Objective:To analyze the impacts of sustainable deterioration of environment quality and demographic structure adjustment on urban residents' health expenditure.Methods:Non-spatial panel model and spatial panel model were applied to use inter-provincial panel data to conduct the empirical analysis.Results:Environment quality,demographic age structure and interaction had significant impact on urban residents' health expenditure.Conclusion:Demographic structure transformation and environment quality deterioration were the two difficulties faced by China's medical and health system.The construction and reform of medical and health system should focus on these challenges.

Objective To compare the prediction probability (Pk) of loss of consciousness (LOC) for the four EEG nonlinear indexes-correlation dimension ( D2), approximate entropy (ApEn) complexity (Cx) and bispectral index (BIS) and their relative accuracy. Methods Twenty ASA Ⅰ-Ⅱ patients aged 22-71 undergoing elective operation on lower limb under epidural anesthesia were studied. The patients were unpremedicated. Epidural catheter was placed at L2,3 or L3,4 interspace. The block height was 95% . Sedation was produced by target-controlled infusion (TCI) of propofol. The target plasma concentration of propofol (Cp) was initially set at 0.5 ?g?ml-1. Cp was gradually increased in increments of 0.3-0.5 ?g?ml-1 every 3 min until LOC. Depth of sedation was assessed using OAA/S scale (5 = alert, 1 = LOC) . LOC was maintained for 12 min. Cp was equal to effect-site concentration (Ce) by the end of 12 minutes. Cp was then gradually decreased in increments of 0.3-0.5 ?g?ml-1 until the patients regained consciousness. The same procedure was repeated 4 times in every patient. BIS, D2 , ApEn and Cx were recorded simultaneously every 3 min. The prediction probability of LOC for D2, ApEn, Cx and BIS was calculated and compared.Results The BIS value was 80.2?6.2 when the patients regained consciousness (T1) and 67.3?7.9 at LOC (T2); D2 was 3.45?0.18 (T1) and3.01?0.16 (T2); ApEn was 0.84?0.05 (T1) and 0.71?0.06 (T2); Cx was 0.55?0.05 (T1) and 0.44?0.05. There was no significant difference in Pk of LOC among the 4 indexes. Conclusion Our results show that all the 4 indexes can be used to monitor the level of sedation produced by propofol.

OBJECTIVE:A fluorospectrophotometric method was established for the determination of lomefoxacin hydrochloride in injection and capsule.METHODS:Samples were diluted with distilled water and detected by fluorospectrophotometry at excitation wavelength of 285nm and emission wavelength of 445nm.RESULTS:Linear relationship was found in the lomefloxacin hydrochloride concentrations ranging from 0.5?g/ml to 2.5?g/ml.The correlation coefficient was 0.9 998.The recoveries of lomefloxacin in injection and capsule were 99.7%(RSD=0.6%,n=5) and 99.6%(RSD=0.8%,n=5),respectively.CONCLUSION:The method is simple,accurate and sensitive and can be used to determine lomefloxacin hydrochloride in injection and capsule.

Objective To investigate the effects of different concentrations of isoflurane on neuronal apoptosis in hippocampus and cerebral cortex in the aged rats. Methods Ninety female pathogen-free SD rats 22-24 months old weighing 497-593 g were randomly divided into 3 groups: group Ⅰ oxygen group inhaled air enriched with 40% O2,groupⅡ and Ⅲ were anesthetized with 1.2% and 1.8% isoflurane for 3 h respectively. Morris water maze was used to assess the cognitive function. The animals were killed at 24 and 72 h and on the 7th day after emergence from anesthesia and their brains were removed. Neuronal apoptosis in hippocampus and cerebral cortex was detected by TUNEL. Results The average escape latency was significantly longer on the 2nd and 3rd day after isoflurane anesthesia in isoflurane group than in oxygen group (P < 0.05 ). The neuronal apoptesis rate was significantly higher in the 2 isoflurane group than in oxygen group (P < 0.05 or 0.01 ). Conclusion Isoflurane anesthesia can result in transient cognitive dysfunction, and the mechanism may be involved in apoptosis in cerebral cortex in the aged rats.

This paper aims to make a comprehensive review about the new generation drug-eluting stents and their effects of anti-thrombosis to decrease stent thrombosis (ST), which are very helpful for interventional radiologists, especially for cardiologists who are engaged in percutaneous coronary interventional therapy. Based on the review of recently published academic papers and the investigation of the manufacturers and market of stent, the main factors related to ST complication which is associated with new generation drug-eluting stents are retrospectively and briefly analyzed. Besides, a variety of new generation drug-eluting stents with anti-thrombosis effect that are being successfully developed recently with new technology and new materials, including the renewal or improvement of the stent platform, loaded drug, carrier and its loading technology, etc. are comprehensively described in this paper in a combination way of vivid pictures with corresponding essay. In addition, the development and the prospect in clinical application of biodegradable drug-eluting stents are also briefly discussed in this paper.

In this paper, all the intrahepatic arterioportal shunts (IHAPSs) that result from the functional redistribution of hepatic arterial and portal venous blood flow are defined as functional IHAPSs (F-IHAPSs) so as to make the differentiation from organic IHAPSs (O-IHAPSs) that result from the intrahepatic arterioportal fistula or direct communication, such as those IHAPSs that are associated with advanced hepatocellular carcinoma (HCC) and other malignant hepatic tumors as well as those IHAPSs that are accompanied by congenital hepatic vascular malformations, hereditary hemorrhagic telangioectasia (HHT) and liver trauma (including iatrogenic injury), etc. In F-IHAPSs, the most common one is formed by the compensatory (or secondary) increase of arterial blood flow that is caused by the decrease of hepatopetal portal blood flow due to a variety of reasons; its formation mechanisms can be divided into three categories:(1) trans-sinusoidal type, such as the F-IHAPSs that is associated with cirrhosis;(2) post-sinusoidal type, such as the F-IHAPSs that is accompanied with the acute stage of Budd-Chiari syndrome; and (3) pre-sinusoidal type, such as the F-IHAPSs that occurs along with the gastrointestinal hemorrhagic shock. Another kind of F-IHAPSs has been commonly seen in some hepatic diseases that have primary increase of hepatic arterial blood flow, including hypervascular hepatic cavernous hemangioma, small hepatocellular carcinoma that has rich blood supply, hepatobiliary inflammatory diseases, etc.;and in this paper they are all classified as F-IHAPSs category, however, the formation mechanisms of such F-IHAPSs vary with their basic diseases. Clinically, imaging diagnosis of F-IHAPSs can be made based on the following three signs:(1) all kinds of hepatic diseases that have concomitant intrahepatic arterioportal fistula or direct communication, as mentioned above, have been definitely excluded:(2) hepatic artery DSA reveals early visualization of portal vein in arterial phase, known as the characteristic sign of F-IHAPSs;and/or: (3) hepatic dynamic enhanced CT/MR scanning demonstrates transient enhancement of liver parenchyma in arterial phase, especially early visualization of portal vein is also present; in this case the diagnosis of F-IHAPSs can be undoubtedly confirmed. However, in making differential diagnosis, F-IHAPSs must be carefully differentiated from O-IHAPSs, local hepatic parenchymal perfusion caused by hepatic aberrant vein or by abnormal hepatopetal draining vein from systemic circulation, etc. In addition, when cirrhosis-related transient hepatic parenchymal enhancement presents as a solitary small nodule, differentiation with small HCC should be taken into consideration. In order to provide the readers with a complete and up-to-date understanding of F-IHAPSs, the relevant example illustrations, figures and graphics are accompanied with the text.

AIM: To investigate the effect of vasodilator-stimulated phosphoprotein (VASP) phosphorylation on the cell migration induced by platelet-derived growth factor BB (PDGF-BB), and to identify which phosphorylation site was more important among the three phosphorylation sites, namely Ser157,Ser239 and Thr278. METHODS: Two phosphorylation mutants of VASP, pcDNA3.1(+)/VASP-S157A and pcDNA3.1(+)/VASP-S239A, were constructed and respectively transfected into the cultured ECV304 cells by means of liposome. The stable expression cells were screened by using antibiotic G418. Protein expression of VASP was measured by Western blotting. The ECV304 cell migration was evaluated using Transwell chamber. RESULTS: Compared to control group, the cell migration was significantly inhibited in ECV304 transfected with VASP-S157A and VASP-S239A (P<0.05), although slight differences existed between VASP-S157A and VASP-S239A transfected cells (P>0.05). CONCLUSION: VASP mutation on the phosphorylation sites of Ser157 and Ser239 inhibits cell migration, and the phosphorylation sites of Ser157 and Ser239 both greatly affect the function of VASP.

Parkinson's disease (PD) is a common neurodegenerative disorder associated with aging. Great progresses have been made toward understanding the pathogenesis over the past decades. It seems that both genetic factors and environmental factors contribute to PD, while the precise pathogenesis still remains unknown. Recently, increasing evidence has suggested that autophagy dysregulation is closely related to PD. Dysregulation of the autophagic pathways has been observed in the brains of PD patients or in animal models of PD, and a number of PD-associated proteins, such as a-synuclein, Parkin and PINK1, were found to involve in autophagy, suggesting a link between autophagy and pathogenesis of PD. In this review, we summarized the role of PD-associated proteins in autophagy pathways. In addition, we described the efficacy of autophagy-modulating compounds in PD models and discussed promising strategies for PD therapy.
Animals ; Autophagy ; Humans ; Parkinson Disease ; physiopathology ; Protein Kinases ; metabolism ; Ubiquitin-Protein Ligases ; metabolism ; alpha-Synuclein ; metabolism

A case of a patient with a unilateral maxillary defect and restricted mouth opening was presented. The two-stage hollow maxillofacial prosthesis can be used to restore the above defect, thus promoting mastication, speaking, swallowing, and sucking, as well as improving the patient's appearance. Satisfactory results were achieved.
Humans ; Mastication ; Maxilla ; Maxillofacial Prosthesis ; Mouth ; Prostheses and Implants

Parkinson's disease (PD) is a common neurodegenerative disorder associated with aging. Great progresses have been made toward understanding the pathogenesis over the past decades. It seems that both genetic factors and environmental factors contribute to PD, while the precise pathogenesis still remains unknown. Recently, increasing evidence has suggested that autophagy dysregulation is closely related to PD. Dysregulation of the autophagic pathways has been observed in the brains of PD patients or in animal models of PD, and a number of PD-associated proteins, such as a-synuclein, Parkin and PINK1, were found to involve in autophagy, suggesting a link between autophagy and pathogenesis of PD. In this review, we summarized the role of PD-associated proteins in autophagy pathways. In addition, we described the efficacy of autophagy-modulating compounds in PD models and discussed promising strategies for PD therapy.