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Objective:To explore the association of inflammatory markers and thromboinflammatory factors before and after thrombolytic intervention with functional outcomes in elderly patients with acute cerebral infarction.Methods:392 patients with acute cerebral infarction admitted to our hospital were randomly selected as study subjects and divided into an observation group(196 cases)treated with arterial thrombolytic therapy and a control group(196 cases)treated with intravenous thrombolysis.Functional outcomes of patients were assessed 72 hours after thrombolysis using the activities of daily living(ADL)scale and, based on the results, patients were divided into a poor functional outcome group and a good functional outcome group.Inflammatory markers such as neutrophil-to-lymphocyte ratio(NLR)and platelet-to-lymphocyte ratio(PLR)and thromboinflammatory factors such as monocyte chemoattractant protein-1(MCP-1), tissue plasminogen activator(t-PA), soluble CD40 ligand(sCD40L)and P-selectin before and after thrombolysis were measured.The relationship of these inflammatory markers and thromboinflammatory factors before thrombolysis with functional outcomes 72 hours after thrombolysis was analyzed.Results:NLR and PLR levels in the two groups after thrombolysis were significantly lower than those before thrombolysis(all P<0.05); Their levels in the observation group were lower than those in the control group(all P<0.05). After thrombolysis, MCP-1 levels in both groups were significantly higher and t-PA, sCD40L, P-selectin levels were significantly lower than pre-thrombolysis levels(all P<0.05); After thrombolysis, the observation group had better results than the control group(all P<0.05). Correlation analysis showed that NLR, PLR, MCP-1 and t-PA were positively correlated with NIHSS score( r=0.336, 0.264, 0.483, 0.549, all P<0.05). NLR, PLR, MCP-1, t-PA and sCD40L levels were significantly lower and P-selectin levels were significantly higher in the good functional outcome group than in the poor functional outcome group both before and 72 hours after thrombolysis( t=13.850, 18.208, 23.636, 22.371, 59.868, 96.646, 378.112, 141.213, 131.160, 110.039, 10.716, 11.108, P<0.05 for all). Logistic regression analysis showed that abnormal levels of NLR, PLR, MCP-1 and t-PA before and after thrombolysis were risk factors for adverse outcomes with thrombolytic intervention( P<0.05). ROC curves showed that the levels of NLR, PLR, MCP-1, t-PA, sCD40L and P-selectin before thrombolysis had a certain predictive value for the risk of adverse functional outcomes with thrombolysis. Conclusions:The levels of these inflammatory markers and thromboinflammatory factors before and after thrombolytic intervention have varying degrees of correlation with functional outcomes in elderly patients with acute cerebral infarction.
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Objective:To investigate the effects of ketogenic diet on seizures, electroencephalogram(EEG) changes and neurobehavioral development in children diagnosed with epilepsy.Methods:A total of 122 children diagnosed with spastic epilepsy in Nanyang Central Hospital from March 2016 to March 2019 were enrolled.The patients were divided into the observation group and the control group, by the computerized random number table method with 61 cases in each group.The children in the control group were treated with conventional therapy, and the children in the observation group were combined with the ketogenic diet on the basis of conventional treatment.The Gesell developmental schedules scale scores were compared between the two groups to evaluate seizure control and EEG improvement.Results:The seizure control in the observation group was significantly better than that in the control group [78.69%(48/61 cases) vs.54.10%(33/61 cases)], and the difference was statistically significant ( χ2 = 12.114, P <0.05). The EEG improvement in the observation group was significantly better than that in the control group [81.97%(50/61 cases) vs.55.74%(34/61 cases)], and the difference was statistically significant ( χ2=13.623, P<0.05). After 12 months of treatment, the children in the observation group had significantly higher fitness, gross motor, fine motor, language, and personal social, and total development quotient scores than the control group [(56.64±13.29) scores vs.(46.04±12.86) scores, (54.84±12.18) scores vs.(47.62±11.91) scores, (54.44±10.70) scores vs.(44.31±11.56) scores, (51.48±12.99) scores vs.(42.04±11.18) scores, (57.88±11.04) scores vs.(47.42±13.16) scores, (275.28±54.71) scores vs.(227.42±55.79) scores], the differences were statistically significant ( t=5.997, 5.887, 6.003, 5.889, 6.007, 6.010, all P<0.05). Conclusion:The ketogenic diet can significantly reduce seizures, improve EEG and neurobehavioral development in children with epilepsy.
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Objective:To explore the correlation of plasma kallikrein and bradykinin receptor 1 with prognosis of cerebral infarction in elderly rats after ischemic stroke.Methods:A total of 40 male Sprague-Dawley rats were randomly divided into 4 groups: the stroke model group(intraperitoneally injected with 150 μl 0.9% saline, n=10), the DX-88 group(intravenously injected with kallikrein inhibitor DX-88 30 μl/time, n=10), the R-954 group(intravenously injected with bradykinin B1 receptor antagonist R-954 30 μl/time, n=10)and the DX-88 combined with R-954 treatment group(intravenously injected with DX-88 and R-954, n=10). Protein expression levels of plasma kallikrein and bradykinin receptor 1 were determined by Western blotting.mRNA expression levels of interleukin-1β(IL-1β), tumor necrosis factor-α(TNF-α)and caspase-3 were analyzed by using qRT-PCR.A neurologic function scale was used to score cerebral nerve injury and calculate the middle cerebral infarction area and cerebral swelling in experimental rats.Cerebral blood-brain barrier permeability was assessed by the cerebral infarction area.Results:Neurological injury scores decreased in the DX-88, R-954 and DX-88 + R-954 groups compared with the stroke model group(5.35±1.35, 6.49±1.16, 4.92±0.92 vs.11.17±2.18, F=15.589, P=0.022). Compared with the stroke model group, the cerebral infarction area was reduced in the DX-88, R-954 and DX-88+ R-954 groups[(4.35±1.05) mm 2, (5.43±0.26) mm 2, (3.88±0.13) mm 2vs.(8.26±1.24) mm 2, F=13.476, P=0.034)]. The extent of brain swelling was smaller in the DX-88, R-954 and DX-88+ R-954 groups than in the stroke model group[(31.28±7.45) %, (35.19±8.57) %, (19.68±3.14) % vs.(74.26±15.66) %, F=16.587, P=0.026)]. Plasma kallikrein protein levels were lower in the DX-88 and DX-88+ R-954 groups than in the stroke model group( P<0.05). The expression of bradykinin-1 receptor mRNA was lower in the R-954 and DX-88+ R-954 groups than in the stroke model group( P<0.05). The above results indicated that antagonism of plasma kallikrein and bradykinin receptor 1 played an important role.mRNA transcription levels of IL-1β, TNF-α and caspase-3 were higher in the stroke model group than in the DX-88, R-954 and DX-88+ R-954 groups( F=12.665、14.574 and 13.665, P=0.021、0.015 and 0.003). Conclusions:Inhibiting plasma kallikrein and bradykinin receptor 1 may provide protection against cerebral nerve injury in cerebral ischemia, and improve the prognosis of cerebral infarction.
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OBJECTIVE:To investigate the clinical efficacy and safety of Memantine hydrochloride tablets combined with Tianzhi granules in the treatment of vascular dementia. METHODS:A total of 94 patients with vascular dementia selected from our hospital during Jun. 2014-Jun. 2016 were divided into observation group and control group according to random number table,with 47 cases each. Besides basic therapy,control group was given Tianzhi granules 5 g,po,tid. Observation group was additionally given Memantine hydrochloride tablets with initial dose of 5 mg,increasing by 5 mg every week,maintaining dose of 20 mg/d at 4th week,po,qd,on the basis of control group. Both groups received treatment for consecutive 4 weeks. Clinical efficacies as well as MMSE,MoCA,ADL scores,the levels of brain-derived neurotrophic factor(BDNF),malondialdehyde(MDA)and super-oxide dismutase(SOD)before and after treatment were observed in 2 groups.The occurrence of ADR was recorded.RESULTS:To-tal response rate of observation group(80.85%)was significantly higher than control group(61.70%),with statistical significance (P<0.05). Before treatment,there was no statistical significance in MMSE,MoCA,ADL scores,the levels of BDNF,MDA or SOD between 2 groups(P>0.05).After treatment,MMSE,MoCA,ADL scores,the levels of BDNF and SOD in 2 groups were increased significantly,while MDA level was decreased significantly;observation group was significantly better than control group,with statistical significance(P<0.05). No obvious ADR was found in 2 groups. CONCLUSIONS:Memantine hydrochlo-ride tablets combined with Tianzhi granules in the treatment of vascular dementia show significant therapeutic efficacy,and can im-prove cognitive function,daily living activity and BDNF,MDA and SOD levels of patients with good safety.
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OBJECTIVE:To investigate the clinical efficacy and safety of Memantine hydrochloride tablets combined with Tianzhi granules in the treatment of vascular dementia. METHODS:A total of 94 patients with vascular dementia selected from our hospital during Jun. 2014-Jun. 2016 were divided into observation group and control group according to random number table,with 47 cases each. Besides basic therapy,control group was given Tianzhi granules 5 g,po,tid. Observation group was additionally given Memantine hydrochloride tablets with initial dose of 5 mg,increasing by 5 mg every week,maintaining dose of 20 mg/d at 4th week,po,qd,on the basis of control group. Both groups received treatment for consecutive 4 weeks. Clinical efficacies as well as MMSE,MoCA,ADL scores,the levels of brain-derived neurotrophic factor(BDNF),malondialdehyde(MDA)and super-oxide dismutase(SOD)before and after treatment were observed in 2 groups.The occurrence of ADR was recorded.RESULTS:To-tal response rate of observation group(80.85%)was significantly higher than control group(61.70%),with statistical significance (P<0.05). Before treatment,there was no statistical significance in MMSE,MoCA,ADL scores,the levels of BDNF,MDA or SOD between 2 groups(P>0.05).After treatment,MMSE,MoCA,ADL scores,the levels of BDNF and SOD in 2 groups were increased significantly,while MDA level was decreased significantly;observation group was significantly better than control group,with statistical significance(P<0.05). No obvious ADR was found in 2 groups. CONCLUSIONS:Memantine hydrochlo-ride tablets combined with Tianzhi granules in the treatment of vascular dementia show significant therapeutic efficacy,and can im-prove cognitive function,daily living activity and BDNF,MDA and SOD levels of patients with good safety.
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BACKGROUND:Col agen-gelatin composite scaffolds have been reported to be able to promote the early recovery of peripheral nerve defects. However, this conclusion has not been further confirmed. OBJECTIVE:To investigate the biocompatibility of the col agen-gelatin scaffold and its treatment outcomes in the repair of peripheral nerve defects. METHODS:The col agen-gelatin scaffold was co-cultured with bone marrow mesenchymal stem cel s (BMSCs) of Sprague-Dawley rats for 5 days, and then the cel growth was observed. Twenty Sprague-Dawley rats were enrol ed, modeled into a left 30-mm peroneal nerve defect and randomized into experimental and control groups. The col agen-gelatin scaffold composited with BMSCs was implanted into the experimental group, and autograft nerve implanted into the control group. Morphology of the middle bridge was observed, and electrophysiology was conducted at 16 weeks after implantation. RESULTS AND CONCLUSION:BMSCs grew and adhered wel onto the scaffold. The myelinated nerve fiber density did not significantly differ between groups (P>0.05). The myelinated nerve fiber diameter, myelin sheaththickness and percentage of nerve tissues in the experimental group were significantly lower than those in the control group (P0.05). The amplitude of motor nerves and the latency of sensory nerves in the experimental group were significantly lower than those in the control group (P<0.05). To conclude, the col agen-gelatin scaffold holds a good cytocompatibity and is ideal for the repair of peripheral nerve defects.
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Objective To observe the effects of different concentrations of baicalin on the mouse model of experimental autoimmune encephalomyelitis (EAE) and to explore its mechanisms.Methods A mouse model of EAE was established with MOG33-55 peptide and bacillus Calmette-Guerin (BGG) vaccine with complete Freund adjuvant (CFA).At the third day after immunization, high and low doses of baicalin were administered to the mice intragastrically once a day for 20 days.The neurological function of mice was evaluated.TUNEL staining was used to detect apoptosis in the spinal cord tissue.The level of ATP in spinal cord tissue was detected by an ATP determination kit.Furthermore, the protein expressions of Bax, Bcl-2, cleaved cas-3 and cleaved cas-9 were detected by western blot, respectively.Results Baicalin improved the neurological function and delayed the onset time in EAE mice.
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BACKGROUND:Several studies have reported that quercetin can inhibit the proliferation and migration but promotes apoptosis of tumor cel s. OBJECTIVE:To explore the effect of quercetin on the proliferation and apoptosis of glioma stem cel s and the signal pathway involved. METHODS:Glioma stem cel s were isolated by immunomagnetic beads and treated in culture medium containingdifferent concentrations of quercetin (0, 25, 50, 100μmol/L). Cel proliferation was measured by MTT and apoptosis measured by flow cytometry at 48 hours after culture. The expression levels of Bcl-2, Bax and survivin, which are related to apoptosis, were detected by western blot. The expression of proliferating cel nuclear antigen (PCNA), which is related to proliferation, was also detected by western blot. The expression of STAT3 and p-STAT3 was also determined by western blot. RESULTS AND CONCLUSION:(1) Compared with the control (0μmol/L) group, quercetin inhibited the proliferation of glioma stem cel s in a dose-depended manner (P<0.05). With the increase of the concentration of quercetin, the expression of PCNA was increased (P<0.05). (2) Quercetin induced apoptosis of glioma stem cel s dose-dependently (P<0.05). With the increase of the concentration of quercetin, the expression of Bcl-2 and survivin was decreased, while the expression Bax was increased. (3) Quercetin could also inhibit phosphorylation of STAT3 dose-dependently, but the level of STAT3 was not changed. To conclude, these results show that quercetin could inhibit the proliferation of glioma stem cel s and promote apoptosis via the STAT pathway.
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BACKGROUND:Increasing evidence has shown that lovastatin with less toxicity to normal cels has crucial effects on proliferation, apoptosis and differentiation of various cancer cels. However, its roles in glioma stem cels remain unclear. OBJECTIVE:To explore the effect of lovastatin on proliferation and apoptosis of glioma stem cels. METHODS: Flow cytometric sorting was used to separate glioma stem cels from human glioblastoma cel line U87. Effects of lovastatin on the proliferation and apoptosis of glioma stem cels were determined by MTT and flow cytometry, respectively. Furthermore, expression levels of Ki67, Bax and Bcl-2 in glioma stem cels treated with lovastatin were detected using western blot analysis. RESULTS AND CONCLUSION: The CD133-positive glioma stem cels were sorted from human glioblastoma cel line U87 with a positive percentage of 85%. MTT assay showed that lovastatin inhibited the proliferation of glioma stem cels in dose (5, 10, 20 μmol/L)- and time (24, 48, 72, 96 hours)-dependent manners. Flow cytometry analysis showed that 10 μmol/L lovastatin (48 hours) induced apoptosis in glioma stem cels. In addition, the expression level of Ki67 was decreased by lovastatin treatment in a dose-dependent manner, and the Bcl-2 and Bax expression levels were reduced and increased by 10 μmol/L lovastatin treatment, respectively. In conclusion, lovastatin can inhibit cel proliferation and induce apoptosis of glioma stem cels, and lovastatin may be a potential drug for treatment of brain tumors.
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BACKGROUND:Cancer stem cel s have self-renewal ability and can differentiate into new tumors. Cancer stem cel s are the source of tumor formation and recurrence, and they can make tumors insensitive to radiotherapy and chemotherapy. OBJECTIVE:To explore the effect of paclitaxel plus cisplatin on the proliferation and apoptosis of nasopharyngeal cancer stem cel s (NPCSCs) and involved signal pathways. METHODS:NPCSCs were sorted by immunomagneticbeads and were treated with paclitaxel, cisplatin or their combination. The expression of caspase-3, activated caspase-3 and Bcl-2, which are related to apoptosis, was determined by western blot. The expression ofβ-catenin and its downstream proto-oncogene, c-myc, was also determined by western blot. The activity of the Wnt/β-catenin pathway was inhibited by knocking downβ-catenin expression orβ-catenin inhibitor XAV939. Proliferation and apoptosis of NPCSCs were detected by MTT and flow cytometry, respectively. RESULTS AND CONCLUSION:Either paclitaxel or cisplatin could inhibit proliferation and induce apoptosis of NPCSCs. The expression of apoptosis marker, activated caspase-3, was increased and the expression of the inhibitor of apoptosis, Bcl-2, was declined. Combined use of paclitaxel and cisplatin had synergistic effect when used together. Either paclitaxel or cisplatin could inhibit the expression ofβ-catenin and c-myc, suppressed the proliferation and induced the apoptosis of NPCSCs by inhibiting the activity of Wnt/β-catenin pathway. These results indicate that the combined use of paclitaxel and cisplatin may inhibit the proliferation of NPCSCs and promote apoptosis via the Wnt/β-catenin pathway.
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BACKGROUND:Previous studies have found that the expression level of miR-486 in glioma stem cels (CD133+) is significantly down-regulated compared with that in glioma non-stem cels (CD133-), but the effect of down-regulation of miR-486 on CD133+ cels remains unclear . OBJECTIVE: To explore the effect of miR-486 on CD133+ cels. METHODS:CD133+ glioma stem cels and CD133- glioma cels were separated from U87 cels by flow cytometer. miR-486 overexpression glioma stem cels were constructed by lipofection transfection. RESULTS AND CONCLUSION:After sorting and purification, the content of the CD133+ fraction was enriched up to 83.5%. The expression level of miR-468 in CD133+ glioma stem cels was obviously down-regulated compared with that in CD133- glioma cels. CD133+ glioma stem cels overexpressing miR-486 were fabricated successfuly. Results from in vitro experiments showed that miR-486 overexpression could dramaticaly decrease the proliferation of glioma stem cels, induce a cel cycle arrest in G1/S phase for CD133+ glioma stem cels and promote cel apoptosis. These findings suggest that miR-486 can be a suppressor of glioma stem cels, which offers a novel potential therapeutic target for glioma stem cels and human glioma.
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BACKGROUND:For treatment of central nervous system diseases, neural stem cel s (NSCs) or bone marrow stromal stem cel s (BMSCs) can be transplanted into the brain, but there are less reports to compare the effects of two kinds of stem cel transplantation. OBJECTIVE:To explore the effect of midbrain NSCs and BMSCs on the behavior and brain morphology of rats with Parkinson’s disease. METHODS:Fifty-eight Sprague-Dawley rats were enrol ed to establish Parkinson’s disease models, and then randomly divided into three groups, which were treated with 5μL midbrain NSCs (n=20), 5μL BMSCs (n=20) and 5μL normal saline (n=18) via two coordinate points of the right striatum at 3 weeks after modeling, respectively. At 5 months after transplantation, the rats underwent intraperitoneal injection of apomorphine to observe behavioral changes, and then, the striatum was taken for immunohistochemistry staining. RESULTS AND CONCLUSION:The number of rotations was reduced significantly in the BMSCs and midbrain NSCs groups at 5 months after transplantation (P0.05). In the BMSCs group, BrdU/Nestin positive cel s were seen in the brain stratium at 1 week after transplantation;BrdU/GFAP and BrdU/NSE positive cel s as wel as TH positive cel s rather than BrdU/TH positive cel s were found in the brain stratium at 1 month after transplantation;after that, the number of BrdU/Nestin positive cel s was reduced gradual y and disappeared ultimately, but there were stil a certain number of BrdU/GFAP and BrdU/NSE positive cel s, especial y the former ones. Meanwhile, the NSCs group also had a similar situation, but no double-labeled cel s were in the normal saline group. These findings indicate that midbrain NSCs and BMSCs transplantation can both improve the behavior of Parkinson’s disease rats, and differentiate into neurons, astrocytes and dopaminergic neurons.
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Staphylococcus epidermidis has the ability to adhere to the surface of shunt tube and to develop the biofilm .It can embed itself in the biofilm so as to escape from the defense of the host .Due to the presence of biofilms , antimicrobial drug resistance , blood brain barrier of central nervous system , the treatment of shunt-related infection caused by Staphylococcus epidermidis is very difficult.This paper reviews the risk factors , prevalence , pathogenesis , treatment and prevention of ventriculoperitoneal shunt-related infections caused by Staphylococcus epidermidis.
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Objective To investigate the relationship between the dynamic changes of hs-CRP and IL-6 with restenosis after stent angioplasty in cerebral arterial stenosis .Methods 65 patients with cerebral artery stenosis stent angioplasty in Nanyang Mu-nicipal Central Hospital from March 2011 to March 2013 were retrospectively analyzed .The changes of hs-CRP and IL-6 levels be-fore operation and at different postoperative time points were observed and their correlation with vascular restenosis was anlyzed . Results (1)The cerebral artery stenosis degree and serum hs-CRP and IL-6 levels were positively correlated(P0 .05);△hs-CRP and △IL-6 had sta-tistically significant differences between the patients with restenosis and the patients without restenosis (P<0 .05) .Conclusion hs-CRP and IL-6 may play an important role in the process of restenosis after stent angioplasty in cerebral arterial stenosis .Monitoring the dynamic changes of hs-CRP and IL-6 has certain value for evaluating vascular restenosis .