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COVID-19 is caused by the 2019 novel coronavirus, which is characterized by hidden onset, long incubation period, and high contagion. The study found that the COVID-19 not only attacks the respiratory system, but also affects other systems such as the heart, kidney, and digestive tract, and could be combined with multiple system diseases such as acute cerebrovascular disease. If doctors, especially non-infective or respiratory doctors, do not pay great attention to the patient when they are receiving patients, and take good care of them, they may easily cause their own infection. This article summarizes the case of a concealed onset COVID-19 patient with cerebral infarction, which caused a medical staff infection after intravenous thrombolytic therapy, explores its clinical characteristics, treatment process and analyzes its prevention and control links to help the epidemic situation. In the prevention and control, the first-time doctor should pay attention to identification, reduce missed diagnosis, and scientific investigation to reduce occupational infection.
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COVID-19 is caused by the 2019 novel coronavirus, which is characterized by hidden onset, long incubation period, and high contagion. COVID-19 not only attacks the respiratory system, but also affects other systems such as the heart, kidney, and digestive tract, and could be combined with multiple system diseases such as acute cerebrovascular disease. If doctors, especially non-infective or respiratory doctors, do not pay great attention to the disease when they are receiving patients, and take good care of them, they may easily be infected. This article summarizes the case of a concealed onset COVID-19 patient with cerebral infarction, which caused a medical staff infection after intravenous thrombolytic therapy, explores its clinical characteristics, treatment process and analyzes its prevention and control links to help the epidemic situation. In the prevention and control of the disease, the first doctor should pay attention to identification, reduce missed diagnosis, and conduct scientific investigation to reduce occupational infection.
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Objective To explore the clinical effect and safety of Shugan-Jianpi-Huayu decoction combined with entecavir for the patients with hepatic cirrhosis of hepatitis B.Methods A total of 150 patients with hepatic cirrhosis of hepatitis B visiting our hospital from Jan. 2013 to Jan. 2015 were enrolled and randomly divided into the observation group and control group, 75 in each group. The control group received entecavir, while the observation group received Shugan-Jianpi-Huayu decoction additionally. The index of liver fuction and liver fibrosis, clinical efficacy and adverse reactions were observed and compared after the treatment.Results After treatment, the AST (42.88 ± 12.57U/Lvs.56.94 ± 14.83U/L,t=6.263), ALT (41.10 ± 10.61U/L vs.53.12 ± 16.78U/L,t=5.243), TBIL (20.15 ± 9.76μmol/Lvs.28.35 ± 12.20μmol/L, t=4.545), PC Ⅲ (103.65 ± 22.84μg/Lvs. 162.44 ± 38.90μg/L,t=11.287),Ⅳ-C (106.72 ± 23.41μg/Lvs.152.94 ± 30.01μg/L, t=10.518), LN (92.75 ± 25.32μg/Lvs.156.64 ± 38.79μg/L,t=11.945), HA (105.58 ± 18.07μg/L vs.159.74 ± 35.50μg/L,t=11.775) of the observation group were significantly better than those of the control group (allP<0.05). The total efficacy rate of the observation group were 85.33% (64/75), which were significantly higher than 64.00% (48/75) of control group (χ2=9.023,P=0.003).Conclusions The Shugan-Jianpi-Huayu decoction combined with entecavir showed efficacy and safey for the patients with hepatic cirrhosis of hepatitis B.
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<p><b>OBJECTIVE</b>To evaluate the efficiency of cell-free fetal DNA detection as a non-invasive prenatal screening (NIPS) method for women of advanced maternal age.</p><p><b>METHODS</b>A total of 10 584 women of advanced maternal age who received NIPS were recruited from the Women's Hospital, Zhejiang University School of Medicine and Jiaxing Maternal and Child Health Hospital during February 2015 and September 2016. The pregnancy outcome was followed-up. The sensitivity, specificity, positive and negative predictive value of fetal chromosomal aneuploidy detected in NIPS were analyzed. And the relationship between maternal age and fetal common chromosomal aneuploidy was analyzed.</p><p><b>RESULTS</b>The sensitivity, specificity, positive and negative predictive value of NIPS were 100.00%, 99.96%, 91.67%, 100.00% for trisomy 21, 100.00%, 99.93%, 68.18%, 100.00% for trisomy 18, and 100.00%, 99.97%, 25.00%, 100.00% for trisomy 13. High-risk rate and true positive rate of trisomy 21 were positively correlated with the maternal age (all<0.01). There were significant differences in high-risk rate and true positive rate between 35-37 year old groups and 38-40 year old groups (all<0.05). Such difference was also found in high-risk rate between 38-40 year old group and ≥ 41 year old group (<0.05), but not in true positive rate between two groups (>0.05).</p><p><b>CONCLUSIONS</b>NIPS is effective for fetal chromosomal aneuploidy screening in women of advanced maternal age. For women under 38 years of age, NIPS is preferred; for women of 41 and above, invasive diagnostic methods are suggested; and for women between 38-41 years old, the option can be determined by themselves after risks and advantages were fully informed.</p>
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<p><b>OBJECTIVE</b>To detect mosaic trisomy 9 missed by conventional cytogenetics.</p><p><b>METHODS</b>Peripheral blood genomic DNA from a girl with mental retardation was analyzed using Affymetrix CytoScan (TM) HD array. Fluorescence in situ hybridization (FISH) was also performed on samples from two patients.</p><p><b>RESULTS</b>The SNP-array analysis has revealed multiple duplications along chromosome 9. FISH analysis showed that, for the peripheral blood sample from one patient, 40 of 100 interphase cells and 15 of 100 metaphase cells carried trisomy 9. For the cord blood sample from another patient, 35 of 100 interphase cells and 10 of 100 cultured cells carried trisomy 9.</p><p><b>CONCLUSION</b>SNP-array is useful for detecting low-level mosaicism which may be missed by conventional cytogenetics. Combined with karyotype and microarray analyses, FISH is a focused and targeted approach for diagnosing mosaic trisomy. They may provide a useful tool for differentiating pseudomosaicisms from true mosaicisms.</p>
Subject(s)
Adult , Female , Humans , Infant , Male , Pregnancy , Chromosomes, Human, Pair 9 , Genetics , In Situ Hybridization, Fluorescence , Mosaicism , Embryology , Oligonucleotide Array Sequence Analysis , Methods , Polymorphism, Single Nucleotide , Prenatal Diagnosis , Trisomy , Diagnosis , Genetics , Uniparental Disomy , Cell Biology , Diagnosis , GeneticsABSTRACT
This study examined the ability of 1,2,3,4,6-penta-O-galloyl-β-D-glucose (β-PGG) to induce the expression of heme oxygenase-1 (HO-1) in the PC12 cells and its regulation in the PC12 cells. One week before treatment with the drug, nerve growth factor (NGF) was added to the cultures at a final concentration of 50 ng/mL to induce neuronal differentiation. After drug treatment, HO-1 gene transcription was analyzed by reverse transcription polymerase chain reaction (RT-PCR). Expression of HO-1 and NF-E2-related factor2 (Nrf2) and activation of extracellular signal-regulated kinase (ERK) and Akt were detected by Western blotting. The viability of the PC12 cells treated with different medicines was examined by MTT assay. The oxidative stress in the PC12 cells was evaluated qualitatively and quantitatively by DCFH-DA. The results showed that β-PGG up-regulated HO-1 expression and this increased expression provided neuroprotection against MPP(+)-induced oxidative injury. Moreover, β-PGG induced Nrf2 nuclear translocation, which was found to be upstream of β-PGG-induced HO-1 expression, and the activation of ERK and Akt, a pathway that is involved in β-PGG-induced Nrf2 nuclear translocation, HO-1 expression and neuroprotection. In conclusion, β-PGG up-regulates HO-1 expression by stimulating Nrf2 nuclear translocation in an ERK- and Akt-dependent manner, and HO-1 expression by β-PGG may provide the PC12 cells with an acquired antioxidant defense capacity to survive the oxidative stress.
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This study examined the ability of 1,2,3,4,6-penta-O-galloyl-β-D-glucose (β-PGG) to induce the expression of heme oxygenase-1 (HO-1) in the PC12 cells and its regulation in the PC12 cells. One week before treatment with the drug, nerve growth factor (NGF) was added to the cultures at a final concentration of 50 ng/mL to induce neuronal differentiation. After drug treatment, HO-1 gene transcription was analyzed by reverse transcription polymerase chain reaction (RT-PCR). Expression of HO-1 and NF-E2-related factor2 (Nrf2) and activation of extracellular signal-regulated kinase (ERK) and Akt were detected by Western blotting. The viability of the PC12 cells treated with different medicines was examined by MTT assay. The oxidative stress in the PC12 cells was evaluated qualitatively and quantitatively by DCFH-DA. The results showed that β-PGG up-regulated HO-1 expression and this increased expression provided neuroprotection against MPP(+)-induced oxidative injury. Moreover, β-PGG induced Nrf2 nuclear translocation, which was found to be upstream of β-PGG-induced HO-1 expression, and the activation of ERK and Akt, a pathway that is involved in β-PGG-induced Nrf2 nuclear translocation, HO-1 expression and neuroprotection. In conclusion, β-PGG up-regulates HO-1 expression by stimulating Nrf2 nuclear translocation in an ERK- and Akt-dependent manner, and HO-1 expression by β-PGG may provide the PC12 cells with an acquired antioxidant defense capacity to survive the oxidative stress.
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Animals , Rats , Cell Death , Genetics , Cell Line, Tumor , Heme Oxygenase-1 , Genetics , Hydrolyzable Tannins , Pharmacology , MAP Kinase Signaling System , Genetics , PC12 Cells , Piperidines , Proto-Oncogene Proteins c-akt , Genetics , PyrazolesABSTRACT
To examine the changes in erythropoietin (Epo) protein and its mRNA expression in rat brain subjected to focal ischemia and possible mechanism of the preconditioning of mitochondrial toxin 3-nitropropionic acid (3-NPA), rats were administrated either vehicle or 3-NPA at a dose of 20 mg/kg, intraperitoneally (ip), 3 days prior to a 2-h middle cerebral artery occlusion followed by 24-h reperfusion. Infarct volumes were measured by using 2, 3, 5 triphenylte trazolinm chloride (TTC) staining, and Epo protein and its mRNA levels were assessed by immunohistochemistry and reverse transcriptase polymerase chain reaction (RT-PCR), respectively. Our results showed that after reperfusion, Epo was found to be expressed extensively in the rat brain. It was most apparent in the basal nuclei and hippocampus, and was, to some extent, present in cortex. Preconditioning with 3-NPA caused a reduction in infarct volume. The expression of both Epo protein and mRNA increased significantly in the different brain areas in the 3-NPA pretreated group as compared with the non-pretreated ischemia model group. These results suggested that preconditioning with low dose 3-NPA could induce ischemic tolerance and neuro-protective effects by increasing the Epo expression in the ischemic and ischemia-related areas.
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To examine the changes in erythropoietin (Epo) protein and its mRNA expression in rat brain subjected to focal ischemia and possible mechanism of the preconditioning of mitochondrial toxin 3-nitropropionic acid (3-NPA), rats were administrated either vehicle or 3-NPA at a dose of 20 mg/kg,intraperitoneally (ip), 3 days prior to a 2-h middle cerebral artery occlusion followed by 24- h reperfusion. Infarct volumes were measured by using 2, 3, 5 triphenylte trazolinm chloride (TTC)staining, and Epo protein and its mRNA levels were assessed by immunohistochemistry and reverse transcriptase polymerase chain reaction (RT-PCR), respectively. Our results showed that after reperfusion, Epo was found to be expressed extensively in the rat brain. It was most apparent in the basal nuclei and hippocampus, and was, to some extent, present in cortex. Preconditioning with 3-NPA caused a reduction in infarct volume. The expression of both Epo protein and mRNA increased significantly in the different brain areas in the 3-NPA pretreated group as compared with the non-pretreated ischemia model group. These results suggested that preconditioning with low dose 3-NPA could induce ischemic tolerance and neuro-protective effects by increasing the Epo expression in the ischemic and ischemia-related areas.
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BACKGROUND: Mainly pathological changes of Parkinson disease (PD)are related to irreversible degeneration and reduction of dopamine neurons of substantia nigra in midbrain; however, oxidative stress reaction plays an important role in onset of PD. 3-nitropropionie acid (3-NP) is an inhibitor of mitochondria compound I, and it can inhibit oxidative phosphorylation so as to restrain energy metabolism. However, professor Riepe from Germany found that small dose of 3-NP can increase the tolerance of neurons to ischemic hypoxia. It is unclear whether it can also strengthen the tolerance of dopamine neurons to neurotoxin.OBJECTIVE: To investigate the possible mechanism and prevention of repetitively preconditioning 3-NP for treating PD.DESIGN: Controlled observational animal study. SETTING: Department of Neurology, Union Hospital affiliated to TongjiMedical College, Huazhong University of Science and Technology. MATERIALS: The experiment was carried out at the Neurological Lab oratory, Union Hospital affiliated to Tongji Medical College, Huazhong U niversity of Science and Technology from March to July 2004. A total of48 C57BL mice, weighing 18-20 g, aged 2-3 months, of both genders, were randomly divided into 6 groups with 8 in each group. ① Blank con trol group: Mice were not medicated. ② 3-NP single administrationgroup: Mice were intraperitoneally injected with 3-NP once. ③ 3-NPrepetitively administrations group: Mice were intraperitoneally injectedwith 3-NP every 5 days for 5 times in total. ④ Neurotoxin group: Micewere intraperitoneally injected with neurotoxin once every day for 5 timesin total. ⑤ 3-NP single preconditioning group: Mice were intraperitoneal ly injected with 3-NP once, and 3 days later, they were intraperitoneallyinjected with neurotoxin once every day for 5 times in total. ⑥ 3-NPrepetitively preconditionings group: Mice were intraperitoneally injectedwith 3-NP and repetitively every 5 days for 5 times in total; 3 days later, mice were intraperitoneally injected with neurotoxin once every day for5 times in total. Dosages of 3-NP and neurotoxin were 20 mg/kg and30 mg/kg, respectively. METHODS: Motor coordination of mice was scored with pole test andtraction test before experiment and at 3 days after the last injection ofneurotoxin. Three days after complete injection, mice were sacrificed rapid ly to measure the contents of malondialdehyde (MDA) and reduced glu tathione (GSH) in the substantia nigra of midbrain. MAIN OUTCOME MEASURES: ① Motor and behavior scores; ② con tent of MDA; ③ content of GSH.~ULTS: All 48 mice were involved in the final analysis. ① Scores of pole test and traction test were decreased in neurotoxin group as compared with those in control group (P＜0.01); but the scores were increased after 3-NP single/repetitively preconditionings, and there were significant difference (P＜0.05, P＜0.01). Meanwhile, there was also significant differencebetween 3-NP repetitively preconditionings group and 3-NP single preconditioning group (P＜0.05). ② Content of MDA was increased in neurotoxin group as compared with that in control group, and there was significant difference (P＜0.01); content of MDA was decreased after 3-NP single preconditioning as compared with that in neurotoxin group, and there was significant difference (P＜0.05); content of MDA was remarkably decreased after 3-NP repetitively preconditionings as compared with that in neurotoxin group, and there was greatly significant difference (P＜0.01); meanwhile, there was also significant difference between 3-NP repetitively preconditionings group and 3-NP single preconditioning group (P＜0.05). ③As compared with that in blank control group, content GSH in 3-NP single administration group was not changed; content of GSH in 3-NP repetitively administrations group was increased (P＜0.05); content of GSH in neurotoxin group was decreased as compared with that in blank control group (P＜0.01); content of GSH in 3-NP single preconditioning group was not changed as compared with that in neurotoxin group (P＞0.05); content of GSH was increased after 3-NP repetitively preconditionings, and there was significant difference (P＜0.05); meanwhile, there was significant difference between 3-NP repetitively preconditionings group and 3-NP single preconditioning group (P＜0.05).CONCLUSION: 3-NP repetitively preconditionings can activate synthesis of GSH, protect dopamine neurons through decreasing production of MDA.
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BACKGROUND: The elevation of plasma fibrinogen(Fbg) is a key risk factor of cerebrovascular diseases. The evaluation of the monomer polymerization function of fibrin has even more important clinical merit than the detection of Fbg level.OBJECTIVE: To investigate the clinical significance of the monomer polymerization function of fibrin in patients with isehemie cerebrovascular diseases and its impacts on rehabilitative intervention.DESIGN: A case control study employing patients and healthy individual as subjects.SETTING: An Institute of Hematology and Department of Neurology of one university.PARTICIPANTS: Totally 110 patients with different ischemic cerebrovascular disease selected from the Department of Neurology, Union Hospital of Tongji Medical College, Huazhong Science and Technology University from September 2001 to March 2002, and 50 healthy individuals were included in the study.METHODS: Rehabilitative intervention was performed in 31 randomly selected cerebral infarct patients, and the parameters indicating the monomer polymerization functions of fibrin in the plasma were detected by the measurement system for the monomer polymerization function of fibrin.MAIN OUTCOME MEASURES: Abnormal condition of monomer polymerization function of fibrin in each parameter.RESULTS: Each parameter indicating the monomer polymerization functions of fibrin in plasma was significantly increased in ischemic cerebrovascular diseases patients than healthy individuals( P ＜ 0.01 ) . The abnormal rate of Fbg leveland fibrin monomer polymerization velocity (FMPV) was significantly elevated in ischemic cerebrovascular disease patients than healthy individuals ( P ＜ 0. 01 ) . The relative risk(RR) of ischemic cerebrovascular diseases in patients with abnormal FMP functions was 4 to 31 times more than healthy control group. In cerebral infarct group, FMPV of anterior circulation infarct subgroup was significantly elevated than that of posterior circulation infarct and lacunar cerebral infarct subgroups( P ＜ 0.05). The FMP function of anterior cerebral infarct patients was significantly higher than that of healthy group before rehabilitative intervention. Although each FMP parameter reduced after rehabilitative intervention, the difference between was not significant compared with that of before therapy.CONCLUSION: FMP function analysis can completely and objectively reflect the coagulation status of the patients with ischemic cerebrovascular diseases, and it can also reflect the range and severity of infarct to some extent. Although common rehabilitative intervention cannot effectively improve the high-coagulation of the blood, the impacts of specific rehabilitative intervention on the coagulation mechanism deserve further investigation.
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BACKGROUND: 3-nitropropionic acid(3-NP) can inhibit the process of oxidative phosphorylation and injure the energy metabolism of the cell and thereby induce cell injury. However, small dose of 3-NP can excite intrinsic cellular protective factor to protect neurons and increase the tolerance of neurons to ischemic hypoxia through mild inhibiting the process of oxidative phosphorylation. It is unclear whether it also has the similar effect on dopaminergic neurons.OBJECTIVE: To investigate whether 3-NP preconditioning could enhance the tolerance of dopaminergic neurons to MPP+(1-methyl-4-phenylpyridine)toxicity.DESIGN: A randomized controlled exploring research based on neuroblastoma SH-SYSY cell that could secrete dopamine.SETTING: Department of neurology of a university hospital.MATERIALS: The study was conducted in the Laboratory of Pathophysiology of Tongji Medical College between March 2003 and November 2003. SH-SYSY cell was obtained from the Cell Center of Peking Union Medical University.INTERVENTIONS: Cells were randomly divided into 6 groups. MPP+ was added into the cultured dopaminergic neuron SH-SY5Y cells for the establishment of the cell model for Parkinson disease. Before the admission of MPP+ (0.25 mmol/L), 3-NP(0. 2 mmol/L) was added once or repetitive times to form preconditioning. Microculture tetrozolium(MTT) was used to detect cell survival rate, and[3H] DA uptake rate was used to test the anterior synaptic function of dopaminergic neurons.MAIN OUTCOME MEASURES: Major consequence: Cell survival rate;Minor consequence: [3H] DA uptake rate.RESULTS: Cell survival rate of MPP+ group was 54.3%, which was significantly lower than that of blank control group( P ＜ 0.01) . After 3-NP preconditioning, cell survival rate significantly elevated, which was 71.8%(single) or 85.2% (repetitive) . There was significant difference between single preconditioning and repetitive preconditioning( P ＜ 0.05 ). The results of[3H] DA uptake rate were similar to that of cell survival rate. [3H] DA uptake rate was 65.8% (single) or 80. 3% (repetitive), which was significantly higher than 50. 1% of MPP+ group. And moreover, repetitive preconditioning had more favorable effect than single preconditioning. Simple admission of 3-NP had no impact on cells.CONCLUSION: 3-NP preconditioning can significantly enhance the tolerance of dopaminergic neuron to MPP+ toxicity, which has significant protective effects on dopaminergic neuron. Repetitive preconditioning have more significant protective effects.
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The involvement of apoptosis in mitochondrial toxin 3-nitropropionic acid (3-NPA)-induced ischemic tolerance to transient focal cerebral ischemia in rats and the mechanism was investigated. 3-NPA at a dose of 20 mg/kg or vehicle control was intraperitoneally into the rats. Three days later, rats were exposed to 2 h of middle cerebral artery occlusion followed by 24 h of reperfusion. Infarct volumes were assessed by 2,3,5-triphenyltetrazolinm chloride (TTC) staining 24 h after reperfusion. Neural cell apoptosis in cerebral ischemic penumbra was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end labeling (TUNEL) and flow cytometry methods (FCM). The results showed that as compared to the vehicle-treated group, pretreatment with 3-NPA could reduce the infarct volume by 23.3% and decrease the number of TUNEL-positive neural cells and apoptotic percentage by 47% (P<0.05) and 44.9% (P<0.01), respectively. It was concluded that the development of 3-NPA-induced ischemic tolerance in brain might be related to the decreases in neural cell apoptosis.
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Animals , Male , Rats , Apoptosis , Cerebral Cortex , Cerebrovascular Circulation , DNA Damage , Infarction, Middle Cerebral Artery , Pathology , Ischemic Attack, Transient , Pathology , Ischemic Preconditioning , Middle Cerebral Artery , Pathology , Nitro Compounds , Propionates , Reperfusion Injury , PathologyABSTRACT
In order to investigate the association of fibrin monomer polymerization function (FMPF) with traditional cerebrovascular risk factors and ischemic cerebrovascular disease in old people, 1:1 paired case-control comparative study was performed for FMPF and traditional cerebrovascular risk factors on 110 cases of old ischemic cerebrovascular disease and 110 controls matched on age, sex and living condition. The results showed that cerebrovascular risk factors were more prevalent in case group than in control group. In the case group, FMPF was significantly higher than in control group. There was a significant positive correlation between hypertension and fibrin monomer polymerization velocity (FMPV), hypertension and fibrinogen (Fbg), alcohol consumption and Fbg, but no significant correlation between diabetic mellitus, smoking and FMPF was found. Among the parameters of blood lipids, there were significant positive correlations between total cholesterol (TC) and parameters of FMPF to varying degrees, triglycerides (TG) and FMPV, TG and Fbg. Our results also showed there were significant linear trends between TC and FMPV (P < 0.001), TC and Fbg (P = 0.0087), TG and FMPV/Amax (maximum absorbance) (P = 0.0143) respectively. Multiple logistic regression analysis revealed that FMPF in case group remained significantly higher than control group after adjustment of all risk factors that were significant in univariate analysis. It was concluded that there is a possible pathophysiological link between FMPF and cerebrovascular risk factors. An elevated FMPF is associated with ischemic cerebrovascular disease and an independent risk factor of this disease. In old people, detection of FMPF might be a useful screening to identify individuals at increased cerebrothrombotic risk.
Subject(s)
Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Case-Control Studies , Cerebral Infarction , Blood , Cerebrovascular Disorders , Blood , Fibrin Fibrinogen Degradation Products , Metabolism , Hypertension , Logistic Models , Polymers , Risk FactorsABSTRACT
To investigate the effects of time interval and cumulative dosage of repetitive mild cellular hypoxia on shape of neurodegeneration and neuroprotection in mice, population spike amplitude (PSA) was measured during hypoxia and posthypoxic recovery in hippocampal slices from untreated control and mice pretreated in vivo with a single or repeatedly intraperitoneal injection of 3-nitropropionate (3-NP). Posthypoxic recovery of PSA was dose-dependent in single pretreated slices, with maximal recovery on pretreatment attained with 20 mg/kg 3-NP (82 +/- 32%, P < 0.01). Upon 5 and 9 treatments with 20 mg/kg 3-NP (dosage interval 3 days), PSA recovered to (38 +/- 9)% with the difference being not significant vs control group and (72 +/- 45)% with the difference being significant (P < 0.05 to control, P < 0.05 to 5 treatments), respectively. In contrast, with 2 days time interval, recovery after 5 and 9 treatments was (30 +/- 25)% and (16 +/- 14)%, respectively (without significant difference from control). Continued neuroprotection was also observed upon increase of dosage interval to 4 and 5 days. It was suggested that repetitive chemical hypoxia is a model for neurodegenerative disease and continued neuroprotection depending on time interval between repetitive hypoxic episodes rather than cumulative dosage. At appropriate time intervals increased neuronal hypoxic tolerance could be induced with number of hypoxic episodes.
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Animals , Male , Mice , Adaptation, Physiological , Cell Hypoxia , Disease Models, Animal , Hippocampus , Cell Biology , Huntington Disease , Ischemic Preconditioning , Neuronal Plasticity , Physiology , Nitro Compounds , Propionates , Time FactorsABSTRACT
Objective To investigate the effect of aging on neuroprotection by preconditioning with 3-nitropropionic acid (3-NPA) and the relationship between aging and adenosine receptor. Methods Population spike amplitude (PSA) in region CA 1 in hippocampal slices was measured during 15 min hypoxia and 45 min posthypoxic recovery from adult and aged mice, which were pretreated in vivo with a single intraperitoneal injection of 3-NPA (20 mg/kg). Posthypoxic PSA recovery was also observed after perfusion with selective agonist or antagonist of adenosine A 1 and A2a receptors. Results Posthypoxic recovery of PSA increased from 26.1?12.2% in control slices to 92.9?15.3% in pretreated slices from adult (P
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AIM: To investigate the relationship between astroglial activation state and ischemic tolerance induced by low dose of 3 nitropropionic acid (3 NPA) in gerbil hippocampus. METHODS: Transient forebrain ischemic model was induced by bilateral common carotid arteries occlution. HE staining and immunohistochemistry were used to identify neuronal and astrocyte response. RESULTS: Preconditioning with 3 NPA produced protective effects of CA 1neurons. The number of glial fibrillary acidic protein positive astrocyte in hippocampal CA 1 region increased slightly in control group, but increased significantly in preconditioning of the brain with 3 nitropropionic acid. CONCLUSION: The state of astroglial activation is related to neuronal survival in ischemic tolerance induced by low dose of 3 nitropropionic acid.
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AIM To investigate antiplatelet agents induced neuroprotection, which is blood perfusion independent, and its gender difference. METHODS Population spike amplitude (PSA) was measured during hypoxia and posthypoxic recovery in blood fsee hippocampal slices from untreated control mice and from in vivo pretreated mice with a single intraperitoneal injection of acetylsalicylic acid (ASA), ticlopidine or clopidogrel. Extracellular recordings and NADH fluorescence spectroscopy were used to determine PSA and NADH fluorescence upon hypoxia in CA1 region in hippocampal slices from ASA treated male and female mice. RESULTS Posthypoxic recovery of PSA was 25 9%?11 6% in control slices. In slices pretreated with ASA, ticlopidine and clopidogrel PSA recovered to 74 7%?35 7% ( P