Neurolytic celiac plexus block (NCPB) is an effective method used to alleviate upper abdominal pain or back pain caused by pancreatic cancer and other malignancies. NCPB can relieve cancer pain to improve the quality of life and cause fewer side effects than conventional analgesic drugs. This article systemically reviewed NCPB methodology and research progress in clinical appli-cations.

The morbidity of pancreatic duct calculus is increasing every year in China. Currently the main therapeutic methods include non-surgical treatment and surgical treatment. Non-surgical treatments contain endoscopic calculus extracting and / or extracorporeal shock wave lithotripsy. Surgical treatment has two categories: drainage of the pancreatic duct decompression and pancreatectomy. Concrete treatment or surgical options should follow the strategy of individual.

Although quinolone resistance results mostly from chromosomal mutations in Enterobacteriaceae,it may also be mediated by plasmid-encoded Qnr determinants.Qnr proteins protect DNA from quinolone action and compromise the effect of quinolones,such as nalidixic acid.Qnr proteins including QnrA,QnrB and QnrS,have been identified worldwide with a quite high prevalence among Asian isolates with a frequent association with clavulanic acid-inhibited expanded-spectrum b-lactamases and plasmid-mediated cephalosporinases.The QnrA genes are embedded in complex sul1-type integrons.A close relative and likely progenitor of the QnrA have been found in the water-borne species Shewanella algae.It may help to determine the location of in vivo transfer of the QnrA genes.Further analyses of the role of quinolones,if any,in enhancing this gene transfer may prevent the spreading of the drug resistance and possibly lead to the finding of a novel mechanism of antibiotic resistance.

To study the general characteristics of cancer pain and to improve cancer pain diagnosis and treatment lev-el by prospective and open cross-sectional assessment of the clinical characteristics of patients with moderate to severe cancer pain. Methods:Patients with moderate to severe cancer pain were observed upon initial admission to the hospital from December 2012 to De-cember 2013. We assessed pain intensity, location, characteristics, and predisposing and mitigating factors and classified the pain by pathophysiology. Results:A total of 310 patients with moderate (101 cases, 32.58%) and severe (209 cases, 67.42%) pains were as-sessed. The top five cancers identified were lung cancer (102 cases, 32.90%), colorectal cancer (30 cases, 9.68%), pancreatic cancer (27 cases, 8.71%), breast cancer (24 cases, 7.74%), and gastric cancer (20 cases, 6.54%). These patients reported 533 cancer pain locations, including waist (132 cases), abdominal (125 cases), chest (88 cases), lower limb (71 cases), shoulder, neck, and upper limb (47 cases), pelvis (33 cases), perineal area (23 cases), and head and face (14 cases). The pain location of the pancreatic cancer was 90.63%consis-tent with the primary tumor site. The pathophysiology of the pain was classified as follows:bone pain (145 cases, 27.20%), visceral pain (138 cases, 25.89%), soft tissue pain (126 cases, 23.64%), and neuropathic pain (124 cases, 23.27%). The incidence of visceral pain in pancreatic cancer was 92.59%. Conclusion:A variety of common malignancies could cause moderate to severe pain, especially lung cancer. The clinical manifestation of pancreatic cancer pain is visceral pain. The location of this cancer was consistent with the pri-mary tumor site. No apparent specificity was observed in other cancer types.

The ampC ?-lactamases gene in Escherichia coli(E.coli) is different from other Gram-negative bacteria.E.coli contains a chromosomal ampC gene which has a weak promoter as well as a transcriptional attenuator.The promoter of the ampC gene in E.coli is part of the preceding frd operon,the attenuator of the ampC gene is a transcription terminator for the frd operon.The ampC regulatory gene,ampR,is absent.Strains carrying the wild-type gene produce a low basal amount of AmpC.Studies on the molecular basis of AmpC overproduction in E.coli have shown that some hyperproducers contain mutation in the promoter region and/or attenautor and/or ampC-coding region of ampC,while others contain more than one copy of ampC.Acquisition of a stronger promoter or insertion of an insertion element containing promoter sequences or regulatory gene ampR has also been proposed as the molecular basis of hyperproduction of AmpC in some E.coli strains.Plasmid-mediated AmpC ?-lactamases have been discovered frequently in E.coli strains.This is another reason for hyperproduction of AmpC ?-lactamases.

This paper expounds the relation between the quality of the blood-pressure meter and the quality of the medical treatment.The good quality of the blood-pressure meter is the basic quality insurance for the medical treatment system.This paper also introduces the method of quality check for the blood-pressure meter and the troubleshooting.

AIM: To investigate the influence of adenosine on human umbilical vein endothelial cells (HUVEC) bFGF protein production and bFGF mRNA expression. METHODS: Immunohistochemistry staining was performed to detect bFGF protein. RT-PCR was performed to detect bFGF mRNA expression. RESULTS: Immunohistochemistry study demonstrated that there was only a small amount of bFGF positive cells and the color was weak in control group (without adenosine). In groups treated with 10~-4 mol/L and 10~-6 mol/L adenosine, bFGF protein was significantly higher than that in control group (P0.05). RT-PCR showed that in 10~-4 mol/L and 10~-6 mol/L adenosine groups, bFGF mRNA expression was higher than that in control group (P0.05). CONCLUSION: Adenosine may promote HUVEC proliferation and angiogenesis partly through inducing bFGF expression.

OBJECTIVE:To establish a method for dissolution determination of Erythromycin ethylsuccinate granules.METHODS:Paddle method was adopted and 0.1 mol?L-1 HCl solution was used as dissolution medium at rotation rate of 50 r?min-1.UV spectrophotometry was used to detect at wavelength of 482 nm.Dissolution rate was calculated.RESULTS:The linear range of erythromycin ethylsuccinate were 4～40 mg?L-1(r=0.999 0,n=5)with an average recovery of 99.19%(RSD=0.56%).Dissolution rate of erythromycin ethylsuccinate was more than 80% within 30 min.CONCLUSION:The method is rapid,simple and accurate for the quality control of Erythromycin ethylsuccinate granules.

Objective To compare the effect of Gegensu Injection and Chinese Traditional Medicine on Chronic Renal Failure.Methods 70 cases of Chronic Renal Failure were selected as group A, treated by Gegensu Injection; During the same term,60 cases of Chronic Renal Failure were selected as group B, treated by Chinese Traditional Medicine and Chinese Traditional Medicine Clyster. The effect of two methods were valued by analyzing the numeral value of Scr and BUN in two groups . Results 1.Significant effective rate is 8.57, effective rate 41.42, ineffective rate 50, total effective rate 50 in group A; 23.33, 41.67, 35, 65 in group B. 2. After treatment, the numeral value of Scr and BUN in group A had significant difference (P

Object To study the effects of SINI TANG (SNT) on the rat aortic rings pre-contracted by high K + and phenylephrine (Phe). Methods The effects of SNT on the aortic rings in the presence of 60 mmol/L KCl and Phe (1?10 -9 -1?10 -4 mmol/L) were observed and t heir me chanisms were studied after treatment with Propranolol (Pro, 3?10 -6 mmol/ L) and Bay K8644 (BK, 1?10 -5 mmol/L) as tool drugs. Results SNT inhibited the contraction induced by cumulative Phe and decreased the maximum tension (T max ); Pro couldn't influe nce the effects of SNT. SNT attenuated the amplitude of contractile effect of hi gh K +; BK couldn't reverse the effects of SNT. Conclusion SNT can shift the dose-response curve to the right and decrease the T max . It shows that SNT is a kind of noncompe titive antagonism. SNT decreases the effect of high K + against contraction of the artery. BK, a L-type Ca 2+ channels activator, couldn't recover the inhibition induced by SNT. The results suggest that SNT inhibit ? 1 recep tor, while calcium channel may not be involved in attenuating the effect of SNT on high K +-induced contraction.