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Biomedical subjects

Ying Zhang

Publications and source records attributed to Ying Zhang.

At least 379 records · Page 21Linked to original sources
PubMed2004

Structural and virological studies of the stages of virus replication that are affected by antirhinovirus compounds.

Pleconaril is a broad-spectrum antirhinovirus and antienterovirus compound that binds into a hydrophobic pocket within viral protein 1, stabilizing the capsid and resulting in the inhibition of cell attachment and RNA uncoating. When crystals of human rhinovirus 16 (HRV16) and HRV14 are incubated with pleconaril, drug occupancy in the binding pocket is lower than when pleconaril is introduced during assembly prior to crystallization. This effect is far more marked in HRV16 than in HRV14 and is more marked with pleconaril than with other compounds. These observations are consistent with virus yield inhibition studies and radiolabeled drug binding studies showing that the antiviral effect of pleconaril against HRV16 is greater on the infectivity of progeny virions than the parent input viruses. These data suggest that drug integration into the binding pocket during assembly, or at some other late stage in virus replication, may contribute to the antiviral activity of capsid binding compounds.

Antiviral Agents↗
PubMed2004

Stimulation of proinsulin biosynthesis by K+ in rat pancreatic islets.

Glucose-stimulated proinsulin biosynthesis is regulated mainly at the translational level. This study aims at investigating the possible role of the B-cell K+ content in such a process. In order to increase the islet cells K+ content, rat pancreatic islets exposed to a low D-glucose concentration (e.g., 2.5 mM) were incubated in the presence of 30 or 60 mM K+, as distinct from a control extracellular K+ concentration of 5 mM. Under these conditions, the K+ content of the islets, as judged from the net uptake of 86Rb+ over 60 min incubation, was increased to a level comparable to that otherwise found in the presence of 16.7 mM D-glucose. In the presence of 2.5-4.0 mM D-glucose, the rise in K+ concentration from 5 to 30 and 60 mM caused a progressive increase in the incorporation of L-[4-3H]phenylalanine into both all islet peptides and (pro)insulin. A preferential stimulation of proinsulin biosynthesis was only observed in islets incubated at 60 mM K+ in the presence of 4.0 mM D-glucose. In relative terms, the K+-induced increase in biosynthetic variables was less pronounced, however, than that otherwise evoked by a rise in D-glucose concentration from 2.5 to 4.0 mM to 5.6 or 16.7 mM. These findings may suggest that the effect of D-glucose to increase the K+ content of islet cells represents one modality for coupling a rise in D-glucose concentration to stimulation of proinsulin biosynthesis.

Animals↗
PubMed2004

Enzyme-to-enzyme channeling in the early steps of glycolysis in rat pancreatic islets.

The enzyme-to-enzyme channeling of metabolic intermediates is not an uncommon process. The present review draws attention to recent experimental work documenting, in rat pancreatic islets, the enzyme-to-enzyme channeling of alpha-D-glucose 6-phosphate between hexokinase isoenzyme(s), mainly glucokinase, and phosphoglucoisomerase. Likewise, the possible enzyme-to-enzyme channeling of beta-D-fructose 6-phosphate between phosphoglucoisomerase and phosphofructokinase is briefly evoked. These considerations are relevant to the anomeric specificity of D-glucose metabolism, even in islets exposed to equilibrated D-glucose, to the perturbation of such an anomeric specificity in the phenomenon of so-called B-cell glucotoxicity, and to the correct interpretation of 3HOH generation from D-[2-(3H)]glucose.

Animals↗
PubMed2004

Stimulation by D-glucose of 36Cl- efflux from prelabeled rat pancreatic islets.

D-glucose was previously reported to cause a concentration-related decrease in the 36Cl- content of prelabeled islets prepared from ob/ob mice, a current animal model of inherited obesity. From these findings, it was inferred that the hexose stimulates Cl- efflux from islet cells and that such an increase in Cl- permeability may partly mediate glucose-induced depolarization of insulin-producing cells. The aim of the present study was to investigate the possible extension of these findings to islets prepared from normal rats by measuring the changes evoked by increasing concentrations of D-glucose in 36Cl- outflow itself from prelabeled isolated islets. After 60 min preincubation at 37 degrees C in the presence of 3 mM D-glucose and 36Cl- (75 microCi/mL), the islets were incubated for 8-10 min at 37 degrees C in the presence of increasing concentrations of the hexose (3-20 mM). The changes in 36Cl- outflow during incubation indicated that D-glucose, in excess of a threshold concentration close to 5 mM, indeed increases effluent radioactivity from the prelabeled islets. It is proposed, therefore, that a gating of volume-sensitive anion channels in glucose-stimulated insulin-producing islet cells participates in the depolarization of the plasma membrane recorded in the range of insulinotropic concentrations of the hexose.

Animals↗
PubMed2004

Evodiamine induces tumor cell death through different pathways: apoptosis and necrosis.

AIM: To study the different death pathways in human cervical cancer HeLa and melanoma A375-S2 cells initiated by evodiamine. METHODS: Viability of evodiamine-induced HeLa and A375-S2 cells was measured by MTT assay. Apoptotic cells with condensed or fragmented nuclei were visualized by Hoechst 33258 staining. Nucleosomal DNA fragmentation was assayed by agarose gel electrophoresis. Proportion of cell death through apoptotic and necrotic pathways was determined by LDH activity-based cytotoxicity assays. Cell cycle distribution was observed by flow cytometry. RESULTS: Evodiamine induced HeLa and A375-S2 cell death dose- and time-dependently. Caspase-3 and -8 were activated in apoptosis induced by evodiamine 15 micromol/L. However, over 24-h incubation of A375-S2 cells, evodiamine 15 micromol/L initiated necrosis related to p38 and ERK (extracellular signal-regulated kinases) activities. Evodiamine-induced HeLa cell death was preceded by an accumulation of cells at the G2/M phase of the cell cycle, but there was no significant effect of evodiamine on A375-S2 cell cycle. CONCLUSION: Evodiamine induces caspase-3,8-dependent apoptosis in HeLa cells which is related to G2/M arrest of the cell cycle. On the other hand, in A375-S2 cells, evodiamine initiates caspase-3,8-mediated apoptosis at early stages and the induction of MAPK-mediated necrosis at later stages of cell culture.

Apoptosis↗
PubMed2004

[Colorectal cancer patients have oligoclonal proliferation of T cells in blood].

OBJECTIVE: To study the clonal characteristics of peripheral T cells and anti-tumor immunology in the patients with colorectal cancer by analyzing T cell receptor beta (TCRbeta) gene repertoire and complementarity determining regions 3 (CDR3) amino acid sequence of the peripheral blood cells (PBL). METHODS: The 24 TCRbetaV genes from PBL in pre-operation and post-operation and colorectal cancer tissues, were amplified by the method of combined reverse transcriptase-polymerase chain reaction (RT-PCR) with denaturation polyacrylamide sequencing gel electrophoresis, which is called TCRbeta gene repertoire. In order to analyze the clonality of the over-expressing bands and the CDR3 sequence, the PCR production was sequenced directly. RESULTS: TCRbeta gene repertoire of PBL in the tumor-bearing patients was clonally expressed, which indicated that there were monoclonal or oligoclonal expansion of T lymphocytes. Some of the clonal T cells in PBL had the same CDR3 amino acid sequence motifs with the clonal T cells in the tumor infiltrating lymphocyte(TIL). The patients with clonal expansion of T cells in PBL had lymph node metastases, but there was no recurrence within 10 months after operation. CONCLUSION: There is oligoclonal proliferation of T cells in the blood of tumor-bearing patients. It is possible that the clonal T lymphocytes are the tumor associated antigen specific anti-tumor T lymphocytes.

Amino Acid Sequence↗
PubMed2004

[Effects of aminoguanidine on the expression of NOS in facial nerve and surrounding tissues of traumatic facial paralysis rats].

OBJECTIVE: To study the effects of inducible NOS inhibitor aminoguanidine on the expression of NOS in facial nerve and surrounding tissue of traumatic facial paralysis rats. METHODS: A small dose of aminoguanidine were intraperitoneally injected into rats before and after facial paralysis. The facial nerve and surrounding tissues were cut at different time point. Immunohistochemical ABC method was used to study the changes of NOS expression in facial nerve and surrounding tissues. RESULTS: The inducible NOS immunoreactivity was obvious inhibited in the facial nerve and surrounding tissues in aminoguanidine group. CONCLUSION: Aminoguanidine chronic treatment can obvious inhibit the inducible NOS expression in the facial nerve and surrounding tissues. Aminoguanidine can improve the regeneration of facial nerve and the recovery of traumatic tissues.

Animals↗
PubMed2004

[Monitoring the breast changes of Chinese postmenopausal women under long-term hormone replacement therapy by mammary ultrasonography].

OBJECTIVE: To investigate the effects of long-term hormone replacement therapy (HRT) on the breasts of postmenopausal women using mammary ultrasonography. METHODS: An open randomized clinical study was designed. The percutaneous estradiol gel was used in a cyclic regimen combined with micronized progesterone (MP) or medroxyprogesterone acetate (MPA). Sixty healthy women (natural menopause for 1 to 5 years) were recruited and divided into four groups according to the dosage of estrogen and two kinds of progestin. All were given for 25 days per month. Mammary ultrasonography was used to observe breast glandular section thickness, breast duct width, the morphology of lobular unit and the blood flow of color Doppler imaging at baseline and every year from the second to seventh year of HRT. The serum estradiol was also measured from the 15th to 25th day of the cycle. Breast pain was recorded by the subjects. RESULTS: (1) The breast glandular section thickness after HRT was larger than that of before HRT. The breast glandular section thickness became larger gradually over time while the breast duct width became smaller over time. The breast duct width of the fifth year of HRT was significantly different from that of the sixth year (P < 0.05). (2) Twenty-two persons had new breast structure changes after HRT, and the accumulated incidence was 41.5%. New solid lesions formation occurred in five subjects (8.3%) and new cyst formation occurred in one subject (1.7%). After the second year of HRT, the serum estradiol level of the subjects with breast structure changes was higher than that of without breast structure changes and in the sixth year of HRT, and the difference was significant (P < 0.05). After the second year of HRT, the breast glandular section thickness of the subjects with breast structure changes was larger than that of without breast structure changes and in the fifth and sixth year of HRT, the difference was significant (P < 0.05). (3) After HRT, the serum estradiol level of subjects with mastalgia was higher than that of without mastalgia and in the second and sixth follow-up year, the difference was significant (P < 0.05). CONCLUSIONS: There is an increasing trend of the percentage of glandular tissues of the breast after HRT. There is an increasing trend of the serum estradiol level and the breast glandular section thickness among the subjects with the breast structure changes; there is an increasing trend of the serum estradiol level among the subjects with mastalgia. Mammary ultrasonography can be used to monitor breast structure changes and breast lesions during HRT.

Aged↗
PubMed2004

[Detection of anti-tubular basement membrane antibodies in sera from patients with tubulointerstitial nephritis].

OBJECTIVE: To detect anti-tubular basement membrane antibodies in sera from patients with tubulointerstitial nephritis (TIN) and investigate its clinical significance. METHODS: The sera were studied from 46 patients with renal biopsy proven TIN. The normal human renal cortex was obtained from patients with nephroectomy, far from carcinoma. Tubules were isolated by a differential sieving technique. The fragments of renal epithelia were removed from tubular basement membrane enriched materials by sonication and centrifugation. Tubular basement membrane antigens were solubilized with 6 mol/L guanidine-HCl. The soluble proteins were used as antigens in Western blot analysis to detect autoantibodies in sera from patients with TIN. The clinical characteristics of positive and negative patients were statistically analyzed. RESULTS: Eleven patients with tubulointerstitial nephritis had anti-tubular basement membrane antibodies by Western blot analysis, and seven protein bands could be blotted by the TIN sera. The positive prevalence of anti-55x10(3) antibody (63.8%) was higher than that of other antibodies. Eight of 27 (29.6%) patients with acute tubulointerstitial nephritis and four of 19 (21.1%) patients with chronic tubulointerstitial nephritis had anti-tubular basement membrane antibodies. ESR,serum IgG and IgM in patients with acute TIN with positive anti-tubular basement membrane antibodies were higher than those of the negative group. There was no significant difference in the other clinical variables such as gender,age,hemoglobin,complement C3,serum IgA,serum creatinine,blood urea nitrogen and creatinine clearance in patients with acute TIN between the positive and negative groups. There was no significant difference in clinical variables mentioned above in patients with chronic TIN between the positive and negative groups. CONCLUSION: Circulating anti tubular basement membrane antibodies could be detected in sera from some patients with TIN, and autoimmunity may play a role in the pathogenesis of TIN.

Adult↗
PubMed2004

[Apoptosis and modulatory mechanism of human AHH-1 T lymphocytes induced by gamma-irradiation].

AIM: To explore the apoptotic characteristics and modulatory mechanism of human AHH-1 T lymphoblast induced by ionizing radiation and provide an experimental basis for preventing and treating immune damage in acute radiation sickness. METHODS: TdT-mediated dUTP nick end labeling (TUNEL) and May-Grunwald Giemsa (MGG) staining, MTT colorimetry and immunohistochemical staining were used to detect the T lymphocyte apoptosis, cell survival and the expressions of Bax, Bcl-XL and caspase-3 proteins. RESULTS: (1) Over a definite dose range, apoptotic rate of AHH-1T lymphocytes increased with the elevation of radiation doses, while the lymphocytic survival rate decreased sharply, both showing a good dose-effect relationship. (2) The expression of apoptosis-accelerating protein Bax enhanced obviously with the increase of radiation doses, while apoptosis-inhibiting protein Bcl-XL trended to persistent decline. (3)The activity of activated apoptosis-executing protein caspase-3 heightened significantly with increased radiation doses, which revealed a better corresponding relationship to apoptotic rate. CONCLUSION: A great number of apoptotic AHH-1 T cells may be one of major accounts for the lymphocyte rapid reduction and depressed organism immune function induced by irradiation. Bax, Bcl-XL and caspase-3 proteins play an important role in the regulation of radiation-induced T cell apoptosis.

Apoptosis↗
PubMed2004

Dissimilar effects of D-mannoheptulose on the phosphorylation of alpha- versus beta-D-glucose by either hexokinase or glucokinase.

D-mannoheptulose inhibits D-glucose phosphorylation by hexokinase isoenzymes. The present study aims at investigating whether the pattern of such an inhibition differs in the case of alpha- versus beta-D-glucose. The phosphorylation of alpha- and beta-D-[U-14C]glucose was measured over 60-min incubation at 4 degrees C in the presence of bovine heart hexokinase and over 10 min at 24 degrees C in the presence of human liver glucokinase. The relative extent of the inhibitory action of D-mannoheptulose (0.02-10.0 mM) was always less marked with alpha- than beta-D-glucose. In the case of hexokinase, the experiments conducted at the high concentration of the D-glucose anomers (1.0 mM) revealed that D-mannoheptulose, at low concentrations (0.2-0.5 mM), may unexpectedly increase the phosphorylation of alpha-D-glucose. These findings thus document anomeric specificity in terms of the inhibitory action of D-mannoheptulose upon alpha- versus beta-D-glucose phosphorylation by either hexokinase or glucokinase.

Animals↗
PubMed2004

Effects of raloxifene hydrochloride on bone mineral density, bone metabolism and serum lipids in Chinese postmenopausal women with osteoporosis: a multi-center, randomized, placebo-controlled clinical trial.

BACKGROUND: Raloxifene has been approved for prevention and treatment of postmenopausal osteoporosis in Caucasian women. It also has some positive effects on serum lipids in Caucasians. The objective of this study was to determine the effect of raloxifene hydrochloride on lumbar spine and total hip bone mineral density (BMD), bone metabolism, and serum lipids in Chinese postmenopausal women with osteoporosis. METHODS: This was a multi-center, randomized, double-blind, placebo-controlled clinical trial in which 204 postmenopausal Chinese women with osteoporosis were assigned to receive raloxifene (60 mg) or placebo treatment daily for 12 months. BMD, serum bone metabolism markers, and serum lipids were measured before and after drug administration. BMD was measured by Dual-Energy X-Ray Absorptiometry (DEXA) and bone metabolism markers were analyzed by one-step enzyme-linked immunosorbent assay. Serum lipids were measured by enzymatic analysis. RESULTS: At the end of the 12-month study, lumbar spine BMD increased in both groups with a mean increase of (3.3 +/- 4.8)% in the raloxifene group and (1.0 +/- 4.9)% in the placebo group (P < 0.001). There was a mean increase in total hip BMD of (1.4 +/- 4.8)% in the raloxifene group and a mean decrease of (0.9 +/- 5.0)% in the placebo group (P < 0.001). No subject in the raloxifene group had a new vertebral fracture and 5 placebo subjects had new fractures (P > 0.05). In the raloxifene group, the median decreases in the biochemical markers of bone metabolism serum osteocalcin and C-telopeptide were 41.7% and 61.5%, respectively. These changes were statistically significant compared with those in the placebo group (10.6% and 35.6%, P < 0.001, respectively). Both total cholesterol and low-density lipoprotein cholesterol decreased significantly in the raloxifene group compared with those in the placebo group (P < 0.001, respectively) and there was no significant effect of raloxifene on high-density lipoprotein cholesterol and triglycerides compared with placebo. CONCLUSIONS: Raloxifene 60 mg/d for 12 months significantly increases lumbar spine and total hip BMD, significantly decreases bone turnover, and has favourable effects on serum lipids in Chinese postmenopausal women with osteoporosis.

Aged↗
PubMed2004

[Time-course of mu-calpain activation, c-Fos, c-Jun, HSP70 and HSP27 expression in hypoxic-ischemic neonatal rat brain].

OBJECTIVE: The cascade of physiological events underlying hypoxic-ischemic brain damage (HIBD) remains to be fully established. The perinatal brain shows both an increased tolerance to hypoxic-ischemic (HI) injury and a faster and more complete recovery than the adult. It is, therefore, important to understand the sequence of events following hypoxia and ischemia in young animals. The present study aimed to clarify the time-course of the activation of the mu-calpain, and the expression of c-Fos, c-Jun, HSP70 and HSP27 proteins following severe HI (2 h hypoxia) and their relationship with each other. METHODS: A modified newborn rat model of HIBD that included a combination of hypoxia and ischemia as described by Rice was used. Forty-two postnatal 7-day-old Sprague-Dawley rats were randomly divided into seven groups (6 rats in each): 6 time-window groups and a normal control group. Samples were collected at 0, 1, 2, 4, 12 and 24 h after HI insults. The protein concentration was determined using a modified Bradford assay. mu-calpain activation, c-Fos, c-Jun, HSP70 and HSP27 expressions were observed respectively by Western blot from cortical and hippocampal samples. RESULTS: The cleavage of cytosolic mu-calpain was observed from both cortical and hippocampal samples in neonatal rats after HI. The ratio 76:80 of mu-calpain was increased significantly post-HI and reached a maximum at 24 h in cortex and at 12 h in hippocampus after HI. The expressions of c-Fos and c-Jun from both cortical and hippocampal samples in neonatal rats were up-regulated and peaked at 2 or 4 h after HI, demonstrating significant differences at 1, 2, 4, and 12 h compared with that observed in the control (P < 0.05). When compared with that observed in cortex, the nuclear c-Fos expression from hippocampal samples was highly elevated at 2, 4 and 12 h but significantly decreased at 24 h after HI (P < 0.05), while the nuclear c-Jun expression from hippocampal samples was highly elevated at 0 and 1 h but significantly decreased at 4 and 24 h after HI (P < 0.05). Similarly, the expressions of HSP70 and HSP27 from both cortical and hippocampal samples were up-regulated and reached a maximum at 12 or 24 h after HI, demonstrating significant differences at 12 or 24 h both in cortex and hippocampus for HSP70, and at 24 h in cerebral cortex as well as at 12 and 24 h in hippocampus for HSP27 compared with the control (P < 0.05). Furthermore, in comparison with that observed in cortex, the HSP70 expression from hippocampal samples was highly elevated at 1 h, but significantly decreased at 4, 12 and 24 h after HI (P < 0.05), while the HSP27 expression was permanently elevated in hippocampus after HI. CONCLUSION: The neuronal injury induced by HI insults appears to involve many ongoing and simultaneous mechanisms. HI activates the calpains immediately, which may contribute to neuron apoptosis, and induces a significant brain neuroprotection, since there is an increased HSP70 expression and a relatively late remarkable HSP27 expression in hypoxic-ischemic neonatal rat brain. Nuclear c-Fos and c-Jun may participate in the pathogenesis of HIBD.

Animals↗
PubMed2004

[Five single nucleotide polymorphisms of casein kinase I gamma 2 gene in children with familial febrile convulsions].

OBJECTIVE: To investigate the association between single nucleotide polymorphisms (SNPs) of casein kinase I gamma 2 (CSNK1G2) gene and children with familial febrile convulsions. METHODS: The study samples were collected from unrelated Chinese Han population of Hebei province, including a cohort of 53 children with familial febrile convulsions(FC) and a control cohort of 101 individuals. Genotypes of SNPs rs2074882, rs740423, rs2277737, rs4806825, rs1059684 were typed by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: The frequencies of the five SNPs complied well with the Hardy-Weinberg equilibrium in FC group and normal group. The distribution of genotype and frequencies of alleles of the SNPs rs740423, rs2277737, rs1059684 in familial febrile convulsions group was significantly different from that in control group. No significant difference was observed in the distribution of genotypes and frequencies of alleles at SNP rs2074882 between two groups. Analysis on rs4806825 was not made owing to its less allele frequency. CONCLUSION: These data indicate that SNPs rs740423, rs2277737, rs1059684 of CSNK1G2 gene may contribute to familial febrile convulsions in children.

Casein Kinase I↗
PubMed2004

[Numerical analysis on ecological gradient of plant communities in Donggou catchment, Hebei Province, China].

Based on DCCA-OAC, the plant communities in Donggou catchment, Bashang region, Hebei Province, were classified into 8 types of community. The environmental gradient, structural gradient and human-disturbance could be well expressed in the ordination plot. Axis 1 reflected the spatial pattern of plant communities along the gradient of altitude and slope, while axis 2 showed the plant community distribution on different aspects. The plant communities showed a distribution gradient along moisture gradient as shown by the combination of both axes of DCCA. The communities exhibited different trends in the synusia and species composition. Betula platyphylla was only existed on the high and steep northern aspect. The dominate species of shrub and herbaceous synusia on northern aspect were Potentilla fruticosa and Carex rigescens respectively, while on southern aspect were Artemisia spp. and Agropyron cristatum. The distribution along altitude and slope also existed among dominate species of each synusia on southern aspect. In addition, human disturbance, including grazing, farming and logging, had significant influence on the temporal and spatial distribution of communities. In general, the better the habitat, the more intensive the human disturbance.

Betula↗
PubMed2004

[Screening of dominant epitopes of antigens related to antibodies in the sera of patients with nasopharyngeal carcinoma].

BACKGROUND & OBJECTIVE: Epstein-Barr virus (EBV) is closely related to nasopharyngeal carcinoma (NPC). Many kinds of methods can be used to examine antibodies in NPC patients sera. This study was to screen the dominant epitopes from random peptide libraries (RPLs) displayed on phage using the EBV-related antibodies purified from the sera of NPC patients, and find new antigens at the epitope level. METHODS: The EBV-related antibodies were eluted from the sera of NPC patients using B95-8 cell EBV proteins as antigen, and the phages from 12-mer RPLs were elutriated for 3 rounds with the antibodies. The positive clones were gained by sandwich ELISA, and competitive inhibition assay from the third elution. The positive clones were sequenced, and the peptide coded by the inserted DNA were blasted with the antigen region of EBV proteins. RESULTS: Sixty-four phage clones were randomly picked up from the third eluate,25 positive clones were picked up using sandwich ELISA assay, the positive percentage was 39.06%. Thirteen clones were picked up for competitive ELISA assay,11 clones showed inhibitory phenomena,the inhibitory rates were between 18.09% and 65.94%. Five positive clones with high absorbency value, and high inhibitory rates were selected out, the sequences of peptides displayed on these clones were -A-T-S-H-L-H-V-R-L-P-W-T- (d15, and d18), -G-S-T-H-K-H-N-H-F-N-K-T- (d19), -K-P-I-H-E-H-P-H-R-F-K-S- (e8), -H-T-H-K-I-K-I-P-L-P-I-Q- (e23). These peptide sequences showed similarity with the amino acid sequences located in antigen regions of EBV integral membrane protein (d15, and d18), EBV thymidine kinase (d19), and EBV major capsid protein (e8, and e23). CONCLUSION: EBV-related epitopes could be obtained by screening the phages from RPLs with polyclonal antibodies purified from the sera of NPC patients, which may offer new methods of antigen preparation for sera diagnosis of NPC.

Amino Acid Sequence↗
PubMed2004

[Progress in the basic research on neurobiological mechanisms of cancer pain].

Pain shows the most disruptive influence on the quality of the life of cancer patients. However, the basic neurobiology of cancer pain is poorly understood, as no appropriate animal model of cancer pain is available. New insights into these mechanisms are now arising from femur, calcaneus, humerus model of cancer pain in murine and tibia model in rats. Cancer pain has its unique mechanisms such as osteolysis, peripheral sensitization, central sensitization and nerve entrapping, which are all involved in the development and maintenance of cancer pain. Here we summarized the study progress of cancer pain animal models, neurochemical mechanisms and drugs for treatment of cancer pain from recent literatures.

Afferent Pathways↗