Patho-morphological study of the supplemental groove

The following results have been obtained in consequence of patho-morphological examination regarding the supplemental groove.1. Light microscopic observation of cross-sectioned supplemental grooves revealed that most of them were shallow in the form of plate or bowl. Some of the supplemental grooves had contents not described in the past and the structure of the contents was not clear under a light microscope. The contents were found in 22% of the supplemental grooves examined.2. The contents in supplemental grooves which were confirmed under a light microscope were found to consist of enamel itself when examined by means of an electron microscope. Microhardness measurements of this enamel showed less than one third the values of normal enamel. By means of microradiography, it was established that radiolucency of this enamel was, for the most part, much higher than normal enamel.3. It was ascertained that enamel with low hardness and high radiolucency constitutes the contents of supplemental grooves. Judging from its tissue properties, the contents were believed to be susceptible to attack by caries. This view was supported by the results of an investigation of caries sites in supplemental grooves.L’examen morpho-pathologique de sillons surnuméraires a donné les résultats suivants:1. En coupes transversales observées en microscopie classique, les sillons surnuméraires apparaissent peu profonds, en forme d’assiette ou de coupe. Dans certains, on trouve un contenu, non encore décrit dans la littérature et dont la structure n’apparaît pas nettement en microscopie classique. On trouve ce contenu dans 22% des sillons surnuméraires étudiés.2. Etudié en microscopie électronique à transmission, le contenu des sillons surnuméraires apparaît fait d’émail. Les mesures de dureté indiquent pour cet émail des valeurs inférieures d’un tiers à celles de l’émail normal. La microradiographie montre que cet émail est, en général, beaucoup moins radiodense que l’émail normal.3. Etant donné que le contenu des sillons surnuméraires s’est révélé être un émail de faible dureté et de faible radiodensité, on peut considérer que, par ses propriétés tissulaires, cet émail est sensible à l’attaque carieuse. Cette hypothèse est corroborée par les résultats de l’étude des sites carieux dans les sillons surnuméraires

On the size of apical foramen in anterior teeth, bicuspids and molars

The present authors have used a replica method to obtain area size measurements for the apical foramen in 4,613 human permanent teeth, and have obtained the following results:1. The morphology of the apical foramen is rich in variety which make it difficult to express its accurate size using foramen diameter measurement. It is therefore more appropriate to determine its size as an area measurement.2. Much variation was observed in the size of the apical foramen even for teeth of the same type. It was, however, also observed that the foramen is smaller in smaller types of teeth and larger in larger types of teeth. It was also observed that, in teeth of the same type, those with a greater number of roots have smaller foramen than those with a smaller number of roots.Les auteurs ont utilisé la méthode des répliques pour mesurer la surface des foramen apicaux de 4.613 dents humaines définitives. Les résultats obtenus ont été les suivants:1. La morphologie du foramen apical est à ce point variée qu’il est difficile d’exprimer sa taille précise en mesurant le diamètre du foramen. De ce fait il est préférable de déterminer sa dimension par une mesure de surface.2. Un grand nombre de variations ont même été observées dans la dimension du foramen apical pour les dents du même type. Cependant, il a été aussi observé que le foramen est plus petit dans les dents de type petit et plus larges dans les dents de grand type. Il a été constaté également que dans les dents de même type, celles comptant un plus grand nombre de racines possèdent des foramen plus petits que ceux des dents dont les racines sont moins nombreuses

Histology of tbe fissure contents in completely impacted teeth

Nous avons étudié les fissures occlusales et leur contenu au niveau de dents complètement incluses à l’aide du microscope optique et électronique et obtenu quelques résultats intéressants. C’est-à-dire au microscope optique, l’examen des coupes de fissures ont montré:a) Un certain nombre de fissures étaient comblées.b) D’autres étaient comblées à certains endroits limités, localisés le long des murs de la fissure.c) D’autres enfin ne contenaient rien et les fissures étaient pratiquement vides.La fine structure du contenu des fissures ne pouvait pas être précisée au microscope optique et l’interprétation ne peut qu’être subjective.Observés au microscope électronique, les dépôts comblant les fissures se sont avérés être de l’émail hypominéralisé

Decrease of miR-146b-5p in Monocytes during Obesity Is Associated with Loss of the Anti-Inflammatory but Not Insulin Signaling Action of Adiponectin

Background: Low adiponectin, a well-recognized antidiabetic adipokine, has been associated with obesity-related inflammation, oxidative stress and insulin resistance. Globular adiponectin is an important regulator of the interleukin-1 receptor-associated kinase (IRAK)/NFkB pathway in monocytes of obese subjects. It protects against inflammation and oxidative stress by inducing IRAK3. microRNA (miR)-146b-5p inhibits NFkB-mediated inflammation by targeted repression of IRAK1 and TNF receptor-associated factor-6 (TRAF6). Therefore, we measured the expression of miR-146b-5p in monocytes of obese subjects. Because it was low we determined the involvement of this miR in the anti-inflammatory, antioxidative and insulin signaling action of globular adiponectin. Methods: miR-146b-5p expression in monocytes of obese subjects was determined by qRT-PCR. The effect of miR-146b-5p silencing on molecular markers of inflammation, oxidative stress and insulin signaling and the association with globular adiponectin was assessed in human THP-1 monocytes. Results: miR-146b-5p was downregulated in monocytes of obese persons. Low globular adiponectin decreased miR-146b-5p and IRAK3 in THP-1 monocytes, associated with increased mitochondrial reactive oxygen species (ROS). Intracellular ROS and insulin receptor substrate-1 (IRS1) protein were unchanged. Silencing of miR-146b-5p with an antisense inhibitor resulted in increased expression of IRAK1 and TRAF6 leading to more NFkB p65 DNA binding activity and TNFa. As

Impact of primary kidney disease on the effects of empagliflozin in patients with chronic kidney disease: secondary analyses of the EMPA-KIDNEY trial

Background: The EMPA KIDNEY trial showed that empagliflozin reduced the risk of the primary composite outcome of kidney disease progression or cardiovascular death in patients with chronic kidney disease mainly through slowing progression. We aimed to assess how effects of empagliflozin might differ by primary kidney disease across its broad population. Methods: EMPA-KIDNEY, a randomised, controlled, phase 3 trial, was conducted at 241 centres in eight countries (Canada, China, Germany, Italy, Japan, Malaysia, the UK, and the USA). Patients were eligible if their estimated glomerular filtration rate (eGFR) was 20 to less than 45 mL/min per 1·73 m2, or 45 to less than 90 mL/min per 1·73 m2 with a urinary albumin-to-creatinine ratio (uACR) of 200 mg/g or higher at screening. They were randomly assigned (1:1) to 10 mg oral empagliflozin once daily or matching placebo. Effects on kidney disease progression (defined as a sustained ≥40% eGFR decline from randomisation, end-stage kidney disease, a sustained eGFR below 10 mL/min per 1·73 m2, or death from kidney failure) were assessed using prespecified Cox models, and eGFR slope analyses used shared parameter models. Subgroup comparisons were performed by including relevant interaction terms in models. EMPA-KIDNEY is registered with ClinicalTrials.gov, NCT03594110. Findings: Between May 15, 2019, and April 16, 2021, 6609 participants were randomly assigned and followed up for a median of 2·0 years (IQR 1·5–2·4). Prespecified subgroupings by primary kidney disease included 2057 (31·1%) participants with diabetic kidney disease, 1669 (25·3%) with glomerular disease, 1445 (21·9%) with hypertensive or renovascular disease, and 1438 (21·8%) with other or unknown causes. Kidney disease progression occurred in 384 (11·6%) of 3304 patients in the empagliflozin group and 504 (15·2%) of 3305 patients in the placebo group (hazard ratio 0·71 [95% CI 0·62–0·81]), with no evidence that the relative effect size varied significantly by primary kidney disease (pheterogeneity=0·62). The between-group difference in chronic eGFR slopes (ie, from 2 months to final follow-up) was 1·37 mL/min per 1·73 m2 per year (95% CI 1·16–1·59), representing a 50% (42–58) reduction in the rate of chronic eGFR decline. This relative effect of empagliflozin on chronic eGFR slope was similar in analyses by different primary kidney diseases, including in explorations by type of glomerular disease and diabetes (p values for heterogeneity all >0·1). Interpretation: In a broad range of patients with chronic kidney disease at risk of progression, including a wide range of non-diabetic causes of chronic kidney disease, empagliflozin reduced risk of kidney disease progression. Relative effect sizes were broadly similar irrespective of the cause of primary kidney disease, suggesting that SGLT2 inhibitors should be part of a standard of care to minimise risk of kidney failure in chronic kidney disease. Funding: Boehringer Ingelheim, Eli Lilly, and UK Medical Research Council

Blockade of class IB phosphoinositide-3 kinase ameliorates obesity-induced inflammation and insulin resistance

Obesity and insulin resistance, the key features of metabolic syndrome, are closely associated with a state of chronic, low-grade inflammation characterized by abnormal macrophage infiltration into adipose tissues. Although it has been reported that chemokines promote leukocyte migration by activating class IB phosphoinositide-3 kinase (PI3Kγ) in inflammatory states, little is known about the role of PI3Kγ in obesity-induced macrophage infiltration into tissues, systemic inflammation, and the development of insulin resistance. In the present study, we used murine models of both diet-induced and genetically induced obesity to examine the role of PI3Kγ in the accumulation of tissue macrophages and the development of obesity-induced insulin resistance. Mice lacking p110γ (Pik3cg−/−), the catalytic subunit of PI3Kγ, exhibited improved systemic insulin sensitivity with enhanced insulin signaling in the tissues of obese animals. In adipose tissues and livers of obese Pik3cg−/− mice, the numbers of infiltrated proinflammatory macrophages were markedly reduced, leading to suppression of inflammatory reactions in these tissues. Furthermore, bone marrow-specific deletion and pharmacological blockade of PI3Kγ also ameliorated obesity-induced macrophage infiltration and insulin resistance. These data suggest that PI3Kγ plays a crucial role in the development of both obesity-induced inflammation and systemic insulin resistance and that PI3Kγ can be a therapeutic target for type 2 diabetes