High-order LP modes based Sagnac interference for temperature sensing with an enhanced optical Vernier effect.

In this paper, high-order LP modes based Sagnac interference for temperature sensing are proposed and investigated theoretically. Based on the specific high-order LP modes excited through the mode selective couplers (MSCs), we design a stress-induced Panda-type few-mode fiber (FMF) supporting 4 LP modes and construct a Sagnac interferometer to achieve a highly sensitive temperature sensor. The performances of different LP modes (LP01, LP11, LP21, and LP02) are explored under a single Sagnac interferometer and paralleled Sagnac interferometers, respectively. LP21 mode has the highest temperature sensitivity. Compared with fundamental mode (LP01), the temperature sensitivity based on LP21 mode improved by 18.2% at least. In addition, a way to achieve the enhanced optical Vernier effect is proposed. It should be noted that two Sagnac loops are located in two temperature boxes of opposite variation trends, respectively. Both two Sagnac interferometers act as the sensing element, which is different from the traditional optical Vernier effect. The temperature sensitivity of novel enhanced optical Vernier effect is magnified by 8 times, which is larger than 5 times the traditional Vernier effect. The novel approach avoids measurement errors and improves the stability of the sensing system. The focus of this research is on high-order mode interference, which has important guiding significance for the development of highly sensitive Sagnac sensors.

Xanthones from securidaca inappendiculata antagonizes the anti-rheumatic effect of methotrexate by inhibiting reduced folate carrier 1.

BACKGROUND: The first-line anti-rheumatic drug methotrexate (MTX) is used in the combination. Because of the unpredictable adverse reactions, optimization of relevant regimens is necessary and meaningful. This study aimed to study the possible interaction between Securidaca inappendiculate Hassk. Derived xanthones and MTX. METHODS: We established adjuvant-induced arthritis (AIA) model, which was treated with MTX and MTX + xanthone-rich fraction (XRF). The clinical efficacy was evaluated by histopathological examination, and LC-MS was used to monitor the blood concentration of MTX. Western blotting and immunohistochemistry were used to detect protein expression. In vitro, we assessed the activity of related transporters by cellular uptake assay based on HEK-293T cells. RESULTS: Compared with MTX-treated rats, inflammation in the immunized rats in the MTX + XRF group was obvious, indicating that XRF antagonized the anti-rheumatic effect of MTX. Meanwhile, XRF reduced liver and kidney injuries caused by MTX in addition to MTX. Results from immunohistochemical and nappendiculat assays suggested that XRF may reduce uptake of MTX by down-regulating reduced folate carrier 1 (RFC1). CONCLUSION: This study indicated that XRF could reduce the plasma concentration of MTX by inhibiting the expression of RFC1, antagonize the therapeutic effect of MTX on AIA rats, and reduce its oral bioavailability. The combination of S. inappendiculate and MTX should be further optimized to achieve the goal of increasing efficiency and reducing toxicity.

The Effect of α7nAChR Signaling on T Cells and Macrophages and Their Clinical Implication in the Treatment of Rheumatic Diseases.

Rheumatoid arthritis (RA) is one of the most common autoimmune disease and until now, the etiology and pathogenesis of RA is not fully understood, although dysregulation of immune cells is one of the leading cause of RA-related pathological changes. Based on current understanding, the priority of anti-rheumatic treatments is to restore immune homeostasis. There are several anti-rheumatic drugs with immunomodulatory effects available nowadays, but most of them have obvious safety or efficacy shortcomings. Therefore, the development of novel anti-rheumatic drugs is still in urgently needed. Cholinergic anti-inflammatory pathway (CAP) has been identified as an important aspect of the so-called neuro-immune regulation feedback, and the interaction between acetylcholine and alpha 7 nicotinic acetylcholine receptor (α7nAChR) serves as the foundation for this signaling. Consistent to its immunomodulatory functions, α7nAChR is extensively expressed by immune cells. Accordingly, CAP activation greatly affects the differentiation and function of α7nAChR-expressing immune cells. As a result, targeting α7nAChR will bring profound therapeutic impacts on the treatment of inflammatory diseases like RA. RA is widely recognized as a CD4+ T cells-driven disease. As a major component of innate immunity, macrophages also significantly contribute to RA-related immune abnormalities. Theoretically, manipulation of CAP in immune cells is a feasible way to treat RA. In this review, we summarized the roles of different T cells and macrophages subsets in the occurrence and progression of RA, and highlighted the immune consequences of CAP activation in these cells under RA circumstances. The in-depth discussion is supposed to inspire the development of novel cell-specific CAP-targeting anti-rheumatic regimens.

In Situ Raman Observation of Oxygen Activation and Reaction at Platinum-Ceria Interfaces during CO Oxidation.

Understanding the fundamental insights of oxygen activation and reaction at metal-oxide interfaces is of significant importance yet remains a major challenge due to the difficulty in in situ characterization of active oxygen species. Herein, the activation and reaction of molecular oxygen during CO oxidation at platinum-ceria interfaces has been in situ explored using surface-enhanced Raman spectroscopy (SERS) via a borrowing strategy, and different active oxygen species and their evolution during CO oxidation at platinum-ceria interfaces have been directly observed. In situ Raman spectroscopic evidence with isotopic exchange experiments demonstrate that oxygen is efficiently dissociated to chemisorbed O on Pt and lattice Ce-O species simultaneously at interfacial Ce3+ defect sites under CO oxidation, leading to a much higher activity at platinum-ceria interfaces compared to that at Pt alone. Further in situ time-resolved SERS studies and density functional theory simulations reveal a more efficient molecular pathway through the reaction between adsorbed CO and chemisorbed Pt-O species transferred from the interfaces. This work deepens the fundamental understandings on oxygen activation and CO oxidation at metal-oxide interfaces and offers a sensitive technique for the in situ characterization of oxygen species under working conditions.

Approaching Charge Separation Efficiency to Unity without Charge Recombination.

Improving the efficiency of charge separation (CS) and charge transport (CT) is essential for almost all optoelectronic applications, yet its maximization remains a big challenge. Here we propose a conceptual strategy to achieve CS efficiency close to unity and simultaneously avoid charge recombination (CR) during CT in a ferroelectric polar-discontinuity (PD) superlattice structure, as demonstrated in (BaTiO_{3})_{m}/(BiFeO_{3})_{n}, which is fundamentally different from the existing mechanisms. The competition of interfacial dipole and ferroelectric PD induces opposite band bending in BiFeO_{3} and BaTiO_{3} sublattices. Consequently, the photoexcited electrons (e) and holes (h) in individual sublattices move forward to the opposite interfaces forming electrically isolated e and h channels, leading to a CS efficiency close to unity. Importantly, the spatial isolation of conduction channels in (BaTiO_{3})_{m}/(BiFeO_{3})_{n} enable suppression of CR during CT, thus realizing a unique band diagram for spatially orthogonal CS and CT. Remarkably, (BaTiO_{3})_{m}/(BiFeO_{3})_{n} can maintain a high photocurrent and large band gap simultaneously. Our results provide a fascinating illumination for designing artificial heterostructures toward ideal CS and CT in optoelectronic applications.

NT3-chitosan elicits robust endogenous neurogenesis to enable functional recovery after spinal cord injury.

Neural stem cells (NSCs) in the adult mammalian central nervous system (CNS) hold the key to neural regeneration through proper activation, differentiation, and maturation, to establish nascent neural networks, which can be integrated into damaged neural circuits to repair function. However, the CNS injury microenvironment is often inhibitory and inflammatory, limiting the ability of activated NSCs to differentiate into neurons and form nascent circuits. Here we report that neurotrophin-3 (NT3)-coupled chitosan biomaterial, when inserted into a 5-mm gap of completely transected and excised rat thoracic spinal cord, elicited robust activation of endogenous NSCs in the injured spinal cord. Through slow release of NT3, the biomaterial attracted NSCs to migrate into the lesion area, differentiate into neurons, and form functional neural networks, which interconnected severed ascending and descending axons, resulting in sensory and motor behavioral recovery. Our study suggests that enhancing endogenous neurogenesis could be a novel strategy for treatment of spinal cord injury.

Differential expression and clinical significance of long non-coding RNAs in the development and progression of lung adenocarcinoma.

With the development of gene testing technology, we have found many different genes, and lncRNA is one of them. LncRNAs refer to a non-protein coding RNA molecule with a length of more than 200bp, which is one of the focuses of research on human malignant diseases such as LUAD. LncRNAs act as an oncogene or inhibitor to regulate the occurrence and progression of tumors. The differential expression of LncRNAs promotes or inhibits the progression of lung adenocarcinoma by affecting cell proliferation, metastasis, invasion, and apoptosis, thus affecting the prognosis and survival rate of patients. Therefore, LncRNAs can be used as a potential target for diagnosis and treatment of cancer. The early diagnosis of the disease was made through the detection of tumor markers. Because lung adenocarcinoma is not easy to diagnose in the early stage and tumor markers are easy to ignore, LncRNAs play an important role in the diagnosis and treatment of lung adenocarcinoma. The main purpose of this article is to summarize the known effects of LncRNAs on lung adenocarcinoma, the effect of differential expression of LncRNAs on the progression of lung adenocarcinoma, and related signal transduction pathways. And to provide a new idea for the future research of lung adenocarcinoma-related LncRNAs.

α-Mangostin Inhibited M1 Polarization of Macrophages/Monocytes in Antigen-Induced Arthritis Mice by Up-Regulating Silent Information Regulator 1 and Peroxisome Proliferators-Activated Receptor γ Simultaneously.

Background: α-Mangostin (MG) showed the potentials in alleviating experimental arthritis, inhibiting inflammatory polarization of macrophages/monocytes, and regulating peroxisome proliferators-activated receptor γ (PPAR-γ) and silent information regulator 1 (SIRT1) signals. The aim of this study was to analyze the correlations among the above-mentioned properties. Methods: Antigen-induced arthritis (AIA) was established in mouse, which was treated with MG in combination with SIRT1/PPAR-γ inhibitors to clarify the role of the two signals in the anti-arthritic actions. Pathological changes were systematically investigated. Phenotypes of cells were investigated by flow cytometry. Expression and co-localization of SIRT1 and PPAR-γ proteins in joint tissues were observed by the immunofluorescence method. Finally, clinical implications from the synchronous up-regulation of SIRT1 and PPAR-γ were validated by experiments in vitro. Results: SIRT1 and PPAR-γ inhibitors (nicotinamide and T0070097) reduced the therapeutic effects of MG on AIA mice, and abrogated MG-induced up-regulation of SIRT1/PPAR-γ and inhibition of M1 polarization in macrophages/monocytes. MG has a good binding affinity to PPAR-γ, and MG promoted the co-expression of SIRT1 and PPAR-γ in joints. Synchronously activating SIRT1 and PPAR-γ was revealed to be necessary by MG to repress inflammatory responses in THP-1 monocytes. Conclusion: MG binds PPAR-γ and excites this signaling to initiate ligand-dependent anti-inflammatory activity. Due to certain unspecified signal transduction crosstalk mechanism, it then promoted SIRT1 expression and further limited inflammatory polarization of macrophages/monocytes in AIA mice.

Retraction: In situ Raman investigation of the phase transition of NaVO2F2 under variable temperature conditions.

[This retracts the article DOI: 10.1039/D1RA02827H.].

α-Mangostin Treats Early-Stage Adjuvant-Induced Arthritis of Rat by Regulating the CAP-SIRT1 Pathway in Macrophages.

BACKGROUND: Studies have found that α-mangostin (MG) can relieve experimental arthritis by activating cholinergic anti-inflammatory pathway (CAP). It affects the polarization of macrophages and the balance of related immune cell subpopulations, but the specific mechanism is still unclear. It has been found that silent information regulator 1 (SIRT1) is closely related to macrophage activity. The purpose of this study is to explore the mechanism of MG intervening in macrophage polarization during treatment of early adjuvant-induced (AIA) rats through the CAP-SIRT1 pathway. METHODS: We investigated the polarization of M1 macrophages and the differentiation of Th1 in AIA rats by flow cytometry. Activity of acetylcholinesterase (AChE) and the level of nicotinic adenine dinucleotide (NAD+) in serum were also detected, and immunohistochemical was used to detect the levels of α7 nicotinic cholinergic receptor (α7nAChR) and SIRT1. Then in macrophages, the molecular mechanism of MG regulating the abnormal activation of macrophages in rats with early AIA through the CAP-SIRT1 pathway was studied. RESULTS: MG can significantly inhibit the polarization of M1 macrophages and the differentiation of Th1 in AIA rats in the acute phase of inflammation. MG can significantly inhibit the activity of AChE and increase the level of NAD+, thereby further up-regulated the expression levels of α7nAChR and SIRT1. Meanwhile, MG inhibited nuclear factor-κB (NF-κB)-mediated inflammation by activating the CAP-SIRT1 pathway in macrophages. CONCLUSION: In summary, the stimulation of MG induced CAP activation, which up-regulated SIRT1 signal, and thereby inhibited M1 polarization through the NF-κB pathway, and improved the pathological immune environment of early-stage AIA rats.

The utility of sputum supernatant as an alternative liquid biopsy specimen for next-generation sequencing-based somatic variation profiling.

Background: Comprehensive genomic profiling has become standard clinical practice in the management of advanced lung cancer. In addition to tissue and plasma, other body fluids are also being actively explored as alternative sources of tumor DNA. This study investigated the utility of induced sputum obtained from patients with non-small-cell lung cancer (NSCLC) for somatic variation profiling. Methods: Our study included 41 treatment-naïve patients diagnosed with locally advanced to advanced NSCLC between October 2018 and June 2019. Capture-based targeted sequencing was performed on matched tumor, plasma, and induced sputum samples of 41 patients using a 168-gene panel. We analyzed the somatic variations detected from each sample type and the concordance of variations detected between matched samples. The concordance rate was defined as the proportion of the total number of variations detected from one sample type relative to the reference sample type. Results: Comparative analysis on the somatic variation detection using matched tumor samples as a reference revealed detection rates of 76.9% for plasma, 72.4% for sputum-supernatant, and 65.7% for sputum-sediment samples. Plasma, sputum-supernatant, and sputum-sediment achieved positive predictive values of 73.3%, 80.4%, and 55.6% and sensitivities of 50.0%, 36.9%, 31.3%, respectively, relative to tumor samples for 168 genes. Sputum-supernatants had significantly higher concordance rates relative to matched tumor samples (69.2% vs. 37.8%; P=0.031) and maximum allelic fraction (P<0.001) than their matched sputum-sediments. Sputum-supernatants had comparable detection rates (71.4% vs. 67.9%; P=1.00) but with significantly higher maximum allelic fraction than their matched plasma samples (P=0.003). Furthermore, sputum-supernatant from smokers had a significantly higher maximum allelic fraction than sputum-supernatant from non-smokers (P=0.021). Conclusions: Our study demonstrated that supernatant fraction from induced sputum is a better sampling source than its sediment and performs comparably to plasma samples. Induced sputum from NSCLC patients could serve as an alternative media for next-generation sequencing (NGS)-based somatic variation profiling.

In situ Raman investigation of the phase transition of NaVO2F2 under variable temperature conditions.

In this study, the phase transition of NaVO2F2 was measured at different temperatures via in situ Raman spectroscopy. The NaVO2F2 compounds were synthesized by a hydrothermal method and were identified to be monoclinic with the P21/c space group at room temperature by XRD. Accordingly, the variations of Raman shifts and intensities of the characteristic peaks for NaVO2F2 associated with temperature were obtained and investigated. It was confirmed that NaVO2F2 had three types of phase transitions, which occurred in the temperature region from 78 K to 573 K. Further, the results indicate that transition from a low-temperature phase (I) to another low-temperature phase (II), low-temperature phase (II) to P21/c phase and P21/c phase to P21/m phase occurred near the three temperature points of 93 K, 233 K, and 453 K, respectively, during the heating process. Therefore, a novel characterization method was provided for further research on the phase transition theory and performance of vanadate compounds.

Ultrasound-guided microwave ablation of benign thyroid nodules: effects on inflammatory factors and thyroid function.

OBJECTIVE: To explore the effects of ultrasound-guided microwave ablation on inflammatory factors and thyroid function in patients with benign thyroid nodules. METHODS: A total of 150 patients with benign thyroid nodules treated in the Huazhong University of Science and Technology Union Shenzhen Hospital from January 2017 to December 2018 were selected as research participants, with 75 patients in each group. Patients in the control group received traditional surgery, while those in the study group were treated with ultrasound-guided percutaneous microwave ablation. The two groups were compared in terms of the following: clinical effect, quality of life scores, white blood cell count (WBC), hypersensitive-C-reactive-protein (hsCRP), tumor necrosis factor α (TNF-α), interleukin (IL)-6, epinephrine (E), norepinephrine (NE), visual analogue scale (VAS) scores, and serum levels of thyroid stimulating hormone (TSH), FT3, FT4, and TT4. RESULTS: The total effective rate of the study group was significantly higher than that of the control group (96.00% vs. 77.33%). Before operation, there was no significant difference in WBC, VAS score, or the levels of hs-CRP, TNF-α, IL-6, E, and NE between the two groups (all P>0.05); After operation, WBC, and the levels of hs-CRP, TNF-α, IL-6, E, and NE increased significantly in both groups and were lower in the study group (all P<0.05). The nodule volume in the study group decreased with time. The serum levels of TSH, FT3, FT4, and TT4 in the study group were better than those in the control group (P<0.05). The study group obtained a lower incidence of postoperative complications than the control group (4.00% vs. 14.00%). In addition, the cosmetic score was higher and the symptom score was lower in the study group compared with the control group (all P<0.05). CONCLUSION: In patients with benign thyroid nodules, the ultrasound-guided microwave ablation could effectively reduce nodule volume, preserve thyroid function, and improve the quality of patients' daily life. This is closely related to a reduced inflammatory response.

Regulation of Sirt1 on energy metabolism and immune response in rheumatoid arthritis.

Rheumatoid arthritis (RA) is a systemic autoimmune disease. Synovial hyperplasia and persistent inflammation serve as its typical pathological manifestations, which ultimately lead to joint destruction and function loss. Both clinical observations and metabolomics studies have revealed the prevalence of metabolic disorders in RA. In inflammatory immune microenvironments, energy metabolism is profoundly changed. Increasingly evidences suggest that this abnormality is involved in the occurrence and development of RA-related inflammation. Unsurprisingly, many energy metabolism sensors have been confirmed with immunoregulatory properties. As a representative, silent information regulator type 1 (Sirt1) controls many aspects of immune cells, such as cell lifespan, polarization, and secretion by functioning as a transcriptional regulator. Because of the profound clinical implication, researches on Sirt1 in the regulation of energy metabolism and immune functions under RA conditions have gradually gained momentum. This signaling balances glycolysis, lipid metabolism and insulin secretion orchestrating with other metabolism sensors, and consequently affects immune milieu through a so-called metabolism-immune feedback mechanism. This article reviews the involvement of Sirt1 in RA by discussing its impacts on energy metabolism and immune functions, and specially highlights the potential of Sirt1-targeting anti-rheumatic regimens. It also provides a theoretical basis for clarifying the mystery about the high incidence of metabolic complications in RA patients and identifying new anti-rheumatic reagents.

Pregnancy-specific glycoprotein 9 acts as both a transcriptional target and a regulator of the canonical TGF-ß/Smad signaling to drive breast cancer progression.

Pregnancy-specific glycoprotein 9 (PSG9) is a placental glycoprotein essential for the maintenance of normal gestation in mammals. Bioinformatics analysis of multiple publicly available datasets revealed aberrant PSG9 expression in breast tumors, but its functional and mechanistic role in breast cancer remains unexplored. Here, we report that PSG9 expression levels were elevated in tumor tissues and plasma specimens from breast cancer patients, and were associated with poor prognosis. Gain- or loss-of-function studies demonstrated that PSG9 promoted breast cancer cell proliferation, migration, and invasionin vitro, and enhanced tumor growth and lung colonization in vivo. Mechanistically, transforming growth factor-ß1 (TGF-ß1) transcriptionally activated PSG9 expression through enhancing the enrichment of Smad3 and Smad4 onto PSG9 promoter regions containing two putative Smad-binding elements (SBEs). Mutation of both SBEs in the PSG9 promoter, or knockdown of TGF-ß receptor 1 (TGFBR1), TGFBR2, Smad3, or Smad4 impaired the ability of TGF-ß1 to induce PSG9 expression. Consequently, PSG9 contributed to TGF-ß1-induced epithelial-mesenchymal transition (EMT) and breast cancer cell migration and invasion. Moreover, PSG9 enhanced the stability of Smad2, Smad3, and Smad4 proteins by blocking their proteasomal degradation, and regulated the expression of TGF-ß1 target genes involved in EMT and breast cancer progression, thus further amplifying the canonical TGF-ß/Smad signaling in breast cancer cells. Collectively, these findings establish PSG9 as a novel player in breast cancer progressionvia hijacking the canonical TGF-ß/Smad signaling, and identify PSG9 as a potential plasma biomarker for the early detection of breast cancer.

First-Principles Study of Thermo-Physical Properties of Pu-Containing Gd2Zr2O7.

A density functional theory plus Hubbard U method is used to investigate how the incorporation of Pu waste into Gd2Zr2O7 pyrochlore influences its thermo-physical properties. It is found that immobilization of Pu at Gd-site of Gd2Zr2O7 has minor effects on the mechanical and thermal properties, whereas substitution of Pu for Zr-site results in remarkable influences on the structural parameters, elastic moduli, elastic isotropy, Debye temperature and electronic structure. The discrepancy in thermo-physical properties between Gd2-yPuyZr2O7 and Gd2Zr2-yPuyO7 may be a result of their different structural and electronic structures. This study provides a direct insight into the thermo-physical properties of Pu-containing Gd2Zr2O7, which will be important for further investigation of nuclear waste immobilization by pyrochlores.

MiR-143-3p regulates early cartilage differentiation of BMSCs and promotes cartilage damage repair through targeting BMPR2.

OBJECTIVE: The aim of this study was to explore the role of microRNA-143-3p (miR-143-3p) in cartilage injury, and to investigate the possible underlying mechanism. MATERIALS AND METHODS: A chondrogenic differentiation cell model was established in bone marrow mesenchymal stem cells (BMSCs). The mRNA expression levels of runt-related transcription factor 2 (RUNX2), miR-143-3p and bone morphogenetic protein 2 (BMPR2) in BMSCs were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) after 0 d, 5 d and 10 d, respectively. Mesenchymal stem cells (MSCs) were transfected with miR-143-3p mimics and its control in accordance with the liposome method. Alcian blue colorimetric assay was used to evaluate proteoglycan deposition of MSCs. Meanwhile, qRT-PCR and Western blot were performed to analyze the expression levels of ACAN and COL2A1. Luciferase reporter gene assay was applied to verify the binding status of miR-143-3p and BMPR2 3'UTR. Also, proteoglycan deposition and the expression of ACAN and COL2A1 were detected after simultaneous transfection of miR-143-3p mimics and BMPR2 overexpression plasmid. RESULTS: 0 d, 5 d and 10 d after inducing cartilage differentiation, the mRNA expression levels of RUNX2 and BMPR2 were markedly increased. However, the expression level of miR-143-3p was significantly decreased with the prolongation of induction period. After transfection with miR-143-3p mimics, the level of miR-143-3p in MSCs was remarkably increased. Alcian blue colorimetric assay and staining assay showed that the deposition of proteoglycans in the mimics group was significantly lower than that of the control group. Meanwhile, after overexpressing miR-143-3p, the levels of cartilage differentiation marker proteins including ACAN and COL2A1 were remarkably reduced. Luciferase report gene assay indicated that miR-143-3p could negatively regulate BMPR2 by binding to its 3'UTR. In addition, overexpression of BMPR2 could strikingly reverse the above effects of overexpressed miR-143-3p. CONCLUSIONS: During chondrogenic differentiation, the level of miR-143-3p was decreased. Moreover, miR-143-3p could regulate the differentiation process by targeting BMPR2 in BMSCs.

MMP-14 aggravates onset of severe preeclampsia by mediating soluble endoglin release.

OBJECTIVE: Gestational hypertension is a pregnancy complication that serious damages the maternal and child health. Early onset severe preeclampsia accounts for about 0.9% of the gestational hypertension disease. Conservative treatment is proposed in recent years to early onset severe preeclampsia through delay delivery. Therefore, it is particularly important to explore the pathogenesis of severe preeclampsia. Soluble endoglin (sEng) has been identified as a central factor to induce endothelium dysfunction of preeclampsia, while its specific mechanism is unclear. MATERIALS AND METHODS: Matrix metallopeptidase 14 (MMP-14) and endoglin expressions and tissue localization in the placenta of preeclampsia and premature were detected by Western blot and immunohistochemistry. Endoglin level, mean arterial blood pressure (MABP), and urinary protein/creatinine ratio were analyzed for correlation to investigate their relationship and the influence of endoglin on eclampsia severity. MMP specific or broad spectrum inhibitor combining MMP-14 siRNA were used in JAR cell line BeWo to explore the regulatory role of MMP-14 on endoglin. RESULTS: MMP-14, endoglin, and sEng expression levels significantly increased in the placenta of severe preeclampsia patients. MMP-14 and endoglin exhibited expression co-localization. Endoglin expression was positively correlated with the severity of eclampsia. MMP-14 directly mediated the release of sEng. CONCLUSIONS: MMP-14 aggravated the onset of severe preeclampsia by mediating sEng release. MMP-14 was proposed as the effective target for the treatment of severe preeclampsia. Blocking the interaction between MMP-14 and endothelial protein may be an important treatment method.

[Development of a near-infrared fluorescence imaging system based on fluorescence properties of methylene blue].

OBJECTIVE: To develop a near-infrared fluorescence imaging system based on the fluorescence properties of methylene blue. METHODS: According to the optical properties of methylene blue, we used a custom-made specific LED light source and an interference filter, a CCD camera and other relevant components to construct the near-infrared fluorescence imaging system. We tested the signal-to-background ratio (SBR) of this imaging system for detecting methylene blue under different experimental conditions and analyzed the SBR in urine samples collected from 15 Wistar rats with intravenous injection of methylene blue at the doses of 0, 1.4, 1.6, 1.8, or 2.0 0 mg/kg methylene blue. RESULTS: The SBR of this imaging system for detecting methylene blue was affected by the concentration of methylene blue and the distance from the sample (P<0.05). In the urine samples from Wistar rats, the SBR varied with the the injection dose, and the rats injected with 1.6 mg/kg methylene blue showed the highest SBR (8.71∓0.20) in the urine (P<0.05). CONCLUSION: This near-infrared fluorescence imaging system is useful for fluorescence detection of methylene blue and can be used for real-time recognition of ureters during abdominal surgery.

HIF-1α promotes inflammatory response of chronic obstructive pulmonary disease by activating EGFR/PI3K/AKT pathway.

OBJECTIVE: Chronic obstructive pulmonary disease (COPD) is an incomplete, reversible disease with progressive inflammation obstruction in airways. This study aims to explore the regulatory mechanism of hypoxia-inducible factor-1α (HIF-1α) in inflammatory response and progression of COPD. PATIENTS AND METHODS: 71 bronchoalveolar lavage fluid (BALF) samples were collected, including 59 samples from COPD patients (COPD group) and 12 from patients with normal pulmonary function (control group). The mRNA and protein levels of HIF-1α and epidermal growth factor receptor (EGFR) in BALF were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot, respectively. Serum levels of interleukin-13 (IL-13), IL-9, IL-1, and tumor necrosis factor-α (TNF-α) were detected by enzyme-linked immunosorbent assay (ELISA). Hypoxia cell model was constructed by COCl2 induction in human embryonic lung cells. Expression levels of HIF-1α, EGFR and p-AKT in NCI-H1563 cells treated with 740Y-P, the phosphoinositide 3-kinase (PI3K) agonist were detected. Finally, we detected proliferation and apoptosis in NCI-H1563 cells with HIF-1α overexpression by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. RESULTS: The mRNA and protein levels of HIF-1α and EGFR were higher in COPD groups compared with those of control group. Serum levels of IL-13, IL-9, IL-1, and TNF-α in COPD patients were elevated. CoCl2 induction in NCI-H1563 cells led to upregulated levels of IL-13, IL-9, IL-1, and TNF-α. 740Y-P treatment remarkably activated EGFR/PI3K/AKT pathway. Overexpressed HIF-1α inhibited proliferation but induced apoptosis of NCI-H1563 cells. CONCLUSIONS: HIF-1α was overexpressed in COPD, which upregulated expressions of inflammatory factors via activating the EGFR/PI3K/AKT pathway. The activated EGFR/PI3K/AKT pathway induced by pulmonary inflammation further upregulated HIF-1α expression in a feedback loop, thus aggravating COPD pathological changes.