appears to be due to its ability to reduce lipid peroxidation.
- Utility of DNA-Specific Stains in Micronuclei Assay as a Marker of Genotoxicity in Oral Potentially Malignant Disorders and Oral Squamous Cell Carcinoma. [Journal Article]
- JCJ Cytol 2019 Apr-Jun; 36(2):111-115
- CONCLUSIONS: Malignant transformation is accompanied by loss of cell capacity to evolve to death in situations of DNA damage. These findings indicate that nuclear anomalies may be misinterpreted as MN with nonspecific DNA stains and lead to false-positive results in studies with cells of epithelial origin.
- A tetravalent single chain diabody (CD40/HER2) efficiently inhibits tumor proliferation through recruitment of T cells and anti-HER2 functions. [Journal Article]
- MIMol Immunol 2019; 109:149-156
- Our aim was to construct a CD40×HER2 single chain diabody (ScDb) and determine its tumor-specific immune activation and anti-HER2 function. Overlap extension-polymerase chain reaction was applied in …
Our aim was to construct a CD40×HER2 single chain diabody (ScDb) and determine its tumor-specific immune activation and anti-HER2 function. Overlap extension-polymerase chain reaction was applied in the construction of ScDb, and the protein was expressed with the pET28a (+)-Rosetta prokaryotic expression system. Soluble ScDb was purified by a nickel-nitrilotriacetic acid column. Dendritic cells (DC) was stimulated by ScDb and inhibited 4T1 cells proliferation in vitro. In 4T1 tumor mice model, lymphocyte infiltration was prominently detected in ScDb group, Caspase-3 expression was significantly upregulated. ScDb was labeled using quantum dots. Immunofluorescence assay indicated ScDb exhibited high affinity to HER2. T6-17 cells were inhibited by ScDb in vitro. The phosphorylation and expression levels of AKT, ERK were markedly decreased. In T6-17 tumor mice model. Compared to CD40 ScFv, HER2 ScFv and normal saline groups, tumor volume diminished significantly in ScDb group, and tumor cells showed extensive deformation, and pervasive karyopyknosis and karyorrhexis were found. In the present study, we successfully constructed a ScDb fragment and expressed it using a prokaryotic expression system. The in vivo and in vitro experimental results indicated that ScDb could inhibit the proliferation of tumor cells by stimulating the tumor-specific immunoreaction and blocking the HER2-related signaling pathway.
- Predictors of differential response to induction therapy in high-risk neuroblastoma: A report from the Children's Oncology Group (COG). [Journal Article]
- EJEur J Cancer 2019; 112:66-79
- CONCLUSIONS: Improved end-induction response in high-risk neuroblastoma is associated with longer survival. Patients with 11q LOH are less likely to respond to induction therapies and should be prioritised for novel approaches in future trials.
- Kolaviron Protects the Prefrontal Cortex and Hippocampus against Histomorphological and Neurobehavioural Changes in Cuprizone Model of Multiple Sclerosis. [Journal Article]
- MJMalays J Med Sci 2018; 25(2):50-63
- CONCLUSIONS: Kv provides protective roles against CPZ-induced neurotoxicity through prevention of ribosomal protein degradation.
- [Evaluation of genetic damage and eating habits in children with normal weight and obesity in school age]. [Journal Article]
- NHNutr Hosp 2019 Apr 10; 36(2):309-314
- Introduction: obesity is a worldwide problem that predisposes to other health conditions. A direct relationship has been shown between obesity and genetic damage; the late is considered as an early m…
Introduction: obesity is a worldwide problem that predisposes to other health conditions. A direct relationship has been shown between obesity and genetic damage; the late is considered as an early marker of cancer in some cases. Objective: to evaluate the genetic damage and eating habits of children with obesity and normal weight. Methods: cross-sectional study conducted in school-age children. Genetic damage was assessed from buccal epithelial mucosal cells, through the quantification of nuclear abnormalities such as micronuclei, karyorrhexis, caryolysis, pyknosis and the presence of two nuclei. The nutritional evaluation was carried out through the analysis of weight, height and the evaluation of their diet through nutritional clinical records. Results: no significant differences were found in the number of nuclear abnormalities between the groups studied. However, some children with obesity showed higher number of nuclear abnormalities compared with children with normal weight. Regarding their eating habits, a positive correlation was found between weight and the consumption of free sugars and proteins in the diet. Conclusions: the lack of evidence that correlates micronuclei with nutritional status suggests that the presence of these abnormalities can be attributed to environmental or epigenetic factors. Special attention requires the study of diets similar to those habitually consumed by this population, in order to avoid their potential consequences. This study represents an important contribution in the evaluation of the possible health risks associated with childhood obesity.
- Periodontitis: Genomic instability implications and associated risk factors. [Journal Article]
- MRMutat Res Genet Toxicol Environ Mutagen 2019; 840:20-23
- Periodontitis is a bacterial infection characterized by the presence of a dense inflammatory infiltrate, which may result in increased DNA damage and other nuclear/cellular abnormalities. Therefore, …
Periodontitis is a bacterial infection characterized by the presence of a dense inflammatory infiltrate, which may result in increased DNA damage and other nuclear/cellular abnormalities. Therefore, it is important to evaluate the periodontal diseases influence on DNA damage and other nuclear/cellular abnomalies formation as cancer risk markers. Thus, the aim of this study was to evaluate the periodontal diseases effect, according to its severity, on the occurrence of DNA damage and other nuclear/cellular abnormalities. This is a cross-sectional study with 77 subjects from the dentistry clinic of the University of Santa Cruz do Sul, Brazil, divided in control group (26 subjects), moderate periodontal disease group (26 subjects) and severe periodontal disease group (25 subjects). All subjects answered self-referenced questionnaires, underwent periodontal clinical examinations and allowed the collection of oral mucosa cells for the BMCyt. In relation to DNA damage biomarkers (micronuclei (MN) and/or nuclear buds (NBUD)), our results indicated no increase in MN frequencies (p > 0.05), however it indicated significant difference in NBUD frequencies between groups (p < 0.024). This result suggests that the periodontal disease status may influence DNA damage. Regarding the other nuclear/cellular abnormalities, was observed a significant difference in the binucleated (BN) frequencies between groups (p < 0.05). Moreover, the periodontitis severity was associated to an increase in the combined (summed) frequency of cells with different levels of DNA damage (MN and/or NBUD), cytokinetic defects (BN cells) and/or cell death (karyorrhexis, pyknotic and karyolytic cells) (r = 0.235; p = 0.040). Periodontal disease depending on its severity, induces nuclear anomalies in buccal cells.
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- Thymoquinone and curcumin modify iNOS, caspase-3, and thioredoxin immunohistochemical expression in acetaminophen (APAP) hepatotoxicity. [Journal Article]
- FMFolia Morphol (Warsz) 2019 Mar 05
- Acetaminophen (APAP) hepatotoxicity is characterized by an extensive oxidative stress due to depletion of glutathione (GSH), which results in massive lipid peroxidation and subsequent liver injury. T…
Acetaminophen (APAP) hepatotoxicity is characterized by an extensive oxidative stress due to depletion of glutathione (GSH), which results in massive lipid peroxidation and subsequent liver injury. The current paradigm suggests that mitochondria are the main source of reactive oxygen species (ROS), which impair mitochondrial function and are responsible for cell signaling resulting in cell death. This study was designed to compare the potential impact of thymoquinone (THQ), and/or curcumin (CURC) on liver injury induced by APAP toxicity in rats. Serum levels of alanine transaminase (ALT), aspartate transaminase (AST), total bilirubin, and total protein were measured. In addition, liver nitric oxide (NO), malondialdehyde (MDA), reduced glutathione (GSH), and superoxide dismutase (SOD) were estimated. Moreover, these biochemical parameters were confirmed by histopathological and immunohistochemical investigations for the expression of thioredoxin, iNOS and caspase 3. Acetaminophen toxicity elevated most of the above-mentioned parameters but decreased GSH, SOD, and total protein levels. Histologically, liver sections demonstrated liver injury characterized by hepatocellular necrosis with nuclear pyknosis, karyorrhexis and karyolysis. Immunohistochemical study revealed increased expression of iNOS and caspase 3 proteins, while the thioredoxin protein expression was decreased. Treatment with the THQ and CURC regulated the biochemical and histopathological alterations induced by APAP toxicity. It was concluded that the combination strategy of THQ and CURC might be considered as a potential antidote in combating liver injury induced by APAP with minimal side effects.