Effect of Propolis mouthwash on plaque and gingival indices over fixed orthodontic patients

In patients with fixed orthodontics, the presence of orthodontic appliances causes dental plaque accumulation and hygiene problems. The purpose of this study was to evaluate the effect of Propolis and chlorhexidine mouthwashes on plaque and gingival indices in patients who are undergoing orthodontic treatment. In this triple blind study, in total, 37 patients aged from 15 to 35 years those who have been undergoing fixed orthodontic treatment were studied. After that, one of the mouthwashes that containing either Propolis or Chlorhexidine was randomly prescribed to patients. The patients were asked to use mouthwashes twice a day after brushing their teeth for three weeks consecutively. Indicators of plaque, gingival and periodontal status (PI, GI, CPI) were determined on Ramford teeth at the beginning and at the end of three weeks for each patient. Then the results were analyzed statistically. The difference between the values of plaque index (P<0.001), gingival index (P=0.006) and periodontal index (P= 0.005) before and after administration of Propolis were statistically significant. The difference was also statistically significant for all three indexes of plaque (P<0.001), gingival (P=0.001) and periodontal (P=0.003) before and after chlorhexidine mouthwash usage. The indices after using mouthwashes were not statistically significant different between two mouthwash groups. It seems that Propolis mouthwash can be used as a suitable alternative in patients with fixed orthodontic treatment without the side effects of chlorhexidine mouthwash

Molecular characterization of Portuguese patients with hereditary cerebellar ataxia

© 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).Hereditary cerebellar ataxia (HCA) comprises a clinical and genetic heterogeneous group of neurodegenerative disorders characterized by incoordination of movement, speech, and unsteady gait. In this study, we performed whole-exome sequencing (WES) in 19 families with HCA and presumed autosomal recessive (AR) inheritance, to identify the causal genes. A phenotypic classification was performed, considering the main clinical syndromes: spastic ataxia, ataxia and neuropathy, ataxia and oculomotor apraxia (AOA), ataxia and dystonia, and ataxia with cognitive impairment. The most frequent causal genes were associated with spastic ataxia (SACS and KIF1C) and with ataxia and neuropathy or AOA (PNKP). We also identified three families with autosomal dominant (AD) forms arising from de novo variants in KIF1A, CACNA1A, or ATP1A3, reinforcing the importance of differential diagnosis (AR vs. AD forms) in families with only one affected member. Moreover, 10 novel causal-variants were identified, and the detrimental effect of two splice-site variants confirmed through functional assays. Finally, by reviewing the molecular mechanisms, we speculated that regulation of cytoskeleton function might be impaired in spastic ataxia, whereas DNA repair is clearly associated with AOA. In conclusion, our study provided a genetic diagnosis for HCA families and proposed common molecular pathways underlying cerebellar neurodegeneration.This work was funded by National Funds through FCT—Fundação para a Ciência e a Tecnologia, I.P., under the project UIDB/04293/2020. It was also supported in part by the FCT grant FCT-ANR/BEX-GMG/0008/2013; the Porto Neurosciences and Neurologic Disease Research Initiative at the i3S (Norte-01-0145-FEDER-000008), supported by Norte Portugal Regional Operational Programme (NORTE 2020) under the PORTUGAL 2020 Partnership Agreement, also through FEDER; and by GenomePT (POCI-01-0145-FEDER-022184). M.S. was the recipient of a fellowship (SFRH/BPD/116046/2016) and acknowledges funding from FCT through program DL 57/2016—Norma Transitória.info:eu-repo/semantics/publishedVersio

Improvement of printing and writing paper properties using PCC Filler Modified by cationic starch modified precipitated calcium carbonate filler

Aim of this study is precipitated calcium carbonate cationic modification and comparison of impact of using its with conventional filler (unmodified) on strength properties of paper. One of the defects of adding fillers to paper is decreasing of mechanical strength of paper because of reduction in bonding area between fibers. In this study whit purpose of maintaining the strength of paper, and change the surface charge of precipitated calcium carbonate and replace it with conventional fillers are used.in this research with aim of precipitated calcium carbonate and replacing it with conventional filler was used. Condition of cationic precipitated calcium carbonate preparation was 90 ċ temperature, 3 hours time and 55% water content of cooking process. loading amount of starch was 9, 12 and 15 percent based on precipitated calcium carbonate weight.Papers made at three level: 10, 16, 30 percent of filler in paper sheets contain conventional fillers were compared. Results indicated that papers containing modified-filler have more values of retention rather than those with unmodified filler, both in 20% and 30% filler dosages.papers contained cationic filler have more mechanical strength index in respect of papers contained conventional fillers

Comprehensive analysis of copy number variation in a Turkish dementia cohort

BACKGROUND: Copy number variants (CNVs) include deletions or multiplications spanning genomic regions. These regions vary in size and may span genes known to play a role in human diseases. As examples, duplications and triplications of SNCA have been shown to cause forms of Parkinson’s disease, while duplications of APP cause early onset Alzheimer’s disease (AD). RESULTS: Here, we performed a systematic analysis of CNVs in a Turkish dementia cohort in order to further characterize the genetic causes of dementia in this population. One hundred twenty-four Turkish individuals, either at risk of dementia due to family history, diagnosed with mild cognitive impairment, AD, or frontotemporal dementia, were whole-genome genotyped and CNVs were detected. We integrated family analysis with a comprehensive assessment of potentially disease-associated CNVs in this Turkish dementia cohort. We also utilized both dementia and non-dementia individuals from the UK Biobank in order to further elucidate the potential role of the identified CNVs in neurodegenerative diseases. We report CNVs overlapping the previously implicated genes ZNF804A, SNORA70B, USP34, XPO1, and a locus on chromosome 9 which includes a cluster of olfactory receptors and ABCA1. Additionally, we also describe novel CNVs potentially associated with dementia, overlapping the genes AFG1L, SNX3, VWDE, and BC039545. CONCLUSIONS: Genotyping data from understudied populations can be utilized to identify copy number variation which may contribute to dementia. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s40246-021-00346-z