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dyscalculia/homa

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NakalaMajaribio ya klinikiHati miliki
5 matokeo

Yellow fever vaccine-associated neurological disease, a suspicious case.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala
Ingia / Ingia
A 70-year-old man with known cardiovascular risk factors, presented with acute onset expression aphasia, agraphia, dyscalculia, right-left disorientation and finger agnosia, without fever or meningeal signs. Stroke was thought to be the cause, but cerebrovascular disease investigation was negative.

[Antiphospholipid syndrome with autoimmune hemolytic anemia which mimics thrombotic thrombocytopenic purpura].

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala
Ingia / Ingia
A 67-year-old woman was admitted to the hospital for lethargy, fever, hemolytic anemia, thrombocytopenia, and consciousness disturbance. Direct Coombs test was positive, and anti-cardiolipin beta2-glycoprotein I antibody was detected. She was diagnosed with antiphospholipid syndrome complicated with

[Multiple intracerebral enhanced lesions strongly suspected to be microsporidiosis. A case report].

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala
Ingia / Ingia
This case of microsporidiosis manifested as mutiple intracranial lesions separated in space and time, and neurological and radiological findings were improved with albendazole administration. A 33-year-old man presented with headache, fever, and dysphasia. His consciousness was clear. Neurological

Postmalaria neurological syndrome: two cases from the Gambia.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala
Ingia / Ingia
We describe 2 patients with severe Plasmodium falciparum malaria whose convalescence was complicated by fever, with acute confusion and acalculia in one patient and a triad of myoclonus, tremor, and dysphasia in the other. Inflammatory changes were found in cerebrospinal fluid samples. Postmalaria
Telomerase reverse transcriptase (TERT) is the protein component of telomerase complex. Evidence has accumulated showing that the nontelomeric functions of TERT are independent of telomere elongation. However, the mechanisms governing the interaction between TERT and its target genes are not clearly
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