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encephalitis/tyrosine

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ČlanciKliničkim ispitivanjimaPatenti
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Tyrosine kinase inhibitors attenuate Japanese encephalitis virus-induced neurotoxicity.

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The cellular signaling molecules that underlie Japanese encephalitis virus (JEV)-induced inflammation and neurotoxicity are not well understood. We examined whether protein tyrosine kinase (PTK) inhibitors play roles in JEV replication and cytopathic effect in neuron/glia cultures. JEV infection

Japanese encephalitis virus infection stimulates Src tyrosine kinase in neuron/glia.

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Japanese encephalitis virus (JEV) is a neurotropic virus. The clinically manifestation of JEV-induced encephalitis is characterized by the brain inflammation and neuronal dysfunction and/or destruction. Currently, the cellular signaling molecules that underlie JEV-induced cerebral inflammation and
Two mosquito STATs, AaSTAT and CtSTAT, have been cloned from Aedes albopictus and Culex tritaeniorhynchus mosquitoes, respectively. These two STATs are more similar to those of Drosophila, Anopheles, and mammalian STAT5 in the DNA binding and Src homology 2 domains. The mRNA transcripts are
Japanese encephalitis virus (JEV), a mosquito-borne flavivirus that causes severe human disease, has been shown to block the interferon (IFN)-induced Janus kinase signal transducer and activation of transcription (Jak-Stat) signaling cascade by preventing Tyk2 tyrosine phosphorylation and Stat

Susceptibility of naïve and differentiated PC12 cells to Japanese encephalitis virus infection.

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Japanese encephalitis is a mosquito-borne disease caused by Japanese encephalitis virus (JEV) infection. Although JEV infects and replicates in cells with multiple tissue origins, neurons are the preferential cells for JEV infection. Currently, the identities of JEV cell tropism are largely unclear.
We analyzed two disease model groups with rats infected by Japanese encephalitis virus (JEV), a 90-day group and a 180-day group after JEV infection. The time measured by the modified pole test showed that motor activities in these two groups were slower than those of age-matched control groups.

A rat model of Parkinson's disease induced by Japanese encephalitis virus.

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In Fischer rats infected with Japanese encephalitis virus (JEV) at 13 days after birth and sacrificed 12 weeks later, the major pathological changes resembled those found in Parkinson's disease. Specifically there was neuronal loss with gliosis which was confined mainly to the zona compacta of the

Amebic Encephalitis in a Patient with Chronic Lymphocytic Leukemia on Ibrutinib Therapy.

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Chronic lymphocytic leukemia (CLL) is the most common type of leukemia in Western countries. A common first-line therapy offered to qualifying patients includes ibrutinib, an oral covalent inhibitor of Bruton's tyrosine kinase. Treatment of CLL with ibrutinib therapy is generally well tolerated;

Association of platelet-derived growth factor-B chain with simian human immunodeficiency virus encephalitis.

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Chemokines and cytokines play a critical role in HIV infection, serving both to modulate virus replication and to recruit target cells to the site of infection. Platelet-derived growth factor (PDGF), a mitogen and chemoattractant for a wide variety of cells, is secreted by macrophages. Since
Isatin, an endogenous monoamine oxidase (MAO) inhibitor, has an important role in the control of neurotransmitter concentration. We previously reported that exogenously administered isatin significantly increased acetylcholine (ACh) and dopamine (DA) levels in the rat striatum. In order to test the

Neurotransmitter synthesizing enzymes in experimental viral encephalitis.

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Stereotactic intracerebral inoculation of a non-neuroadapted strain of herpes simplex virus type 1 into the left neostriatum of Sprague-Dawley rats induced clinical acute encephalitis within 3 to 5 days postinoculation, with microscopic evidence of inflammation in brain parenchyma, but with no gross

Inhibition of tyrosine hydroxylase expression within the substantia nigra of mice infected with canine distemper virus.

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Experimental infection of mouse brain with a neuroadapted strain of canine distemper virus (CDV) leads to early acute encephalitis, followed by late neurological diseases such as motor pathologies (paralysis and turning behavior) or obesity syndrome. We have previously shown that, during the early
Thyrotropin-releasing hormone (TRH) has been reported to have some possibilities toward the treatment of affective CNS disorders. However, long term treatments with daily injections are often required. Effects of TRH-SR (sustained release microspheres of TRH) which is encapsulated in copoly

Fulminant Acanthamoeba castellanii Encephalitis in an Ibrutinib-Treated Patient.

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We report a case of fulminant Acanthamoeba castellanii encephalitis in a patient with chronic lymphocytic leukemia treated with ibrutinib. The unusually rapid neurologic decline and fatal outcome observed are probably related to alterations in immunologic function associated with inhibition
Background: Given the active research on targeted therapy using tyrosine kinase (TK) inhibitors (TKIs) in the field of oncology, further studies have recently been conducted to evaluate their use in autoimmune disorders. Based on
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