Search

A patient, diagnosed with a combination of level 3 endemic dental fluorosis and degree 1 tetracycline staining, was treated sequentially by macroabrasion techniques and nightguard vital bleaching. Various pairings of diamond and carbide burs, abrasive disks, rotary polishing points, and diamond polishing pastes were tested to obtain the optimal combination for macroabrasion. This conservative treatment regimen produced results that were termed "excellent" by the patient and met the goals of the dentists. (Quintessence Int 2003;34: 87-91) [ABSTRACT FROM AUTHOR]

Background: Delayed gastric emptying is a non-motor symptom of Parkinson's disease. Few data exist on gastric emptying in early-stage Parkinson's disease. In idiopathic rapid-eye-movement sleep behavior disorder, a presumable pre-motor stage of Parkinson's disease, gastric emptying has not yet been investigated.Methods: Twenty healthy controls, 13 patients with idiopathic rapid-eye-movement sleep behavior disorder, and 39 patients with Parkinson's disease patients underwent standardized testing for gastric emptying with the (13)C-octanoate breath test.Results: Gastric emptying was significantly delayed in drug-naïve (P < .001) and in treated Parkinson's disease patients (P < .001), but normal in patients with idiopathic rapid-eye-movement sleep behavior disorder.Conclusions: Our study confirms delayed gastric emptying in drug-naïve, early-stage Parkinson's disease. Normal gastric emptying in idiopathic rapid-eye-movement sleep behavior disorder might be explained by the fact that neurodegenerative changes in structures modulating gastric motility are not severe enough to cause a functional deficit that can be detected by the (13)C-octanoate breath test. [ABSTRACT FROM AUTHOR]

Previous studies have shown a correlation between the production of certain matrix metalloproteinases (MMPs), especially the gelatinases, by malignant tumors and the progression of these cancers as they invade and metastasize through the extracellular matrix and basement membranes. However, very few of these studies examined this relation- ship in human oral cancer in vivo, and none addressed the issue of how combinations of the MMPs may further enhance tumor progression. To determine which MMPs are produced in vivo by human oral cancers, we used specific anti-human-MMP antibodies and immunocytochemistry (ICC) methods to examine oral cancer tissue specimens from 20 surgery patients. The ICC data indicated that 72-kDa (72K-GL) and 92-kDa gelatinases (92K-GL) were produced in vivo by discreet clusters of tumor cells and by stromal fibroblasts, vascular endothelial cells (72K-GL), and PMNs (92K-GL). Some stromal fibroblasts near the tumors also appeared to produce fibroblast-type collagenase (FIB-CL), a finding confirmed by Western blot analysis of media conditioned by oral tumor explant cultures. ICC results indicated that 5 of the 20 tumors coincidentally produced all three MMPs. To examine how the two gelatinases and FIB-CL may interact in vitro to degrade fibrillar type I collagen, a major structural component of the extracellular matrix, we used a modified FIB-CL activity assay. Combinations of the gelatinases and FIB-CL were incubated with a ³H-collagen substrate, with the results compared with the combination of stromelysin-1 (SL-1, a superactivator of FIB-CL) and FIB-CL. 92K-GL caused a nine-fold increase in collagenase activity, equivalent to SL-1, while 72K-GL produced a four-fold increase. These results indicate that human oral cancers produce 92K-GL, 72K-GL, and FIB-CL in vivo and that the gelatinases and FIB-CL cooperate to enhance collagen degradation greatly in vitro. [ABSTRACT FROM AUTHOR]

Matrix metalloproteinases (MMPs) are a family of nine or more highly homologous Zn++- endopeptidases that collectively cleave most if not all of the constituents of the extracellular matrix. The present review discusses in detail the primary structures and the overlapping yet distinct substrate specificities of MMPs as well as the mode of activation of the unique MMP precursors. The regulation of MMP activity at the transcriptional level and at the extracellular level (precursor activation, inhibition of activated, mature enzymes) is also discussed. A final segment of the review details the current knowledge of the involvement of MMP in specific developmental or pathological conditions, including human periodontal diseases. [ABSTRACT FROM AUTHOR]

A critical outcome of periodontal disease is degradation of the collagenous periodontal ligament that connects teeth to bone in the dental arch. Periodontal diseases occur in response to bacterial colonization of the teeth, but their molecular pathogenesis is still speculative. One family of enzymes, known as the matrix metalloproteinases (MMPs), has been implicated in the degradation of the periodontal ligament. MMPs, which are also suspected to play a role in many other physiologic and pathologic remodeling processes, can be secreted by epithelial cells surrounding the teeth and are found in relative abundance in tissues and fluids near periodontally diseased sites. Since most MMPs are secreted as inactive zymogens which may be activated by limited proteolysis, it has been suggested that proteinases expressed by the infecting periodontal pathogens might activate latent host MMPs to initiate or accelerate degradation of the collagenous periodontal ligament. The aim of this work was to examine interactions between purified host MMPs and bacterial proteinase. In this article, we demonstrate that a proteinase isolated from the periodontopathogen Porphyromonas gingivalis can activate MMP-1, MMP-3, and MMP-9 and can catalyze the superactivation of MMP-1 by MMP-3. Activation of these MMPs is demonstrated to result from initital hydrolysis within their propeptide. Also, for MMP-1 and MMP-9, the P. gingivalis proteinase cleaves the MMP propeptide following a lysine residue at a previously unreported site which, for both MMPs, is one residue NH2- terminal to the known autocatalytic cleavage site. These data describe a mode of virulence for the periodontopathogen Porphyromonas gingivalis that involves activation of host-degradative enzymes. [ABSTRACT FROM AUTHOR]

Background: Web-based self-help interventions for parents of children with ADHD and other externalizing disorders have been proven to be effective. In order to recommend individualized and optimized interventions, a better understanding of the acceptance and utilization of this innovative treatment approach is needed. Previous research has frequently employed subjective reports of utilization, but the validity of these studies may be limited., Methods: Data from the German WASH study were used. Participants (n = 276) were randomly assigned to the intervention condition (a) web-based self-help or (b) web-based self-help with optional telephone-based support calls. Data collection took place at baseline (T1) and 12 weeks later (T2). Utilization data were tracked using a log file generated for each participant at T2. Prediction models were calculated using CART (Classification and Regression Trees), a method known mostly from the field of machine learning., Results: Acceptance, of the intervention as defined in this paper was very high on objective (89.4% have taken up the intervention) and subjective measures (91.4% reported having used the intervention and 95.3% reported they would recommend the intervention to a friend). The average number of logins corresponded to recommendations. Predictors of acceptance and predictors of utilization were similar and included, e.g., child's externalizing symptoms, parental psychopathology, and above all additional telephone-based support by counselors., Conclusions: Through a detailed identification of acceptance and utilization, and the predictors thereof, we were able to gain a better understanding of the acceptance and utilization of web-assisted self-help for a parent management intervention in the treatment of children with ADHD and ODD. These findings can be used to recommend web-based interventions to particularly suitable families. It should be noted that some form of support is required for an intensive engagement with the content of the program., Trial Registration: The protocol of the study (German Clinical Trials Register DRKS00013456 conducted on January 3rd, 2018) was approved by the Ethics Committee of the University Hospital, Cologne., (© 2024. The Author(s).)

NKG2D is an activating receptor of natural killer cells that recognizes stress-induced ligands (NKG2DL) expressed by many tumor cells. Nevertheless, NKG2DL downregulation or shedding can still allow cancer cells to evade immune surveillance. Here, we used lentiviral gene transfer to engineer clinically usable NK-92 cells with a chimeric antigen receptor (NKAR) which contains the extracellular domain of NKG2D for target recognition, or an NKAR, together with the IL-15 superagonist RD-IL15, and combined these effector cells with recombinant NKG2D-interacting bispecific engagers that simultaneously recognize the tumor-associated antigens epidermal growth factor receptor (EGFR) or ErbB2 (HER2). Applied individually, in in vitro cell-killing assays, these NKAB-EGFR and NKAB-ErbB2 antibodies specifically redirected NKAR-NK-92 and NKAR&#95;RD-IL15-NK-92 cells to glioblastoma and other cancer cells with elevated EGFR or ErbB2 levels. However, in mixed glioblastoma cell cultures, used as a model for heterogeneous target antigen expression, NKAR-NK cells only lysed the EGFR- or ErbB2-expressing subpopulations in the presence of one of the NKAB molecules. This was circumvented by applying NKAB-EGFR and NKAB-ErbB2 together, resulting in effective antitumor activity similar to that against glioblastoma cells expressing both target antigens. Our results demonstrate that combining NK cells carrying an activating NKAR receptor with bispecific NKAB antibodies allows for flexible targeting, which can enhance tumor-antigen-specific cytotoxicity and prevent immune escape.