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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.
ABSTRACT
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 discuss the individualizing schedule of endovascular treatment for intracranial venous sinus thrombosis based on the clinical feature and the stage of the disease.Methods Forty-three patients diagnosed with intracranial venous sinus thrombosis in Xuanwu Hospital,Capital University of Medical Sciences and in Zhongshan Hospital Xiamen University during period of August 2010 to August 2011 were treated with endovascular therapy designed individually based on the clinical stage of the disease development.Of all 43 cases,22 cases with acute onset (＜ 1 week after the onset) were treated with standard anticoagulant therapy ; 11 cases who failed to respond to anticoagulant therapy and 8 cases with subacute onset (1 week to 1 month) received intravenous thrombolysis and mechanical thrombus maceration;and 13 cases with chronic course (＞ 1 month) were given mechanical thrombus maceration combined with balloon dilation vascular surgery or stent-assisted venous sinus surgery,with taking anticoagulant for 12months.The patients were followed up for 3 to 6 months (mean 4.5 months).Results Their symptoms and signs were all significantly improved,with headache relief in 29 cases(67.4％),vision improvement in 28cases (28/31,90.3％),cerebrospinal fluidpressure decrease to normal level in 32 cases(32/43,74.4％) ;no improvement in 1 case,and a complication of subdural hematoma in 1 case.Three months follow-up of 39 patients,symptoms disappeared,the pressure cerebrospinal fluid in 36 cases returned to normal (94.3％),the papilledema in 37 cases subsided (94.9％).After 6 months,16 patients were followed up with an angiography; 8 of them were found venous sinus clear,5 were found partial recanalization of venous sinus trunk,cortical veins and deep venous was partially compensation,and 3 cases with stent-assisted venous sinus surgery were found the stent not shifted or collapsed,and venous sinuses maintained patency.Conclusions Endovascular treatment for patients with intracranial venous sinus thrombosis should be treated with individually designed therapy based on their clinical features and the stage of the disease.The individualized treatment was effective and safe.
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The Sonic hedgehog (SHH) signaling pathway plays a pivotal role in neurogenesis and brain damage repair. Our previous work demonstrated that the SHH signaling pathway was involved in the neuroprotection of cortical neurons against oxidative stress. The present study was aimed to further examine the underlying mechanism. The cortical neurons were obtained from one-day old Sprague-Dawley neonate rats. Hydrogen peroxide (H(2)O(2), 100 μmol/L) was used to treat neurons for 24 h to induce oxidative stress. Exogenous SHH (3 μg/mL) was employed to activate the SHH pathway, and cyclopamine (20 μmol/L), a specific SHH signal inhibitor, to block SHH pathway. LY294002 (20 μmol/L) were used to pre-treat the neurons 30 min before H(2)O(2) treatment and selectively inhibit the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. The cell viability was measured by MTT and apoptosis rate by flow cytometry analysis. The expression of p38, p-p38, ERK, p-ERK, Akt, p-Akt, Bcl-2, and Bax in neurons was detected by immunoblotting. The results showed that as compared with H(2)O(2) treatment, exogenous SHH could increase the expression of p-Akt by 20% and decrease the expression of p-ERK by 33%. SHH exerted no significant effect on p38 mitogen-activated protein kinase (p38 MAPK) pathway. Blockade of PI3K/Akt pathway by LY294002 decreased the cell viability by 17% and increased the cell apoptosis rate by 2-fold. LY294002 treatment could up-regulate the expression of the pro-apoptotic gene Bax by 12% and down-regulate the expression of the anti-apoptotic gene Bcl-2 by 54%. In conclusion, SHH pathway may activate PI3K/Akt pathway and inhibit the activation of the ERK pathway in neurons under oxidative stress. The PI3K/Akt pathway plays a key role in the neuroprotection of SHH. SHH/PI3K/Bcl-2 pathway may be implicated in the protection of neurons against H(2)O(2)-induced apoptosis.
ABSTRACT
The Sonic hedgehog (SHH) signaling pathway plays a pivotal role in neurogenesis and brain damage repair. Our previous work demonstrated that the SHH signaling pathway was involved in the neuroprotection of cortical neurons against oxidative stress. The present study was aimed to further examine the underlying mechanism. The cortical neurons were obtained from one-day old Sprague-Dawley neonate rats. Hydrogen peroxide (H(2)O(2), 100 μmol/L) was used to treat neurons for 24 h to induce oxidative stress. Exogenous SHH (3 μg/mL) was employed to activate the SHH pathway, and cyclopamine (20 μmol/L), a specific SHH signal inhibitor, to block SHH pathway. LY294002 (20 μmol/L) were used to pre-treat the neurons 30 min before H(2)O(2) treatment and selectively inhibit the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. The cell viability was measured by MTT and apoptosis rate by flow cytometry analysis. The expression of p38, p-p38, ERK, p-ERK, Akt, p-Akt, Bcl-2, and Bax in neurons was detected by immunoblotting. The results showed that as compared with H(2)O(2) treatment, exogenous SHH could increase the expression of p-Akt by 20% and decrease the expression of p-ERK by 33%. SHH exerted no significant effect on p38 mitogen-activated protein kinase (p38 MAPK) pathway. Blockade of PI3K/Akt pathway by LY294002 decreased the cell viability by 17% and increased the cell apoptosis rate by 2-fold. LY294002 treatment could up-regulate the expression of the pro-apoptotic gene Bax by 12% and down-regulate the expression of the anti-apoptotic gene Bcl-2 by 54%. In conclusion, SHH pathway may activate PI3K/Akt pathway and inhibit the activation of the ERK pathway in neurons under oxidative stress. The PI3K/Akt pathway plays a key role in the neuroprotection of SHH. SHH/PI3K/Bcl-2 pathway may be implicated in the protection of neurons against H(2)O(2)-induced apoptosis.
Subject(s)
Animals , Rats , Cerebral Cortex , Metabolism , Hedgehog Proteins , Metabolism , Neurons , Metabolism , Neuroprotective Agents , Metabolism , Oxidative Stress , Physiology , Phosphatidylinositol 3-Kinase , Metabolism , Proto-Oncogene Proteins c-akt , Metabolism , Rats, Sprague-DawleyABSTRACT
The effects of Sonic hedgehog (Shh) signaling pathway activation on S-type neuroblastoma (NB) cell lines and its role in NB tumorigenesis were investigated. Immunohistochemistry was used to detect the expression of Shh pathway components-Patched1 (PTCH1) and Gli1 in 40 human primary NB samples. Western blotting and RT-PCR were used to examine the protein expression and mRNA levels of PTCH1 and Gli1 in three kinds of S-type NB cell lines (SK-N-AS, SK-N-SH and SHEP1), respectively. Exogenous Shh was administrated to activate Shh signaling pathway while cyclopamine was used as a selective antagonist of Shh pathway. S-type NB cell lines were treated with different concentrations of Shh or/and cyclopamine for different durations. Cell viability was measured by using MTT method. Apoptosis rate and cell cycle were assayed by flow cytometry. The xenograft experiments were used to evaluate the role of Shh pathway in tumor growth in immunodeficient mice. High-level expression of PTCH1 and Gli1 was detected in both NB samples and S-type NB cell lines. Cyclopamine decreased the survival rate of the three cell lines while Shh increased it, and the inhibition effects of cyclopamine could be partially reversed by shh pre-treatment. Cyclopamine induced the cell apoptosis and the cell cycle arrest in G(0)/G(1) phase, while Shh induced the reverse effects and could partially prevent effects of cyclopamine. Cyclopamine could also inhibit the growth of NB in vivo. Our studies revealed that activation of the Shh pathway is important for survival and proliferation of S-type NB cells in vivo and in vitro through affecting cell apoptosis and cell cycle, suggesting a new therapeutic approach to NB.
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Polycomb group proteins Bmi-1 is the core subunits of the PRC1 complex,and also plays important roles in the regulation of neural development. This review introduces the construction of Bmi-1 and the recent study for Bmi-1 in the nervous system development and tumor generation. The important roles of Bmi-1 for sustain of the neural stem cell proliferation,regulation mechanism of neural development and tumor generation are discussed.