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Malignant ascites in hepatocellular carcinoma is usually a sign of advanced disease and poor prognosis and is also thought to be associated with chronic inflammation mediated by neutrophil extracellular trap networks (NETs). Whereas ozone, a strong oxidant, has significant antibacterial and anti-inflammatory effects, its effectiveness in treating malignant liver ascites is unclear.cOzone showed significant anti-peritoneal fluid production properties in H22 tumor-bearing mice, and ozone reduced peritoneal fluid production by activating AMPK and up-regulating SR-A phagocytosis damage-associated molecular patterns (DAMPs) to reduce the production of NETs. This suggests that ozone could be used as a new drug for the treatment of malignant ascites in hepatocellular carcinoma.

Malignant glioma is the most common and deadly brain tumor. A marked reduction in the levels of sGC (soluble guanylyl cyclase) transcript in the human glioma specimens has been revealed in our previous studies. In the present study, restoring the expression of sGCβ1 alone repressed the aggressive course of glioma. The antitumor effect of sGCβ1 was not associated with enzymatic activity of sGC since overexpression of sGCβ1 alone did not influence the level of cyclic GMP. Additionally, sGCβ1-induced inhibition of the growth of glioma cells was not influenced by treatment with sGC stimulators or inhibitors. The present study is the first to reveal that sGCβ1 migrated into the nucleus and interacted with the promoter of the TP53 gene. Transcriptional responses induced by sGCβ1 caused the G0 cell cycle arrest of glioblastoma cells and inhibition of tumor aggressiveness. sGCβ1 overexpression impacted signaling in glioblastoma multiforme, including the promotion of nuclear accumulation of p53, a marked reduction in CDK6, and a significant decrease in integrin α6. These anticancer targets of sGCβ1 may represent clinically important regulatory pathways that contribute to the development of a therapeutic strategy for cancer treatment.

With abundant research on group 2 innate lymphoid cells (ILC2s) published over the years, ILC2s are widely known to be implicated in regulating various pathological processes, including anti-helminth immunity, tissue repair, thermogenesis, and autoimmune diseases such as asthma and allergic rhinitis (AR). ILC2s permanently reside in peripheral tissues such as the skin, gut, lungs, and nasal cavity; however, there is limited information about their exact functions in nasal mucosal immunity. CD226 is an activating costimulatory molecule, mainly expressed on natural killer (NK) cells, T cells, and inflammatory monocytes. However, whether ILC2s express CD226 or play a role in the pathogenesis of ILC2s-related diseases remains unknown. Here, we established a method to isolate and identify ILC2s from the nasal mucosa and detected CD226 expression on ILC2s obtained from healthy and AR mice. Herein, we describe this protocol for the isolation and identification of ILC2s from mouse nasal mucosa, which will help explore the internal pathological mechanism of immunological disorders in nasal mucosal diseases.

Surgical management of spontaneous hypertensive brainstem hemorrhage remains a challenge for neurosurgeons, especially when the hemorrhage is located the ventral brainstem. Recently endoscopic endonasal approach has been applied for resection of ventral brainstem lesions, though no published literature has explored its utility in treating brainstem hemorrhage. Here we reported a successful evacuation of severe hypertensive brainstem hemorrhage through endoscopic endonasal transclival approach. A 37 years-old male with a 5-year history of uncontrolled hypertension was brought to the Emergency Department with sudden vomiting, limb convulsions, and loss of consciousness for 2 hours. Computed tomography demonstrated a hemorrhage measuring 2.5 × 2.2 cm in the ventral midbrain and pontine. He presented with a Glasgow coma scale (GCS) score of 3 and disrupted vitals, and was intubated in the Emergency Department. Considering the ventral location of the hemorrhage and the need for emergent surgical decompression, an endoscopic endonasal approach was applied. Evacuation of the brainstem hemorrhage was achieved and his spontaneous respiration improved immediately after surgery. He was weaned off the ventilator and extubated on postoperative day 1, along with an improved GCS score of 5 (E2V1M2). At 1 month postoperatively his GCS score improved to 11 (E4V2M5) and he is currently under rehabilitation. Endoscopic endonasal approach is a feasible alternative for emergent surgery of ventrally located brainstem hemorrhage in carefully selected cases by providing direct visualization of the area and a good working angle, which facilitate evacuation of the hemorrhage with minimal damage to the brainstem.

In the past two decades, miRNAs have been demonstrated to play critical roles in development and progression of malignant diseases. To identify the role and mechanism of miRNA are urgent for the application of miRNA-based therapeutics in cancers. MiR-205 is a conserved miRNA from the invertebrate to mammalian species. Previous studies showed a large body of evidence to demonstrate the oncogenic or tumor suppressive role of it in different types of cancers. Our aim here is to clarify the role and novel mechanism of miR-205 in solid tumors. In the present study, we found that a high level of miR-205 is an independent biomarker for favorable prognosis in LIHC, HNSCC and LUSC. In the functional experiment, we stably expressed miR-205 in tumor cell lines derived from above mentioned cancers. The result showed that overexpression of miR-205 significantly inhibits cancer cell proliferation. Mechanistically, we identified that the lysophosphatidylcholine acyltransferase-1 (LPCAT1) is a novel target of miR-205 in multiple cancer cells. Furthermore, we found that LPCAT1 is required for sustained proliferation of cancer cells and a high level of it is closely associated with poor prognosis in clinical patients. Collectively, we revealed the important prognostic value of a miR-205-LPCAT1 axis in multiple cancers and highlighted an essential role of LPCAT1 in miR-205-regulated cancer cell proliferation. All these discoveries make a miR-205-LPCAT1 axis to shed light upon a potential therapeutic target in cancer treatment.

It has been reported since late 1970 that magnetic field interacts strongly with biological systems. Cold atmospheric plasma (CAP) has also been widely studied over the past few decades in physics, biology, and medicine. In this study, we propose a novel idea to combine static magnetic field (SMF) with CAP as a tool for cancer therapy. Breast cancer cells and wild type fibroblasts were cultured in 96-well plates and treated by CAP with or without SMF. Breast cancer cells MDA-MB-231 showed a significant decrease in viability after direct plasma treatment with SMF (compared to only plasma treatment). In addition, cancer cells treated by the CAP-SMF-activated medium (indirect treatment) also showed viability decrease but was slightly weaker than the direct plasma-SMF treatment. By integrating the use of SMF and CAP, we were able to discover their advantages that have yet to be utilized. Bioelectromagnetics. 38:53-62, 2017. © 2016 Wiley Periodicals, Inc.

We have shown that rutaecarpine extracted from the dried fruit of Chinese herb Evodia rutaecarpa (Juss) Benth (Wu Zhu Yu) promotes glucose consumption and anti-inflammatory cytokine expression in insulin-resistant primary skeletal muscle cells. In this study we investigated whether rutaecarpine ameliorated the obesity profiles, lipid abnormality, glucose metabolism and insulin resistance in rat model of hyperlipidemia and hyperglycemia.Rats fed on a high-fat diet for 8 weeks, followed by injection of streptozotocin (30 mg/kg, ip) to induce hyperlipidemia and hyperglycemia. One week after streptozotocin injection, the fat-fed, streptozotocin-treated rats were orally treated with rutaecarpine (25 mg·kg(-1)·d(-1)) or a positive control drug metformin (250 mg·kg(-1)·d(-1)) for 7 weeks. The body weight, visceral fat, blood lipid profiles and glucose levels, insulin sensitivity were measured. Serum levels of inflammatory cytokines were analyzed. IRS-1 and Akt/PKB phosphorylation, PI3K and NF-κB protein levels in liver tissues were assessed; pathological changes of livers and pancreases were examined. Glucose uptake and AMPK/ACC2 phosphorylation were studied in cultured rat skeletal muscle cells in vitro.Administration of rutaecarpine or metformin significantly decreased obesity, visceral fat accumulation, water consumption, and serum TC, TG and LDL-cholesterol levels in fat-fed, streptozotocin-treated rats. The two drugs also attenuated hyperglycemia and enhanced insulin sensitivity. Moreover, the two drugs significantly decreased NF-κB protein levels in liver tissues and plasma TNF-α, IL-6, CRP and MCP-1 levels, and ameliorated the pathological changes in livers and pancreases. In addition, the two drugs increased PI3K p85 subunit levels and Akt/PKB phosphorylation, but decreased IRS-1 phosphorylation in liver tissues. Treatment of cultured skeletal muscle cells with rutaecarpine (20-180 μmol/L) or metformin (20 μmol/L) promoted the phosphorylation of AMPK and ACC2, and increased glucose uptake.Rutaecarpine ameliorates hyperlipidemia and hyperglycemia in fat-fed, streptozotocin-treated rats via regulating IRS-1/PI3K/Akt signaling pathway in liver and AMPK/ACC2 signaling pathway in skeletal muscles.

Modern research has shown that BanXia BaiZhu TianMa decoction (BBT) has the potential effect of lowering BP in vitro and in vivo. However, its therapeutic mechanism has not been clearly defined. The present study was designed to evaluate the protective effect of BBT on the heart by examining heart functioning and anti-inflammatory characteristics and to obtain scientific evidence for its further medical applications. BBT was extracted by decocting the herb extraction and analysed by HPLC. The left ventricular mass index (LVMI) was measured, and a histological examination of samples of the heart was performed. Inflammatory status was investigated by measuring tissue levels of interleukin-1 (IL-1), interleukin-6 (IL-6), tumour necrosis factor (TNF-α), inducible nitric oxide synthase (iNOS), and molecules of the nuclear factor κB (NF-κB) pathway. The BBT treatment significantly reversed the course of hypertension-derived heart damage. Meanwhile, the herb formula markedly reduced levels of IL-1, IL-6, TNF-α, and iNOS. In addition, the traditional compound suppressed the activity of the NF-κB pathway. The present study provides evidence of heart protection by BBT in SHRs. The action mechanisms may be partially attributable to the anti-inflammatory characteristic of the formula. Understanding the pharmacological action of BBT will benefit its impending use.

With the development of the IT industry, the information resources and services that people come into contact with have been growing. The sharing and interaction of these two types of information has led to further growth in data resulting in the advent of the era of big data. However, due to the complexity of information, such as low utilization, the confusion, and disorder, it will be a great challenge for service providers to offer customers services with high quality and accurate quality. The recommendation system is a solution adopted by e-marketers for such problems. This paper proposes a SPARK-based recommendation algorithm called SARF. The SARF first reads the original data from the HDFS and uses Spark to yield the datasets. Then, by using these datasets, the optimal recommended model is generated through iterative process. Finally, we gain the results which are recommended to the user by the optimal model. The final experimental results show that our SARF framework can effectively reduce the recommendation error and solve the problem of cold start.

Histone deacetylases (HDACs) are enzymes that regulate protein functions by catalyzing the removal of acetyl and acyl groups from lysine residues. They play pivotal roles in governing cell behaviors and are indispensable in numerous biological processes. HDAC11, the last identified and sole member of class IV HDACs, was reported over a decade ago. However, its physiological function remains poorly understood. Here, we report that HDAC11 knockout mice are resistant to high-fat diet-induced obesity and metabolic syndrome, suggesting that HDAC11 functions as a crucial metabolic regulator. Depletion of HDAC11 significantly enhanced insulin sensitivity and glucose tolerance, attenuated hypercholesterolemia, and decreased hepatosteatosis and liver damage. Mechanistically, HDAC11 deficiency boosts energy expenditure through promoting thermogenic capacity, which attributes to the elevation of uncoupling protein 1 (UCP1) expression and activity in brown adipose tissue. Moreover, loss of HDAC11 activates the adiponectin-AdipoR-AMPK pathway in the liver, which may contribute to a reversal in hepatosteatosis. Overall, our findings distinguish HDAC11 as a novel regulator of obesity, with potentially important implications for obesity-related disease treatment., Highlights • Obesity is a serious and widespread health problem that has become a growing concern in many societies. Most currently available weight-loss medications do not work for everyone, and the effects decline over time. Thus, there is an urgent need to identify new molecular targets to improve drug development for the treatment of obesity and obesity-related diseases. In this study, we discovered that the histone deacetylase 11 (HDAC11) enzyme is a key regulator of metabolism and obesity, and the absence of HDAC11 prevents obesity in mice. Our findings will facilitate the development of novel therapeutics to treat obesity by targeting HDAC11.

Inducible nitric oxide synthase (iNOS) plays an important role in inflammation, which has also been considered as a major driver of breast cancer disease progression. Radix Glycyrrhiza (RG) has been broadly used for its anti-inflammatory and antitumorigenic effects. However, the mechanisms of regulation of iNOS in inflammation and cancer have not been fully explored. Total flavonoids isolated from RG (TFRG) exhibited anti-inflammatory activity through the regulation of ERK/NF-κB/miR-155 signaling and suppression of iNOS expression in LPS/IFN-γ stimulated RAW264.7 macrophages without cytotoxicity. TFRG also markedly reduced tumor mass of breast cancer cell MDA-MB-231 xenografts with suppression of iNOS expression, formation of 3-nitrotyrosine (3-NT), and inactivation of protumorigenic JAK2/STAT3 signaling pathway. These results suggested that TFRG limited the development of breast cancer and inflammation due to its property of iNOS inhibition.

Significance StatementObesity is a serious and widespread health problem which has become a growing concern in many societies. Most currently available weight-loss medications do not work for everyone, and the effects decline over time. Thus, there is an urgent need to identify new molecular targets to improve drug development for the treatment of obesity and obesity-related diseases. In this study, we discovered that the histone deacetylase 11 (HDAC11) enzyme is a key regulator of metabolism and obesity, and the absence of HDAC11 prevents obesity in mice. Our findings will facilitate the development of novel therapeutics to treat obesity by targeting HDAC11.AbstractObesity and its associated metabolic syndromes are the consequence of susceptible genes and obesogenic environments. We report here that histone deacetylase 11 (HDAC11) plays a critical role in the development of obesity and in metabolic homeostasis. HDAC11 knockout mice display resistance to high-fat diet-induced obesity and associated syndromes by enhancing glucose tolerance and insulin sensitivity, attenuating hypercholesterolemia and hyperinsulinemia, and blocking hepatosteatosis and liver damage. Mechanistically, HDAC11 deficiency boosts energy expenditure through promoting thermogenic capacity, which attributes to the elevation of uncoupling protein 1 (UCP1) expression and activity in brown adipose tissue. Moreover, loss of HDAC11 stimulates mitochondrial oxidation, elevates plasma adiponectin, and activates the adiponectin-AdipoR-AMPK pathway in the liver, which may contribute to a reversal in hepatosteatosis. These findings establish HDAC11 as a key regulator of metabolism and indicate that HDAC11 inhibitors may hold promise for treating overweight and obesity-related diseases.

Objective: To systematically study various surgical approaches for treating complex hypopharyngeal and/or laryngotracheal stenoses at a variety of sites and levels. Patients and Methods: We retrospectively analyzed the treatment of 17 patients with severe and complex hypopharyngeal and/or laryngotracheal stenosis at various sites and levels of severity. All of the 17 patients initially had a tracheostomy. Thirteen had failed the previous laser lysis and/or dilation treatment. Given the high severity and complexity of stenosis, all of these patients were treated by open surgical reconstruction techniques using repairing grafts (flaps), followed by stenting. Results: Thirteen of 17 patients had successful decannulation 1-8 months post-operation and had stable airway and adequate vocal and swallow function. Two patients with complex hypopharyngeal and esophageal stenosis had unsuccessful decannulation. Follow-up was lost in 1 patient with complex hypopharyngeal and esophageal stenosis and 1 patient with original hypopharyngeal stenosis and recurrent thoracotracheal stenosis. Conclusion: Despite the failure by the regular treatments using laser lysis and/or dilation therapy, severe and complex hypopharyngeal and/or laryngotracheal stenosis may be successfully treated by variable open surgical reconstruction techniques using different grafts (flaps) depending on the site and severity of the stenosis.

// Ka Bian 2 , Naveen Reddy Muppani 1 , Lobna Elkhadragy 1 , Wei Wang 3 , Cheng Zhang 1 , Tenghui Chen 4 , Sungyun Jung 3 , Ole Morten Seternes 5 and Weiwen Long 1,2 1 Department of Biochemistry and Molecular Biology, Wright State University, Dayton, OH, USA 2 Department of Otorhinolaryngology, Tangdu Hospital, The Fourth Military Medical University, Xi’an, China 3 Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA 4 Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA 5 Department of Pharmacy, University of Tromsoe, N-Tromsoe, Norway Correspondence to: Weiwen Long, email: // Keywords : ERK3, TDP2, Top2 inhibitors, DNA damage, chemoresistance Received : June 01, 2015 Accepted : December 12, 2015 Published : December 19, 2015 Abstract Posttranslational modifications (PTMs), such as phosphorylation and ubiquitination, play critical regulatory roles in the assembly of DNA damage response proteins on the DNA damage site and their activities in DNA damage repair. Tyrosyl DNA phosphodiesterase 2 (TDP2) repairs Topoisomerase 2 (Top2)-linked DNA damage, thereby protecting cancer cells against Top2 inhibitors-induced growth inhibition and cell death. The regulation of TDP2 activity by post-translational modifications in DNA repair, however, remains unclear. In the current study, we have found that ERK3, an atypical MAPK, phosphorylates TDP2 at S60 and regulates TDP2’s phosphodiesterase activity, thereby cooperatively protecting lung cancer cells against Top2 inhibitors-induced DNA damage and growth inhibition. As such, our study revealed a post-translational regulation of TDP2 activity and discovered a new role of ERK3 in increasing cancer cells’ DNA damage response and chemoresistance to Top2 inhibitors.

The gold nanoparticles and cold plasma have been widely investigated separately in cancer therapy. In this paper, the two agents were combined in order to achieve a more profound understanding of their interactions in glioblastoma (U87) and normal human astrocytes (E6/E7). Gold nanoparticles were endocytosed at an accelerated rate in the U87 cell membrane due to the plasma treatment. This caused many divots across the cell membrane which made it more porous. On the contrary, in E6/E7 cells, there was no significant difference for penetration of gold nanoparticles or the cell membrane morphology. As proven in previous experiments the addition of the nanoparticles decrease cell viability, allowing the cold plasma to be more efficient. Present work demonstrated the synergistic effect of the two agents, which can be correlated in order to maximize the efficiency.

GarciniaLinn. plants having rich natural xanthones and benzophenones with anti-inflammatory activity attracted a great deal of attention to discover and develop them as potential drug candidates. Through screening targeting nitric oxide accumulation in stimulated macrophage, we found that 1,3,5,7-tetrahydroxy-8-isoprenylxanthone (TIE) had potential anti-inflammatory effect. To understand how TIE elicits its anti-inflammatory activity, we uncovered that it significantly inhibits the production of nitric oxide (NO) and prostaglandin E2 (PGE2) in LPS/IFNγ-stimulated RAW264.7 cells. In further study, we showed that TIE reduced the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), two key molecules responsible for the production of NO and PGE2 during inflammation progress. Additionally, TIE also suppressed the expression of inflammatory cytokines IL-6, IL-12, and TNF-α. TIE-led suppression in iNOS, COX-2, and cytokines production were probably the consequence of TIE’s capability to block ERK and p38MAPK signaling pathway. Moreover, TIE blocked activation of nuclear factor-kappa B (NF-κB) as well as NF-κB regulation of miR155 expression. Our study suggests that TIE may represent as a potential therapeutic agent for the treatment of inflammatory diseases.

Introduction: Multiple organ failure syndrome (MOFS) is a pathology associated to unspecified and severe trauma, characterized by elevated morbidity and mortality. The complex inflammatory MOFS-related reactions generate important ischemia-reperfusion responses in the induction of this syndrome. Nitric oxide elevation, through the activation of cyclic guanosine monophosphate (cGMP), has the potential of counteracting the typical systemic vasoconstriction, and platelet-induced hypercoagulation. Tadalafil would possibly act protectively by reducing cGMP degradation with consequent diffuse vasodilatation, besides reduction of platelet-induced hypercoagulation, thus, preventing multiple organ failure syndrome development. Methods: The experimental protocol was previously approved by an institution animal research committee. Experimental MOFS was induced through the stereotaxic micro-neurosurgical bilateral anterior hypothalamic lesions model. Groups of 10 Wistar rats were divided into: a) Non-operated control; b) Operated control group; c) 2 hours after tadalafil-treated operated group; d) 4 hours after tadalafil-treated operated group; e) 8 hours after post-treated operated group. The animals were sacrificed 24 hours after the neurosurgical procedure and submitted to histopathologic examination of five organs: brain, lungs, stomach, kidneys, and liver. Results: The electrolytic hypothalamic lesions resulted in a full picture of MOFS with disseminated multiple-organs lesions, provoked primarily by diffusely spread micro-thrombi. The treatment with tadalafil 2 hours after the micro-neurosurgical lesions reduced the experimental MOFS lesions development, in a highly significant level (P

// Xiang Zhang 1,* , Shu-Li Cheng 2,* , Ka Bian 3,4,* , Lei Wang 1 , Xiao Zhang 1 , Bo Yan 1 , Lin-Tao Jia 1 , Jing Zhao 1 , Noor Gammoh 5 , An-Gang Yang 4 and Rui Zhang 1 1 State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, the Fourth Military Medical University, Xi’an, Shaanxi, China 2 Department of Orthodontics, School of Stomatology, the Fourth Military Medical University, Xi’an Shaanxi, China 3 Department of Otolaryngology, Tangdu Hospital, the Fourth Military Medical University, Xi’an Shaanxi, China 4 State Key Laboratory of Cancer Biology, Department of Immunology, the Fourth Military Medical University, Xi’an, Shaanxi, China 5 Edinburgh Cancer Research Centre, The University of Edinburgh, Western General Hospital, Edinburgh EH4 2XR, United Kingdom * These authors contributed equally to this work Correspondence: Rui Zhang, email: // An-Gang Yang, email: // Keywords : microRNA-26a, ITGA5, human hepatocellular carcinoma, anoikis, tumor metastasis Received : October 13, 2014 Accepted : December 09, 2014 Published : December 10, 2014 Abstract Metastasis is the major reason for the death of patients suffering from malignant diseases such as human hepatocellular carcinoma (HCC). Among the complex metastatic process, resistance to anoikis is one of the most important steps. Previous studies demonstrate that microRNA-26a (miR-26a) is an important tumor suppressor that inhibits the proliferation and invasion of HCC cells by targeting multiple oncogenic proteins. However, whether miR-26a can also influence anoikis has not been well established. Here, we discovered that miR-26a promotes anoikis of HCC cells both in vitro and in vivo. With a combinational analysis of bioinformatics and public clinical databases, we predicted that alpha5 integrin (ITGA5), an integrin family member, is a putative target of miR-26a. Furthermore, we provide experimental evidence to confirm that ITGA5 is a bona fide target of miR-26a. Through gain- and loss-of-function studies, we demonstrate that ITGA5 is a functional target of miR-26a-induced anoikis in HCC cells. Collectively, our findings reveal that miR-26a is a novel player during anoikis and a potential therapeutic target for the treatment of metastatic HCC.

Despite a regain of interest recently in ERK3 kinase signaling, the molecular regulations of both ERK3 gene expression and protein kinase activity are still largely unknown. While it is shown that disruption of ERK3 gene causes neonatal lethality, cell type-specific functions of ERK3 signaling remain to be explored. In this study, we report that ERK3 gene expression is upregulated by cytokines through c-Jun in endothelial cells; c-Jun binds to the ERK3 gene and regulates its transcription. We further reveal a new role for ERK3 in regulating endothelial cell migration, proliferation and tube formation by upregulating SRC-3/SP-1-mediated VEGFR2 expression. The underlying molecular mechanism involves ERK3-stimulated formation of a transcriptional complex involving coactivator SRC-3, transcription factor SP-1 and the secondary coactivator CBP. Taken together, our study identified a molecular regulatory mechanism of ERK3 gene expression and revealed a previously unknown role of ERK3 in regulating endothelial cell functions.

Recent studies report that a conflict between information from the visual system and vestibular system is one of the main reasons for induction of motion sickness (MS). We may be able to clarify the integration mechanism of visual and vestibular information using an animal model with a visual defect, the retinal degeneration fast (rdf) mouse, and the role of vestibular information in the pathogenesis of MS. The rdf mice and wild-type Kunming mice were subjected to rotary stimulation to induce MS. Conditioned taste anorexia to saccharin solution and behavior score were used to observe the differences in MS sensitivity between two types of mice. The decrease in intake of saccharin solution and the behavior score in rdf mice were greater than those in normal mice. After rotatory stimulation, the reduction of intake mass and the behavior score were greater in rdf mice compared to those of normal mice. The rdf mice were more sensitive to rotation than normal mice. We conclude that visual information plays a role in the pathogenesis of MS. Visual information and vestibular information impact each other and integrate through certain channels in the central nervous system in mice.

Inflammation plays a pivotal role in the development and progression of cardiovascular diseases, in which, the endothelium dysfunction has been a key element. The current study was designed to explore the vasodilatory effect of anti-inflammatory herbs which have been traditionally used in different clinical applications. The total saponins fromActinidia argutaradix (SAA), total flavonoids fromGlycyrrhizaeradix et rhizoma (FGR), total coumarins fromPeucedaniradix (CPR), and total flavonoids fromSpatholobicaulis (FSC) were extracted. The isometric measurement of vasoactivity was used to observe the effects of herbal elements on the isolated aortic rings with or without endothelium. To understand endothelium-independent vasodilation, the effects of herb elements on agonists-induced vasocontractility and on the contraction of endothelium-free aortic rings exposed to a Ca2+-free medium were examined. Furthermore, the role of nitric oxide signaling in endothelium-dependent vasodilation was also evaluated. In summary, FGR and FSC exhibit potent anti-inflammatory effects compared to CPR and SAA. FGR exerts the strongest vasodilatory effect, while CPR shows the least. The relaxation induced by SAA and FSC required intact endothelia. The mechanism of this vasodilation might involve eNOS. CPR-mediated vasorelaxation appears to involve interference with intracellular calcium homeostasis, blocking Ca2+influx or releasing intracellular Ca2+.