Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This work is to study the ultrastructure of the neuronal lipofuscin that occurred in the brain and the spinal cord of an autopsy case of familial Alzheimer's disease and to compare with those in several other diseases. The patient was a 46-year-old male, whose father and elder brother were diagnosed as Alzheimer's disease and died at the age of 42, respectively. He became afflicted with forgetfulness and disorientation at the age of 36. He developed a grand mal seizure at the age of 39 and thereafter, his clinical course was characterized by pyramidal signs, dysarthria and the symptoms of Gerstmann's syndrome, visuo-spatial agnosia, apraxia for dressing and constructive apraxia. He became bedridden at 45 years old and died of general prostration. The brain weighed 1,250 g, and the cerebral cortex showed mild atrophy. The neuronal loss, senile plaques and Alzheimer's neurofibrillary tangles were found throughout the cerebral cortex. The senile plaques were also found in the basal ganglia, the cerebellar medulla and cortex. There was severe amyloid angiopathy in the occipital and cerebellar cortices. The specimens for electron microscopy were taken from the cerebral cortex, the basal ganglia, the thalamus, the midbrain, the medulla oblongata, the cerebellum and the spinal cord. The ultrastructural study revealed three different types of the neuronal lipofuscin, though different stainability between these lipofuscin granules could not be manifested by several histochemical methods. Their morphological differences seemed to be based on the sites of the central nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ultrastructural study of the neuronal lipofuscin--an autopsy case of familial Alzheimer's disease]. 648 35

All 302 children treated at the rheumatology clinic of a children's hospital in Santo Domingo between September 1985 and September 1986 were included in a prospective study of the causes of joint pain in children. The 137 girls and 165 boys were grouped in five categories according to the underlying condition. The largest group, reactive arthritic conditions, affected 78 patients (25.9%). 72 of the 78 had rheumatic fever. The second largest category, hematological processes, affected 75 patients (22.6%); 40 of the 75 patients had sickle cell disease, 25 had hemophilia or other conditions, and 8 had neoplasias. 63 patients (20.8%) had infectious processes, including 33 with septic arthritis, 17 with abscesses and cellulitis, 7 with arthritis and osteomyelitis, and 6 with osteomyelitis. Prostration and pain on movement were more pronounced in patients with septic arthritis. 42 children (12.6%) had collagen vascular disease. 32 had juvenile rheumatoid arthritis, 4 had lupus, 3 vasculitis, 2 dermatomyositis, and 1 each had scleroderma and erythum nodosum. 25 patients (8.2%) had a miscellaneous array of other conditions. Sickle cell disease or neoplasia were most likely when anemia was also present. Extreme prostration and signs of inflammation suggested infectious processes. The small joints were primarily affected in juvenile rheumatoid arthritis and sickle cell disease.
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PMID:[Causes of joint pain in children]. 1229 May 50

The authors report the clinical case of a 21-year-old man, with " straight back " syndrome, admitted due to prostration and fever. He developed acute pulmonary oedema and shock, caused by chordae tendineae rupture of a mixomatous and prolapsing mitral valve, with endocarditis. He had also a mixomatous tricuspid valve, reduced calibre distal thoracic aorta and celiac trunk stenosis. Mitral valve replacement and Vega annuloplasty were performed. This case illustrates the association between " straight back " syndrome and valvular and vascular disease and emphasizes that structural heart and vascular abnormalities may be present more often in these patients than previously anticipated.
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PMID:["Straight back" syndrome]. 2261 35