Observation of delocalization transition in topological waveguide arrays with long-range interactions.

Topological edge states are a generic feature of topological insulators, and the long-range interactions, which break certain properties of topological edge states, are always non-negligible in real physical systems. In this Letter, we investigate the influence of next-nearest-neighbor (NNN) interactions on the topological properties of the Su-Schrieffer-Heeger (SSH) model by extracting the survival probabilities at the boundary of the photonic lattices. By introducing a series of integrated photonic waveguide arrays with different strengths of long-range interactions, we experimentally observe delocalization transition of light in SSH lattices with nontrivial phase, which is in good agreement with our theoretical predictions. The results indicate that the NNN interactions can significantly affect the edge states, and that the localization of these states can be absent in topologically nontrivial phase. Our work provides an alternative way to investigate the interplay between long-range interactions and localized states, which may stimulate further interest in topological properties in relevant structures.

Ultralow birefringent glass waveguide fabricated by femtosecond laser direct writing.

Optical waveguides prepared by femtosecond laser direct writing have birefringent properties, which can affect polarization encoding and entanglement on chips. Here, we first propose a shape-stress dual compensation fabrication scheme to decrease birefringence. Ultralow birefringent waveguides (1 × 10-9) were obtained by controlling the cross sectional shape of the main waveguide and adjusting the position of the auxiliary lines. In addition, we prepared polarization-independent directional coupler and demonstrated the evolution of polarization-independent waveguide array with different polarized light. In the future, ultralow birefringent waveguides will be widely applied in polarization encoding and entangled quantum photonic integrated circuits.

Arbitrarily rotated optical axis waveguide induced by a trimming line.

Rotated optical axis waveguides can facilitate on-chip arbitrary wave-plate operations, which are crucial tools for developing integrated universal quantum computing algorithms. In this paper, we propose a unique technique based on femtosecond laser direct writing technology to fabricate arbitrarily rotated optical axis waveguides. First, a circular isotropic main waveguide with a non-optical axis was fabricated using a beam shaping method. Thereafter, a trimming line was used to create an artificial stress field near the main waveguide to induce a rotated optical axis. Using this technique, we fabricated high-performance half- and quarter-wave plates. Subsequently, high-fidelity (97.1%) Pauli-X gate operation was demonstrated via quantum process tomography, which constitutes the basis for the full manipulation of on-chip polarization-encoded qubits. In the future, this work is expected to lead to new prospects for polarization-encoded information in photonic integrated circuits.

Single NV centers array preparation and static magnetic field detection.

To solve the problem of static magnetic field detection accuracy and consistency, we prepared an array of single NV centers for static magnetic field vector and gradient detection using the femtosecond laser direct writing method. The prepared single NV centers are characterized by fewer impurity defects and good stress uniformity, with an average spatial positioning error of only 0.2 µm. This array of single NV centers can achieve high accuracy magnetic field vector and gradient measurement with GBZ≈-0.047 µT/µm in the Z-axis. This result provides a new idea for large-range, high-precision magnetic field vector and gradient measurements.

Phase customization in photonic integrated circuits with trimmed waveguides.

Accurate photon phase control on a chip is essential to improve the expandability and stability of photonic integrated circuits (PICs). Here, we propose a novel, to the best of our knowledge, on-chip static phase control method in which a modified line is added close to the normal waveguide with a lower-energy laser. By controlling the laser energy and the position and length of the modified line, the optical phase can be precisely controlled with low loss and a three-dimensional (3D) path. Customizable phase modulation ranging from 0 to 2π is performed with a precision of λ/70 in a Mach-Zehnder interferometer. The proposed method can customize high-precision control phases without changing the waveguide's original spatial path, which is expected to control the phase and solve the phase error correction problem during processing of large-scale 3D-path PICs.

Selective granulocyte and monocyte apheresis in inflammatory bowel disease: Its past, present and future.

The etiology and pathogenesis of inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease, are not fully understood so far. Therefore, IBD still remains incurable despite the fact that significant progress has been achieved in recent years in its treatment with innovative medicine. About 20 years ago, selective granulocyte and monocyte apheresis (GMA) was invented in Japan and later approved by the Japanese health authority for IBD treatment. From then on this technique was extensively used for IBD patients in Japan and later in Europe. Clinical trials from Japan and European countries have verified the effectiveness and safety of GMA therapy in patients with IBD. In 2013, GMA therapy was approved by China State Food and Drug Administration for therapeutic use for the Chinese IBD patients. However, GMA therapy has not been extensively used in China, although a few clinical studies also showed that it was effective in clinical and endoscopic induction of remission in Chinese IBD patients with a high safety profile. This article reviews past history, present clinical application as well as the future prospective of GMA therapy for patients with IBD.

Correlation of plasma MMP-1 and TIMP-1 levels and the colonic mucosa expressions in patients with ulcerative colitis.

BACKGROUND: Both plasma and mucosal levels of matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) have been shown to be independently correlated with ulcerative colitis (UC), but their relationship with each other and to disease severity remains unclear. This study aims to evaluate the relationship between colonic mucosal and plasma levels of MMP-1 and TIMP-1 with each other and with the severity of ulcerative colitis (UC). METHODS: Colonic mucosal lesions and venous blood samples were collected from 30 patients with UC and 15 normal subjects. Real-time reverse transcription-PCR and immunohistochemistry were used to determine colonic mucosal MMP-1 and TIMP-1 expression; ELISA was used to measure plasma levels of MMP-1 and TIMP-1. RESULTS: Expression of colonic mucosal and plasma MMP-1 and TIMP-1 in patients with UC was significantly higher than that of controls (P < .05), and was positively correlated with disease severity (P < .05). Plasma MMP-1 and TIMP-1 levels were well correlated with their corresponding expression in colonic mucosa (P < .05, r = 0.805 and 0.908). CONCLUSION: Plasma MMP-1 and TIMP-1 levels reflect their colonic mucosal expression to some extent in patients with UC. Plasma MMP-1 and TIMP-1, in particular, demonstrate the potential to become biomarkers to clinically diagnose UC, predict its severity, and guide further therapy.

[Meta-analysis of terlipressin in treatment of hepatorenal syndrome: an update].

OBJECTIVE: To evaluate the efficacy, adverse effect and safety of terlipressin in the treatment of hepatorenal syndrome (HRS). METHODS: Correlated randomized controlled clinical trials (RCTs) comparing terlipressin with other therapies in the treatment of HRS were searched in Medline, Embase, Cochrane Library, VIP and National Knowledge Infrastructure (CNKI). Stata 9.0 was used for meta-analysis. RESULTS: 7 RCTs including 305 cases were selected for analysis in accordance with the enrollment criteria. HRS reversal rate of terlipressin was superior to that of placebo (total OR = 6.76, 95% CI = 3.37-13.56, P = 0.000); Myocardial infarction rate (total OR = 1.37, 95% CI = 0.26-7.31, P = 0.715), arrhythmic rate (total OR = 3.25, 95% CI = 0.49-21.31, P = 0.222), suspected intestinal ischemic rate (total OR = 2.14, 95% CI = 0.46-10.02, P = 0.336) and peripheral ischemic rate (total OR = 1.72, 95% CI = 0.34-8.76, P = 0.516) of terlipressin were similar with those of placebo; Mortality rate of terlipressin was a little lower than that of placebo (total OR = 0.55, 95% CI = 0.31-0.98, P = 0.044). HRS reversal rate (total OR = 0.92, 95% CI = 0.32-2.67, P = 0.877), myocardial infarction rate (total OR = 0.92, 95% CI = 0.06-15.34, P = 0.952), arrhythmic rate (total OR = 0.32, 95% CI = 0.03-3.73, P = 0.364), suspected intestinal ischemic rate (total OR = 0.92, 95% CI = 0.06-15.34, P = 0.952), peripheral ischemic rate (total OR = 0.92, 95% CI = 0.06-15.34, P = 0.952) and mortality rate (total OR = 0.80, 95% CI = 0.29-2.24, P = 0.673) of terlipressin were similar to those of noradrenalin. CONCLUSION: Terlipressin and noradrenalin are effective and safe in the treatment of HRS, the relationship between terlipressin and HRS mortality rate should be elucidated with further studies.

Protective effect of ilomastat on trinitrobenzenesulfonic acid-induced ulcerative colitis in rats.

AIM: To evaluate the protective effects of ilomastat, an exogenous matrix metalloproteinase (MMP) inhibitor, on trinitrobenzenesulfonic acid (TNB)-induced ulcerative colitis (UC) in rats. METHODS: Male SD rats were randomly divided into model group, protective groups A and B, and normal control group. Rats in the model group received only intra-colonic TNB. Rats in the protective groups A and B received intra-peritoneal ilomastat of 10 mg/kg and 20 mg/kg, respectively, beside TNB. Rats in the normal control group received only intra-colonic normal saline. After 3 wk, segments of colon were obtained. RT-PCR and immunohistochemistry were used to examine the expression of MMP-1 and TIMP-1. Hematoxylin-eosin (HE) staining was used for pathological study. RESULTS: The model of UC was successfully induced in rats. Inflammation of colonic mucosa greatly improved in protective groups A and B. Expression of MMP-1 and TIMP-1 in the model group, protective groups A and B was significantly higher than that in the normal control group (P < 0.0001) with MMP-1 expression increased more significantly than TIMP-1 expression. Expression of MMP-1 in protective groups A and B was significantly lower than that in the model group (P < 0.0001) . Expression of MMP-1 in protective group B was significantly lower than that in protective group A (P < 0.0001). CONCLUSION: Ilomastat improves TNB-induced UC in rats by inhibiting the MMP-1 activity.

Expression of matrix metalloproteinase-1 and tumor necrosis factor-alpha in ulcerative colitis.

AIM: To examine the expression of matrix metallo-proteinase-1 (MMP-1) and tumor necrosis factor-alpha (TNF-alpha) in the colon mucosa of patients with ulcerative colitis (UC). METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry were used to examine the expression of MMP-1 and TNF-alpha at both mRNA and protein levels in the colon mucosa of patients with UC. Correlation between MMP-1 and TNF-alpha and their correlation with the severity of the disease were also analyzed statistically. RESULTS: The expression of MMP-1 and TNF-alpha in the ulcerated and inflamed colon mucosa of patients with UC was significantly higher than that in the non-inflamed mucosa of normal controls at both mRNA and protein levels. Furthermore, the expression of MMP-1 and TNF-alpha in the ulcerated area was significantly higher than that in the inflamed area of patients with UC (0.9797 +/- 0.1433 vs 0.6746 +/- 0.0373, 0.8669 +/- 0.0746 vs 0.5227 +/- 0.0435, P < 0.05). There was no statistically significant difference in the non-inflamed area of normal controls. There was a significant correlation between MMP-1 and TNF-alpha expression (0.9797 +/- 0.1433 vs 0.8669 +/- 0.0746, P < 0.05), the correlating factor was 0.877. MMP-1 and TNF-alpha showed a significant correlation with the severity of the disease (0.0915 +/- 0.0044 vs 0.0749 +/- 0.0032 , 0.0932 +/- 0.0019 vs 0.0724 +/- 0.0043, P < 0.05), their correlating factors were 0.942 and 0.890, respectively. CONCLUSION: Excessively expressed MMP-1 directly damages the colon mucosa by degrading extracellular matrix (ECM) in patients with UC. While damaging colon mucosa, excessively expressed TNF-alpha stimulates MMPs secreting cells to produce more MMP-1 and aggravates the mucosa damage. MMP-1 promotes secretion of TNF-alpha in a positive feedback manner to cause further injury in the colon mucosa. MMP-1 and TNF-alpha correlate well with the severity of the disease, and therefore, can be used clinically as biological markers to judge the severity of UC.

Expression of matrix metalloproteinase-1 and tissue inhibitor of metalloproteinase-1 in ulcerative colitis.

AIM: To examine the expression of metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in the colonic mucosa of patients with ulcerative colitis (UC). METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry were used to study the expression of MMP-1 and TIMP-1 at both mRNA and protein levels in patients with UC and controls. The relationship between MMP-1 mRNA, TIMP-1 mRNA, MMP-1 mRNA/TIMP-1 mRNA ratio and the severity of clinical symptoms of the patients with UC were also analyzed. RESULTS: The expression of MMP-1 mRNA and TIMP-1 mRNA in the ulcerated and inflamed colonic mucosa was significantly higher than that in the non-inflamed colonic mucosa (P < 0.001), but there was no statistically significant difference in the non-inflamed colonic mucosa of UC patients and normal controls (P > 0.05). The mRNA expression of MMP-1 and TIMP-1 in ulcerated colonic mucosa of UC patients was increased by 80-fold and 2.2-fold, respectively when compared with the normal controls. In the inflamed colonic mucosa, the increase was 30-fold and 1.6-fold, respectively. Immunohistochemical analysis showed that among the ulcerated, inflamed, and non-inflamed colonic mucosae of UC patients and the normal controls, the positive rate of MMP-1 expression was 87%, 87%, 40% and 35% respectively, and the positive rate of TIMP-1 expression was 89%, 89%, 80% and 75%, respectively. Furthermore, the expression of MMP-1 mRNA, TIMP-1 mRNA and the MMP-1 mRNA/ TIMP-1 mRNA ratio were correlated with the severity of clinical symptoms (P <0.05). CONCLUSION: Excessive expression of MMP-1 in the diseased colonic mucosa causes excessive hydrolysis of the extracellular matrix (ECM) and ulceration in UC patients. MMP-1 mRNA, TIMP-1 mRNA and MMP-1 mRNA/TIMP-1 mRNA ratio can be used as biomarkers to judge the severity of clinical symptoms in patients with UC. Exogenous TIMP-1 or MMP-1 inhibitor therapy is a novel treatment for patients with UC.

Intestinal mucosal barrier dysfunction participates in the progress of nonalcoholic fatty liver disease.

Intestinal mucosal barrier dysfunction is closely related to liver diseases, which implies impaired gut-liver axis may play a role in the pathogenesis of NAFLD. In our study, rats were divided into three groups: normal chow diet (NCD) group, high-fat diet (HFD) group and TNBS-induced colitis with high-fat diet (C-HFD) group. Liver tissues were obtained for histological observation and TNF-α, IL-6 mRNA determination and blood samples were collected for liver enzymes and LPS analysis. Ultrastructural changes of jejuna epithelium, SIBO and amounts of CD103(+)MHCII(+)DCs and CD4(+)CD25(+)FoxP3(+)T-regs in terms of percentage in mesenteric lymph nodes (MLN) were observed by electron microscope, bacterial cultivation and flow cytometry, respectively. The results demonstrated the pathological characteristics accorded with nonalcoholic simple fatty liver (NAFL) and NASH in HFD group by week 8 and 12, respectively. Besides, the degree of hepatic steatosis and steatohepatitis was more severe in C-HFD group compared with HFD-group at the same time point. NAFLD activity score (NAS), liver enzymes, concentration of LPS and mRNA expressions of TNF-α, IL-6 were higher significantly in C-HFD group compared with HFD and NCD group at week 4, 8 and 12, respectively. In HFD group, epithelium microvilli atrophy, disruptive tight junctions and SIBO were present, and these changes were more severe in NASH compared with NAFL. The percentage of CD103+MHCII+DCs and CD4+CD25+FoxP3+T-regs decreased significantly in NAFL and NASH compared with NCD group. Our conclusion was that gut-liver axis was impaired in NAFLD, which played crucial role in the pathogenesis of NAFLD.

Flt3/Flt3L Participates in the Process of Regulating Dendritic Cells and Regulatory T Cells in DSS-Induced Colitis.

The immunoregulation between dendritic cells (DCs) and regulatory T cells (T-regs) plays an important role in the pathogenesis of ulcerative colitis (UC). Recent research showed that Fms-like tyrosine kinase 3 (Flt3) and Flt3 ligand (Flt3L) were involved in the process of DCs regulating T-regs. The DSS-induced colitis model is widely used because of its simplicity and many similarities with human UC. In this study, we observe the disease activity index (DAI) and histological scoring, detect the amounts of DCs and T-regs and expression of Flt3/Flt3L, and investigate Flt3/Flt3L participating in the process of DCs regulating T-regs in DSS-induced colitis. Our findings suggest that the reduction of Flt3 and Flt3L expression may possibly induce colonic immunoregulatory imbalance between CD103(+)MHCII(+)DCs and CD4(+)CD25(+)FoxP3(+)T-regs in DSS-induced colitis. Flt3/Flt3L participates in the process of regulating DCS and T-regs in the pathogenesis of UC, at least, in the acute stage of this disease.

Influence of Rosiglitazone on the Expression of PPARγ, NF-κB, and TNF-α in Rat Model of Ulcerative Colitis.

Aim. To observe the disease activity index (DAI) and the colonic mucosa damage index (CMDI), detect the colonic mucosal expression of PPARγ, NF-κB, and TNF-α in rats with ulcerative colitis (UC), and to investigate the protective role of rosiglitazone in UC. Methods. Sprague-Dawley (SD) rats were divided into three groups: a control group, a rosiglitazone treatment group, and a UC model group. Rats were sacrificed on days 7, 14, 21, or 35 following administration of treatment after enema and DAI, CMDI and colonic expression of PPARγ, NF-κB, and TNF-α were assessed. Results. In the UC model group, DAI, CDMI and the colonic expression of NF-κB and TNF-α increased significantly compared to the control group at all timepoints, but PPARγ decreased significantly. Furthermore, in the rosiglitazone treatment group, DAI and CMDI decreased significantly on the 14-day, 21-day, and 35-day timepoints compared to the UC model group; the colonic expression of NF-κB and TNF-α decreased compared to UC model group at all timepoints, but the PPARγ expression increased significantly. Conclusions. Rosiglitazone can alleviate colonic mucosal inflammation and have the protective role on UC by upregulating PPARγ expression and downregulating NF-κB and TNF-α expression.

Protective role of metalloproteinase inhibitor (AE-941) on ulcerative colitis in rats.

AIM: To evaluate the protective role of AE-941, a matrix metalloproteinase (MMP) inhibitor, on ulcerative colitis (UC) in rats. METHODS: Sprague Dawley (SD) rats were randomly divided into three groups: a control group, an AE-941 treatment group, and an UC model group. Rats were sacrificed on days 7, 21, or 56 following administration of treatment by enema and the disease activity index (DAI), colonic mucosa damage index (CMDI) and colonic expression of MMP-2 and MMP-9 were assessed. RESULTS: DAI and CDMI scores in the UC model group increased significantly compared to the control group at all timepoints (P < 0.001), and also increased significantly at the 21- and 56-d timepoints compared to the AE-941-treated group (DAI: 21- and 56-d = 2.09 ± 0.25, 1.52 ± 0.30 vs 1.55 ± 0.28, 0.59 ± 0.19, respectively, P = 0.040 and 0.007, CMDI: 21- and 56-d = 3.03 ± 0.42, 1.60 ± 0.35 vs 2.08 ± 0.46, 0.86 ± 0.37, respectively, P = 0.040 and 0.005). Furthermore, the colonic expression of MMP-2 and MMP-9 in the UC model group increased significantly compared to the control group (P < 0.001), and also increased compared to the AE-941-treated group on the 21- and 56-d timepoints (MMP-2: 21- and 56-d = 0.6048 ± 0.0522, 0.4163 ± 0.0330 vs 0.3983 ± 0.0218, 0.1093 ± 0.0072, respectively, P = 0.010; MMP-9: 21- and 56-d = 0.6873 ± 0.0472, 0.4328 ± 0.0257 vs 0.5179 ± 0.0305, 0.2673 ± 0.0210, respectively, P = 0.010 and 0.040). CONCLUSION: Expression of MMP-2 and MMP-9 increased significantly in rats with UC. AE-941 can reduce colonic mucosal damage by downregulating the expression of MMP-2 and MMP-9.

Effect of Etiasa on the expression of matrix metalloproteinase-2 and tumor necrosis factor-α in a rat model of ulcerative colitis.

The aim of this study was to determine the disease activity index (DAI) and the colonic mucosa damage index (CMDI), and to detect the colonic mucosal expression levels of matrix metalloproteinase-2 (MMP-2) and tumor necrosis factor-α (TNF-α) in rats with ulcerative colitis (UC). We also aimed to investigate the protective role of Etiasa in UC. Sprague Dawley (SD) rats were randomly divided into three groups: the control, an Etiasa-treated group and a UC model group. Rats were sacrificed on days 14, 21, 35 or 56 following the administration of treatment by enema and the DAI, CMDI and colonic expression levels of MMP-2 and TNF-α were assessed. In the UC model group, the DAI and CDMI scores and the colonic expression levels of MMP-2 and TNF-α increased significantly compared with the control at all timepoints, and were also significantly higher than those in the Etiasa-treated group. In conclusion, the expression levels of MMP-2 and TNF-α increased significantly in rats with UC. Etiasa reduces colonic mucosal damage by downregulating the expression of MMP-2 and TNF-α.