Status and progress of treatment methods for root caries in the last decade: a literature review

The aim of this literature review is to explore the treatment methods for root caries in laboratory and clinical research in the last decade. A systematic search of publications in PubMed and Web of Science databases was performed. The timespan was limited to the last 10 years and English language. Further retrieval was conducted using the search terms of specific therapies or treatments. Eighty‐two articles were included in this systematic review and full texts were retrieved. Types of studies included laboratory studies and clinical trials. Therapeutic approaches for root caries without risk of pulp exposure can be categorized into non‐invasive and restorative treatment. Non‐invasive treatments which targeted different causative factors of root caries have been developed in the last decade. Accordingly, several artificial caries model systems have been proposed for the study of root caries in the laboratory. Carious tissue excavation techniques and restorative materials and procedures have been modified to improve the prognosis of invasive treatment. It is of importance to determine the most appropriate therapy for root caries and further clinical trials are needed to draw firm conclusions concerning the efficacy and consistency of the various treatment methods proposed.     

The opposing roles of NOTCH signalling in head and neck cancer: a mini review

NOTCH signalling can exert oncogenic or tumour suppressive effects in both solid and haematological malignancies. Similar to T‐cell acute lymphoblastic leukaemia (T‐ALL), early studies suggested a pro‐tumorigenic role of NOTCH in head and neck squamous cell carcinoma (HNSCC), mainly based on the increased expression levels of the genes within the pathway. Recently, data from exome sequencing analyses unexpectedly pointed to a tumour suppressor role for NOTCH in HNSCC by identifying loss‐of‐function mutations in the NOTCH1 gene in a significant proportion of patients. These data have questioned the accepted role of NOTCH in HNSCC and the possible rationale of targeting NOTCH in this disease. This review summarises the current information on NOTCH signalling in HNSCC and discusses how this pathway can apparently exert opposing effects within the same disease.     

Phenotype study of fresh and cultured hairy cells with the use of immunologic markers and electron microscopy

The phenotype of fresh and cultured leukemic cells from patients with hairy cell leukemia was studied using a panel of monoclonal antibodies in addition to the detection of peroxidase activity under electron microscopy. In fresh samples, the leukemic cells from 11 patients displayed predominantly a B phenotype, as judged by their reactivity with the B1 monoclonal antibody and surface immunoglobulin expression. Ultrastructural peroxidase activity, characteristic of hairy cells, was observed in all cases studied. When hairy cells were cultured in the presence of phytohemagglutinin and irradiated T cells, their phenotype converted from surface Ig+, B1+, OKT3-, OKT11- to surface Ig-, B1+, OKT3-, OKT11+. In contrast, the peroxidase activity remained unchanged. Some hairy cells were also OKM1+, but no conclusion could be made about the MO2 antigen, a more specific marker of monocytes. The variability of the phenotype in vivo and in vitro indicates that reliable markers are required for identifying hairy cells. When studied together, the staining by B1 monoclonal antibody and the ultrastructural detection of peroxidase, enable the identification of hairy cells with certainty.     

Differentiation-linked expression of cell surface markers on HL-60 leukemic cells

The cell surface antigenic phenotype of HL-60, a human acute promyelocytic leukemia cell line, has been analyzed before and after maturation induction with dimethylsulfoxide (DMSO) using a panel of markers including a "library" of monoclonal antibodies and "conventional" antisera in conjunction with the fluorescene-activated cell sorter. HL-60 cells express granulocyte and "leukocyte" differentiation antigens but not antigens of the lymphoid, platelet, and erythroid lineages. DMSO-induced morphological maturation was found to be associated with a decrease in the proportion of cells in mitotic cycle, induction of C3d receptors, increased expression of granulocytic and leukocyte antigens, and diminished expression of HLA-A,B,C and beta 2-microglobulin determinants. HL-60 cells have no detectable expression of HLA-DR-associated determinants as assayed by rabbit anti-p28,33 monoclonal anti-HLA-DR (monomorphic determinant), and HLA-DRw typing alloantisera. The relationship of these changes in cell surface properties to normal granulocytic differentiation is discussed.     

Clonal rearrangement and expression of the T cell receptor beta gene and involvement of the breakpoint cluster region in blast crisis of CGL

A case of lymphoid blast crisis of Ph1-positive CGL is described in which the blast cells had an immature T cell phenotype, clonal rearrangement and expression of the T cell receptor beta gene, and a rearrangement of the breakpoint cluster region (bcr) on chromosome 22. This case therefore provides definite evidence for transformation involving a common myeloid-T lineage progenitor, penetrance of the Ph1 molecular alteration into the T cell lineage, and clonal selection in blast crisis at the level of a committed T lineage precursor.     

New glucose-6-phosphate dehydrogenase mutations associated with chronic anemia

We have identified the glucose-6-phosphate dehydrogenase mutations responsible for enzyme deficiency in nine individuals with chronic nonspherocytic hemolytic anemia. We found the variants Tokyo, Iowa, Shinshu, and Guadalajara in British subjects and Kobe in an Italian. In addition we have determined the variant Corum has the mutation 820 G-- >A and have found in British subjects the mis-sense mutations 224 T-- >C, 488 G-->A and 833 C-->T which have not been described before. Some, but not all, of the mutations involve amino acids located near putative substrate binding sites.     

Body weight, metabolism and clock genes

Background

The metabolic syndrome has been described in children; however, a standard criterion has not been established for its diagnosis. Also, few studies have been conducted to specifically observe the possible existence of agreement among the existing diagnostic criteria. The purpose of the study is to evaluate agreement concerning prevalence rates of the metabolic syndrome diagnosed by six different criteria in overweight schoolchildren in the city of Botucatu - SP -Brazil.

Methods

This is a cross-sectional study on 128 overweight schoolchildren. Clinical examination included anthropometry, pubertal staging evaluation, and blood pressure. Triacylglycerol, glycemia, HDL-cholesterol, insulin levels, and HOMA-IR were determined. The Kappa index, the Mann-Whitney test and the chi-square test were used for statistical analysis.

Results

The prevalence of the metabolic syndrome varied from 10 to 16.5% according to different diagnostic criteria. Results were similar for boys and girls and pubertal stage. Great agreement was observed among the six different diagnostic criteria for the metabolic syndrome.

Conclusions

Different diagnostic criteria, when adopted for subjects with similar demographic characteristics, generate similar and compatible prevalence. Results suggest that it is possible to adopt any of the analyzed criteria, and the choice should be according to the components available for each situation.