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Removable partial denture is one of the most important means of treating dental defects for its high strength, low price, wide range of indications, minimal trauma and repairability. With the aging of the population becoming more and more prominent, removable partial dentures will continue to be a common restorative method in the future. The production of removable partial denture cannot be separated from the accurate impression technology, and there are many shortcomings in the process of taking impressions of traditional removable partial denture, such as the number of visits, time-consuming, complex production process, high pollution, waste, low efficiency, and the quality is not easy to control, etc. However, the emergence of digital impression provides new technical support for the taking of removable partial denture impression. Digital impression technology has the advantages of high precision, comfort, high efficiency, shortened treatment time and personalized design, which helps to improve the effect of removable partial denture restoration and patient satisfaction. As the premise and foundation of the whole digital removable partial denture restoration treatment, accuracy of the reconstruction of the oral model directly affects the final denture restoration effect. At present, digital impression technology has been widely used in the field of oral restoration. This paper will review the current status of the application of digital impression technology in removable partial denture, in order to further guide the clinical application.

The authors inadvertently included grant numbers OT3HL147741 & U24CA233032, which are grant-specific. This was an oversight on the authors’ part as these grants did not support the research in this publication.

Cytogenetic risk stratification at diagnosis has long been one of the most useful tools to assess prognosis in acute lymphoblastic leukemia (ALL). To examine the prognostic impact of cytogenetic abnormalities on outcomes after allogeneic hematopoietic cell transplantation, we studied 1731 adults with Philadelphia-negative ALL in complete remission who underwent myeloablative or reduced intensity/non-myeloablative conditioning transplant from unrelated or matched sibling donors reported to the Center for International Blood and Marrow Transplant Research. A total of 632 patients had abnormal conventional metaphase cytogenetics. The leukemia-free survival and overall survival rates at 5 years after transplantation in patients with abnormal cytogenetics were 40% and 42%, respectively, which were similar to those in patients with a normal karyotype. Of the previously established cytogenetic risk classifications, modified Medical Research Council-Eastern Cooperative Oncology Group score was the only independent prognosticator of leukemia-free survival (P=0.03). In the multivariable analysis, monosomy 7 predicted post-transplant relapse [hazard ratio (HR)=2.11; 95% confidence interval (95% CI): 1.04-4.27] and treatment failure (HR=1.97; 95% CI: 1.20-3.24). Complex karyotype was prognostic for relapse (HR=1.69; 95% CI: 1.06-2.69), whereas t(8;14) predicted treatment failure (HR=2.85; 95% CI: 1.35-6.02) and overall mortality (HR=3.03; 95% CI: 1.44-6.41). This large study suggested a novel transplant-specific cytogenetic scheme with adverse [monosomy 7, complex karyotype, del(7q), t(8;14), t(11;19), del(11q), tetraploidy/near triploidy], intermediate (normal karyotype and all other abnormalities), and favorable (high hyperdiploidy) risks to prognosticate leukemia-free survival (P=0.02). Although some previously established high-risk Philadelphia-negative cytogenetic abnormalities in ALL can be overcome by transplantation, monosomy 7, complex karyotype, and t(8;14) continue to pose significant risks and yield inferior outcomes.

ObjectivesTo describe the prevalence of, types of, and characteristics associated with self-reporting multiple (≥ 2) barriers to medication use in older women using long-term cardiovascular and oral hypoglycemic medications.MethodsThis cross-sectional study set at the Women's Health Initiative during 2005-2010 included women who were using any chronic medication from 3 target classes (i.e., antilipemics, antihypertensives, oral hypoglycemics) for at least 1 month and who had answered questions about barriers to medication use at year 4 (2009) of the study period (N = 59,054). Measurements included common self-reported barriers to medication use, and sociodemographic, health characteristic, medication use, and access to care variables were evaluated. Multivariable logistic regression models were used to examine associations between participant characteristics and barriers to medication use.ResultsAmong the participants, 47,846 (81%) reported no barriers, 7105 (12%) reported 1 barrier, and 4103 (6.9%) reported 2 or more barriers to medication use. The most common barriers reported were having concerns about adverse effects, not liking to take medications, and medications costing too much. Several characteristics were found to be associated with reporting 2 or more barriers in multivariable modeling, including demographic (e.g., lower age, black race, Hispanic ethnicity) and health or medication (e.g., lower quality of life, lower physical function, higher number of concurrent medications) characteristics.ConclusionAmong older women using chronic cardiovascular and oral hypoglycemic medications, approximately 20% reported at least 1 barrier to medication use, with 7% of women reporting multiple barriers. Pharmacists should prioritize identifying barriers to medication use in older women using chronic medications to improve patient care.

Urban heat island (UHI) has posed a threat to sustainable development, and the identification of the spatial characteristics of UHI is a prerequisite for the mitigation of UHI effects. Taking Kunming City and Guiyang City in the karst region of Southwest China as two examples, this study utilized spatial econometric modeling and random forest regression to identify and compare the spatial distribution and impact of urban heat islands related to topographic and urban morphology. The results indicated that the UHI in Kunming and Guiyang mainly monocentrically and polycentrically distributed, respectively, and the urban heat island intensity (UHII) in Kunming was significantly higher than that in Guiyang. The spatial error model effectively reflected the influence of topography and urban form on UHII, and the random forest regression model objectively measured the contribution of different influencing factors to UHII. Enhanced vegetation index (EVI), population density (PD), percentage of impervious surface (PIS), ground sky view factor (GSVF), building density (BD) and percentage of water bodies (PW) had similar effects and contributions to the UHII in the two cities, while urban surface roughness (USR) contributed less than topographic slope (SLOPE) on UHII in Kunming, and the SLOPE contributed less than USR in Guiyang. In the karst ecologically fragile zone, the morphology of Kunming and Guiyang are mainly shaped by the topography, which can be characterized as monocentric and polycentric, respectively. And the UHI distribution and UHII were also closely related to topographic patterns. EVI, SLOPE and PW, all showed inhibitory effects on UHII, and EVI contributed the most. PD, PIS, USR and BD, exacerbate the UHII, with PD contributing the most. The above conclusions can provide a reference for policymakers and urban planners to optimize urban morphology and mitigate urban heat island. [ABSTRACT FROM AUTHOR]

Summary: Severe aplastic anaemia (SAA) is a rare and life‐threatening bone marrow failure disorder. We used data from the transplant outcomes in aplastic anaemia study to characterize mosaic chromosomal alterations (mCAs) in the peripheral blood of 738 patients with acquired SAA and evaluate their associations with telomere length (TL) and survival post‐haematopoietic cell transplant (HCT). The median age at HCT was 20.4 years (range = 0.2–77.4). Patients with SAA had shorter TL than expected for their age (median TL percentile for age: 35.7th; range <1–99.99). mCAs were detected in 211 patients (28.6%), with chr6p copy‐neutral loss of heterozygosity (6p‐CNLOH) in 15.9% and chr7 loss in 3.0% of the patients; chrX loss was detected in 4.1% of female patients. Negative correlations between mCA cell fraction and measured TL (r = −0.14, p = 0.0002), and possibly genetically predicted TL (r = −0.07, p = 0.06) were noted. The post‐HCT 3‐year survival probability was low in patients with chr7 loss (39% vs. 72% in patients with chr6‐CNLOH, 60% in patients with other mCAs and 70% in patients with no mCAs; p‐log rank = 0.001). In multivariable analysis, short TL (p = 0.01), but not chr7 loss (p = 0.29), was associated with worse post‐HCT survival. TL may guide clinical decisions in patients with SAA. [ABSTRACT FROM AUTHOR]

Summary: Individuals with telomere biology disorders (TBDs) have very short telomeres, high risk of bone marrow failure (BMF), and reduced survival. Using data from TBD patients, a mean leukocyte Southern blot telomere length (TL) of 5 kilobases (kb) was estimated as the 'telomere brink' at which human survival is markedly reduced. However, the shortest telomere, not the mean TL, signals replicative senescence. We used the Telomere Shortest Length Assay (TeSLA) to tally TL of all 46 chromosomes in blood‐derived DNA and examined its relationship with TBDs. Patients (n = 18) had much shorter mean TL (TeSmTL) (2.54 ± 0.41 kb vs. 4.48 ± 0.52 kb, p < 0.0001) and more telomeres <3 kb than controls (n = 22) (70.43 ± 8.76% vs. 33.05 ± 6.93%, p < 0.0001). The proportion of ultrashort telomeres (<1.6 kb) was also higher in patients than controls (39.29 ± 10.69% vs. 10.40 ± 4.09%, p < 0.0001). TeS <1.6 kb was associated with severe (n = 11) compared with non‐severe (n = 7) BMF (p = 0.027). Patients with multi‐organ manifestations (n = 10) had more telomeres <1.6 kb than those with one affected organ system (n = 8) (p = 0.029). Findings suggest that TBD clinical manifestations are associated with a disproportionately higher number of haematopoietic cell telomeres reaching a telomere brink, whose length at the single telomere level is yet to be determined. [ABSTRACT FROM AUTHOR]

Background While Alzheimer disease (AD) and vascular dementia (VaD) may be accelerated by hypercholesterolemia, the mechanisms underlying this association are unclear. We tested whether dysregulation of cholesterol catabolism, through its conversion to primary bile acids (BAs), was associated with dementia pathogenesis. Methods and findings We used a 3-step study design to examine the role of the primary BAs, cholic acid (CA), and chenodeoxycholic acid (CDCA) as well as their principal biosynthetic precursor, 7[alpha]-hydroxycholesterol (7[alpha]-OHC), in dementia. In Step 1, we tested whether serum markers of cholesterol catabolism were associated with brain amyloid accumulation, white matter lesions (WMLs), and brain atrophy. In Step 2, we tested whether exposure to bile acid sequestrants (BAS) was associated with risk of dementia. In Step 3, we examined plausible mechanisms underlying these findings by testing whether brain levels of primary BAs and gene expression of their principal receptors are altered in AD. Step 1: We assayed serum concentrations CA, CDCA, and 7[alpha]-OHC and used linear regression and mixed effects models to test their associations with brain amyloid accumulation (N = 141), WMLs, and brain atrophy (N = 134) in the Baltimore Longitudinal Study of Aging (BLSA). The BLSA is an ongoing, community-based cohort study that began in 1958. Participants in the BLSA neuroimaging sample were approximately 46% male with a mean age of 76 years; longitudinal analyses included an average of 2.5 follow-up magnetic resonance imaging (MRI) visits. We used the Alzheimer's Disease Neuroimaging Initiative (ADNI) (N = 1,666) to validate longitudinal neuroimaging results in BLSA. ADNI is an ongoing, community-based cohort study that began in 2003. Participants were approximately 55% male with a mean age of 74 years; longitudinal analyses included an average of 5.2 follow-up MRI visits. Lower serum concentrations of 7[alpha]-OHC, CA, and CDCA were associated with higher brain amyloid deposition (p = 0.041), faster WML accumulation (p = 0.050), and faster brain atrophy mainly (false discovery rate [FDR] p = 4 million registrants from general practice clinics in the United Kingdom, we tested whether patients using BAS (BAS users; 3,208 with [greater than or equal to]2 prescriptions), which reduce circulating BAs and increase cholesterol catabolism, had altered dementia risk compared to those on non-statin lipid-modifying therapies (LMT users; 23,483 with [greater than or equal to]2 prescriptions). Patients in the study (BAS/LMT) were approximately 34%/38% male and with a mean age of 65/68 years; follow-up time was 4.7/5.7 years. We found that BAS use was not significantly associated with risk of all-cause dementia (hazard ratio (HR) = 1.03, 95% confidence interval (CI) = 0.72-1.46, p = 0.88) or its subtypes. We found a significant difference between the risk of VaD in males compared to females (p = 0.040) and a significant dose-response relationship between BAS use and risk of VaD (p-trend = 0.045) in males. Step 3: We assayed brain tissue concentrations of CA and CDCA comparing AD and control (CON) samples in the BLSA autopsy cohort (N = 29). Participants in the BLSA autopsy cohort (AD/CON) were approximately 50%/77% male with a mean age of 87/82 years. We analyzed single-cell RNA sequencing (scRNA-Seq) data to compare brain BA receptor gene expression between AD and CON samples from the Religious Orders Study and Memory and Aging Project (ROSMAP) cohort (N = 46). ROSMAP is an ongoing, community-based cohort study that began in 1994. Participants (AD/CON) were approximately 56%/36% male with a mean age of 85/85 years. In BLSA, we found that CA and CDCA were detectable in postmortem brain tissue samples and were marginally higher in AD samples compared to CON. In ROSMAP, we found sex-specific differences in altered neuronal gene expression of BA receptors in AD. Study limitations include the small sample sizes in the BLSA cohort and likely inaccuracies in the clinical diagnosis of dementia subtypes in primary care settings. Conclusions We combined targeted metabolomics in serum and amyloid positron emission tomography (PET) and MRI of the brain with pharmacoepidemiologic analysis to implicate dysregulation of cholesterol catabolism in dementia pathogenesis. We observed that lower serum BA concentration mainly in males is associated with neuroimaging markers of dementia, and pharmacological lowering of BA levels may be associated with higher risk of VaD in males. We hypothesize that dysregulation of BA signaling pathways in the brain may represent a plausible biologic mechanism underlying these results. Together, our observations suggest a novel mechanism relating abnormalities in cholesterol catabolism to risk of dementia., Author(s): Vijay R. Varma 1, Youjin Wang 2, Yang An 3, Sudhir Varma 4, Murat Bilgel 3, Jimit Doshi 5, Cristina Legido-Quigley 6, João C. Delgado 7, Anup M. Oommen [...]