Objective: To study the effect of Butylphthalide combined with Urinary Kallidinogenase on the pathological course of nerve damage in patients with massive cerebral infarction. Methods:The patients with massive cerebra...Objective: To study the effect of Butylphthalide combined with Urinary Kallidinogenase on the pathological course of nerve damage in patients with massive cerebral infarction. Methods:The patients with massive cerebral infarction who received treatment in our hospital between January 2016 and December 2017 were selected and randomly divided into the group A receiving Butylphthalide treatment, the group B receiving Urinary Kallidinogenase treatment and the group C receiving Butylphthalide combined with Urinary Kallidinogenase treatment on the basis of conventional treatment. 14 d after treatment, serum levels of nerve markers, coagulation indexes, growth factors and oxidative stress indexes were determined. Results:After treatment, visinin-like protein-1 (VILIP-1), neuron-specific enolase (NSE), S100B protein (S100B), thromboxane A2 (TXA2), lysophosphatidic acid (LPA), D-dimer (D-D), 8-isoprostanes F2α (8-iso-PGF2α) and malondialdehyde (MDA) levels of 3 groups significantly decreased whereas nitric oxide (NO), nitric oxide synthase (NOS), vascular endothelial growth factor (VEGF), brain-derived neurotrophic factor (BDNF), insulin-like growth factor-I (IGF-I), superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) levels significantly increased, and VILIP-1, NSE, S100B, TXA2, LPA, D-D, 8-iso-PGF2α and MDA levels of the group C after treatment were significantly lower than those of the group A and group B whereas NO, NOS, VEGF, BDNF, IGF-I, SOD and T-AOC levels were significantly higher than those of the group A and group B. Conclusion: Butylphthalide combined with Urinary Kallidinogenase is better than monotherapy in improving the pathological course of nerve damage in patients with massive cerebral infarction.展开更多
Myasthenia gravis(MG)is neuromuscular disorder induced neurotransmission defects at the neuromuscular junctions.MG is an autoimmune disease in which the autologous immune system,including the corresponding antibodies,...Myasthenia gravis(MG)is neuromuscular disorder induced neurotransmission defects at the neuromuscular junctions.MG is an autoimmune disease in which the autologous immune system,including the corresponding antibodies,immune cells and complement systems,attacks the cholinergic receptor(AChRs)of the postsynaptic membrane,resulting in weakness of skeletal muscle.A rare portion of MG cases is mediated with antibodies specific to muscle specific kinase(MuSK)and low-density lipoprotein receptor related protein 4(LRP4).The major clinical symptoms of MG are presented as weakness of skeletal muscle,fatigue prone,which are worsened after exercise.Adequate rest and treatment with cholinesterase inhibitors could significantly relieve and reduce the symptoms.The average onset rate is about 8-20 cases per 100,000 people.展开更多
Neuromyelitis optica(NMO)is an autoimmune demyelinating disease that mainly affects the optic nerve and spinal cord,potentially resulting in blindness and paralysis.Once thought to be a clinical variant of multiple sc...Neuromyelitis optica(NMO)is an autoimmune demyelinating disease that mainly affects the optic nerve and spinal cord,potentially resulting in blindness and paralysis.Once thought to be a clinical variant of multiple sclerosis,NMO is currently considered as a different disease with its own features due to the identification of a specific autoantibody against aquaporin 4.Given the high risk of disability,treatment should be launched once the diagnosis is established.Evidence from clinical practice showed that traditional immunosuppressive agents affecting the function of T and B cells could attenuate disease exacerbation.Recently,with better understanding pathogenesis of NMO,increasing bodies of novel therapies and therapeutic targets have been discovered.In this review,the authors discuss the current strategies of treating NMO in details and briefly introduce the potential therapies in future.展开更多
Myasthenia gravis(MG)is an acquired autoimmune disease affecting synaptic transmission via the neuromuscular junction mainly due to the presence of auto-antibodies targeting acetylcholine receptors.Ocular or generaliz...Myasthenia gravis(MG)is an acquired autoimmune disease affecting synaptic transmission via the neuromuscular junction mainly due to the presence of auto-antibodies targeting acetylcholine receptors.Ocular or generalized MG is clinically diagnosed when the extra-ocular muscles or other muscle groups beyond the extra-ocular muscles are involved.MG occurs in both sexes at any ages from all races but shows a wide variability in incidence and prevalence.Differences in clinical phenotypes of MG patients between West and East countries have been observed.Herein,we review the current concept on epidemiology,classification,and generalized progression in MG,mainly focusing on the differential features from China's Mainland.展开更多
文摘Objective: To study the effect of Butylphthalide combined with Urinary Kallidinogenase on the pathological course of nerve damage in patients with massive cerebral infarction. Methods:The patients with massive cerebral infarction who received treatment in our hospital between January 2016 and December 2017 were selected and randomly divided into the group A receiving Butylphthalide treatment, the group B receiving Urinary Kallidinogenase treatment and the group C receiving Butylphthalide combined with Urinary Kallidinogenase treatment on the basis of conventional treatment. 14 d after treatment, serum levels of nerve markers, coagulation indexes, growth factors and oxidative stress indexes were determined. Results:After treatment, visinin-like protein-1 (VILIP-1), neuron-specific enolase (NSE), S100B protein (S100B), thromboxane A2 (TXA2), lysophosphatidic acid (LPA), D-dimer (D-D), 8-isoprostanes F2α (8-iso-PGF2α) and malondialdehyde (MDA) levels of 3 groups significantly decreased whereas nitric oxide (NO), nitric oxide synthase (NOS), vascular endothelial growth factor (VEGF), brain-derived neurotrophic factor (BDNF), insulin-like growth factor-I (IGF-I), superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) levels significantly increased, and VILIP-1, NSE, S100B, TXA2, LPA, D-D, 8-iso-PGF2α and MDA levels of the group C after treatment were significantly lower than those of the group A and group B whereas NO, NOS, VEGF, BDNF, IGF-I, SOD and T-AOC levels were significantly higher than those of the group A and group B. Conclusion: Butylphthalide combined with Urinary Kallidinogenase is better than monotherapy in improving the pathological course of nerve damage in patients with massive cerebral infarction.
文摘Myasthenia gravis(MG)is neuromuscular disorder induced neurotransmission defects at the neuromuscular junctions.MG is an autoimmune disease in which the autologous immune system,including the corresponding antibodies,immune cells and complement systems,attacks the cholinergic receptor(AChRs)of the postsynaptic membrane,resulting in weakness of skeletal muscle.A rare portion of MG cases is mediated with antibodies specific to muscle specific kinase(MuSK)and low-density lipoprotein receptor related protein 4(LRP4).The major clinical symptoms of MG are presented as weakness of skeletal muscle,fatigue prone,which are worsened after exercise.Adequate rest and treatment with cholinesterase inhibitors could significantly relieve and reduce the symptoms.The average onset rate is about 8-20 cases per 100,000 people.
基金supported by the New Clinical Technique or Program of Tangdu Hospital in 2013,2014.
文摘Neuromyelitis optica(NMO)is an autoimmune demyelinating disease that mainly affects the optic nerve and spinal cord,potentially resulting in blindness and paralysis.Once thought to be a clinical variant of multiple sclerosis,NMO is currently considered as a different disease with its own features due to the identification of a specific autoantibody against aquaporin 4.Given the high risk of disability,treatment should be launched once the diagnosis is established.Evidence from clinical practice showed that traditional immunosuppressive agents affecting the function of T and B cells could attenuate disease exacerbation.Recently,with better understanding pathogenesis of NMO,increasing bodies of novel therapies and therapeutic targets have been discovered.In this review,the authors discuss the current strategies of treating NMO in details and briefly introduce the potential therapies in future.
基金This work was supported by the National Natural Science Foundation of China(Nos.31200665,31270952 and 81301069).
文摘Myasthenia gravis(MG)is an acquired autoimmune disease affecting synaptic transmission via the neuromuscular junction mainly due to the presence of auto-antibodies targeting acetylcholine receptors.Ocular or generalized MG is clinically diagnosed when the extra-ocular muscles or other muscle groups beyond the extra-ocular muscles are involved.MG occurs in both sexes at any ages from all races but shows a wide variability in incidence and prevalence.Differences in clinical phenotypes of MG patients between West and East countries have been observed.Herein,we review the current concept on epidemiology,classification,and generalized progression in MG,mainly focusing on the differential features from China's Mainland.