Development and validation of a reliable method for automated measurements of psoas muscle volume in CT scans using deep learning-based segmentation: a cross-sectional study.

OBJECTIVES: We aimed to develop an automated method for measuring the volume of the psoas muscle using CT to aid sarcopenia research efficiently. METHODS: We used a data set comprising the CT scans of 520 participants who underwent health check-ups at a health promotion centre. We developed a psoas muscle segmentation model using deep learning in a three-step process based on the nnU-Net method. The automated segmentation method was evaluated for accuracy, reliability, and time required for the measurement. RESULTS: The Dice similarity coefficient was used to compare the manual segmentation with automated segmentation; an average Dice score of 0.927 ± 0.019 was obtained, with no critical outliers. Our automated segmentation system had an average measurement time of 2 min 20 s ± 20 s, which was 48 times shorter than that of the manual measurement method (111 min 6 s ± 25 min 25 s). CONCLUSION: We have successfully developed an automated segmentation method to measure the psoas muscle volume that ensures consistent and unbiased estimates across a wide range of CT images.

Direct Hybridization of Hydrophobic Nanocrystals with Colloidal Silica via van der Waals Force.

We present a novel, direct approach to hybridize hydrophobic quantum dot (QD) nanocrystals with colloidal silica (A) via van der Waals (vdW) force only. The A is constructed by aggregation of 15-25 nm sized hydrophobic silica nanoparticles with octadecyl groups. For hybridization, the hydrophobic QDs sit on the crevices of A via reinforced vdW force by interdigitation of long-chained hydrocarbons along the enlarged contact area of the crevices. The hybrids (B) are easily encapsulated with silica with/without functional groups, yielding QD-layer-incorporated silica particles (C) with greatly enhanced PL (up to 690%) and astonishing photostability compared with their free QDs under an identical QD concentration. This approach is simple, novel, versatile, and extended to the cases of three different sized QDs. The hydrophobic product C with phenylethyl groups is applicable to fabricate a white LED, and its hydrophilic analogues can be a promising material for bioapplications.

Decreased expression of VLDLR is inversely correlated with miR-200c in human colorectal cancer.

Colorectal cancer (CRC) is one of the most common cancers and has a high rate of morbidity and mortality worldwide. Very-low-density-lipoprotein receptor (VLDLR), a member of the low-density-lipoprotein receptor (LDLR) superfamily, is a multifunctional receptor that regulates cellular signaling by binding numerous ligands. Several studies reported the altered expression of VLDLR and suggested that VLDLR may play a critical role in tumor development by affecting cell proliferation and metastasis. However, the function of VLDLR and regulation of its expression by miRNAs have not been investigated in CRC. In the present study, we investigated the expression of VLDLR in CRC patients and found it to be significantly decreased in tumors in comparison with paired adjacent non-tumor tissues. Moreover, VLDLR over-expression inhibited the proliferation and migration of CRC cells. We also found that VLDLR expression was negatively regulated by miR-200c in CRC cells and that their expression levels were inversely correlated in CRC patients. These data suggest that VLDLR down-regulation mediated by the increased expression of miR-200c may be involved in the development of CRC.

Mouse-specific up-regulation of Ccnb1 expression by miR-199a-5p in keratinocyte.

MicroRNA (miRNA) are a class of single-stranded, small non-coding RNA that regulate various biological processes, including skin and hair cycle regulation, by modulating the expression of specific genes at the post-transcriptional level. Recently, several studies reported that miRNA directly or indirectly up-regulate target genes. Previously, we performed microarray analysis to identify the target genes of miR-199a-5p in a mouse skin keratinocyte cell line and detected more than 200 genes whose expression was significantly increased by miR-199a-5p overexpression (> 1.5-fold). In this study, we further investigated these genes and found that cyclin B1 (Ccnb1) expression was positively regulated by miR-199a-5p in keratinocyte. Moreover, Ccnb1 expression was inversely correlated with miR-199a-5p expression during the mouse hair cycle. Cell cycle analysis showed that the proportion of cells in S phase was slightly increased, while the proportion of cells in G2/M phase decreased by miR-199-5p. Using luciferase assay, we found that the 3' untranslated region of Ccnb1 was a direct target of miR-199a-5p. We also found that the regulation of Ccnb1 expression by miR-199a-5p is mouse specific. CCNB1 expression was not affected in the human and monkey cell lines. These results provide a new relationship between Ccnb1 and miR-199a-5p in both mouse keratinocyte and miRNA biology.

Regulation of Srpr Expression by miR-330-5p Controls Proliferation of Mouse Epidermal Keratinocyte.

Srpr is a gene encoding α subunit of the signal recognition particle receptor which is involved in the targeting and translocation of nascent secretory and membrane proteins to the endoplasmic reticulum. Previous studies showed aberrant expression of Srpr in several cell types with abnormal growth rate. Although Srpr is expressed in various tissues including skin, the role of Srpr in keratinocytes and regulation of its expression by miRNAs have not been studied. In this study, we investigated the role of SRPR and regulation of its expression by miRNA in skin keratinocytes. We found that SRPR was highly expressed in epidermal keratinocytes and regulated keratinocyte proliferation by affecting cell cycle progression. We also demonstrated that miR-330-5p directly inhibits Srpr expression. These data suggest that miR-330-5p-mediated regulation of the SRPR level is needed for the regulation of proliferation of epidermal keratinocytes.

MicroRNA-330-5p negatively regulates ITGA5 expression in human colorectal cancer.

Colorectal cancer (CRC), one of the most prevalent malignant cancers, has high rates pf incidence and is the fourth leading cause of cancer-related deaths for both men and women worldwide. MicroRNAs (miRNAs) play critical roles in the development of various types of cancers. miRNA­330-5p has been implicated in the progression of prostate, neuronal and pancreatic cancers by regulating proliferation, migration, invasion and epithelial-mesenchymal transition of cells. The purpose of the present study was to investigate the expression of miR-330-5p in CRC and identify its target gene(s) that may act in CRC tumorigenesis. We found that miR-330-5p expression was significantly lower in CRC tissues than that in adjacent non-tumorous tissues. Furthermore, we identified integrin α5 (ITGA5) as a new target of miR-330-5p and found that it inhibits ITGA5 expression by directly binding to the 3' untranslated region of ITGA5 mRNA. These results suggest that downregulation of miR-330-5p expression may affect CRC development via modulation of ITGA5 expression.

miR-330-5p inhibits proliferation and migration of keratinocytes by targeting Pdia3 expression.

The microRNAs (miRNAs) are a class of small non-coding RNA molecules that play important roles in cellular processes by regulating gene expression at the post-transcriptional level. In skin biology, several miRNAs have been shown to be associated with differentiation, migration and apoptosis of keratinocytes, and regulation of the hair cycle. Although the biological role of miR-330-5p has been reported in several cancers and cells, the function and molecular mechanism of miR-330-5p in skin keratinocytes have not been identified. In this study, we found that miR-330-5p inhibited the proliferation and migration of mouse keratinocytes. Among the candidate target genes of miR-330-5p searched using microarray analysis, we found that the expression of Pdia3 was directly regulated by miR-330-5p in the mouse keratinocyte. Moreover, inhibition of Pdia3 expression caused decreased proliferation and migration ability of mouse keratinocytes. Additionally, expressions of miR-330-5p and Pdia3 displayed an inverse correlation with respect to the hair cycle stage. These results indicated that regulation of Pdia3 expression by miR-330-5p is important in maintaining the hair cycle through regulation of the proliferation and migration capability of keratinocytes.

Quantum dot-layer-encapsulated and phenyl-functionalized silica spheres for highly luminous, colour rendering, and stable white light-emitting diodes.

Although the quantum efficiencies of quantum dots (QDs) are approaching unity through advances in the synthesis of QD materials, their luminescence efficiencies after mixing with resin and thermal curing for white light-emitting diodes (LEDs) are seriously lowered because of aggregation and oxidation of QDs and poor adhesion of QDs to the resin. To overcome these problems, QD-layer-encapsulated and phenyl-functionalized silica (SQS(Ph)) spheres were synthesized and applied for white LEDs, whereby the QDs were homogeneously distributed at radial equidistance from the center and near the surface of approximately 100 nm-sized silica spheres and the surface was functionalized with phenylethyl groups. The inter-core distances of QDs were over ∼14 nm, which is over the limit (<10 nm) for Förster resonance energy transfer (FRET) that leads to photoluminescence (PL) reduction. This hierarchical nanostructure excludes a chance of FRET between QDs and provides the QDs a gradually refractive index matching environment, which yields ∼4-fold enhanced PL in SQS(Ph). More importantly, the SQS(Ph) acquired a highly adhesive property to silicone resin due to their phenyl functional group matching, which resulted in remarkably improved light extraction in white LEDs. When incorporated along with a yellow-emitting Y3Al5O12:Ce(3+) (YAG:Ce) phosphor and silicone resin on blue LED chips, the SQS(Ph) spheres presented significantly improved performance [luminous efficiency (LE) = 58.2 lm W(-1); colour rendering index Ra = 81.8; I/I0 = 0.98 after 60 h operation] than their original QDs (LE = 39.6 lm W(-1); Ra = 78.1; I/I0 = 0.91 after 60 h operation) under a forward bias current of 60 mA.

FZD6 expression is negatively regulated by miR-199a-5p in human colorectal cancer.

Colorectal cancer (CRC), the third most common cancer worldwide, also has the highest rate of cancer-related morbidity and mortality. WNT signaling is initiated by binding of WNT to various receptors, including frizzleds (FZDs), and plays a critical role in CRC and other tumor development by regulating proliferation, differentiation, migration, apoptosis, and polarity. Among the members of the FZD family, FZD6 is broadly expressed in various tissues, and its overexpression has been reported in several cancers, suggesting an important role in cancer development. In this study, we investigated the expression of FZD6 in patients with CRC and found it to be increased in tumors, as compared to paired adjacent non-tumor tissues. Additionally, we found that FZD6 expression was negatively regulated by miR199a5p in CRC cells. These results suggest that overexpression of FZD6, mediated by reduced expression of miR-199a-5p, may play an important role in the development of CRC.

Highly sensitive immunoassay for the diagnosis of acute myocardial infarction using silica spheres encapsulating a quantum dot layer.

Commercial ELISA kits for substance P (SubP), which are helpful for the clinical diagnosis of acute myocardial infarction, are limited in efficacy because of low sensitivity. A highly sensitive immunoassay was developed using silica spheres encapsulating a quantum dot-layer (SQS) and labeling antibodies, on a Parylene A-modified plate. The high sensitivity was possible by taking advantage of the enhanced photoluminescence of the SQS and dense immobilization of SubP on a Parylene A-modified plate. Glutaraldehyde was used for cross-linking of SQS to the anti-SubP antibody and SubP to the Parylene A coating. The SQS-linked immunosorbent assay (SQSLISA) was optimized and validated. The dynamic range for the assay was 1-10000 pg/mL with a linear correlation factor of 0.9992 when the competitive SQSLISA was employed. The intra- and interday accuracies were 93-100% and 87-122%, respectively. The reproducibility was lower than 11%. The developed method was applied to clinical samples collected from healthy controls (n = 30) and acute myocardial infarction (n = 16) and it displayed a high correlation with the commercial ELISA kit, with a limit of detection that was 30-fold lower. Clinical sample analysis confirmed that SubP is a promising diagnostic marker for acute myocardial infarction. The SQSLISA is expected to be a practical and useful assay tool.

Salinomycin sensitizes antimitotic drugs-treated cancer cells by increasing apoptosis via the prevention of G2 arrest.

Here, we investigated whether Sal could sensitize cancer cells to antimitotic drugs. We demonstrated that Sal sensitized paclitaxcel (PAC)-, docetaxcel (DOC)-, vinblastin (VIN)-, or colchicine (COL)-treated cancer cell lines, suggesting that Sal has the ability to sensitize the cells to any form of microtubule-targeting drugs. Sensitization to the antimitotic drugs could be achieved with very low concentrations of Sal, suggesting that there is a possibility to minimize Sal toxicity associated with human cancer patient treatments. Sensitization by Sal increased apoptosis, which was observed by C-PARP production. Sal sensitized the cancer cells to antimitotic drugs by preventing G2 arrest, suggesting that Sal contributes to the induction of mitotic catastrophe. Sal generally reduced cyclin D1 levels in PAC-, DOC-, and VIN-treated cells. In addition, Sal treatment increased pH2AX levels and reduced p21 levels in antimitotic drugs-treated cells. These observations suggest that the mechanisms underlying Sal sensitization to DNA-damaging compounds, radiation, and microtubule-targeting drugs are similar. Our data demonstrated that Sal sensitizes cancer cells to antimitotic drugs by increasing apoptosis through the prevention of G2 arrest via conserved Sal-sensitization mechanisms. These results may contribute to the development of Sal-based chemotherapy for cancer patients treated with antimitotic drugs.