1.Expression and modulation of connective tissue growth factor in renal interstitial fibrosis
Chinese Journal of Pathophysiology 1999;0(09):-
CTGF, a member of the CCN family of immediate early genes, is a recently discovered profibrotic growth factor, which is involved in many pathophysiologic procedures. CTGF acts as a downstream effector of TGF-? acting on interstitial cells to enhance the progression of fibrotic renal diseases. It has been shown that CTGF gene expression can be induced or blocked by some kinds of cytokine and drugs. It is an interesting candidate target for future intervention strategies of renal interstitial fibrosis. [
2.Analysis of lidocaine in human spinal fluid by high-performance liquid chromatography
Ming JIN ; He HUANG ; Junming LIU
Chinese Journal of Forensic Medicine 1988;0(04):-
=3) in spinal fluid. The intra and inter-day relative standard deviation of analysis were less than 3.0 % (n = 5). The recovery of lidocaine was between 98.3 % - 102.7 % . Lidocaine assay was carried out in a medical case by using the method established. Conclusion Spinal fluid is suitable for assay lidocain in forensic toxicological analysis and other medical studies by using the HPLC method which is sensitive, rapid and accurate.
3.The changes of acetylcholinesterase and nitric oxide synthase neuron in rat enteric nervous system after intestine congestion
Junming ZHANG ; Fen LIU ; Yanhua REN
Medical Journal of Chinese People's Liberation Army 2001;0(08):-
Objective To explore the nervous mechanism of intestinal function disorder after intestine congestion through observing the changes of acetylcholinesterase (AchE) neuron and nitric oxide synthase neuron (NOS) expression in nervous system of rat intestinal tract. Methods Sprague Dawley rats were divided into experimental groups (intestine congestion 20min and 60min group) and the control group. Then the spreading specimens of intestinal myen-teric plexus of ileums were collected and stained by AchE and nicotinamide-adenine dinucleotide phosphate-D (NADPH-d) histochemistry, to observe and compare the density of distribution and staining of AchE and NOS positive neurons. Result Compared to the control group, the number and positive expression of AchE positive neuron in intestinal myen-teric plexus of ileums in the experimental group rats decreased (P
4.Professor LIU Huilin's experience in treating cluster headache with acupuncture-moxibustion
Qi AN ; Huilin LIU ; Junming AN ; Fuqing ZHANG
Journal of Acupuncture and Tuina Science 2024;22(6):514-520
This paper introduces chief physician LIU Huilin's empirical characteristics in treating cluster headache based on holism and pattern-identification-based treatment,with spirit-regulating filiform needling,filiform fire needle pricking,and collateral-pricking for bloodletting sequential therapy,which inherits the academic thoughts of"acupuncture-moxibustion for treating spirit"from Professor ZHOU De'an and"three-unblocking acupuncture therapy"from HE Puren,thus providing a reference for treating cluster headache with acupuncture-moxibustion therapy.
5.Distribution pattern of GPRC6A mRNA in mouse tissue by in situ hybridization
Junming LUO ; Zhaoqian LIU ; Jinshi LIU ; Y.eugene CHIN
Journal of Central South University(Medical Sciences) 2010;35(1):1-10
Objective To explore the distribution pattern of G protein-coupled receptor family C, group 6, subtype A (GPRC6A) mRNA in adult mice. Methods The distribution of GPRC6A mRNA in paraffin embedded adult mouse tissues was determined by highly sensitive nonradioactive cRNA probe in situ hybridization (ISH). We compared ISH with and without addition of tyramide signal amplification (TSA). GPRC6A wild-type and littermate GPRC6A null mice tissue sections were investigated by ISH. Results TSA greatly increased the sensitivity of ISH to detect GPRC6A mRNA in wild type mouse tissues. There was no detection of GPRC6A mRNA in GPRC6A gene specific knockout tissue in paraffin embedded tissue section. The mRNA of GPRC6A was detectable in the digestive gland or accessory digestive gland including salivary gland and pancreas, as well as in the tissues including kidney, testis, brain, muscle, and fat. Conclusion The mRNA distribution pattern of GPRC6A gene is compatible with the phenotype of GPRC6A knockout mice.
6.Surgical treatment of aortic coarctation associated type B aortic dissection
Ningning LIU ; Lizhong SUN ; Yongmin LIU ; Junming ZHU
Chinese Journal of Thoracic and Cardiovascular Surgery 2015;31(5):290-292
Objective To summarize the methods and results of surgical treatment of coarctation of the aorta associated with aortic dissection.Methods Analyzed the clinical data of 10 patients with aortic coarctation associated type B aortic dissection who underwent one-stage surgical repair between 2011 and 2013 in Anzhen Hospital.There were 7 males and 3 females with the age ranged from 23 to 56 years,average at 41.2 years.All patients were diagnosed by UCG and CTA.There are three key points to determine the operation method,diameter of the aortic arch and descending aorta,and the extent of dissection.Descending thoracic aortic replacement with short stented elephant trunk was performed in 3 patients,thoracic and abdominal aortic replacement in 1 patient,ascending-abdominal aorta bypass with arch or descending aortic ligature in 3 patients.Results One hospital death occurred(10%).There was no severe surgical complication.No death or reoperation occurred during follow up period.Conclusion Aortic coarctation associated type B aortic dissection is a rare and complex disease.Surgical treatment is an effective and safe method for the disease.
7.Relationship between antiproliferation effects of aloe-emodin on growth of gastric cancer cells and cell cycle arrest
Bingxiu XIAO ; Junming GUO ; Donghai LIU ; Shun ZHANG ; Qiong LIU
Chinese Traditional and Herbal Drugs 1994;0(05):-
Objective To investigate the relationship between the antiproliferation effects of aloe-emodin on growth of gastric cancer cells and cell cycle arrest.Methods Human gastric cancer SGC-7901 cells were treated with 2.5,5,10,20,and 40 ?mol/L aloe-emodin for 1—5 d.The cell growth was determined by MTT assay.Cell proliferation and cycle distributions were analyzed by flow cytometry.Western blotting assay was used to detect the changes of cell cycle regulators,cyclins,and cyclin-dependent kinases(CDK).Results Aloe-emodin inhibited the growth of gastric cancer cells in a dose-dependent manner.Treatment of aloe-emodin resulted in cell cycle arresting at G2/M phase.Its molecular mechanisms involved the decrease of the expression of cyclin A and CDK2,the increase of the expression of cyclin B1 and CDK1.Conclusion One of the antitumor mechanism of aloe-emodin on the growth of gastric cancer SGC-7901 cells is to arrest the cell cycle,which indicates that aloe-emodin has a potential value for the treatment of gastric cancer in clinic.
8.The expression of CD14 in rat Kupffer cells
Junming FENG ; Jingquan SHI ; Yousheng LIU ; Yusong YIN
Chinese Journal of Pathophysiology 1986;0(02):-
AIM: To explore the expression of CD14 in rat Kupffer cells (KCs). METHODS: In rat KCs induced by LPS or the mediators from KCs induced by LPS,the changes of CD14 expression were measured by RT-PCR and immunohistochemistry.The expressions of TNF? mRNA?IL-6 mRNA or the concentrations of TNF??IL-6 were estimated by in situ hybridization and radioimmunoassay,respectively. RESULTS: LPS increased the expression of CD14 in KCs in a dose-dependent fashion (LPS,1 ?g/L-10 mg/L) and in a time-dependent fashion(0.5 h-24 h,peaked at 3-6 hours). While the expression of CD14 in KCs stimulated by the active mediators from KCs which had been exposed to LPS 1 hour were obviously increased. CONCLUSIONS: There was a close relationship between LPS or the active mediators from KCs induced by LPS and the expressions of CD14. It is implied that the increase in CD14 expression may be induced by LPS and the cytokines produced by KCs,it also reveals that there is a auto-regulated loop in CD14 expression.
9.Clinical Observation of Jintiange Capsules Combined with Zoledronic Acid Injection in the Treatment of Pa-tients with Postmenopausal Diabetic Osteoporosis
Ying PAN ; Suhui QIE ; Guoqiang LIU ; Junming CAO
China Pharmacy 2016;27(35):4953-4955,4956
OBJECTIVE:To investigate the effects of Jintiange capsules combined with zoledronic acid on bone mineral densi-ty(BMD),VAS scores and lab indexes of patients with postmenopausal diabetic osteoporosis. METHODS:140 patients with post-menopausal diabetic osteoporosis were divided into control group and treatment group according to randomized blocks,with 70 cas-es in each group. Both group received 0.9% Sodium chloride injection 100 ml intravenously before and after treatment,and were given vitamin D and calcium. Control group was given Zoledronic acid injection 5 mg intravenously for more than 15 min,once ev-ery 4 weeks. Treatment group was additionally given Jintiange capsules 1.2 g,po,tid,on the basis of control group. Both groups received 6 months of treatment. BMD,VAS score,lab indexes before and after treatment and the occurrence of ADR were com-pared between 2 groups. RESULTS:After treatment,BMD of 2 groups were increased significantly compared to before treatment, and the treatment group was significantly higher than the control group,with statistical significance (P<0.05). VAS score of 2 groups after treatment were significantly lower than before treatment,and VAS score of treatment group was significantly lower than that of control group after treatment,with statistical significance(P<0.05). The levels of blood calcium and serium inorganic phosphorus had no change in 2 groups;but the level of osteocalcin was significantly higher than before treatment,while the level of bone-specific alkaline phosphatase was significantly lower than before treatment,and the levels of osteocalcin and bone-specific alkaline phosphatase in treatment groups were significantly better than in control group,with statistical significance (P<0.05). There was no statistical significance in the incidence of ADR between 2 groups(P>0.05). CONCLUSIONS:Jintiange capsules combined with Zoledronic acid injection in the treatment of postmenopausal osteoporosis patients with diabetes can significantly in-crease BMD,relieve pain and improve lab index levels. Moreover,it doesn’t increase the risk of ADR.
10.Protective effect of PPAR-αagonist on PAN-induced podocyte injury
Junming XU ; Fangyu PAN ; Yuan LIU ; Xiaoyang YUE ; Jun ZOU
Chinese Pharmacological Bulletin 2014;(10):1377-1381,1382
Aim To investigate the function of fenofi-brate on PAN ( puromycin aminonucleoside )-induced podocyte injury. Methods SD female rats of 18-week-old were randomly assigned into 3 groups ( n =6 ) . Mice in PAN group and fenofibrate treated group received a single intravenous injection of PAN ( 65 mg ·kg-1 ) , while those in control group received equal volume of saline. Mice in fenofibrate treated group re-ceived 40 mg · kg-1 · d-1 of fenofibrate ( intragastric administration ) on day 1 after PAN injection , while those in PAN group and control group received equal volume of vehicle. 24 hours urine samples from all group were collected on day 0(1 day before PAN injec-tion), day 6, day 10. The 24 hours urine protein was detected by Bradford assay. All the rats were sacrificed 10 days after the induction of podocyte injury, and glo-merulus sample were collected. The expression of podocyte injury marker and transcription level in apop-tosis, podocyte cytoskeleton protein, slit diaphragm protein were evaluated by Western blot and real-time PCR. Results Compared with the control group, 10 days after injection of PAN, 24 hours urine protein was obviously increased, and the expression and transcrip-tion level of podocyte injury marker desmin, apoptosis, podocyte cytoskeleton protein, slit diaphragm protein were upregulated greatly, however, those were signifi-cantly lower in fenofibrate treated group as compared with those in PAN group. Conclusions PPAR-α ago-nist fenofibrate can ameliorate PAN-induced glomerulus podocyte injury, and the mechanism involved may be associated with inhibition of the mitochondria apopto-sis, TGF-β/Smad pathway and p38 pathway.