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Biomedical subjects

M Saeki

Publications and source records attributed to M Saeki.

At least 145 records · Page 8Linked to original sources
PubMed1982

Movement disorders of familial neuroacanthocytosis syndrome.

Characteristic movement disorders were observed in two siblings who had neuroacanthocytosis syndrome with normal serum lipoprotein levels. The disorders included orolingual tic-like movements associated with vocalization, biting of the lip and tongue, peculiar dysphagia with bird-like drinking, and postural lapse with abrupt buckling of the knees. In addition, subtle features of parkinsonism and chorea were observed. These movement problems are strikingly similar to those described in cases of neuroacanthocytosis syndrome in several other familial and sporadic cases. Careful observations of these unusual movement disorders may provide a clue to the diagnosis of this rare syndrome.

Acanthocytes↗
PubMed1981

Delta waves in the EEGs of patients with intracerebral hemorrhage.

Localized polymorphic delta wave activity appears ipsilaterally in patients with intracerebral hematoma without a shift of midline structures, regardless of the location of hematoma. Appearance of delta wave slowing after thalamic bleeding is quite variable, however, and may produce localized slowing or unilateral diffuse polymorphic delta wave activity. Unilateral diffuse polymorphic delta wave activity is seen in patients with larger hematomas of 30 mL or more, which cause a shift of the midline structures. The shift of midline structures, including the hypothalamus and surrounding structures, is thought to be one of the main factors responsible for the production of unilateral responsible for the production of unilateral diffuse polymorphic delta wave slowing.

Brain Diseases↗
PubMed1977

Serum amylase isozymes in patients with chronic pancreatitis with hyperamylasemia.

In order to clarify the relationship between hyperamylasemia and clinical states in chronic pancreatitis, serum amylase isozymes were studied in 39 cases of chronic pancreatitis including 13 cases of alcoholic pancreatitis. Hyperamylasemia in chronic pancreatitis is generally due to high pancreatic type isoamylase (P-amylase) activity in acute exacerbation, sometimes accompanied by a transient elevation in salivary type isoamylase (S-amylase). On remission, however, hyperamylasemia due to high S-amylase activity has been found. These were cases of advanced alcoholic pancreatitis, which exhibited a characteristic pattern of low serum P-amylase and high serum S-amylase activities while the clearance ratio (Cam/Ccr) was normal despite high S-amylase activity. It should be noted that hyperamylasemia in chronic pancreatitis may be caused by high S-amylase activity in addition to high P-amylase activity, especially in alcoholic pancreatitis.

Amylases↗