Dentin Materials as Biological Scaffolds for Tissue Engineering

Vital tooth-derived demineralized dentin matrix (DDM) has a bone-inductive ability, while non-vital tooth-derived DDM lost it. Acid treatment for dentin provides the increase of surface area, the release of matrix-binding growth factors such as BMPs, and the decrease of the infection risk. Human autograft of vital tooth-derived DDM was achieved first in Japan 2002, while first bone autograft was noted in Italy 1820. This paper introduced dentin/bone biology and a unique clinical case, combined with two types of non-vital tooth-derived DDM (roots, granules) for lateral bone augmentation. A 63-year-old woman revealed highly atrophic mandible in 2015. Three non-vital teeth were extracted, changed in shape, demineralized in 2% HNO3, were rinsed, and were grafted immediately. The CT images at 3 months after the graft showed remarkable lateral augmentation. DDM scaffolds were received to host, and two fixtures were placed into the DDM-augmented bone. The patient was successfully restored with their own DDM scaffolds and implant surgery

Long-term effect of cardiac pacing on sleep-disordered breathing in patients with conventional indications for a permanent pacemaker

Background: The effect of cardiac pacing on sleep-disordered breathing is controversial. We investigated the long-term effect of cardiac pacing on sleep disordered breathing in patients with conventional indications for permanent pacemakers Methods: Subjects comprised 40 patients (29 men; mean age 69±9 years, mean left ventricle ejection fraction 69±8%, and body mass index 23.6±3.5 kg/m2) who were diagnosed with indications for permanent pacemakers (sick sinus syndrome in 23 patients, atrioventricular block in 15, and brady atrial fibrillation in 2). All patients received polysomnographic evaluations before implantation of permanent pacemakers. After implantation of permanent pacemakers, all patients received polysomnographic evaluations during use of the pacemaker settings (AAI/DDD/VVI at 70 beats per minute). Results: The mean follow-up period was 35±13 months. Before implantation, the distribution of sleep-disordered breathing was as follows: 93% had apnea hypopnea index >5, 58% had apnea hypopnea index >15, and 20% had apnea hypopnea index >30. The mean apnea hypopnea index for all patients was 20±15, for those with obstructive type apnea was 4.9±5.3, and for those with central type apnea was 3.0±4.5. The mean Epworth Sleepiness Score was 5.9±4.0. No patient received continuous positive airway pressure therapy or any other therapy for sleep-disordered breathing during the follow up period. The mean apnea hypopnea index at 1 week after implantation of permanent pacemakers was 21±14 (P=0.8) and the mean apnea hypopnea index at end of follow-up was 11±7 (P<0.0001). Conclusion: Long term cardiac pacing significantly reduces the number of episodes of sleep apnea in patients with conventional permanent pacemaker indications

Inverse Relation between Condition of Heart Failure and Intrathoracic Impedance Measured by Implantable Cardioverter Defibrillator—A case report—

The patient was a 78-year-old man with dilated cardiomyopathy. His cardio-thoracic ratio was 60.4% and left ventricular ejection fraction (LVEF) was 33%. He had been repeatedly admitted for congestive heart failure. He underwent implantation of an implantable cardioverter-defibrillator (ICD) for ventricular fibrillation. We compared the values of BNP and shock impedance stored by the ICD. The correlation coefficient (p-value) between BNP and shock impedance was −0.700 (p < 0.0005), increase of BNP and shock impedance was −0.778 (p < 0.0001), percent increase of BNP and shock impedance was −0.767 (p < 0.0005). In conclusion, there is an inverse relation between BNP and shock impedance, and measurements of shock impedance may be useful in the management of congestive heart failure

Empagliflozin in Patients with Chronic Kidney Disease

Background The effects of empagliflozin in patients with chronic kidney disease who are at risk for disease progression are not well understood. The EMPA-KIDNEY trial was designed to assess the effects of treatment with empagliflozin in a broad range of such patients. Methods We enrolled patients with chronic kidney disease who had an estimated glomerular filtration rate (eGFR) of at least 20 but less than 45 ml per minute per 1.73 m(2) of body-surface area, or who had an eGFR of at least 45 but less than 90 ml per minute per 1.73 m(2) with a urinary albumin-to-creatinine ratio (with albumin measured in milligrams and creatinine measured in grams) of at least 200. Patients were randomly assigned to receive empagliflozin (10 mg once daily) or matching placebo. The primary outcome was a composite of progression of kidney disease (defined as end-stage kidney disease, a sustained decrease in eGFR to &lt; 10 ml per minute per 1.73 m(2), a sustained decrease in eGFR of &amp; GE;40% from baseline, or death from renal causes) or death from cardiovascular causes. Results A total of 6609 patients underwent randomization. During a median of 2.0 years of follow-up, progression of kidney disease or death from cardiovascular causes occurred in 432 of 3304 patients (13.1%) in the empagliflozin group and in 558 of 3305 patients (16.9%) in the placebo group (hazard ratio, 0.72; 95% confidence interval [CI], 0.64 to 0.82; P &lt; 0.001). Results were consistent among patients with or without diabetes and across subgroups defined according to eGFR ranges. The rate of hospitalization from any cause was lower in the empagliflozin group than in the placebo group (hazard ratio, 0.86; 95% CI, 0.78 to 0.95; P=0.003), but there were no significant between-group differences with respect to the composite outcome of hospitalization for heart failure or death from cardiovascular causes (which occurred in 4.0% in the empagliflozin group and 4.6% in the placebo group) or death from any cause (in 4.5% and 5.1%, respectively). The rates of serious adverse events were similar in the two groups. Conclusions Among a wide range of patients with chronic kidney disease who were at risk for disease progression, empagliflozin therapy led to a lower risk of progression of kidney disease or death from cardiovascular causes than placebo

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field