Photoacoustic Spectroscopy Gas Detection Technology Research Progress.

Photoacoustic spectroscopy (PAS) can be utilized as an ultrasensitive gas detection method. The basic principles of gas detection using PAS are discussed in this paper. First, the basic instrumentation for a PAS gas detection system is introduced focusing on the photoacoustic cell. The discussion includes non-resonant photoacoustic cells and the different types of resonant photoacoustic cells, including the longitudinal photoacoustic cell, the Helmholtz photoacoustic cell, the T-type photoacoustic cell, and the high-frequency resonant photoacoustic cell. The basic working principles of each of these, cells as well as the advantages and disadvantages of photoacoustic cells are discussed, and the development of newer types of photoacoustic cells in recent years is outlined in detail. This review provides detailed reference information and guidance for interested researchers who would like to design and build advanced photoacoustic cells for gas detection.

Significance of m6A in subtype identification, immunological evolution, and therapeutic sensitivity of RA.

N6-methyladenosine (m6A) is one kind of important epigenetic modification pattern which is extensively involved in immune regulation. The development and progression of autoimmune diseases are closely related to immune dysregulation. Considering that rheumatoid arthritis (RA) is a typical autoimmune disease, the m6A process might be one of the important regulatory mechanisms in the pathogenesis of RA. In this study, we identified five differentially expressed m6A regulators in normal and RA samples from the GEO database. With these five regulators, we constructed the nomogram, and it could accurately identify the risk of RA morbidity. Next, we identified 121 differentially expressed genes (DEGs) between normal and RA samples, of which 36 DEGs were co-expressed with these five m6A regulators. We noted that these DEGs were highly enriched in multiple immunoregulatory signaling pathways, such as cytokine-mediated immune cell chemotaxis, adhesion, and activation. To further characterize the heterogeneity of immunological features, we clustered the RA samples into two subtypes. The C2 subtype has higher infiltration levels of pro-inflammatory cells and activity of pro-inflammatory signaling pathways. Thus, the inflammatory response might be more vigorous in the C2 subtype. Next, we constructed the m6Asig system with the SVM machine learning algorithms and least absolute shrinkage and selection operator (LASSO) regression. The m6Asig could accurately distinguish the C1 and C2 subtypes, which indicated that the m6Asig could be a potential biomarker for the inflammatory activity of RA. Finally, by comparing the information from the CellMiner, TTD, and DrugBank databases, we determined 25 drugs. The targets of these drugs were positively correlated with m6Asig. To be clarified, the above findings were derived from bioinformatics and statistical analyses, and further experimental validation still requires. In summary, this study further revealed the m6A and immunoregulation mechanisms in RA pathogenesis. Also, the m6Asig could be a novel biomarker with potential applicability in the clinical management of RA.

Irisin mitigates rheumatoid arthritis by suppressing mitochondrial fission via inhibiting YAP-Drp1 signaling pathway.

BACKGROUND: Irisin is a hormone-like factor secreted by muscle cells and produced by cleavage of the membrane protein fibronectin type III domain protein 5 (FNDC5), which exerts anti-inflammatory and anti-proliferative effects. However, the effects and the underlying mechanisms of irisin in rheumatoid arthritis (RA) are still unclear. METHOD: Collagen-induced arthritis (CIA) model was induced in DBA/1 mice and then treated with irisin. Arthritis index, paw thickness, weight, number of affected paws, serum inflammatory factors and related pathological tests were measured. RA fibroblast-like synoviocytes (RA-FLSs) were pretreated with IL-1ß and irisin, and the migration, proliferation, invasion, oxidative stress and mitochondrial related function of RA-FLSs were detected. RESULTS: Irisin significantly improved arthritis symptoms in CIA mice, as indicated by reduced arthritis index, alleviated paw thickness, decreased the number of affected paws and inhibited release of inflammatory factors. Irisin alleviated joint destruction, FLSs proliferation and the expression of YES-associated protein (YAP) and mitochondrial dynamic related protein 1 (Drp1) in the FLSs of CIA mice. In vitro experiment, irisin inhibited the proliferation, migration and invasion of RA-FLSs and improved oxidative stress induced by IL-1ß, thereby restraining the pathogenic transformation of RA-FLSs. Mechanically, irisin suppressed the nuclear translocation of YAP, in turn, could reduce the synthesis of Drp1 protein and inhibit the mitochondrial fission of RA-FLSs, which was reversed by YAP agonists. Therefore, irisin has a protective effect on RA. CONCLUSION: Irisin inhibits the proliferation, migration, invasion and inflammatory response of RA-FLSs by inhibiting the YAP-Drp1 signaling pathway, which implies a potential therapeutic effect on RA.

Bifunctional Interface Passivation via Copper Acetylacetonate for Efficient and Stable Perovskite Solar Cells.

Manipulating interface defects can minimize interfacial nonradiative recombination, thus increasing the stability and performance of perovskite solar cells (PSCs). Here, copper acetylacetonate [Cu(acac)2] as a passivator is used to treat the interface between Spiro-OMeTAD and perovskite. Owing to the strong chelation, the uncoordinated Pb2+ could react with -C═O/-COH functional groups, firmly anchoring acetylacetonate at this interface or the grain boundaries (GBs) of perovskite films to construct multiple ligand bridges, accompanied by the p-type copper iodide formation with copper substituting lead. Simultaneously, Cu+-Cu2+ pairs transfer electrons from Pb0 to I0, suppressing deep level defects of Pb0 and I0 near the perovskite interface. These can be beneficial to hole-transferring. Moreover, the Schiff base complexes with hydrophobicity, from the reaction of acetylacetonate with perovskite, can lead to tightly packed adjacent perovskite surfaces and self-seal the GBs of the perovskite, inhibiting moisture diffusion for long-term stability. Consequently, the Cu(acac)2-based PSC has achieved more than 24% champion efficiency while retaining ca. 92% of the initial power conversion efficiency after 1680 h of storage.

Lead-Free Halide Double Perovskite for High-Performance Photodetectors: Progress and Perspective.

Lead halide perovskite has become a promising candidate for high-performance photodetectors (PDs) due to its attractive optical and electrical properties, such as high optical absorption coefficient, high carrier mobility, and long carrier diffusion length. However, the presence of highly toxic lead in these devices has limited their practical applications and even hindered their progress toward commercialization. Therefore, the scientific community has been committed to searching for low-toxic and stable perovskite-type alternative materials. Lead-free double perovskite, which is still in the preliminary stage of exploration, has achieved inspiring results in recent years. In this review, we mainly focus on two types of lead-free double perovskite based on different Pb substitution strategies, including A2M(I)M(III)X6 and A2M(IV)X6. We review the research progress and prospects of lead-free double perovskite photodetectors in the past three years. More importantly, from the perspective of optimizing the inherent defects in materials and improving device performance, we propose some feasible pathways and make an encouraging perspective for the future development of lead-free double perovskite photodetectors.

Noninvasive Imaging OX40+ Activated T Cells Provides Early Warning of Rheumatoid Arthritis.

PURPOSE: The goal of this study was to develop an imaging probe-IRDye-680RD-OX40 mAb-that can be used for noninvasive imaging and optical imaging of rheumatoid arthritis (RA). OX40/OX40 ligand (OX40L) interactions have been shown to exert potent costimulatory effects on T cell activation. Detectable change in T cell activation profiles was observed in early RA. METHODS: OX40 expression pattern was analyzed by flow cytometry. N-hydroxysuccinimide (NHS) esters are used to label proteins selectively on free amino groups of OX40 monoclonal antibody (mAb). Characterization of IRDye-680RD-OX40 mAb was measured and a fluorescence spectrum gathered. Cell binding assay was also performed between activated and naïve murine T cells. Longitudinal near-infrared fluorescence (NIRF) imaging of the probe was performed on day 8, day 9, day 10, and day 11 of adjuvant-induced arthritis (AIA) mouse model. Paw thickness and body weight were compared between the OX40 mAb and IgG injection groups. RESULTS: NIRF imaging with IRDye-680RD-OX40 mAb revealed strong OX40-positive responses with high specificity. Flow analysis showed that OX40 was specifically expressed on the surface of T cells in RP and spleen of AIA model. The AIA group was significantly differentiated from the control group at all time points with imaging monitoring. The region of interest (ROI) was in line with ex vivo imaging and biodistribution study. This study highlights the potential utility of the OX40 NIRF imaging as a new strategy for RA prediction and T cell monitoring. CONCLUSION: The results provide evidence that IRDye-680RD-OX40 mAb detects organized T cells activation in early RA. The optical probe was capable of detection of RA pathogenesis. It identified transcriptional responses to RA that mediate its immune functions. Thus, it may be an ideal probe for RA imaging.

Precise diagnosis and successful surgical intervention of the median arcuate ligament syndrome: A case report.

INTRODUCTION AND IMPORTANCE: The median arcuate ligament syndrome (MALS) is a rare disorder that produces a spectrum of symptoms due to compression of the arcuate ligament, clinically manifested primarily by abdominal pain, nausea, vomiting, and weight loss. The mechanism of these symptoms has not yet been revealed, and the current treatment methods are still somewhat controversial. CASE PRESENTATION: We present a 54-year-old woman who presented with intermittent epigastric pain for nine months. During the onset, she lost 7.5 kg. After routine examinations in a nearby hospital, no abnormality was found. She was referred to us. CTA showed compression of the celiac artery. Further selective celiac angiography at the end of inspiration and expiration confirmed MALS. After consultation with the patient, the decision to have a laparotomy was made. The celiac artery was completely skeletonized, and external compression on the artery was released. Postoperative symptoms improved significantly. One-year follow-up after the operation, she had a weight gain of 4.8 kg and was satisfied with the surgical results. CLINICAL DISCUSSION: The manifestations of MALS are varied and challenging. Our patient presented with weight loss and intermittent abdominal pain. The mutual confirmation of multiple investigations can provide a more comprehensive overview of celiac artery compression. We confirmed using ultrasonography, CT angiography, and selective digital subtraction angiography in this case. The celiac artery compression was relieved after open surgery. Our patient's symptoms improved significantly after surgery. We hope our treatment method can provide a reference for MALS diagnosis and treatment. CONCLUSION: It is challenging to diagnose MALS. Cross-confirmation of multiple examinations can provide a more comprehensive view of celiac compression. Surgical decompression of the celiac artery (open or laparoscopic surgery) may be an effective therapy for MALS, especially in centers with experience.

CXCR4 antagonist AMD3100 enhances therapeutic efficacy of transcatheter arterial chemoembolization in rats with hepatocellular carcinoma.

This study aims to discover the therapeutic effect of chemokine (CXC motif) receptor 4 (CXCR4) antagonist AMD3100 combined with transcatheter arterial chemoembolization (TACE) in a rat model with hepatocellular carcinoma (HCC). An orthotopic model of HCC was established and treated with TACE (doxorubicin-lipiodol emulsion) with or without AMD3100. The tumor volume was measured by magnetic resonance imaging (MRI). Histopathological changes were detected by hematoxylin-eosin (HE) staining. HCC cell apoptosis was assessed by terminal deoxyribonucleotidyl transferase (TdT)-mediated biotin-16-dUTP nick-end labeling (TUNEL) staining. Immunohistochemistry was used to detect the expression of CD34, hypoxia-inducible factor 1α (HIF-1α), vascular endothelial growth factor (VEGF), and Ki67. Gene and protein expressions were quantified by quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and western blotting, respectively. Both TACE and AMD3100 reduced the tumor volume in orthotopic rat model of HCC with the decreased CXCR4 expression in tumor tissues, and the combination had better effect. However, TACE increased the microvessel density (MVD) in HCC tissues of rats, while AMD3100 treatment reduced MVD in HCC tissues. AMD3100 reduced the TACE induced MVD in HCC tissues with the reduction of HIF-1α and VEGF expression. Either AMD3100 or TACE could promote HCC cell apoptosis accompanying by decreased cell proliferation, and their combined use had better therapeutic effects. CXCR4 antagonist AMD3100 enhance therapeutic efficacy of TACE in rats with HCC via promoting the HCC cell apoptosis, reducing cell proliferation, and inhibiting MVD, thus reducing tumor volume.

The protective effects of S14G-humanin (HNG) against mono-sodium urate (MSU) crystals- induced gouty arthritis.

Gout is a common and complex form of arthritis that has brought great inconveniences to the normal lives of patients. It is reported that oxidative stress and nod-like receptor family protein 3 (NLRP3) inflammasome-mediated inflammatory reactions are involved in the pathogenesis of gout arthritis. S14G-humanin (S14G-HNG) is a modified peptide of HNG with higher inhibitory activity on the accumulation and deposition of Aß. Recently, S14G-HNG has been reported to exert great anti-inflammatory effects. The present study proposed to explore the possible therapeutic property of S14G-HNG against gout arthritis. An animal model was established by stimulation with mono-sodium urate (MSU) crystals, followed by treatment with colchicine and S14G-HNG, respectively. The elevated Gait score promoted synovitis score and activated myeloperoxidase (MPO) observed in MSU crystals-treated mice were significantly reversed by colchicine and S14G-HNG. Bone marrow-derived macrophages (BMDMs) were isolated from mice and stimulated with MSU crystals, followed by being treated with 25 and 50 µM S14G-HNG. The increased mitochondrial reactive oxygen species (ROS) and Malondialdehyde (MDA) levels, upregulated NADPH oxidase-4 (NOX-4), activated NLRP3 inflammasome, and elevated production of inflammatory factors in MSU crystals-treated BMDMs were dramatically reversed by S14G-HNG, accompanied by the upregulation of sirtuin type-1 (SIRT1). Lastly, the protective effects of S14G-HNG against MSU crystals-induced NLRP3 inflammasome activation were significantly abolished by the knockdown of SIRT1. In conclusion, our data reveal that S14G-HNG could possess potential benefits against MSU crystals-induced gout arthritis, with colchicine displaying a better effect.

LncRNA SNHG14 contributes to proinflammatory cytokine production in rheumatoid arthritis via the regulation of the miR-17-5p/MINK1-JNK pathway.

Rheumatoid arthritis (RA) is a widespread autoimmune disorder of the joints. Long noncoding RNAs (lncRNAs) have been reported to participate in the pathogenesis of RA by serving as competitive endogenous RNAs. LncRNA small nucleolar RNA host gene 14 (SNHG14) is involved in the development of various diseases. Here, we found that high expression of SNHG14 in RA was closely related to the disease activity. Functional assays indicated that SNHG14 knockdown obviously hampered phorbol myristate acetate-activated THP-1 (pTHP-1) cell proliferation and proinflammatory cytokines production. In mechanism, SNHG14 served as a sponge of microRNA-17-5p (miR-17-5p), and misshapen like kinase 1 (MINK1) was a target of miR-17-5p. SNHG14 depletion-induced inhibitory effects on cell proliferation and inflammatory response were reversed by MINK1 overexpression in macrophages. Moreover, SNHG14 promoted the jun N-terminal kinase (JNK) signaling via the miR-17-5p/MINK1 axis. Overall, SNHG14 boosted the process of RA by MINK1 activating the JNK pathway.

Application of Automated Hand Ultrasound Scanning and a Simplified Three-Joint Scoring System for Assessment of Rheumatoid Arthritis Activity.

Ultrasound can be used to objectively diagnose and evaluate disease activity in patients with rheumatoid arthritis (RA). We aimed to determine the value of a new automated hand ultrasound (AHUS) scanning device and a simplified 3-joint ultrasound scoring system (US3) in detecting synovitis in RA. We compared AHUS and traditional ultrasound (US) scanning in detecting synovial hyperplasia (SH), joint effusion, bone erosion and power Doppler (PD) synovitis in 49 patients. In addition, we compared the value of US3 (in which 3 proximal interphalangeal [PIP] and/or metacarpophalangeal [MCP] joints with the highest scores for swelling and tenderness were evaluated) with the 22-joint ultrasound scoring system (US22) in 26 patients. Almost perfect κ coefficients (0.86-0.937) were obtained between AHUS and traditional US in detecting SH, joint effusion, bone erosion and PD synovitis (p < 0.001). The intra-class correlation coefficient (ICC) between AHUS and traditional US was 0.955-0.995. Of the US3 findings in AHUS, SH synovitis and PD synovitis were positively correlated with DAS28-CRP (adjusted R2 = 0.421, p < 0.0001; adjusted R2 = 0.365, p < 0.0001). US3 was highly correlated with US22 in detecting SH and PD synovitis (R = 0.792, p < 0.01; R = 0.948, p < 0.01). Compared with US22, a more significant correlation was identified between US3 scores and most clinical and laboratory values. In conclusion, AHUS performed comparably to traditional US in detecting synovitis in RA, and US3 was highly consistent with US22 in assessing synovitis and was positively correlated with RA disease activity.

Baicalein modulates the radiosensitivity of cervical cancer cells in vitro via miR-183 and the JAK2/STAT3 signaling pathway.

BACKGROUND: Increasing radiosensitivity of cancer cells can enhance the efficacy of cervical cancer treatment. OBJECTIVES: This study evaluated the potential roles and mechanism of baicalein in regulating the radiosensitivity of cervical cancer cells in vitro. MATERIAL AND METHODS: Real-time quantitative polymerase chain reaction (RT-qPCR) was used to assess miR-183 expression in End1/E6E7 cells, Hela cells and Hela cells irradiated with X-ray (0 Gy, 1 Gy, 3 Gy, 5 Gy, and 10 Gy). Cell Counting Kit-8 (CCK-8) method measured cell viability of Hela cells after miR-183 regulation, baicalein or RO8191 treatment. Apoptosis rates were detected using flow cytometry. Thereafter, expression of Bcl-2, Bax and caspase-3 RNA was also detected through RT-qPCR. Protein concentrations of E-cadherin, N-cadherin, Vimentin in epithelial-mesenchymal transition (EMT), phospho-JAK2/STAT3, and total Janus kinase 2/signal transducer and activator of transcription 3 STAT3 (JAK2/STAT3) were examined using enzyme-linked immunosorbent assay (ELISA) methods. RO8191, a JAK2/STAT3 activator, was used to activate the JAK2/STAT3 signaling pathway. RESULTS: The miR-183 expression was significantly lower in Hela cells compared to End1/E6E7 cells. Following upregulation of miR-183 in Hela cells, cell viability was inhibited while apoptosis was promoted. Moreover, EMT was inhibited after miR-183 over-expression. X-ray treatment markedly reduced the cell survival rate and increased miR-183 RNA expression. Baicalein treatment severely reduced the cell viability of 10-Gy X-ray-irradiated Hela cells, partially reversing the effect of miR-183, and also increased apoptosis and prevented EMT in irradiated cells. Y1007/8 in JAK2 and tyrosine (Tyr) residue 705 of STAT3 were phosphorylated, resulting in high expression of JAK2/STAT3, which was decreased by irradiation and baicalein treatment. RO8191 activated JAK2/STAT3 signaling, promoted cell viability and EMT, and inhibited cell apoptosis, while baicalein partly reversed the functions of RO8191. CONCLUSIONS: Baicalein inhibited cell viability and EMT, and induced cell apoptosis of Hela cells, through upregulating miR-183 via inactivation of the JAK2/STAT3 signaling pathway.

Dysregulation of intercellular signaling by MOF deletion leads to liver injury.

Epigenetic mechanisms that alter heritable gene expression and chromatin structure play an essential role in many biological processes, including liver function. Human MOF (males absent on the first) is a histone acetyltransferase that is globally downregulated in human steatohepatitis. However, the function of MOF in the liver remains unclear. Here, we report that MOF plays an essential role in adult liver. Genetic deletion of Mof by Mx1-Cre in the liver leads to acute liver injury, with increase of lipid deposition and fibrosis akin to human steatohepatitis. Surprisingly, hepatocyte-specific Mof deletion had no overt liver abnormality. Using the in vitro coculturing experiment, we show that Mof deletion-induced liver injury requires coordinated changes and reciprocal signaling between hepatocytes and Kupffer cells, which enables feedforward regulation to augment inflammation and apoptotic responses. At the molecular level, Mof deletion induced characteristic changes in metabolic gene programs, which bore noticeable similarity to the molecular signature of human steatohepatitis. Simultaneous deletion of Mof in both hepatocytes and macrophages results in enhanced expression of inflammatory genes and NO signaling in vitro. These changes, in turn, lead to apoptosis of hepatocytes and lipotoxicity. Our work highlights the importance of histone acetyltransferase MOF in maintaining metabolic liver homeostasis and sheds light on the epigenetic dysregulation in liver pathogenesis.

Somatic mutations in colorectal cancer are associated with the epigenetic modifications.

Colorectal cancer (CRC) mostly arises from progressive accumulation of somatic mutations within cells. Most commonly mutated genes like TP53, APC and KRAS can promote survival and proliferation of cancer cells. Although the molecular alterations and landscape of some specific mutations in CRC are well known, the presence of a somatic mutation signature related to genomic regions and epigenetic markers remain unclear. To find the signatures from a random distribution of somatic mutations in CRCs, we carried out enrichment analysis in different genomic regions and identified peaks of epigenetic markers. We validated that the mutation frequency in miRNA is dramatically higher than in flanking genomic regions. Moreover, we observed that somatic mutations in CRC and colon cancer cell lines are significantly enriched in CTCF binding sites. We also found these mutations are enriched for H3K27me3 in both normal sigmoid colon and colon cancer cell lines. Taken together, our findings suggest that there are some common somatic mutations signatures which provide new directions to study CRC.

[Research progress on the application of lower limb alignment in discoid meniscus injury].

Discoid meniscus injury is a kind of common sports injury. Its treatment methods include arthroscopic discoid meniscus plasty, discoid meniscus subtotal resection, discoid meniscus total resection and so on. Although the short-term clinical effect is good, the long-term clinical effect is not ideal. At present, different scholars have different views on the choice of surgical methods for discoid meniscus injury. In recent years, many scholars have shown that the choice of operation and the change of lower limb force line are related to the therapeutic effect of discoid meniscus injury. This paper mainly summarizes the current situation of the treatment of discoid meniscus injury and the changes of the force line of the lower limbs after operation, and expounds therole of the evaluation of the force line of the lower limbs in the treatment of discoid meniscus, so as to provide the basis for the clinical individualized treatment of discoid meniscus injury.

Peripheral Vascular Disease and Implication of Nursing Practice: A Brief Literature Review.

Nowadays nurse practitioners are working in several acute hospital settings in different specialized departments. For decades, studies have shown the implications of nurse practice in peripheral vascular disease (PVD) and peripheral vascular intervention (PVI) to have several major benefits. However, there are very limited studies and data on this particular aspect. In this literature review, we briefly discuss the implication of nursing practice in PVD/PVI. This review briefly shows that nursing practice has a major contribution and implication in the treatment of patients with PVD or PVI, especially in patients with diabetes mellitus. From available research, we briefly discuss the implication of nursing practice pre- and postoperatively for PVI. Nurses also contribute significantly in catheter-directed thrombolytic therapy, in smoking cessation programs organized for patients with PVD, and in screening patients for PVD. The vascular nurse practitioners are also involved in providing healthcare advice in order to reduce the risk of disease progression. The major lack of research in this particular field should further inspire scientists to develop and carry out research to further investigate and demonstrate the contribution of nurses in the treatment and management of PVD or PVI, which is gradually becoming a major issue.

Menin inhibitor MI-3454 induces remission in MLL1-rearranged and NPM1-mutated models of leukemia.

The protein-protein interaction between menin and mixed lineage leukemia 1 (MLL1) plays a critical role in acute leukemias with translocations of the MLL1 gene or with mutations in the nucleophosmin 1 (NPM1) gene. As a step toward clinical translation of menin-MLL1 inhibitors, we report development of MI-3454, a highly potent and orally bioavailable inhibitor of the menin-MLL1 interaction. MI-3454 profoundly inhibited proliferation and induced differentiation in acute leukemia cells and primary patient samples with MLL1 translocations or NPM1 mutations. When applied as a single agent, MI-3454 induced complete remission or regression of leukemia in mouse models of MLL1-rearranged or NPM1-mutated leukemia, including patient-derived xenograft models, through downregulation of key genes involved in leukemogenesis. We also identified MEIS1 as a potential pharmacodynamic biomarker of treatment response with MI-3454 in leukemia, and demonstrated that this compound is well tolerated and did not impair normal hematopoiesis in mice. Overall, this study demonstrates, for the first time to our knowledge, profound activity of the menin-MLL1 inhibitor as a single agent in clinically relevant PDX models of leukemia. These data provide a strong rationale for clinical translation of MI-3454 or its analogs for leukemia patients with MLL1 rearrangements or NPM1 mutations.

In vivo monitoring of rashes caused by systemic lupus erythematosus disease using snapshot spectral imaging.

Monitoring the activity of systemic lupus erythematosus (SLE) is important to patient management. Blood biochemical indexes are commonly assessed but are both time demanding and traumatizing. In this study, a noninvasive and real-time spatial-spectral data tool was used to monitor SLE patients through rash spectral data. To build the relationship between the rash spectrum changes and changes in the patients' status, a snapshot hyperspectral Fourier transform imaging spectrometer was built to monitor the rash reflectance changes of hospitalized SLE patients. A simple rash activity index (RAI) which was normally distributed with the doctor's visual rating of rash severity was calculated from hyperspectral images. The sensitivity of the change in RAI is higher than complement 3/4 levels. RAI and anti-dsDNA antibodies both decreased as the patients recovered. Anti-dsDNA and complement 3/4 were important indicators of SLE activity suggesting that the RAI directly correlated with patient status. The snapshot spectrometer therefore provides an auxiliary method to monitor SLE disease.

[The risk factors of periprosthetic fracture after hip arthroplasty:a meta-analysis].

OBJECTIVE: To explore risk factors of the periprosthetic fracture after hip arthroplasty. METHODS: Potential studies were searched in databases including Pubmed, Embase, Cochrane Library, CNKI as well as Wanfang Database up to November 2018 and references in related literatures. The methodological quality of literature was estimated by Newcastle-Ottawa Scale. Raw data were merged and tested mainly by Revmain 5.3. RESULTS: Seventeen studies in total were appropriate with 90 632 patients. The results revealed that it increased the risk of periprosthetic fracture after hip arthroplasty, including female (OR=1.62, 95%CI:1.44 to 1.82, P<0.01), revision(OR=3.78, 95%CI:1.88 to 7.58, P<0.01), preoperative diagnosis of rheumatoid arthritis(OR=1.60, 95%CI:1.07 to 2.37, P=0.02). Conversely, patients involved with cemented prosthesis fixation(OR=0.43, 95%CI:0.27 to 0.68, P<0.01) were less likely to suffer periprosthetic fracture after hip arthroplasty. Other factors were not significantly relevant to periprosthetic fracture after hip arthroplasty, including the age, preoperative diagnosis(femoral head necrosis, osteoarthritis, developmental dysplasia of the hip, femoral fracture, concomitant heart diseases) and American Society of Anesthesiologists >=3. CONCLUSIONS: Orthopedics doctors should constantly be cantious about the risk factors including female, revision and diagnosis of rheumatoid arthritis. They are supposed to prevent the periprosthetic fracture by gentle operation during hip arthroplasty and monitoring the functional exercise after operations when the above risk factors occur.

A temperature-sensitive phase-change hydrogel of tamoxifen achieves the long-acting antitumor activation on breast cancer cells.

Background: Breast cancer is one of the foremost threats to female health nowadays. Tamoxifen, an antagonist of estrogen receptor-α (ERα), is the first choice for endocrine-dependent breast cancer (ERα-positive breast cancer) treatment. However, ERα has an important function in the normal physical regulation of estrogen, and current oral administration of tamoxifen has potential side effects on normal endocrine secretion. In the present work, we aim to develop novel approaches to increase the antitumor effect of tamoxifen on breast cancer cells and decrease the potential side effects in the human body during treatment. Methods: A temperature-sensitive phase-change hydrogel for tamoxifen (Tam-Gel) was generated. After establishing subcutaneous tumors formed by MCF-7, an ERα-positive breast cancer cell line, in nude mice, an intratumoral injection of Tam-Gel was performed to examine whether Tam-Gel facilitated the slow-release or antitumor effect of tamoxifen. A metastatic breast cancer model was established using the intrahepatic growth of MCF-7 cells in immunodeficient rats. Results: Tam-Gel can transform from liquid to hydrogel at room temperature. An intratumoral injection of Tam-Gel facilitated the slow-release or antitumor effect of tamoxifen. Once Tam-Gel, but not Tam-Sol, was administered by intratumoral injection, it significantly decreased the uptake of radionuclide probes (18F-fluoroestradiol or 18F-fluorodeoxyglucose) by cells in rats' livers and the intrahepatic growth of MCF-7 cells in rats' livers. Conclusion: A novel slow-release system was successfully prepared to facilitate the long-term release of tamoxifen in breast cancer tissues, and achieved an antitumor effect in the long term.