Objective To explore the effect of microRNA‐21(miR‐21) on the migration and invasion ability in human laryn‐geal squamous carcinoma cell Hep2 .Methods The MTT method was used to detect the viability of Hep2 cells at 48 h after miR‐21 inhibitor and miR‐21 NC transferring into Hep2 cells by LipofectamineTM 2000 .The cell migration ability was detected by using the scratch test .The cell invasion ability was detected by using the Transwell method .The activation of phosphatase and tensin homo‐logue deleted on chromosome 10 (PTEN)/phosphatidylinositol 3 kinase (PI3K) /protein kinase B(Akt) signal pathway and the expression of matrix metalloproteinase 2 (MMP2) ,MMP9 ,reversion inducing cysteine rich protein with kazal motif (RECK) was detected by using the Western blotting .Results Compared with miR‐21 NC ,miR‐21 inhibitor could significantly reduce the Hep2 cellviability[(0.688±0.043)vs.(0.375±0.012)],inhibitedthemigrationability[(6.57±0.02)μm vs.(20.49±2.18)μm]and invasion ability[(100 .7 ± 10 .2) vs .(46 .8 ± 4 .3)] ,and the differences were statistically significant (P<0 .01) ,meanwhile miR‐21 inhibitor could down‐regulate the expression of PI3K ,MMP2 and MMP9(P<0 .01) ,and reduced the phosphorylation level of Akt (P<0 .01) ,up‐regulated the expression of PTEN and RECK (P<0 .01) .Conclusion miR‐21 inhibitor can significantly suppress the migration and invasion ability of Hep2 ,which may be related with the PTEN/PI3K/Akt signal pathway .

Objective:To investigate the expression and clinical significance of PD-L1 in colorectal cancer (CRC). Methods:A total of 210 CRC patients who accepted radical surgery in our hospital from January 2015 to January 2016 were divided into three groups, namely, high-frequency microsatellite instability (MSI-H), low-frequency microsatellite instability (MSI-L), and microsatellite stable (MSS). The expression of PD-L1 was detected by immunohistochemistry, and the expression characteristics of PD-L1 in different types of CRC were analyzed. Results:CRC cases with low differentiation had a higher expression of PD-L1 than CRC patients with high differ-entiation (P<0.05). PD-L1 had a positive rate of 75.8%in the MSI-H group and a rate of 9.3%in the MSI-L and MSS groups, wherein the difference between the two groups was statistically significant (P<0.05). Conclusion:PD-L1 was positively expressed in some CRC tu-mor tissues, and its positive rate was significantly higher in MSI-H than in MSI-L and MSS. The therapeutic effect of a PD-L1 blocker for patients with MSI-H CRC might be preferable.

BACKGROUND:Osteoporosis caused by chemotherapy has become one of the serious side effects that impact the skeletal system. Icarin shows a strong anti-osteoporosis activity, which can have protective effect on osteoporosis induced by chemotherapy. OBJECTIVE: To study the protective effect and mechanism of icarin against cyclophosphamide-induced obstacle of mouse bone marrow mesenchymal stem cels differentiating into osteoblasts. METHODS:MTT assay and alkaline phosphatase (ALP) staining were used to determine the optimal protective concentration of icarin against cyclophosphamide-induced obstacle of mouse bone marrow mesenchymal stem cels differentiating into osteoblasts. mRNA expressions of osteoblast-specific transcription factors, OC, ALP, Runx2, and Wnt/β-catenin signaling pathway target genes, β-catenin, C-Myc, cyclin D1, were determined using RT-PCR method at different time after intervention with the optimal concentration of icarin. Expressions of Runx2, β-catenin, c-Myc, cyclin D1 regulated by the optimal concentration of icarin were detected using western blot assay at the protein level. RESULTS AND CONCLUSION:Cel viability and ALP activity decreased significantly in the cyclophosphamide group compared with the control group, but there was no significant difference in cel viability between icarin group and cyclophosphamide group. Icarin at 100 μmol/L showed the best protective effect against cyclophosphamide-induced obstacle of osteogenic differentiation of bone marrow mesenhymal stem cels. Compared with the control group, cyclophosphamide chemotherapy reduced the expressions of ALP, OC, Runx2 at mRNA level and Runx2 at protein level, weakened the expressions ofβ-catenin, cyclin D1 at mRNA level and active β-catenin, Cyclin D1, c-myc at protein level, and increased the expression of DKK1. Compared with the cyclophosphamide group, 100 μmol/L icarin increased the expression of osteoblast-specific transcription factors and Wnt/β-catenin signaling pathway genes at mRNA and protein levels, and reduced the expression of DKK1 protein. These results show that cyclophosphamide can lead to osteogenic differentiation disorder of mouse bone marrow mesenchymal stem cels, and in contrast, icarin shows a protective effect and its optimal intervention concentration is 100 μmol/L. Additionaly, the protective roleof icarin is probably related to activation of Wnt/β-catenin signal pathway.

Objective To investigate the effect and mechanism of estrodial (E2) on intracellular free calcium in the endometrial-myometrial interface (EMI) smooth muscle cells from uteri with adenomyosis.MethodsFrom March 2011 to October 2011,16 uterus specimens were collected from patients with adenomyosis undergoing hysterectomy in Beijing Obstetrics and Gynecology Hospital,which included 9 proliferative endometrium and 7 secretory endometrium.EMI smooth muscle cells from the uterus were cultured and loaded with calcium ion ( Ca2 + ) fluorescent probe fluo-4/AM.The labeled cells were stimulated with the various concentration of E2 ( 1 × 102,1 × 103,1 × 104,1 × 105 pmol/L,respectively),then the changes of intracellular Ca2+ fluorescence intensity were measured by laser scanning microscopy.The most suitable concentration of E2 was selected,and the reaction difference between the EMI smooth muscle cells of two menstrual phases were also investigated; The changes of intracellular Ca2 + fluorescence intensity were detected proliferative and secretory smooth muscle cells in E2 conjugated to bovine serum albumin (17β-E2-BSA) group,cycloheximide (CHX) group,fulvestrant (ICI182780) group and pertussis toxin (PTX) group.Results ( 1 ) The cell viability of primary cultured EMI smooth muscle cells was well at 24 hours culture.(2) 1 × 102 - 1 × 105 pmol/L E2 can rapidly increase the intracellular Ca2+ fluorescence intensity within 1 min ( P ＜ 0.01 ) ;The increased amplitudes caused by 1 × 104 pmol/L and 1 × 105 pmoL/L E2 were the most significant,but there was no significant difference between them (P ＞0.05).1 × 104 pmol/L was the most suitable concentration.( 3 ) With the 1 × 104 pmol/L E2,the Ca2+ fluorescence intensity changes showed no significant difference between the EMI smooth muscle cells from the proliferative phase and secretory phase uterus (P ＞ 0.05 ).The Ca2+ fluorescence intensity changes were 646 ± 32 in 17β-E2-BSA group and 602 ±31 in CHX group,when compared with 513 ±26 and 617 ±35 in respective control group,no significant difference was observed (P ＞ 0.05 ).The increased amplitude of 188 ± 20 in the PTX group and 302 ± 11 in ICI182780 group exhibited significant difference with 632 ± 33 and 635 ± 24 in respective control group ( P ＜ 0.01 ).Conclusion E2 could increase the intracellular Ca2 + of EMI through a membrane receptor dependent and nongenomic mechanism of action.

Purpose: Leptin interacts not only with leptin receptor (LEPR) but also engages with other receptors. While the pro-oncogenic effects of the adrenergic receptor β2 (ADRB2) are well-established, the role of leptin in activating ADRB2 in triple-negative breast cancer (TNBC) remains unclear. Materials and Methods: The pro-carcinogenic effects of LEPR were investigated using murine TNBC cell lines, 4T1 and EMT6, and a tumor-bearing mouse model. Expression levels of LEPR, NADPH oxidase 4 (NOX4), and ADRB2 in TNBC cells and tumor tissues were analyzed via western blot and quantitative real-time polymerase chain reaction. Changes in reactive oxygen species (ROS) levels were assessed using flow cytometry and MitoSox staining, while immunofluorescence double-staining confirmed the co-localization of LEPR and ADRB2. Results: LEPR activation promoted NOX4-derived ROS and mitochondrial ROS production, facilitating TNBC cell proliferation and migration, effects which were mitigated by the LEPR inhibitor Allo-aca. Co-expression of LEPR and ADRB2 was observed on cell membranes, and bioinformatics data revealed a positive correlation between the two receptors. Leptin activated both LEPR and ADRB2, enhancing intracellular ROS generation and promoting tumor progression, which was effectively countered by a specific ADRB2 inhibitor ICI118551. In vivo, leptin injection accelerated tumor growth and lung metastases without affecting appetite, while treatments with Allo-aca or ICI118551 mitigated these effects. Conclusion This study demonstrates that leptin stimulates the growth and metastasis of TNBC through the activation of both LEPR and ADRB2, resulting in increased ROS production. These findings highlight LEPR and ADRB2 as potential biomarkers and therapeutic targets in TNBC.

Purpose: Leptin interacts not only with leptin receptor (LEPR) but also engages with other receptors. While the pro-oncogenic effects of the adrenergic receptor β2 (ADRB2) are well-established, the role of leptin in activating ADRB2 in triple-negative breast cancer (TNBC) remains unclear. Materials and Methods: The pro-carcinogenic effects of LEPR were investigated using murine TNBC cell lines, 4T1 and EMT6, and a tumor-bearing mouse model. Expression levels of LEPR, NADPH oxidase 4 (NOX4), and ADRB2 in TNBC cells and tumor tissues were analyzed via western blot and quantitative real-time polymerase chain reaction. Changes in reactive oxygen species (ROS) levels were assessed using flow cytometry and MitoSox staining, while immunofluorescence double-staining confirmed the co-localization of LEPR and ADRB2. Results: LEPR activation promoted NOX4-derived ROS and mitochondrial ROS production, facilitating TNBC cell proliferation and migration, effects which were mitigated by the LEPR inhibitor Allo-aca. Co-expression of LEPR and ADRB2 was observed on cell membranes, and bioinformatics data revealed a positive correlation between the two receptors. Leptin activated both LEPR and ADRB2, enhancing intracellular ROS generation and promoting tumor progression, which was effectively countered by a specific ADRB2 inhibitor ICI118551. In vivo, leptin injection accelerated tumor growth and lung metastases without affecting appetite, while treatments with Allo-aca or ICI118551 mitigated these effects. Conclusion This study demonstrates that leptin stimulates the growth and metastasis of TNBC through the activation of both LEPR and ADRB2, resulting in increased ROS production. These findings highlight LEPR and ADRB2 as potential biomarkers and therapeutic targets in TNBC.

Purpose: Leptin interacts not only with leptin receptor (LEPR) but also engages with other receptors. While the pro-oncogenic effects of the adrenergic receptor β2 (ADRB2) are well-established, the role of leptin in activating ADRB2 in triple-negative breast cancer (TNBC) remains unclear. Materials and Methods: The pro-carcinogenic effects of LEPR were investigated using murine TNBC cell lines, 4T1 and EMT6, and a tumor-bearing mouse model. Expression levels of LEPR, NADPH oxidase 4 (NOX4), and ADRB2 in TNBC cells and tumor tissues were analyzed via western blot and quantitative real-time polymerase chain reaction. Changes in reactive oxygen species (ROS) levels were assessed using flow cytometry and MitoSox staining, while immunofluorescence double-staining confirmed the co-localization of LEPR and ADRB2. Results: LEPR activation promoted NOX4-derived ROS and mitochondrial ROS production, facilitating TNBC cell proliferation and migration, effects which were mitigated by the LEPR inhibitor Allo-aca. Co-expression of LEPR and ADRB2 was observed on cell membranes, and bioinformatics data revealed a positive correlation between the two receptors. Leptin activated both LEPR and ADRB2, enhancing intracellular ROS generation and promoting tumor progression, which was effectively countered by a specific ADRB2 inhibitor ICI118551. In vivo, leptin injection accelerated tumor growth and lung metastases without affecting appetite, while treatments with Allo-aca or ICI118551 mitigated these effects. Conclusion This study demonstrates that leptin stimulates the growth and metastasis of TNBC through the activation of both LEPR and ADRB2, resulting in increased ROS production. These findings highlight LEPR and ADRB2 as potential biomarkers and therapeutic targets in TNBC.

Within six months of the discovery of X-ray in 1895, the technology was used to scan the interior of the human body, paving the way for many innovations in the field of medicine, including an ultrasound device in 1950, a CT scanner in 1972, and MRI in 1980. More recent decades have witnessed developments such as digital imaging using a picture archiving and communication system, computer-aided detection/diagnosis, organ-specific workstations, and molecular, functional, and quantitative imaging. One of the latest technical breakthrough in the field of radiology has been imaging genomics and robotic interventions for biopsy and theragnosis. This review provides an engineering perspective on these developments and several other megatrends in radiology.
Biological Markers/analysis ; Biomedical Engineering ; Diagnosis, Computer-Assisted/*trends ; Diagnostic Imaging/*trends ; Equipment Design ; Genomics ; Humans ; Image Processing, Computer-Assisted/*trends ; Radiology Information Systems/*trends ; Robotics ; Systems Integration ; User-Computer Interface

OBJECTIVES: Nail has been a substitute DNA source for genotyping. To investigate the integrity and consistency of nail DNA amplification for biomarker study, nail clippings from 12 subjects were collected at monthly intervals. The possibility of longer amplification and existence of GAPDH RNA/protein, were also investigated with three nail samples. METHODS: Three primer sets were designed for quantitative amplification of nuclear and mitochondrial genes and analysis of their consistency. The mean threshold cycles in amplification of the target genes were compared to test the consistency of polymerase chain reaction (PCR) performance among individual factors including age groups, sex, family, the nail source, and by the size of the amplification segments. RESULTS: The amplification of the target genes from nail DNA showed similar integrity and consistency between the nail sources, and among the serial collections. However, nail DNA from those in their forties showed earlier threshold cycles in amplification than those in their teens or seventies. Mitochondrial DNA (mtDNA) showed better DNA integrity and consistency in amplification of all three targets than did nuclear DNA (nucDNA). Over 9 kb of mtDNA was successfully amplified, and nested quantitative PCR showed reliable copy numbers (%) between the two loci. Reverse transcription PCR for mRNA and immunoblotting for GAPDH protein successfully reflected their corresponding amounts. Regarding the existence of RNA and protein in nails, more effective extraction and detection methods need to be set up to validate the feasibility in biomarker study. CONCLUSIONS: Nail DNA might be a feasible intra-individual monitoring biomarker. Considering integrity and consistency in target amplification, mtDNA would be a better target for biomarker research than nucDNA.
Adult ; Age Factors ; Aged ; Biological Markers/analysis ; Child ; DNA/*analysis/isolation & purification ; DNA Primers ; DNA, Mitochondrial/analysis ; Feasibility Studies ; Female ; Gene Amplification ; Humans ; Male ; Middle Aged ; Nails/*chemistry ; Pilot Projects

OBJECTIVE:To establish HPLC fingerprints of Miao medicine Ardisia crenata.METHODS:HPLC method was adopted.The determination was performed on Diamonsil C18 column with mobile phase consiste of methanol-water (gradient elution) at the flow rate of 1.0 mL/min.The detection wavelength was 220 nm,and column temperature was maintained at 30 ℃.The sample size was 10 μL.Using 11-O-(3',4',5'-three-o-galloylhyperin)-bergeninum as reference,HPLC fingerprints of 16 batches of samples were determined.Common identification and similarity evaluation were performed by using TCM Chromatographic Fingerprint Similarity Evaluation Software (2012 edition).Cluster analysis of fmgerprrints was conducted.RESULTS:There were 6 common peaks in HPLC fingerprints of 16 batches of samples.The similarity among 8 batches was more than 0.9.The 16 batches of samples could be clustered into 4 categories.CONCLUSIONS:Established fingerprints can provide reference for identification and quality evaluation ofA.crenata.