Luminescent Coordination Polymer for Picric Acid Detection and Treatment on Spinal Cord Injury Model Via Upregulating the trka Expression.

A luminescent coordination polymer based on Tb(III) has been synthesized with the tripodal carboxylic acid ligand containing N,O codonors (H2PBA = 5-[4-pyridin-3-yl-benzoylamino]-isophthalic acid) as ligand under solvothermal conditions. The chemical formula of this polymer is {[Tb2(PBA)3(H2O)3]·DMF·3H2O}n (1). Complex 1 has good sensitivity and selectivity to picric acid (PA). At 0-30 µmol/L, 1's quenching constant is 4.5 × 104 L/mol. In the biological function study, the motor function of spinal cord-injured animals after different treatments was evaluated using the blood-brain barrier (BBB) method. The trka expression level on the neural stem cells after treatment was measured to reveal the underlying mechanism.

Anti-inflammatory effect of delphinidin on intramedullary spinal pressure in a spinal cord injury rat model.

Delphinidin, a flavonoid polyphenolic compound, is widely found in nature and is used as a food supplement due to its pharmacological activity. The aims of the present study were to examine the anti-inflammatory effect of delphinidin in alleviating spinal cord injury (SCI)-induced inflammation in a rat model and to determine the underlying mechanisms in SCI. The Basso, Beattie, Bresnahan (BBB) scores of rats were assessed to evaluate the effect of delphinidin on the recovery of motor function. ELISA kits were also used to analyze the activities of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2) and caspase-3. In addition, the protein expression levels of nuclear factor (NF)-κB, activator protein 1 (AP-1) and p38-MAPK protein expression were measured using western blot analysis. Treatment with delphinidin significantly increased the BBB scores, as well as inhibited the intramedullary spinal pressure in SCI rats. Delphinidin treatment also significantly suppressed the levels of inflammatory factors and NF-κB protein expression in SCI rats. Finally, treatment with delphinidin significantly inhibited NF-κB stimulation, COX-2 activity, PGE2 production, and AP-1 and p38-MAPK protein expression in SCI rats. These results suggest that the anti-inflammatory effect of delphinidin alleviated inflammation in the SCI rat model via alleviation of the intramedullary spinal pressure through the NF-κB and p38-MAPK signaling pathways.

Comparison of high-viscosity cement vertebroplasty and balloon kyphoplasty for the treatment of osteoporotic vertebral compression fractures.

BACKGROUND: Percutaneous vertebroplasty is a widely used vertebral augmentation procedure for treating osteoporotic vertebral compression fractures (OVCFs). But high cement leakage rate caused by a low-viscosity cement and high injection pressure has limited its general use. Balloon kyphoplasty (BKP) and high-viscosity cement vertebroplasty (HVCV) are 2 modifications of vertebroplasty designed to decrease cement leakage. OBJECTIVE: To assess the safety and efficacy of HVCV compared with BKP. STUDY DESIGN: A prospective cohort study. SETTING: Department of Spine Surgery, an affiliated hospital of a medical university. METHOD: One hundred seven patients suffering from painful OVCFs were randomly assigned into HVCV or BKP groups. Visual Analog Scale (VAS), Oswestry Disability Index (ODI), cement leakage, and vertebral height restoration were evaluated. All occurring complications and injected cement volumes were recorded. The follow-up time was one year. RESULTS: VAS and ODI scores improved in both groups, and did not differ significantly between the 2 groups. More cement was used in the BKP group than in HVCV group (4.22 vs. 3.31 mL, P < 0.0001). The incidence of cement leakage in the HVCV group was lower than that of the BKP group (13.24% vs 30.56%, P < 0.05). No symptomatic cement leakages occurred in the HVCV group. In the BKP group, one patient experienced discogenic back pain related to a disc leak, and another patient had asymptomatic cement emboli in the lung related to venous leakage. The mean compression rate before the procedure was 29.98% in the HVCV group and 28.67% in the BKP group (P = 0.94). The vertebral height was improved significantly and maintained at one-year follow-up in both groups. BKP was more effective in vertebral height restoration than HVCV (44.87% vs. 23.93%, P < 0.0001). There was one case of a new adjacent vertebral fracture in the HVCV group (2%), and 4 cases of new nonadjacent vertebral fractures in the BKP group (7.84%) (P = 0.18). LIMITATIONS: A single-center and relatively small-sample size study. CONCLUSION: HVCV and BKP are safe and effective in improving quality of life and relieving pain. HVCV has a lower cement leakage rate, whereas BKP is more effective in vertebral height restoration. Subsequent fractures are not different between the 2 groups.

Tumor M2-pyruvate kinase in stool as a biomarker for diagnosis of colorectal cancer: A meta-analysis.

OBJECTIVE: The aim of this meta-analysis was to evaluate the diagnosis value of tumor M2-pyruvate kinase (M2-PK) in stool as a biomarker for diagnosis of colorectal cancer. MATERIALS AND METHODS: By searching the databases of Cochrane Library, PubMed, China national knowledge Information and Wanfang, the diagnosis study related to tumor M2-PK in stool as a biomarker for diagnosis of colorectal cancer were screened and included in this study. The pooled sensitivity, specificity, positive likelihood ratio (+LR), negative likelihood ratio (-LR) and the receiver operating characteristic curve (ROC) were calculated by stata 11.0 software. RESULTS: According to the including criteria, 14 trials including 1990 subjects were finally included in this meta-analysis. The pooled diagnosis sensitivity, specificity, +LR, -LR and area under curve were 0.78 (95% confidence interval [CI]: 0.74-0.81), 0.77 (95% CI: 0.76-0.79), 4.38 (95% CI: 3.27-5.88), 0.28 (95% CI: 0.23-0.34) and 0.86 (95% CI: 0.834-0.89). No statistical publication bias was found in this study. CONCLUSION: Tumor M2-PK in stool can be a useful biomarker in the diagnosis of colorectal cancer with relative high sensitivity and specificity.

Ultraviolet (UV) and hydrogen peroxide activate ceramide-ER stress-AMPK signaling axis to promote retinal pigment epithelium (RPE) cell apoptosis.

Ultraviolet (UV) radiation and reactive oxygen species (ROS) impair the physiological functions of retinal pigment epithelium (RPE) cells by inducing cell apoptosis, which is the main cause of age-related macular degeneration (AMD). The mechanism by which UV/ROS induces RPE cell death is not fully addressed. Here, we observed the activation of a ceramide-endoplasmic reticulum (ER) stress-AMP activated protein kinase (AMPK) signaling axis in UV and hydrogen peroxide (H2O2)-treated RPE cells. UV and H2O2 induced an early ceramide production, profound ER stress and AMPK activation. Pharmacological inhibitors against ER stress (salubrinal), ceramide production (fumonisin B1) and AMPK activation (compound C) suppressed UV- and H2O2-induced RPE cell apoptosis. Conversely, cell permeable short-chain C6 ceramide and AMPK activator AICAR (5-amino-1-ß-D-ribofuranosyl-imidazole-4-carboxamide) mimicked UV and H2O2's effects and promoted RPE cell apoptosis. Together, these results suggest that UV/H2O2 activates the ceramide-ER stress-AMPK signaling axis to promote RPE cell apoptosis.

Protective role of Wallerian degeneration slow (Wld(s)) gene against retinal ganglion cell body damage in a Wallerian degeneration model.

Nerve distal axon injury-induced Wallerian degeneration is significantly delayed in Wallerian degeneration slow (Wld(s)) mutant mice, although the associated mechanisms are not completely clear and the role of Wld(s) in retinal ganglion cell (RGC) body damage is not fully understood. In the present study, a Wallerian degeneration model was established in wild-type (WT) and Wld(s) mutant mice by creating mechanical injury in the optic nerves. Wallerian degeneration and RGC body collapse were observed to be significantly delayed in the Wld(s) mice. Electroretinograms (ERG) and visual evoked potentials (VEPs) in Wld(s) mice were also significantly improved at the earlier stages (one week) following injury. The retina immunohistochemistry results showed that Wld(s) mice had more ordered cells and improved inner granular cell layer arrangement compared with the WT mice. Optic nerve Luxol Fast Blue (LFB) staining showed greater axon demyelination in WT mice than in Wld(s) mice. A large number of apoptotic cells were also observed in the WT mice. The present results suggest that the Wld(s) gene may also protect the RGC body following nerve injury.

TNF-α promotes human retinal pigment epithelial (RPE) cell migration by inducing matrix metallopeptidase 9 (MMP-9) expression through activation of Akt/mTORC1 signaling.

Tumor necrosis factor-alpha (TNF-α) promotes in vitro retinal pigment epithelial (RPE) cell migration to initiate proliferative vitreoretinopathy (PVR). Here we report that TNF-α promotes human RPE cell migration by inducing matrix metallopeptidase 9 (MMP-9) expression. Inhibition of MMP-9 by its inhibitor or its neutralizing antibody inhibited TNF-α-induced in vitro RPE cell migration. Reversely, exogenously-added active MMP-9 promoted RPE cell migration. Suppression Akt/mTOR complex 1(mTORC1) activation by LY 294002 and rapamycin inhibited TNF-α-mediated MMP-9 expression. To introduce a constitutively active Akt (CA-Akt) in cultured RPE cells increased MMP-9 expression, and to block mTORC1 activation by rapamycin inhibited its effect. RNA interference (RNAi)-mediated silencing of SIN1, a key component of mTOR complex 2 (mTORC2), had no effect on MMP-9 expression or secretion. In conclusion, this study suggest that TNF-α promotes RPE cell migration by inducing MMP-9 expression through activation of Akt/ mTORC1, but not mTORC2 signaling.

Metastatic pattern of lymph node and surgery for gastric stump cancer.

BACKGROUND AND OBJECTIVES: Metastatic pattern of lymph node (LN) and surgery options for gastric stump cancer (GSC) remain controversial. The aim of this study was to investigate LN metastasis and lymphadenectomy for GSC for curative purposes. METHODS: Sixty-seven patients with GSC were analyzed retrospectively. RESULTS: The metastatic rates of LN were as follows: 63.3% in right cardia (No. 1), 33.3% in left cardia (No. 2), 75.0% in lesser curvature (No. 3), 53.3% in greater curvature (No. 4), 40.0% in celiac artery (No. 9), 60.0% in splenic hilus (No. 10), 72.7% in splenic artery (No. 11), 36.1% in hepatoduodenal ligament (No. 12), 8.3% in retropancreatic (No. 13), 21.4% in para-aortic (No. 16), 50% in supra-diaphragm (No. 111), 16.7% in LN within jejunal mesentery, respectively. All nine patients who only received simple laparotomy died within 1 year. The overall 5-year survival rate of GSC was 17.9% (12/67), including 100% for stage I, 80.0% for stage II, 12.1% for stage III, and 0% for stage IV. Moreover, the 5-year survival rate (36.7%, 11/30) for curative patients was significantly better than that (3.6%, 1/28) of non-curative patients (chi(2) = 7.76, P < 0.01). CONCLUSIONS: Our results imply that GSC has a wide range of LN metastases, including LN within jejunal mesentery in B-II reconstruction cases, and curable resection may obtain better results. Therefore, we suggest that radical operation for B-I patients needs removal of gastroduodenectomy anastomosis and the above LNs, and that B-II patients need removal of 10 cm of jejunum besides gastrojejunostomy anastomosis, and clearance of LN within its mesentery, in addition to B-I GSC.