Granulocyte colony-stimulating factor (G-CSF) has been demonstrated to have neuroprotective effects in rat model with focal cerebral ischemia through anti-apoptotic pathways and by promoting proliferation of neural stem cells. In the present study, we examined the neuroprotective effect of G-CSF in an acute focal cerebral ischemia rat model with lipid metabolism disorder. Eighty male SD rats were randomly divided into normal diet control group (NC group) and high-fat diet group (HFD group) (n = 40 in each). In HFD group, rats were fed on high fat diet to induce atherosclerosis. After 29 days, 4 rats from each group were sacrificed to evaluate the effects of different diets, and the middle cerebral artery occlusion (MCAO) was performed in the rest of the rats. MCAO rats received either G-CSF (50 μg·kg(-1)·mL(-1)) or phosphate buffered saline (PBS) injection through the external jugular vein for 5 days, which was followed by 5-bromo-deoxy uridine (BrdU, i.p., 50 mg/kg) injection for another 7 days. To evaluate the effects of G-CSF treatment on neurological function, the modified neurological severity score (mNSS) was calculated. The vascular distribution, ischemic cells proliferation, cell apoptosis and the expression of vascular endothelial growth factor (VEGF) were measured to determine the effects of G-CSF treatment. Our results showed that G-CSF-treated rats had a lower mNSS than PBS-treated rats in both NC group and HFD group. G-CSF injection promoted endothelial cell proliferation and vascular regeneration, and inhibited cell apoptosis. The serum and tissue levels of VEGF were significantly increased after G-CSF treatment. It is concluded that G-CSF exerts its neuroprotective effect in focal cerebral ischemia rats with hyperlipidemia by enhancing angiogenesis, promoting cells proliferation, decreasing cell apoptosis, and increasing local VEGF expression.

Objective:To clarify the contribution of endogenous bFGF, bFGF mRNA and FGFR1 to the abnormal growth and phenotypic transformation of neoplastic tumors cells.Methods:The antisense oligonucleotide primers was used to evaluate the influence of endogenous bFGF on growth of human glioma malignant cell lines SWO-38 in vitro. MTT was used to examine the variety of cells growth treated with bFGF antisense oligonucleotide primers. The methods of ELISA, in situ hybridization, immuno-hischemistry and image analysis were used to detect the expression level of bFGF, bFGF mRNA and FGFR1. The colony formation of cells in soft agar was used to assess the cloning efficiency of the cells after exposed to bFGF antisense oligo-nucleotide primers.Results:The cells multiplication, expression of bFGF mRNA and FGFR1 was inhibited by bFGF antisense oligonucleotide primers,and the cells multiplication was dose-dependent. Treated with antisense oligo-nucleotide primers, the expression of FGFR1 and secretion of bFGF were distinctly reduced, and the inhibition efficiency of cells multiplication of WSO-38 was 48% and the inhibition efficiency of colonies of SWO-38 in soft agar was 35%. The inhibition of cells multiplication can be reversed completely by external bFGF, and the reverse efficiency was 8%.Conclusion:The synthesis of bFGF mRNA and expression of bFGF can be specifically inhibited by antisense oligonucleotide, but the inhibition can be cleared up with the addition of external bFGF. The study suggested that the bFGFantisense oligonucleotide could have good effect in inhibiting of tumor under special condition.

Granulocyte colony-stimulating factor (G-CSF) has been demonstrated to have neuroprotective effects in rat model with focal cerebral ischemia through anti-apoptotic pathways and by promoting proliferation of neural stem cells. In the present study, we examined the neuroprotective effect of G-CSF in an acute focal cerebral ischemia rat model with lipid metabolism disorder. Eighty male SD rats were randomly divided into normal diet control group (NC group) and high-fat diet group (HFD group) (n = 40 in each). In HFD group, rats were fed on high fat diet to induce atherosclerosis. After 29 days, 4 rats from each group were sacrificed to evaluate the effects of different diets, and the middle cerebral artery occlusion (MCAO) was performed in the rest of the rats. MCAO rats received either G-CSF (50 μg·kg(-1)·mL(-1)) or phosphate buffered saline (PBS) injection through the external jugular vein for 5 days, which was followed by 5-bromo-deoxy uridine (BrdU, i.p., 50 mg/kg) injection for another 7 days. To evaluate the effects of G-CSF treatment on neurological function, the modified neurological severity score (mNSS) was calculated. The vascular distribution, ischemic cells proliferation, cell apoptosis and the expression of vascular endothelial growth factor (VEGF) were measured to determine the effects of G-CSF treatment. Our results showed that G-CSF-treated rats had a lower mNSS than PBS-treated rats in both NC group and HFD group. G-CSF injection promoted endothelial cell proliferation and vascular regeneration, and inhibited cell apoptosis. The serum and tissue levels of VEGF were significantly increased after G-CSF treatment. It is concluded that G-CSF exerts its neuroprotective effect in focal cerebral ischemia rats with hyperlipidemia by enhancing angiogenesis, promoting cells proliferation, decreasing cell apoptosis, and increasing local VEGF expression.
Animals ; Brain Ischemia ; metabolism ; Disease Models, Animal ; Granulocyte Colony-Stimulating Factor ; metabolism ; Hyperlipidemias ; metabolism ; Male ; Neuroprotective Agents ; metabolism ; Rats ; Rats, Sprague-Dawley

Objective:To explore the predictive value of different critical values of slow gait speed on adverse outcomes in elderly maintenance hemodialysis (MHD) patients.Methods:The study was a prospective cohort study. The clinical data of elderly patients (≥ 60 years old) who received MHD treatment in the Third Affiliated Hospital of Guangzhou Medical University from March 1 to June 30, 2021 were collected, including demographic characteristics, diseases-related data and laboratory examination results. The follow-up period was one year. The six-meter walking test was used to measure the gait speed (m/s), and 0.6 m/s, 0.8 m/s and 1.0 m/s were used as the different critical values of the gait speed for grouping. The differences of clinical data between different groups were compared. Logistic regression analysis method was used to assess the association of slow gait speed with adverse outcomes (falls and hospitalization) in elderly MHD patients. The receiver operating characteristic (ROC) curve was performed to evaluate the best critical value of slow gait speed to predict the risk of falls and hospitalization.Results:A total of 108 elderly patients with MHD were included, with 57 males and 51 females. There were 43 patients (39.8%) of falls and 34 patients (31.5%) of hospitalization. There were statistically significant differences in age, Charlson's comorbidity index, and the proportions of hypertension, family support needed in daily life, walking aids needed, falls and hospitalization events among the four groups of the patients grouped according to gait speed (all P < 0.05). Multivariate logistic regression analysis results showed that the risk of falls predicted by gait speed of 0.6- < 0.8 m/s was higher than that by gait speed of > 1.0 m/s ( OR=3.973, 95% CI 1.116-14.136, P=0.033). The risk of hospitalization predicted by gait speed < 0.6 m/s was higher than that by gait speed > 1.0 m/s ( OR=9.147, 95% CI 1.658-50.453, P=0.011). The logistic regression analysis was performed with the critical values of 0.6 m/s, 0.8 m/s and 1.0 m/s as the classification variables, and the results showed that the gait speed of < 0.8 m/s was an influencing factor of the falls risk in elderly MHD patients (≥ 0.8 m/s as reference, OR=3.200, 95% CI 1.099-9.318, P=0.033). The gait speed < 0.8 m/s and < 0.6 m/s were influencing factors of hospitalization (≥ 0.8 m/s as reference, OR=3.899, 95% CI 1.355-11.216, P=0.012; ≥ 0.6 m/s as reference, OR=4.226, 95% CI 1.107-16.140, P=0.035). The area under the ROC curve for gait speed of < 0.6 m/s, < 0.8 m/s and < 1.0 m/s to predict the risk of falls were 0.605(95% CI 0.493-0.717, P=0.065), 0.668(95% CI 0.562-0.774, P=0.003), and 0.634 (95% CI 0.529-0.739, P=0.019), respectively. The best critical value of slow gait speed to predict the risk of fall was 0.73 m/s, and the area under the ROC curve was 0.720(95% CI 0.623-0.817, P < 0.001), with the sensitivity and specificity of 0.846 and 0.512, respectively. The area under the ROC curve for gait speed of < 0.6 m/s, < 0.8 m/s and < 1.0 m/s to predict the risk of hospitalization were 0.629(95% CI 0.509-0.749, P=0.032),0.683(95% CI 0.573-0.793, P=0.002), and 0.608(95% CI 0.497- 0.719, P=0.073). The best critical value of slow gait speed to predict the risk of hospitalization was 0.81 m/s, and the area under the ROC curve was 0.688(95% CI 0.576-0.800, P=0.002), with the sensitivity and specificity of 0.689 and 0.676, respectively. Conclusion:The critical value of gait speed 0.8 m/s can be used to predict the risk of falls and hospitalization in elderly MHD patients.

The residents who had lived for at least 5 years and aged over 20 years old were sampled from urban to rural districts of Jiangsu Province with a stratified cluster sampling technique. B mode ultrasonography and thyroid function determination were carried out in 6 128 persons. The location, diameter, number, boundary, and calcification in thyroid nodules were described by using 7.5 MHz/50 mm transducer of thyroid ultrasonography. TSH was measured by chemiluminescence immunoassay. Free triiodothyronine(FT3)and free thyroxin(FT4)were measured when TSH was abnormal. The crude prevalence of thyroid nodules was 21.12% in total population, 14.55% in male, and 25.24% in female. The standardized prevalence was 15.69%, 11.20%, and 20.40%, respectively. The prevalence was lower in male than in female, and increased with age(P＜0.05). Thyroid nodules in Jiangsu Province were highly prevalent and more attention should be paid to the follow-up, early diagnosis, and treatment.