Shijiazhuang, China

Hebei Medical University

www.hebmu.edu.cn
Shijiazhuang, China

Hebei Medical University is a university in Shijiazhuang, Hebei, People's Republic of China,under the provincial government.... a capital city of Hebei Province which is 4 hours away from Beijing by car and 1 and a half hours by train, Hebei Medical University Established in 1894, it is one of the oldest and AAA graded medical schools in China. Wikipedia.

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News Article | April 5, 2017
Site: www.medicalnewstoday.com

The human body's peripheral nervous system could be capable of interpreting its environment and modulating pain, neuroscientists have established, after successfully studying how rodents reacted to stimulation. Until now, accepted scientific theory has held that only the central nervous system - the brain and spinal cord - could actually interpret and analyse sensations like pain or heat. The peripheral system that runs throughout the body was seen to be a mainly wiring network, relaying information to and from the central nervous system by delivering messages to the 'control centre' (the brain), which then tells the body how to react. In recent years there has been some evidence of a more complex role for the peripheral nervous system, but this study by the Hebei Medical University in China and the University of Leeds highlights a crucial new role for the ganglia, a collection of 'nodules'. Previously these were believed to act only as an energy source for messages being carried through the nervous system. In addition, researchers now believe they also have the ability to act as 'mini brains', modifying how much information is sent to the central nervous system. The five year study found that nerve cells within the ganglia can exchange information between each other with the help of a signalling molecule called GABA, a process that previously believed to be restricted to the central nervous system. The findings are published in the Journal of Clinical Investigation and have potential future implications for the development of new painkillers, including drugs to target backache and arthritis pain. Current pain relief drugs are targeted at the central nervous system and often have side effects including addiction and tolerance issues. The new research opens up the possibility of a route for developing non-addictive and non-drowsy drugs, targeted at the peripheral nervous system. Safe therapeutic dosage of these new drugs can also be much higher, potentially resulting in higher efficacy. Whilst the study showed a rodent's peripheral nervous system was able to interpret the type of stimulation it was sensing, further research is still needed to understand how sensations are interpreted and whether these results apply to humans. In addition, the theory would need to be adopted by drug development companies and extensively tested before laboratory and clinical trials of a drug could be carried out. Should the findings be adopted, a timescale of at least 15-20 years might be required to produce a working drug. Neuroscientist Professor Nikita Gamper, who led the research at both universities, said: "We found the peripheral nervous system has the ability to alter the information sent to the brain, rather than blindly passing everything on to the central nervous system. "We don't yet know how the system works, but the machinery is definitely in place to allow the peripheral system to interpret and modify the tactile information perceived by the brain in terms of interpreting pain, warmth or the solidity of objects. "Further research is needed to understand exactly how it operates, but we have no reason to believe that the same nerve arrangements would not exist in humans. "When our research team looked more closely at the peripheral system, we found the machinery for neuronal communication did exist in the peripheral nervous system's structure. It is as if each sensory nerve has its own 'mini-brain', which to an extent, can interpret incoming information." Co-author of the study, Professor Xiaona Du from Hebei Medical University, added: "This dramatically changes our understanding of pain medication because in theory it is now possible to target drugs at the peripheral nervous system which could widen the type of treatments available." Professor Gamper believes the findings may present a challenge to the accepted 'Gate Control Theory of Pain'. The theory holds that a primary 'gate' exists between the peripheral and central nervous systems, controlling what information is sent to the central system. The study now suggests the transmission of information to the central nervous system must go through another set of gates, or more accurately a process similar to a volume control, where the flow of information can be controlled by the peripheral nervous system. "Peripheral nerves have the ability to dial up or down the signal which goes through these gates to the brain", said Professor Gamper. "Importantly, we believe that these gates can be exploited for therapeutic control of pain." Dr Kathryn Adcock, Head of Neurosciences and Mental Health at the Medical Research Council, which part funded the work, said: "These findings are an interesting step in advancing scientists' understanding of the mechanisms underpinning pain perception. We are committed to supporting work such as this to aid the continued search for new and better pain treatments." Lishuang Cao, head of Membrane Physiology at GlaxoSmithKline R&D in Shanghai commented on this research: "This interesting finding could pave the way for developing novel pain medicines by targeting the peripheral GABA signaling pathway and at the same time avoiding or reducing the side effects of many existing pain killers. "Further work is needed to understand the physiological role of GABA in painful situations like inflammatory, neuropathic and chronic pain. More importantly we need to know if the same mechanism is present in human beings' peripheral nervous systems."


RATIONALE:: Abdominal aortic aneurysms (AAAs) are characterized by pathological remodeling of the aortic wall. Although both increased Krüppel-like factor 5 (KLF5) expression and macrophage infiltration have been implicated in vascular remodeling, the role of KLF5 in macrophage infiltration and AAA formation remains unclear. OBJECTIVE:: To determine the role of KLF5 in AAA formation and macrophage infiltration into AAAs. METHODS AND RESULTS:: KLF5 expression was significantly increased in human AAA tissues and in two mouse models of experimental AAA. Moreover, in myeloid-specific Klf5 knockout mice (myeKlf5 mice), macrophage infiltration, medial smooth muscle cell loss, elastin degradation, and AAA formation were markedly decreased. In cell migration and time-lapse imaging analyses, the migration of murine myeKlf5 macrophages was impaired, and in luciferase reporter assays, KLF5 activated Myo9b transcription by direct binding to the Myo9b promoter. In subsequent co-immunostaining studies, Myo9b was colocalized with F-actin, cortactin, vinculin, and Tks5 in the podosomes of phorbol 12,13-dibutyrate-treated macrophages, indicating that Myo9b participates in podosome formation. Gain- and loss-of-function experiments showed that KLF5 promoted podosome formation in macrophages by upregulating Myo9b expression. Furthermore, RhoA-GTP levels increased after KLF5 knockdown in macrophages, suggesting that KLF5 lies upstream of RhoA signaling. Finally, Myo9b expression was increased in human AAA tissues, located in macrophages, and positively correlated with AAA size. CONCLUSIONS:: These data are the first to indicate that KLF5-dependent regulation of Myo9b/RhoA is required for podosome formation and macrophage migration during AAA formation, warranting consideration of the KLF5–Myo9b–RhoA pathway as a therapeutic target for AAA treatment. © 2017 American Heart Association, Inc.


Xue L.,Hebei Medical University
Arteriosclerosis, Thrombosis, and Vascular Biology | Year: 2017

OBJECTIVE—: To investigate the relationship between 3 markers of apoptosis, that is, FADD (Fas-associated death domain–containing protein), caspase-3, and caspase-8, and incidence of coronary events (CEs) in a population-based cohort study. APPROACH AND RESULTS—: In vitro experiments were performed to assess the response of the apoptotic biomarkers after Fas stimulation of peripheral blood mononuclear cells. The experiments showed significantly increased releases of FADD, caspase-3, and caspase-8 after Fas stimulation. The relationship between FADD, caspase-3, and caspase-8, respectively, and incidence of CEs was studied in 4284 subjects from the population-based Malmö Diet and Cancer Study. Cox’ proportional hazards regression was used to examine the association between the apoptotic biomarkers and incidence of CE over a mean follow-up of 19 years. A total of 381 individuals had CE during the follow-up. High FADD at baseline was significantly associated with incident CE. In the highest compared with the lowest quartile of FADD, the risk factor adjusted hazards ratio for CE was 1.82 (95% confidence interval, 1.35–2.46; P for trend =0.001). A significant association was also found between caspase-8 and CE; the hazards ratio (Q4 versus Q1) was 1.90 (95% confidence interval, 1.39–2.60; P for trend =0.001) after adjustment for risk factors. No association was found between caspase-3 and CEs. CONCLUSIONS—: High levels of FADD and caspase-8, but not caspase-3, were associated with increased incidence of CE in subjects from the general population. The in vitro experiments support the view that these biomarkers could reflect activation of the extrinsic apoptotic pathway. © 2017 American Heart Association, Inc.


Sun Y.,Hebei Medical University
Circulation Research | Year: 2017

RATIONALE:: Neuregulin-1 (NRG-1) includes an extracellular EGF-like domain and an intracellular domain (NRG-1-ICD). In response to transforming growth factor (TGF)-β1, its cleavage by proteolytic enzymes releases a bioactive fragment, which suppresses the vascular smooth muscle cell (VSMC) proliferation by activating ErbB receptor. However, NRG-1-ICD function in VSMCs remains unknown. OBJECTIVE:: Here, we characterize the function of NRG-1-ICD and underlying mechanisms in VSMCs. METHODS AND RESULTS:: Immunofluorescence staining, Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) showed that NRG-1 was expressed in rat, mouse and human VSMCs and was upregulated and cleaved in response to TGF-β1. In the cytoplasm of HASMCs, the NRG-1-ICD participated in filamentous actin formation by interacting with smooth muscle α-actin (α-SMA). In the nucleus, the Nrg-1-ICD induced circular ACTA2 (circACTA2) formation by recruitment of the zinc-finger transcription factor IKZF1 to the first intron of α-SMA gene. We further confirmed that circACTA2, acting as a sponge binding microRNA (miR)-548f-5p, interacted with miR-548f-5p targeting 3ʼ untranslated region (3ʼ-UTR) of α-SMA mRNA, which in turn relieves miR-548f-5p repression of the α-SMA expression and thus upregulates α-SMA expression, thereby facilitating stress fiber formation and cell contraction in HASMCs. Accordingly, in vivo studies demonstrated the localization of the interaction of circACTA2 with miR-548f-5p is significantly decreased in human intimal hyperplastic arteries compared with normal arteries, implicating that dysregulation of circACTA2 and miR-548f-5p expression is involved in intimal hyperplasia. CONCLUSIONS:: These results suggest that circACTA2 mediates NRG-1-ICD regulation of α-SMA expression in HASMCs via the NRG-1-ICD/circACTA2/miR-548f-5p axis. Our data provide a molecular basis for fine-turning α-SMA expression and VSMC contraction by transcription factor, circular RNA and microRNA. © 2017 American Heart Association, Inc.


Zhou H.,Hebei Medical University | Li Y.-J.,Hebei Medical University
Current Pharmaceutical Design | Year: 2012

The small GTPase RhoA and its downstream effector, Rho kinase (ROCK), appear to mediate numerous pathophysiological signals, including smooth muscle cell contraction, actin cytoskeleton organization, cell adhesion and motility, proliferation, differentiation and the expression of several genes. Clinical interest in the RhoA/ROCK pathway has increased, due to emerging evidence that this signaling pathway is involved in the pathogenesis of several diseases, including hypertension, coronary vasospasm, stroke, atherosclerosis, heart failure and diabetes; ROCK is considered an important future therapeutic target. Several pharmaceutical companies are already actively engaged in the development of ROCK inhibitors as the next generation of therapeutic agents for these diseases. This review discusses the relationship between diabetes and hyperglycemia-induced RhoA/ROCK activation, highlights recent findings on the roles of ROCK inhibitors from experimental models of diabetes and clinical studies in cardiovascular patients, and elucidates major challenges for developing more selective ROCK inhibitors. Accumulating evidence suggests the potential of ROCK inhibitors as therapeutic agents for diabetes and its complications. © 2012 Bentham Science Publishers.


Previous reports indicate a potential role for calcitonin (CT) in the treatment of osteoarthritis (OA). To evaluate this potential therapeutic role, we investigated the effect of CT pretreatment on the activation of mitogen-activated protein kinase (MAPK) signaling and the expression of matrix metalloproteinase-13 (MMP-13) in interleukin-1β (IL-1β)-induced chondrocytes, and further assessed its protective effect in a rat model of anterior cruciate ligament transection (ACLT), using sham-operated and saline-treated controls. Using western blotting in vitro, we found that CT pretreatment inhibited the IL-1β-induced phosphorylation of 38,000-dalton protein (p38) and extracellular regulated protein 1/2 (ERK1/2) and reduced the expression of MMP-13 protein. For the in vivo experiment, 30 male rats were randomly divided into three groups of 10, subjected to bilateral ACLT or sham surgery, and then treated for 12 weeks with subcutaneous injections of CT or normal saline. Histological observations showed that CT treatment reduced the severity of the cartilage lesions stemming from the ACLT surgery and provided a lower Mankin score when compared with that determined for rats in the saline-treated ACLT group. Immunohistochemical staining revealed that CT treatment increased type II collagen expression and decreased MMP-3 and a disintegrin and metalloproteinase with thrombospondin motifs-4 (ADAMTS-4) expression when compared with the saline-treated group. Subchondral bone analysis indicated that CT treatment inhibited the reduction in bone mineral density observed in the saline-treated ACLT group and reduced the ACLT-induced destruction to the subchondral trabecular microstructure. Our data demonstrate that CT induces its protective effects by reducing the chondrocyte response to inflammatory stimuli, cartilage extracellular matrix degradation, and subchondral trabecular microstructure damages brought on by OA.


Liu C.,Hebei Medical University
Cochrane database of systematic reviews (Online) | Year: 2013

Pulmonary arterial hypertension is a devastating disease, which leads to right heart failure and premature death. Recent evidence suggests that endothelin receptor antagonists may be promising drugs in the treatment of pulmonary arterial hypertension. To evaluate the efficacy of endothelin receptor antagonists in pulmonary arterial hypertension. We searched CENTRAL (Cochrane Central Register of Controlled Trials), MEDLINE, EMBASE, and the reference section of retrieved articles. Searches are current as of January 2012. We included randomised trials (RCTs) and quasi-randomised trials involving patients with pulmonary arterial hypertension. Five review authors independently selected studies, assessed study quality and extracted data. We included 12 randomised controlled trials involving 1471 patients. All the trials were of relatively short duration (12 weeks to six months). After treatment, patients treated with endothelin receptor antagonists could walk on average 33.71 metres (95% confidence interval (CI) 24.90 to 42.52 metres) further than those treated with placebo in a six-minute walk test. Endothelin receptor antagonists improved more patients' World Health Organization/New York Heart Association (WHO/NYHA) functional class status than placebo (odds ratio (OR) 1.60; 95% CI 1.20 to 2.14), and reduced the odds of functional class deterioration compared with placebo (OR 0.26; 95% CI 0.16 to 0.42). There was a reduction in mortality that did not reach statistical significance on endothelin receptor antagonists (OR 0.57; 95% CI 0.26 to 1.24), and limited data suggest that endothelin receptor antagonists improve the Borg dyspnoea score and cardiopulmonary haemodynamics in symptomatic patients. Hepatic toxicity was not common, and endothelin receptor antagonists were well tolerated in this population. However, several cases of irreversible liver failure caused by sitaxsentan have been reported that led to license holder for sitaxsentan to withdraw the product from all markets worldwide. Endothelin receptor antagonists can increase exercise capacity, improve WHO/NYHA functional class, prevent WHO/NYHA functional class deterioration, reduce dyspnoea and improve cardiopulmonary haemodynamic variables in patients with pulmonary arterial hypertension with WHO/NYHA functional class II and III. However, there was only a trend towards endothelin receptor antagonists reducing mortality in patients with pulmonary arterial hypertension. Efficacy data are strongest in those with idiopathic pulmonary hypertension. The irreversible liver failure caused by sitaxsentan and its withdrawal from global markets emphasise the importance of hepatic monitoring in patients treated with endothelin receptor antagonists.


Jia J.,Hebei Medical University
Investigative ophthalmology & visual science | Year: 2013

To explore the regulation of inducible nitric oxide synthase (iNOS) expression by nuclear factor kappa B (NF-κB) in human lens epithelial cells (LECs) treated with high levels of glucose, and to elucidate the impact of this in the pathogenesis of cataracts associated with diabetes. LECs (SRA01/04) were cultured in vitro. NF-κB nuclear translocation and iNOS expression were measured at different glucose concentrations and at various time points, and the optimal concentration for detecting changes in the patterns of NF-κB nuclear translocation and iNOS expression was chosen. As a specific NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC) was used to assess the effect of inhibiting NF-κB. Western blotting and inverted fluorescence microscopy were used to monitor the nuclear translocation of NF-κB. PCR and Western blotting were used to measure iNOS expression. Using the University of California, Santa Cruz database and the TFSEARCH program, we searched the DNA sequence upstream of iNOS for the core binding sequence for NF-κB. Chromatin immunoprecipitation (ChIP) was used to measure the binding of NF-κB. The nuclear translocation of NF-κB was measured upon glucose treatment, and the concentration of NF-κB in the nucleus was found to peak at 25 to 30 minutes of treatment with 25 mM glucose. iNOS mRNA and protein levels also increased significantly in a time- and concentration-dependent manner and iNOS mRNA and protein reached their peak values after 8 hours of treatment with 25 mM glucose. The binding of NF-κB to the promoter of the iNOS gene was enhanced in the 25 mM glucose group compared with the 5.5 mM glucose group or the 25 mM glucose + 100 μL PDTC group, and this difference was statistically significant (P < 0.05). NF-κB regulates iNOS expression in a time- and concentration-dependent manner. Under high glucose conditions, NF-κB is activated and rapidly translocates to the nucleus, leading to increased binding to the iNOS promoter and a consequent increase in iNOS expression. The findings of this study provide important experimental evidence that clarifies the pathogenesis of cataracts associated with diabetes and contributes to the search for therapeutic targets of these cataracts.


The use of celecoxib is associated with a significant decrease in breast cancer risk. However, the long-term use of high-dose celecoxib might be limited owing to cardiovascular side effects. In this study, we found that acetylbritannilactone (ABL), extract from a Chinese medicinal herb, could reduce celecoxib dose and potentiate the growth-inhibitory effect in breast cancer cells. ABL enhanced the apoptotic effect of celecoxib in COX-2-expressing cells, but had little effect in COX-2-negative cells. The apoptosis induced by the combination treatment disappeared when COX-2 was knocked down, whereas the lack of apoptotic effects in COX-2-negative cells was reversed after COX-2 transfection. However, the combination treatment induced a G(0)/G(1) phase arrest independent of whether or not the cells expressed COX-2. The G(0)/G(1) arrest was attributed to a decreased expression of cyclinD1, cyclinE, CDK2 and CDK6, especially the upregulation of p21. In addition, inhibition of Akt and p38 signaling pathways was required by the synergism, as the constitutively active Akt and p38 protected cells against apoptosis and cell cycle arrest induced by the combination treatment. In vivo, administration of celecoxib and ABL were more effective than the individual agents against xenograft tumor growth. Thus, our data suggested that the combinatorial approach of celecoxib and ABL might be helpful for breast cancer treatment.


Patent
Hebei Medical University | Date: 2013-06-06

A bionic elastic fixing device relates to orthopedic medical devices, and is used to implement bionic elastic internal fixing for joint dislocation. The device consists of an elastic component (1) and a fixing assembly (2, 3, 4). The elastic component (1) may be multiple strip-shaped elastic mesh pieces, and has the assembly direction being the same as the ligament fibers at the joint required to be fixed. The elastic modulus of the elastic component (1) matches the elastic modulus of the ligament fibers at the joint required to be fixed. Two ends of the elastic component (1) are fixedly connected to the dislocated joint by the fixing assembly (2, 3, 4). The elastic component (1) has the same shape as the ligament fibers at the joint required to be fixed.

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