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1.

Objective

To determine the effect of laser needle-knife on PI-3K, AKT and VEGF mRNA expression of vertebral arteries in a rabbit model of cervical spondylotic arteriopathy (CSA) and the mechanism of action involved.

Methods

Forty healthy general-grade rabbits were divided into a normal control group, model group, acupuncture group, and laser needle-knife group (n?=?10 rabbits per group), and the CSA rabbit model was established in all but groups but the normal control group. CSA model rabbits in the acupuncture group were treated by acupuncture at the Fengchi (GB 20) and Cervical Jiaji (EX-B 2) points, whereas rabbits in the laser needle-knife group were treated with laser needle-knife targeting the Jiaji points near the C5 spinous process. Rabbits in the normal control and model groups were fixed using similar methods. Behavioral characteristics of all rabbits were evaluated before and after treatment. Peak systolic velocity (PSV) of the right carotid and vertebral arteries in each group were examined using beside B ultrasound, and PI-3K, AKT, VEGF mRNA expression in vertebral arteries were determined by real-time PCR.

Results

The behavioral signs of rabbits were improved after treatment in both the acupuncture and laser needle-knife groups. In comparison with control group, PSV of right carotid arteries in acupuncture group and laser needle-knife group were enhanced significantly (P?<?0.05 and P?<?0.01), PSV of right vertebral arteries in acupuncture group and laser needle-knife group were enhanced significantly too (P?<?0.01 and P?<?0.05). PI-3K mRNA expression in laser needle-knife and acupuncture group was significantly higher than that in control group (P?<?0.01, P?<?0.05). AKT mRNA expression in laser needle-knife and acupuncture group was significantly higher than that in control group (P?<?0.01). VEGF mRNA expression in laser needle-knife and acupuncture group was significantly higher than that in control group too (P?<?0.01, P?<?0.05). No significant differences were found in PI-3K, AKT and VEGF mRNA expression levels among acupuncture and laser needle-knife groups (P?>?0.05).

Conclusion

Laser needle-knife could effectively intervene the mRNA expression of PI-3K, AKT and VEGF, this may be one of the mechanisms of the effect of laser needle-knife in treating CSA in rabbits.  相似文献   

2.

Background

This paper presents quantitative analysis of blood flow shear stress by measuring the carotid arterial wall shear stress (WSS) and the intima-media thickness (IMT) of experimental rabbits fed with high-fat feedstuff on a weekly basis in order to cause atherosclerosis.

Methods

This study is based on establishing an atherosclerosis model of high-fat rabbits, and measuring the rabbits’ common carotid arterial WSS of the experimental group and control group on a weekly basis. Detailed analysis was performed by using WSS quantification.

Results

We have demonstrated small significant difference of rabbit carotid artery WSS between the experimental group and the control group (P<0.01) from the 1st week onwards, while the IMT of experimental group had larger differences from 5th week compared with the control group (P<0.05). Next, we have shown that with increasing blood lipids, the rabbit carotid artery shear stress decreases and the rabbit carotid artery IMT goes up. The decrease of shear stress appears before the start of IMT growth. Furthermore, our receiver operator characteristic (ROC) curve analysis showed that when the mean value of shear stress is 1.198 dyne/cm2, the rabbit common carotid atherosclerosis fatty streaks sensitivity is 89.8%, and the specificity is 81.3%. The area under the ROC curve is 0.9283.

Conclusions

All these data goes to show that WSS decreasing to 1.198 dyne/cm2 can be used as an indicator that rabbit common carotid artery comes into the period of fibrous plaques. In conclusion, our study is able to find and confirm that the decrease of the arterial WSS can predict the occurrence of atherosclerosis earlier, and offer help for positive clinical intervention.
  相似文献   

3.

Objective

To investigate the levels of blood fat, C-reactive protein (CRP) and hemorheological indicators in the elder patients with coronary heart disease (CHD), so as to provide evidence for prospective study and treatment of elder CHD.

Methods

We collected the clinical data of 127 elder CHD patients who admitted to this hospital between July 2016 and December 2017 to detect the levels of blood fat, CRP and hemorheological indicators.

Results

In elder CHD patients, levels of the total cholesterol (TC), triglyceride (TG) and low density lipoprotein cholesterin (LDL-C) were significantly higher than the normal reference, and comparison with the control group also showed significant increases (p?<?0.01); average levels of the high-density lipoprotein cholesterin (HDL-C), phospholipid (PL), lipoprotein a [LP (a)] and free fatty acid were in the range of normal reference. Abnormal levels of TC, TG, LDL-C and HDL-C were identified in 59.06%, 58.27%, 51.18% and 18.11% of the elder CHD patients, most of which were concomitant with obesity or hypertension, and levels of these indicators were significantly higher than those in the control group with statistically significant differences (p?<?0.01). Comparisons of the age, gender distribution, hypotension, exercise and sleep showed that differences had no statistical significance (p?>?0.05). In comparison with the control group, the levels of CRP, the whole blood viscosities at high and low shears, plasma viscosity, hematocrit value, aggregation index and rigidity index of red blood cells (RBC) were all higher than those in the control group, and the differences had statistical significance (p?<?0.01). However, the erythrocyte sedimentation rate (ESR), deformity index of RBC, blood flow rates in the bilateral middle cerebral arteries (MCA), anterior cerebral arteries (ACA), terminal internal carotid artery (TICA), posterior cerebral arteries (PCA), vertebral arteries (VA) and basilar artery (BA) were significantly lower than those in the control group, and the differences had statistical significance (p?<?0.05 or 0.01).

Conclusion

In elder CHD patients, anomaly is mainly seen in levels of TC, TG and LDL-C with concentrated, adhesive and aggregating blood.  相似文献   

4.

Background

Neutralization of vascular endothelial growth factor receptor 1 (VEGFR1) and/or VEGFR2 is a widely used means of inhibiting tumor angiogenesis.

Methods

Based on the complex X-ray structures of VEGFA/VEGFR1, VEGFA/VEGFR2, and VEGFB/VEGFR1, a peptide (referred to as VGB) was designed to simultaneously bind to VEGFR1 and VEGFR2, and binding, antiangiogenic and antitumor properties of the peptide was investigated in vitro.

Results

VGB bound to both VEGFR1 and VEGFR2 in human umbilical vein endothelial cells (HUVECs) and 4?T1 mammary carcinoma tumor (MCT) cells, and inhibited the proliferation of HUVE, 4?T1 MCT, and U87 glioblastoma cells. Through abrogation of AKT and ERK1/2 phosphorylation, VEGFA-stimulated proliferation, migration, and two- and three-dimensional tube formation in HUVECs were inhibited more potently by VGB than by bevacizumab. In a murine 4?T1 MCT model, VGB strongly inhibited tumor growth without causing weight loss, accompanied by inhibition of AKT and ERK1/2 phosphorylation, a significant decrease in tumor cell proliferation (Ki-67 expression), angiogenesis (CD31 and CD34 expression), an increase in apoptosis index (increased TUNEL staining and p53 expression and decreased Bcl-2 expression), and the suppression of systematic spreading of the tumor (reduced NF-κB and MMP-9 and increased E-cadherin expression).

Conclusion

The dual specificity of VGB for VEGFR1 and VEGFR2, through which the PI3K/AKT and MAPK/ERK1/2 signaling pathways can be abrogated and, subsequently, angiogenesis, tumor growth, and metastasis are inhibited.

General significance

This study demonstrated that simultaneous blockade of VEGFR1 and VEGFR2 downstream cascades is an effective means for treatment of various angiogenic disorders, especially cancer.  相似文献   

5.
6.

Objective

To explore the expression level of FGF5 in the peripheral blood of primary hypertension patients and its clinical significance.

Methods

The 34 patients with primary hypertension treated in this hospital from June 2012 to June 2014 were selected as the observation group, while the 25 patients at this hospital who had physical exam with heathy results were selected as control group. Venous blood was drawn early in the morning after an overnight fast. FGF5, mRNA and protein level changes in the peripheral blood cells and peripheral blood serum were analyzed by real-time fluorescence based quantitative PCR (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). FGF5 gene SNP (rs16998073) were amplified by PCR and inserted into T vector, and its genetic variation were analyzed by sequencing. The relationship of FGF5 protein levels and genetic variation with diastolic/systolic blood pressure was also analyzed.

Results

Comparing with the control group, the observation group’s FGF5 mRNA and protein levels significantly increased in the peripheral blood cells and peripheral blood. The difference was statistically significant (P?<?.05). Correlation analysis showed that FGF5 protein level and systolic/diastolic blood pressure were positively correlated (P?<?.05). T/A genetic variation of FGF5 gene SNP (rs16998073) and diastolic/systolic blood pressure were positively correlated (P?<?.05).

Conclusion

The FGF5 mRNA and protein expression levels of the patients with primary hypertension were abnormal and had genetic variation, which were associated with blood pressure of the patients with primary hypertension.  相似文献   

7.

Background

Biologic sex can influence response to pharmacologic therapy. The purpose of this proof-of-concept study was to evaluate the medicating effects of estrogen in the efficacy of acute antiplatelet loading therapy on stroke outcome in the rabbit small clot embolic model.

Methods

Female and male (20/group) New Zealand White rabbits were embolized to produce embolic stroke by injecting small blood clots into the middle cerebral artery via an internal carotid artery catheter. Two hours after embolization, rabbits were treated with standard dose antiplatelet loading (aspirin 10 mg/kg plus clopidogrel 10 mg/kg). Primary outcome measures were platelet inhibition, behavioral outcome P50 (the weight of microclots (mg) that produces neurologic dysfunction in 50% of a group of animals), and effect of endogenous estrogen on outcome.

Results

For the first time in a non-rodent model of stroke, it was found that higher endogenous estrogen levels resulted in significantly better behavioral outcome in female subjects (rs ?0.70, p?<?0.011). Platelet inhibition in response to collagen, arachidonic acid, and adenosine diphosphate (ADP) was not significantly different in females with higher vs. lower estrogen levels.

Conclusions

Behavioral outcomes are improved with females with higher endogenous estrogen levels treated with standard dose antiplatelet loading. This is the first non-rodent study to demonstrate that higher endogenous estrogen levels in female rabbits appear to be neuroprotective in ischemic stroke. This research supports the further study of the effect of endogenous estrogen levels on outcome with standard dose antiplatelet loading in stroke patients not eligible for revascularization therapies.
  相似文献   

8.

Objective

The present study aimed at evaluating the efficacy of an improved phage lysate marker vaccine for haemorrhagic septicaemia in mice and rabbit model and development of a DIVA ELISA based on iron restricted outer membrane protein (IROMP).

Method

The experimental vaccine was prepared by lysing P. multocida B:2 grown under iron restricted conditions with a Pasteurella bacteriophage and addition of an alum adjuvant to enhance the immunogenicity. The vaccine was administered in mice and rabbits divided into two group each. Phage lysate vaccine (PL-VacI) was administered to group I mice and rabbits whereas group II mice and rabbits received alum precipitated HS vaccine (HS-VacII). Antibody titres were monitored 0, 30, 60, 90, 210 and 240 dpv. An IROMP (130 kDa) based indirect ELISA was also developed to differentiate between infected and vaccinated animals. The Pasteurella phage isolated in present study was sequenced at Georgia Genomic Facilty, Georgia.

Result

The sequence of PMP-GAD-IND (Pasteurella bacteriophage) was deposited in GenBank under no KY203335. The group I mice and rabbits vaccinated with Phage lysate vaccine (PL-VacI) group revealed significantly higher antibody titres than group II mice and rabbits receiving alum-precipitated bacterin (HS-VacII) by MAT, IHA and ELISA (P < 0.05 and P < 0.001). The peak log 10 values (3.46) in case of group I mice by ELISA were attained at 90DPI whereas in group II mice the peak values at 90DPI were 2.82. Mean log10 titres by ELISA in group I and II rabbits were 2.43 and 2.35 respectively at 30DPI whereas at 120DPI the titres were 3.29 and 2.75, respectively. The DIVA ELISA detected presence of a novel 137 kDa IROMP/siderophore antibody in sera of group I mice and rabbits (PL-VacI) absent in sera of mice and rabbits given HS-VacII.

Conclusion

The bacteriophage based marker vaccine (PL-VacI) had a more effective and longer immune response against HS in mice and rabbit in comparison to the widely used alum precipitated HS vaccine (HS-VacII). Moreover, the development of a recombinant IROMP based indirect ELISA could serve as an excellent tool to differentiate between infected and vaccinated cattle and buffaloes for effective control of HS.  相似文献   

9.

Objective

To investigate the role of DR4 gene in the occurrence, development and prognosis of acute myeloid leukemia (AML), find a new regulatory gene of Decitabine for the treatment of AML, namely DR4 gene, and explore the molecular mechanism of AML in the treatment of AML.

Methods

The methylation level and the mRNA expression level of DR4 gene promoters of bone marrow mononuclear cells in 122 patients with newly diagnosed AML and 24 patients with iron deficiency anemia (IDA) were detected using Methylation specific PCR (MS-PCR) and Q-RT-PCR, respectively, and a correlation analysis of them was conducted. The effects of Decitabine on the proliferation of K562 cells were detected using CCK-8 assay. Then, the effects of Decitabine on the methylation level and the mRNA expression level of DR4 genes of K562 cells treated with Decitabine were detected using MS-PCR and Q-RT-PCR, respectively. The effects of Decitabine on the cell cycle and apoptosis of K562 cells were detected using flow cytometry.

Results

Compared with the control group, the methylation level (P?=?.002) of DR4 genes of bone marrow mononuclear cells in patients with newly diagnosed AML was high. The methylation level (P?=?.01) of DR4 genes of bone marrow mononuclear cells in patients of the positive group of enlargement of liver, spleen and lymph node was lower than that of the negative group, and the methylation level (P?=?.006) of DR4 genes in patients of the high risk group of clinical stage was lower than that of the low risk group, and the methylation level (P?=?.03) of DR4 genes in patients of the group where patients did not achieve complete remission (CR1) after a course of induction chemotherapy was lower than that of the group where patients achieved complete remission (CR1) after a course of induction chemotherapy. There was a significant negative correlation (P?<?.01) between the methylation level and the mRNA expression level of DR4 genes of bone marrow mononuclear cells in 122 patients with newly diagnosed AML. After the K562 cells were treated with Decitabine for 48?h, the methylation level of DR4 gene promoters gradually decreased, while the mRNA expression level of DR4 genes gradually increased, both of which showed a concentration-dependent relationship. After the K562 cells were treated with 5?µmol/L Decitabine for 48?h, the K562 cells in G0/G1 phase and G2/M phase increased significantly, and the K562 cells in S phase decreased significantly.

Conclusion

DR4 gene played an important role in the occurrence and development of AML. Decitabine can effectively inhibit the proliferation of K562 cells, which probably partly because it can terminate the methylation effect of DR4 gene promoters and restore the mRNA expression of DR4 genes.  相似文献   

10.

Objectives

This study aimed to observe the changes in tumor angiogenesis after heated lipiodol (60°C) infusion via the hepatic artery in a rabbit model of VX2 liver cancer.

Materials and Methods

Twenty rabbits with VX2 hepatic tumors were randomly divided into 2 groups (10 rabbits in each group). Under anesthesia, a trans-catheter hepatic arterial infusion was performed, and lipiodol (37°C; control group) or heated lipiodol (60°C; treated group) was injected into the hepatic arteries of the animals. Then, changes in tumor angiogenesis were assessed using the following markers and methods. 1. Vascular endothelial growth factor receptor (VEGFR) and vascular endothelial growth factor (VEGF) expression levels in the tumor were assessed using western blotting and real-time quantitative polymerase chain reaction (PCR). 2. Proliferating cell nuclear antigen (PCNA) expression in the tumor was assessed through immunohistochemical staining. 3. The morphological changes in tumor vascular endothelial cells were observed using transmission electron microscopy (TEM).

Results

VEGFR and VEGF mRNA and protein expression levels were reduced in the treated group compared to the control group. PCNA protein showed reduced expression levels in the treated group compared to the control group. TEM indicated that the endothelial cell endoplasmic reticulum expanded, the chondriosome was swollen, and the endothelial cell microvilli were decreased after heated lipiodol infusion.

Conclusions

The tumor angiogenesis of rabbits with VX2 cancer was inhibited after arterial heated lipiodol infusion compared to lipiodol infusion.  相似文献   

11.

Objectives

Female reproductive dysfunction occurs in patients with pathological loss of adipose tissue, i.e. lipodystrophy (LD). However, mechanisms remain largely unclear and treatment effects of adipocyte-derived leptin have not been assessed in LD animals.

Methods

In the current study, C57Bl/6 LD mice on a low-density lipoprotein receptor knockout background were treated with leptin or saline for 8?weeks and compared to non-LD controls.

Results

The number of pups born was 37% lower in breeding pairs consisting of LD female mice x non-LD male mice (n?=?3.3) compared to LD male mice x non-LD female mice (n?=?5.2) (p?<?0.05). Mean uterus weight was significantly lower in the saline-treated LD group (18.8?mg) compared to non-LD controls (52.9?mg; p?<?0.0001) and increased significantly upon leptin treatment (46.5?mg; p?<?0.001). The mean number of corpora lutea per ovary was significantly lower in saline-treated LD animals compared to non-LD controls (p?<?0.01) and was restored to non-LD control levels by leptin (p?<?0.05). Mechanistically, mRNA expression of ovarian follicle-stimulating hormone receptor (p?<?0.01) and estrogen receptor β (p?<?0.05), as well as of pituitary luteinizing hormone β subunit (p?<?0.001) and follicle-stimulating hormone β subunit (p?<?0.05), was significantly upregulated in LD mice compared to non-LD controls. In addition, mean time to vaginal opening as a marker of puberty onset was delayed by 12.5?days in LD mice (50.9?days) compared to non-LD controls (38.4?days; p?<?0.001).

Conclusions

Female LD animals show impaired fertility which is restored by leptin. Future studies should assess leptin as a subfertility treatment in human leptin-deficiency disorders.  相似文献   

12.

Background

Deteriorated arterial function and high incidence of cardiovascular events characterise diabetes mellitus. Metformin and recent antidiabetic drugs, SGLT2 inhibitors, reduce cardiovascular events. We explored the possible effects of empagliflozin’s effect on top of metformin treatment on endothelial function and arterial stiffness parameters in type 1 diabetes mellitus (T1DM) patients.

Methods

Forty T1DM patients were randomised into three treatment groups: (1) empagliflozin (25 mg daily), (2) metformin (2000 mg daily) and (3) empagliflozin/metformin (25 mg daily and 2000 mg daily, respectively). The fourth group received placebo. Arterial function was assessed at inclusion and after 12 weeks treatment by: endothelial function [brachial artery flow-mediated dilation (FMD), reactive hyperaemia index (RHI)], arterial stiffness [pulse wave velocity (PWV) and common carotid artery stiffness (β-stiffness)]. For statistical analysis one-way analysis of variance with Bonferroni post-test was used.

Results

Empagliflozin on top of metformin treatment significantly improved endothelial function as did metformin after 12 weeks of treatment: FMD [2.6-fold (P?<?0.001) vs. 1.8-fold (P?<?0.05)] and RHI [1.4-fold (P?<?0.01) vs. 1.3-fold (P?<?0.05)]. Empagliflozin on top of metformin treatment was superior to metformin in improving arterial stiffness parameters; it significantly improved PWV and β-stiffness compared to metformin [by 15.8% (P?<?0.01) and by 36.6% (P?<?0.05), respectively]. Metformin alone did not influence arterial stiffness.

Conclusion

Empagliflozin on top of metformin treatment significantly improved arterial stiffness compared to metformin in T1DM patients. Endothelial function was similarly improved in all treatment groups. Empagliflozin seems to possess a specific capacity to decrease arterial stiffness, which could support its cardioprotective effects observed in large clinical studies.Trial registration Clinical trial registration: NCT03639545
  相似文献   

13.

Objective

Proteoglycan 4 (Prg4) has emerged from human association studies as a possible factor contributing to weight gain, dyslipidemia and insulin resistance. In the current study, we investigated the causal role of Prg4 in controlling lipid and glucose metabolism in mice.

Methods

Prg4 knockout (KO) mice and wild-type (WT) littermates were challenged with an obesogenic high-fat diet (45% of total calories as fat) for 16?weeks. To further stimulate the development of metabolic alterations, 10% fructose water was provided starting from week 13.

Results

Prg4 deficiency only tended to reduce diet-induced body weight gain, but significantly improved glucose handling (AUC: ?29%; p?<?0.05), which was also reflected by a tendency towards a reduced HOMA-IR score (?49%; p?=?0.06 as compared to WT mice). This coincided with lower hepatic expression of glycolysis (Gck: ?30%; p?<?0.05) and lipogenesis (Acc: ?21%; p?<?0.05 and Scd1: ?38%; p?<?0.001) genes, which translated in significantly lower hepatic triglyceride levels (?56%; p?<?0.001) in Prg4 KO mice as compared to WT mice. Prg4 KO mice likely had lower glucose utilization by skeletal muscle as compared to WT mice, judged by a significant reduction in the genes Glut4 (?29%; p?<?0.01), Pfkm (?21%; p?<?0.05) and Hk2 (?39%; p?<?0.001). Moreover, Prg4 KO mice showed a favorable white adipose tissue phenotype with lower uptake of triglyceride-derived fatty acids (?46%; p?<?0.05) and lower gene expression of inflammatory markers Cd68, Mcp1 and Tnfα (?65%, ?81% and ?63%, respectively; p?<?0.01) than WT mice.

Conclusion

Prg4 KO mice are protected from high-fat diet-induced glucose intolerance and fatty liver disease.  相似文献   

14.
15.

Background

Oncogenic activation of the PI3K signalling pathway plays a pivotal role in the development of glioblastoma multiforme (GBM). A central node in PI3K downstream signalling is controlled by the serine-threonine kinase AKT1. A somatic mutation affecting residue E17 of the AKT1 gene has recently been identified in breast and colon cancer. The E17K change results in constitutive AKT1 activation, induces leukaemia in mice, and accordingly, may be therapeutically exploited to target the PI3K pathway. Assessing whether AKT1 is activated by somatic mutations in GBM is relevant to establish its role in this aggressive disease.

Methodology/Principal Findings

We performed a systematic mutational analysis of the complete coding sequence of the AKT1 gene in a panel of 109 tumor GBM samples and nine high grade astrocytoma cell lines. However, no somatic mutations were detected in the coding region of AKT1.

Conclusions/Significance

Our data indicate that in GBM oncogenic deregulation of the PI3K pathway does not involve somatic mutations in the coding region of AKT1.  相似文献   

16.

Objective

Explore the possible protective effect of Sargentodoxa cuneata total phenolic acids on cerebral ischemia reperfusion injury rats.

Methods

Focal cerebral ischemia reperfusion rats model were established by linear thrombus. Nimodipine group, Naoluotong group, the high, middle and low dose of Sargentodoxa cuneata total phenolic acids groups were given related drugs via intragastric administration before operation for seven days, once a day. At the same time sham operation group, and ischemia reperfusion group were given the same volume of physiological saline. One hour after the last administration, establish focal cerebral ischemia- reperfusion model in rats by thread method, and the thread was taken out after 2?h ischemia to achieve cerebral ischemia reperfusion injury in rats. After reperfusion for 24?h, the rats were given neurologic deficit score. The brain tissue was taken to measure the levels of IL-6, IL-1β, TNF-α, Bcl-2, Bax, Casp-3 and ICAM-1; HE staining observed histopathological changes in the hippocampus and cortical areas of the brain; Immunohistochemistry was used to observe the expression of NGF and NF-KBp65.

Result

Focal cerebral ischemia reperfusion rats model was copyed successed. Compared with model group, each dose group of Sargentodoxa cuneata total phenolic acids could decreased the neurologic deficit score (P?<?0.05 or P?<?0.01), decreased the levels of IL-6, IL-1β, ICAM-1, TNF-α, Bax and Caspase-3 in brain tissue (P?<?0.05 or P?<?0.01), increased the levels of IL-10, Bcl-2, NGF in brain tissue (P?<?0.05 or P?<?0.01), decreased the express of NF-KBp65 in brain (P?<?0.05 or P?<?0.01).

Conclusion

Sargentodoxa cuneata total phenolic acids can improve focal cerebral ischemia reperfusion injury rats tissue inflammation, apoptosis pathway, increase nutrition factor to protect the neurons, reduce the apoptosis of nerve cells, activate brain cells self-protect, improve the histopathological changes in the hippocampus and cortical areas of the brain, reduce cerebral ischemia reperfusion injury.  相似文献   

17.

[Purpose]

The purpose of this study was to investigate the effects of aquatic exercise and CES treatment on the cognitive function by using K-WAB and BDNF, IGF-1, and VEGF of persons with intellectual disabilities.

[Methods]

All subjects were 15 male with intellectual disabilities who were participating in the aquatic training program and CES treatment during 12 weeks at rehabilitation center. The subjects were divided into control group, exercise group, and exercise+CES group. Blood samples for BDNF, IGF-1, and VEGF were taken from brachial vein at rest between before and after treatment.

[Results]

The results are summarized as follows: Cognitive function level increased significantly in the exercise+CES group compared to those in the exercise and control group. The changes of blood IGF-1 concentration were no significant difference among groups. The changes of blood BDNF and VEGF concentration were significantly increased in exercise group and exercise+CES group than control group. However, blood BDNF and VEGF concentration were significantly difference between exercise group and exercise+CES group.

[Conclusion]

In conclusion, it can be concluded that CES treatment with exercise can amend cognitive function of persons with intellectual disabilities more effectively and increase of BDNF and VEGF by exercise can explain the cognitive function improvement of persons with intellectual disabilities.  相似文献   

18.
19.

Objective

Observing the effect of nano-silver hydrogel coating film on deep partial thickness scald model of rabbit.

Method

We prepared boiling water scalded rabbits with deep II degree scald models and applied high, medium and low doses of nano-silver hydrogel coating film for different time and area. Then we compared the difference of burned paper weight before administration and after administration model burns, burn local skin irritation points infection, skin crusting and scabs from the time, and the impact of local skin tissue morphology.

Result

Rabbits deep II degree burn model successful modeling; on day 12, 18, high, medium and low doses of nano-silver hydrogel coating film significantly reduced skin irritation of rabbits infected with the integral value (P < 0.01, P < 0.05); high, medium and low doses of nano-silver hydrogel coating film group significantly decreased skin irritation, infection integral value (P < 0.01, P < 0.05); high, medium and low doses of nano-silver hydrogel coating film significantly reduced film rabbits’ scalded skin crusting time (P < 0.01), significantly shortened the rabbit skin burns from the scab time (P < 0.01), and significantly improved the treatment of skin diseases in rabbits scald model change (P < 0.01, P < 0.05).

Conclusion

The nano-silver hydrogel coating film on the deep partial thickness burns has a significant therapeutic effect; external use has a significant role in wound healing.  相似文献   

20.

Background

Nitric oxide (NO) plays a major role in physiology as a biological mediator. NO has been identified in nervous, immune and vascular systems and is a critical parameter in numerous pathologies, such as cancer. This article describes the electrochemical biomeasurements of NO synthase (NOS) activity from cultured endothelial cells using a multiple microelectrode array.

Methods

Firstly, the effect of biocompatible fibronectin coating on electrochemical measurements was investigated. Secondly, endothelial cells were deposited on the fibronectin coated sensor and NO release was triggered with vascular endothelial growth factor (VEGF). NG-nitro-l-arginine methyl ester (L-NAME) was used as an inhibitor of NO production, and different kinase blockers were investigated. Change in NOS activity was quantified using differential pulse voltammetry before and after addition of VEGF.

Results

Our results show that carefully applied layers of fibronectin have a very limited effect on electrochemistry and that VEGF induces an increase in NOS activity that is mainly mediated through the phosphatidylinositol 3 kinase (PI-3), and not by the extracellular signal-regulated kinases 1/2. Results obtained using electrochemical sensors were supported by wound healing assay demonstrating the critical role of phosphatidylinositol 3 kinase and extracellular signal-regulated kinases 1/2 for angiogenesis.

Conclusion

Electrochemical study of the intracellular transduction of the VEGF signal leading to NO synthesis was achieved, showing the critical role of PI-3 kinase.

General significance

This study presents an electrochemical sensor allowing measurements of NOS activity in cell cultures and tissue samples.  相似文献   

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