Development of liver fibrosis is closely associated with angiogenesis and abnormal vascular remodeling. Recent studies have highlighted the importance of angiogenesis and vascular remodeling in fibrogenesis, the results that inhibition of angiogenesis is effective in suppression of liver fibrosis demonstrate that therapies with several molecular targets against angiogenesis, inflammation and fibrosis might be beneficial for the treatment of cirrhosis. However, there is some evidence that inhibition of angiogenesis can even worsen fibrosis. This article outlines recent advances regarding the interplay between inflammation, angiogenesis and fibrogenesis in terms of cellular and molecular mechanisms, and suggests a requirement of greater understanding to intervene in these key processes, such as liver sinusoidal endothelial cell fenestration and impact distinct chemokine actions driving monocyte migration and differentiation, for therapeutic benefit in the future.
Humans ; Inflammation ; therapy ; Liver Cirrhosis ; therapy ; Neovascularization, Pathologic ; therapy ; Vascular Remodeling

Innate immunity initially resists the infection of pathogenic microorganism in host immune response.Recent researches confirmed that mitochondria participated in a wide range of innate immune pathways,mainly including contributing to innate immune activation,regulating antiviral signaling pathways and antibacterial immunity.Therefore,further studies on the relationship among mitochondria,hepatitis B virus(HBV)infection and innate immune response might contribute to elucidate the mechanism of chronic HBV infection and explore the mechanism of host immune to clear HBV.Here,mitochondria playing a vital role in regulations of innate immune response,HBV infection tending to chronicity by suppressing innate immune response and chronic HBV infection by regulating the innate immune response through injuring mitochondria,were reviewed.

Objective To observe the efficacy of lipoic acid combined with mosapride in the treatment of diabetic neurogenic bladder.Methods 30 patients with type 2 diabetes complicated with diabatic neurogenic bladder were treated with lipoic acid and mosapride for three weeks,on the base of good controlling of blood glucose,blood lipids,and other metabolic indicators.The residual urine volume of bladder and urodynamic indicators were compared before and after treatment.Results The residual urine volume of bladder and urodynamic indicators after treatment for three weeks and withdrawal for four weeks were (62.5 ± 27.8) ml and (61.3 ± 21.6) ml,(8.3 ± 1.9) ml/s and (7.9 ±2.1)ml/s,(10.7 ± 1.8)ml/s and (10.3 ± 1.6) ml/s,(25.6 ±2.7)cm H2O and (24.5 ±2.3)cm H2O,which were significiantly better than those before treatment [(128.3 ± 72.5) ml,(5.2 ± 1.3) ml/s,(8.4 ± 1.2) ml/s,(18.1 ±1.2)cm H2O](t=4.01,4.21,3.45,3.52,3.68,3.47,3.33,3.24,all P ＜0.01).Conclusion Lipoic acid combined with mosapride has good effect in the treatment of diabetic neurogenic bladder.

Objective:To establish a highly sensitive, rapid and selective liquid chromatography mass spectrometry (LC-MS) method for the determination of metoprolol in rat plasma.Methods:A simplified liquid-liquid extraction with acetidin was employed for the sample preparation. The separation was carried out on a Thermo ODS-C_(18)(5 μm,100 mm×2.1 mm).The mobile phase consisted of acetonitrile-methanol-water(20∶20∶60). Propranolol was used as the internal standard. The detection was performed on a liquid chromatography mass spectrometry by selected ion monitoring(SIM) scan mode electrospray ionization(ESI).Results and Conclusion:The range of calibration curve was 0.1-50 ng/ml and the limit of quantification was 0.1 ng/ml. The intra- and inter-day precision RSD was less than 15%.This method is sensitive, simple,rapid and suitable for the pharmacokinetic study of metoprolol.

Chronic pain is a common clinical disease,which brings great burden to the patients.However,the pathogenesis underlying of chronic pain is complicated,which is affected by many factors,such as physiology,psychology and society.Therefore,the treatment of chronic pain has been a problem in clinical practice.Considering its complexity,a single way of treatment usually could not reach satisfactory results,so combination therapy is often used to treat chronic pain at present.The combination therapy includes pharmacological treatment,psychological approaches,interventional treatment,self management and so on.The treatment plans are distinct for different types of chronic pain,even the individual patients with the same kind of pain.The emergence of interdisciplinary rehabilitation programs shed light upon the treatment of chronic pain recent years.This paper reviewed the research on chronic pain treatment,in order to provide theoretical basis for clinical practice.

Objective To evaluate the possible molecular pathogenesis of intractable temporal lobe epilepsy. The potassium ion channel gene KCNJ4 encodes one of the subfamilies of Kir channels, Kir2.3 subunit, which may play an important role in modulating neuronal excitation. Interference in the function or expression of this gene would cause disturbance of ionic concentrations, thus leading to seizure activity. Methods Reverse transcription polymerase chain reaction (RT-PCR) and Western-blot analysis were used to measure the expression alterations of KCNJ4 mRNA as well as its protein product Kir2.3 channel in temporal cortex samples from patients who had undergone temporal lobectomy for intractable epilepsy (n=12). Tissue from 10 subjects who did not have epilepsy served as controls. Results The expression of KCNJ4 mRNA (0.438?0.178) and its protein Kir2.3 (M 50=0.063) were significantly decreased in epileptic brain compared with the controls (P

Objective To discuss the feasibility and curative effect of broncho-alveolar lavage(BAL)through bronchofiberscope in the treatment of severe toxic pulmonary edema caused by irritative gas.Methods 16 cases se- vere toxic pulmonary edema caused by irritative gas were performed BAL through bronchofiberseope.The index of oxygen in arterial blood,clinical and radiological changes before,during and 2 hours after BAL were observed.Results 2 hours after BAL through bronchofiberscope,the partial pressure of oxygen in arterial blood(PaO2)obviously in- creased,the partial pressure of carbon dioxide in arterial blood(PaCO_2)did not change much.PaO_2 and PaCO_2 had no obvious change before and during BAL.The shadow area in the X-ray film of chest obviously decreased 24 hours af- ter BAL.In all 16 cases,13 cases were cured,1 case got improvement,and 2 cases died.The curative rate was 81%. Conclusion BAL through bronchofiberscope could clear the noxious substance in airway and improve the ventilation function.It was safe and had confirmed curative effect.

Objective To investigate the curative effect of modified tracheal catheter in acute respiratory failure caused by central airway stenosis.Methods 16 cases inpatient with acute respiratory failure caused by central airway stenosis were involved.Found out the position and range of stenosis of central airway by X-ray and CT of chest and fiberbronchoscope,chose the suitable silicon suction tube and cut it to make a tracheal catheter,then guided the catheter through the stenosis by fiberbronchoscope to construct artificial airway.Results The dyspnea of all 16 cases of acute respiratory failure caused by central airway stenosis could by relieved in short time,the PaO_2 raised from(39?12)mm Hg to(72?10)mm Hg,SaO_2 raised from(75?13)% to(93?3)%,PaCO_2 dropped from(102?21)mm Hg to(62?13)mm Hg after therapy.The effective rate is 100%.There was no other serious complication except for 2 cases of little amount of bleeding in trachea.15 cases survived and one died of serious muhisystem organ failure.Conclusions The use of modified tracheal catheter in treatment of acute respiratory failure caused by central airway stenosis can relieve the acute dyspnea in short time,it also can dilate central airway,save the cost of tracheal balloon dilatation for the follow-up therapy.

Objective To investigate the alterations and molecular mechanism of transient outward potassi- um currents(I_(to)) in ventricular myocytes from diabetic rats and explore the mechanism of predisposition of arrhyth- mias in diabetes.Methods The diabetes model was established by a single injection of streptozocin(STZ,65 mg/ kg,pH=4.5) I.P.in male Sprague-Dawley rats with weight 150-200 g.Ventricular myocytes were isolated by enzymatic perfusion.The currents were recorded with the whole-cell patch clamp technique,and gene expres- sions of channel-forming subunits (Kv4.2,Kv4.3 and Kv1.4) were semi-quantified by the technique of reverse transcriptase-polymerase chain reaction(RT-PCR).Results The I_(to) density (+70 mV) decreased significantly in diabetic rats compared with controls[control:(30.6?3.8)pA/pF(n=9) vs diabetes:(18.9?3.3)pA/pF(n= 29)(P

Objective] To explore the humoral and cellular immune responses in mice to eukaryotic expression recombinant plasmid encoding histidine rich protein 2 (HRP\|Ⅱ) of Plasmodium falciparum. [Methods] The start and stop codes were introduced into HRP\|Ⅱ gene fragment, the reading frame and the position of start and stop codes in HRP\|Ⅱ were identified by sequencing. HRP\|Ⅱ fragment containing the start and stop codes was cloned into pcDNA3 1(\|) to form pcDNA3 1(\|)/HRP\|Ⅱ. The BALB/c mice were immunized i.m. with the plasmids for 3 times in 3 weeks intervals. Two weeks after the last immunization, the sera and splenocytes were collected to investigate anti\|HRP\|Ⅱ antibodies by ELISA and the splenocytes proliferation response to HRP\|Ⅱ. [Results] Sequence data show that the reading frame and the position of start and stop codes are correct. Restriction enzyme digestion indicated that the HRP\|Ⅱ gene fragment containing start and stop codes was successfully cloned into pcDNA3 1(\|). Mice raised significant anti\|HRP\|Ⅱ antibodies after pcDNA3 1(\|)/HRP\|Ⅱ immunization, and the splenocytes proliferated prominently when stimulated with HRP\|Ⅱ protein. [Conclusion] Eukaryotic expression recombinant plasmid \{encoding\} HRP\|Ⅱ gene can induce significantly humoral and cellular immune response in mice. HRP\|Ⅱ gene may be a good candidate for P.falciparum blood\|stage multiple DNA vaccine.