Current trend for maxillary implant overdenture

The purpose of this review was to provide the current research trend for the maxillary implant overdenture, and to provide an update of recent research focused on the numbers of implants and attachment types. A literature search was conducted on the maxillary overdenture research which was published during 2020. We excluded studies that contained tooth-supported overdenture and denture fabrication, or designed a case report or pilot study. After screening the title, abstract, and full-text, sixteen studies were included for this review. Although many studies were tried to reduce the numbers of implants, in conclusion, four regular implants with proper attachment systems are still recommended for the overdenture in contemporary dentistry with proper attachment systems, excepting magnet attachment.ope

Comparison Between Semi-Quantitative Frequency Methods and 7-day Dietary Records Methods in Food and Nutrition Intake Status For Hemodialysis Patients

Objectives: The valid assessment of food and nutrients intakes using appropriate dietary intake method is necessary to improve the nutritional status of the hemodialysis (HD) patients. This study was conducted to compare the method between newly developed, semi-quantitative food frequency questionnaire (Semi-FFQ) and 7-day dietary records (7-DRs) for hemodialysis patients. Methods: We conducted both methods on 53 maintenance HD patients in two university hospitals. We calibrated the frequency, portion size and daily intake of 47 food items reported in Semi-FFQ. The food and nutrients intake was compared and the correlation of the two methods was analyzed. Also each nutrient intake was compared to recommended dietary allowance for Korean (KDRIs) and recommended nutrient reference value for HD patients. Results: Energy and energy-yielding nutrients intakes were significantly higher in the two methods (p<0.01). These support the possible reliability between Semi-FFQ and 7-DRs that is similar with regard to most mineral and vitamin intakes. Thus, the Semi-FFQ used in this study for the assessment of nutrient intakes of HD patients can be reliable for the assessment of the nutrient intake along with the 7-DRs. The correlation coefficients were higher for foods consumed daily, such as steamed rice, meat and chicken, bean, egg, milk, coffee and alcohol than for those of foods eaten rarely (p<0.01). Conclusions: The Semi-FFQ used in this study can be a reliable tool for the assessment of the HD patients’ nutrient intake along with the 7-DRs, despite its limitations.ope

Postoperative acute kidney injury

Acute kidney injury (AKI) after cardiac surgery is a common and serious complication. Several definitions of AKI have been proposed recently, and include both increases in serum creatinine levels and decreases in urine output as diagnostic criteria. The pathophysiology of postoperative AKI is complex and involves both ischemic injury and systemic inflammation. Identifying risk factors, such as old age, underlying diabetes, heart failure, and obesity, may aid in the application of preventative methods for postoperative AKI. Additionally, recognizing different risks after different types of surgical procedures would be valuable. Novel biomarkers that could detect AKI more precisely at an earlier time point are being investigated. Several new biomarkers have been assessed in large multi-center studies and are believed to accommodate conventional clinical findings in diagnosing postoperative AKI. In high-risk patients, preventative measures, such as the maintenance of adequate hemodynamics and sufficient fluid resuscitation, could lower the incidence of postoperative AKI. Avoiding nephrotoxic agents and optimizing preoperative hemoglobin levels to avoid excessive transfusions would also be beneficial. In situations in which medical management fails to maintain sufficient urine output and acid-base and electrolyte homeostasis, early initiation of renal replacement therapy should be considered.ope

MicroRNAs and the glomerulus

MicroRNAs (miRNAs) are short non-coding RNAs regulating gene expression at the post-transcriptional level by blocking translation or promoting cleavage of their target mRNAs. Increasing evidence shows that miRNAs play central roles in gene transcription, signal transduction and pathogenesis of human diseases. Diabetic nephropathy (DN) is a severe microvascular complication that can lead to end-stage renal disease. Increased expansion (hypertrophy) and accumulation of extracellular matrix (ECM) proteins such as collagen (fibrosis) in the glomerular mesangium along with glomerular podocyte dysfunction are major features of DN. Profiling of miRNAs and study\ of their functions in renal glomeruli can provide critical new information to advance our knowledge of DN as well as other kidney diseases and thereby uncover much needed new therapeutic targets. In this review, we summarize the biogenesis of miRNAs and their functions in the glomerulus, with particular emphasis on glomerular mesangial cells and podocytes related to the pathogenesis of DN.ope

FOG2 protein down-regulation by transforming growth factor-β1-induced microRNA-200b/c leads to Akt kinase activation and glomerular mesangial hypertrophy related to diabetic nephropathy

Glomerular hypertrophy is a hallmark of diabetic nephropathy. Akt kinase activated by transforming growth factor-β1 (TGF-β) plays an important role in glomerular mesangial hypertrophy. However, the mechanisms of Akt activation by TGF-β are not fully understood. Recently, miR-200 and its target FOG2 were reported to regulate the activity of phosphatidylinositol 3-kinase (the upstream activator of Akt) in insulin signaling. Here, we show that TGF-β activates Akt in glomerular mesangial cells by inducing miR-200b and miR-200c, both of which target FOG2, an inhibitor of phosphatidylinositol 3-kinase activation. FOG2 expression was reduced in the glomeruli of diabetic mice as well as TGF-β-treated mouse mesangial cells (MMC). FOG2 knockdown by siRNAs in MMC activated Akt and increased the protein content/cell ratio suggesting hypertrophy. A significant increase of miR-200b/c levels was detected in diabetic mouse glomeruli and TGF-β-treated MMC. Transfection of MMC with miR-200b/c mimics significantly decreased the expression of FOG2. Conversely, miR-200b/c inhibitors attenuated TGF-β-induced decrease in FOG2 expression. Furthermore, miR-200b/c mimics increased the protein content/cell ratio, whereas miR-200b/c inhibitors abrogated the TGF-β-induced increase in protein content/cell. In addition, down-regulation of FOG2 by miR-200b/c could activate not only Akt but also ERK, which was also through PI3K activation. These data suggest a new mechanism for TGF-β-induced Akt activation through FOG2 down-regulation by miR-200b/c, which can lead to glomerular mesangial hypertrophy in the progression of diabetic nephropathy.ope

Epigenetic modifications and diabetic nephropathy

Diabetic nephropathy (DN) is a major complication associated with both type 1 and type 2 diabetes, and a leading cause of end-stage renal disease. Conventional therapeutic strategies are not fully efficacious in the treatment of DN, suggesting an incomplete understanding of the gene regulation mechanisms involved in its pathogenesis. Furthermore, evidence from clinical trials has demonstrated a “metabolic memory” of prior exposure to hyperglycemia that continues to persist despite subsequent glycemic control. This remains a major challenge in the treatment of DN and other vascular complications. Epigenetic mechanisms such as DNA methylation, nucleosomal histone modifications, and noncoding RNAs control gene expression through regulation of chromatin structure and function and post-transcriptional mechanisms without altering the underlying DNA sequence. Emerging evidence indicates that multiple factors involved in the etiology of diabetes can alter epigenetic mechanisms and regulate the susceptibility to diabetes complications. Recent studies have demonstrated the involvement of histone lysine methylation in the regulation of key fibrotic and inflammatory genes related to diabetes complications including DN. Interestingly, histone lysine methylation persisted in vascular cells even after withdrawal from the diabetic milieu, demonstrating a potential role of epigenetic modifications in metabolic memory. Rapid advances in high-throughput technologies in the fields of genomics and epigenomics can lead to the identification of genome-wide alterations in key epigenetic modifications in vascular and renal cells in diabetes. Altogether, these findings can lead to the identification of potential predictive biomarkers and development of novel epigenetic therapies for diabetes and its associated complications.ope

Transforming growth factor β1 (TGF-β1) enhances expression of profibrotic genes through a novel signaling cascade and microRNAs in renal mesangial cells

Increased expression of transforming growth factor-β1 (TGF-β1) in glomerular mesangial cells (MC) augments extracellular matrix accumulation and hypertrophy during the progression of diabetic nephropathy (DN), a debilitating renal complication of diabetes. MicroRNAs (miRNAs) play key roles in the pathogenesis of DN by modulating the actions of TGF-β1 to enhance the expression of profibrotic genes like collagen. In this study, we found a significant decrease in the expression of miR-130b in mouse MC treated with TGF-β1. In parallel, there was a down-regulation in miR-130b host gene 2610318N02RIK (RIK), suggesting host gene-dependent expression of this miRNA. TGF-β receptor 1 (TGF-βR1) was identified as a target of miR-130b. Interestingly, the RIK promoter contains three NF-Y binding sites and was regulated by NF-YC. Furthermore, NF-YC expression was inhibited by TGF-β1, suggesting that a signaling cascade, involving TGF-β1-induced decreases in NF-YC, RIK, and miR-130b, may up-regulate TGF-βR1 to augment expression of TGF-β1 target fibrotic genes. miR-130b was down-regulated, whereas TGF-βR1, as well as the profibrotic genes collagen type IV α 1 (Col4a1), Col12a1, CTGF, and PAI-1 were up-regulated not only in mouse MC treated with TGF-β1 but also in the glomeruli of streptozotocin-injected diabetic mice, supporting in vivo relevance. Together, these results demonstrate a novel miRNA- and host gene-mediated amplifying cascade initiated by TGF-β1 that results in the up-regulation of profibrotic factors, such as TGF-βR1 and collagens associated with the progression of DN.ope

Evaluating a shared decision-making intervention regarding dialysis modality: development and validation of self-assessment items for patients with chronic kidney disease

Background: Shared decision-making is a two-way symmetrical communication process in which clinicians and patients work together to achieve the best outcome. This study aimed to develop self-assessment items as a decision aid for choosing a dialysis modality in patients with chronic kidney disease (CKD) and to assess the construct validity of the newly developed items. Methods: Five focus group interviews were performed to extract specific self-assessment items regarding patient values in choosing a dialysis modality. After survey items were refined, a survey of 330 patients, consisting of 152 hemodialysis (HD) and 178 peritoneal dialysis (PD) patients, was performed to validate the self-assessment items. Results: The self-assessment for the decision aid was refined to 35 items. The structure of the final items appeared to have three dimensions of factors; health, lifestyle, and dialysis environment. The health factor consisted of 12 subscales (α = 0.724), the lifestyle factor contained 11 subscales (α = 0.624), and the dialysis environment factor was represented by 12 subscales (α = 0.694). A structural equation model analysis showed that the relationship between the decision aid factors (health, lifestyle, and dialysis environment), patients' CKD perception, and cognition of shared decision-making differed between HD patients and PD patients. Conclusion: We developed and validated self-assessment items as part of a decision aid to help patients with CKD. This attempt may assist CKD patients in making informed and shared decisions closely aligned with their values when considering dialysis modality.ope

Regulation of inflammatory phenotype in macrophages by a diabetes-induced long noncoding RNA

The mechanisms by which macrophages mediate the enhanced inflammation associated with diabetes complications are not completely understood. We used RNA sequencing to profile the transcriptome of bone marrow macrophages isolated from diabetic db/db mice and identified 1,648 differentially expressed genes compared with control db/+ mice. Data analyses revealed that diabetes promoted a proinflammatory, profibrotic, and dysfunctional alternatively activated macrophage phenotype possibly via transcription factors involved in macrophage function. Notably, diabetes altered levels of several long noncoding RNAs (lncRNAs). Because the role of lncRNAs in diabetes complications is unknown, we further characterized the function of lncRNA E330013P06, which was upregulated in macrophages from db/db and diet-induced insulin-resistant type 2 diabetic (T2D) mice, but not from type 1 diabetic mice. It was also upregulated in monocytes from T2D patients. E330013P06 was also increased along with inflammatory genes in mouse macrophages treated with high glucose and palmitic acid. E330013P06 overexpression in macrophages induced inflammatory genes, enhanced responses to inflammatory signals, and increased foam cell formation. In contrast, small interfering RNA-mediated E330013P06 gene silencing inhibited inflammatory genes induced by the diabetic stimuli. These results define the diabetic macrophage transcriptome and novel functional roles for lncRNAs in macrophages that could lead to lncRNA-based therapies for inflammatory diabetes complications.ope

Epigenetic modifications in the pathogenesis of diabetic nephropathy

Diabetic nephropathy (DN) is a leading cause of end-stage renal disease. Diabetic vascular complications such as DN can progress despite subsequent glycemic control, suggesting a metabolic memory of previous exposure to hyperglycemia. Diabetes profoundly impacts transcription programs in target cells through activation of multiple signaling pathways and key transcription factors leading to aberrant expression of pathologic genes. Emerging evidence suggests that these factors associated with the pathophysiology of diabetic complications and metabolic memory also might be influenced by epigenetic mechanisms in chromatin such as DNA methylation, histone lysine acetylation, and methylation. Key histone modifications and the related histone methyltransferases and acetyltransferases have been implicated in the regulation of inflammatory and profibrotic genes in renal and vascular cells under diabetic conditions. Advances in epigenome profiling approaches have provided novel insights into the chromatin states and functional outcomes in target cells affected by diabetes. Because epigenetic changes are potentially reversible, they can provide a window of opportunity for the development of much-needed new therapies for DN in the future. In this review, we discuss recent developments in the field of epigenetics and their relevance to diabetic vascular complications and DN pathogenesis.ope