Two new variants of the lipocalin allergen Bos d 2.

Allergens from various sources have been shown to comprise several isoforms. In the present study, a series of chromatographic steps was carried out to separate the lipocalin allergen Bos d 2 isoforms present in cow dander. Subsequent HPLC-MS-MS analyses revealed two new Bos d 2 variants. In one of the proteins, tyrosine (Y83) was substituted by aspartic acid, and in the other protein valine (V102) was replaced by alanine. We propose the three Bos d 2 variants be named as Bos d 2.0101 (previously sequenced Bos d 2), Bos d 2.0102 and Bos d 2.0103. Our results suggest that molecular polymorphism is a common property among lipocalin allergens. Since allergen isoforms may show variation in their IgE binding and/or T-cell reactivity, all of the many allergen forms should be taken into account when planning preparations for immunotherapy.

Creatine kinase isoenzymes in acute brain injury.

Brain-type creatine kinase (CK) isoenzyme (CK-BB) was detected in the serum in 13 out of 26 patients with acute brain injury (50%). The peak of CK-BB activity ranged from 5 to 188 U/liter, constituting, on average, 10.5% of the total CK activity. The highest activities were seen in patients with gunshot wounds. High CK-BB activity was associated with poor prognosis, but minimal CK-BB elevations did not have prognostic significance. Heart-type creatine kinase isoenzyme (CK-MB) was detected in the serum in 17 out of 26 patients (65%). The peak activity ranged from 5 to 115 U/liter, constituting, on average, 6.6% of total CK activity. Electrocardiogram taken from 20 patients revealed transient T-wave inversions in the precordial leads in four patients; three of them also showed serum CK-MB activity. Subendocardial hemorrhage was detected at autopsy in three of the five CK-MB-positive patients, but in none of the four CK-MB-negative cases. Present findings suggest that acute brain injury may be secondarily cause myocardial damage.

The effect of gemfibrozil on serum lipids in diabetic patients.

The effect of gemfibrozil, a new hypolipidaemic compound, on serum lipids, lipoproteins and ophthalmic signs was studied in 20 diabetics during a 28 week trial. Ten of the patients were taking oral hypoglycaemic agents and another ten insulin. Genfibrozil elevated the proportion of alpha-lipoproteins (HDL) (P less than 0.005) in patients on oral agents to the same level as in those using insulin, who experienced no change in HDL. The pre-beta-lipoprotein proportion (VLDL) decreased (P less than 0.001) along with the serum triglyceride level in patients on oral agents only. The proportion of beta-lipoproteins (LDL) remained unchanged in both groups. The serum cholesterol and total lipid levels decreased significantly whether the patients were on oral treatment or insulin. The gemfibrozil was well tolerated. A minor increase in diabetic therapy was made in 9 patients in order to control the blood sugar levels. The ophthalmic signs were generally unchanged.

Myasthenia gravis and monoclonal IgG gammopathy.

Monoclonal IgG gammopathy of the lambda light-chain type was detected in a 51-year-old woman who had unexplained fever, muscle fatigue, and myalgia. One year later, myasthenia gravis was diagnosed. There was no evidence of myelomatosis or other malignancy. On the assumption that her M-component (gammopathic paraprotein) was related to myasthenia, she was treated with melphalan and cyclophosphamide, but her clinical condition was not improved. Despite therapeutic trials of other agents and a time course of 6 years, the quantity of the M-component remained unchanged. Serum AChR antibody activity was not located in the paraprotein peak. The findings do not support a relationship between the M-component and myasthenia gravis.

Heart type creatine kinase isoenzyme (CK MB) in acute cerebral disorders.

Heart type creatine kinase isoenzyme (CK MB) was detected in the serum in 23 out of 53 patients (43%) with acute cerebrovascular, traumatic, or infectious brain damage. Electrocardiogram disclosed abnormalities suggestive of acute myocardial injury in 15 of these 23 patients. Eleven of them also showed increased LD1 activity. Subendocardial haemorrhage was detected in 3 out of 8 necropsied patients with serum CK MB activity. Among those 30 patients in whom no CK MB activity was found electrocardiographic abnormalities suggestive of acute myocardial injury were observed in 2 and increased LD1 was seen in 4 cases. The mortality was higher if either CK MB isoenzyme or electrocardiographic abnormalities suggestive of acute myocardial injury were present, compared with the patients lacking these signs (P less than 0.01). Present findings suggest that acute brain damage may secondarily cause myocardial damage more often than has been believed before. Results also indicate that a combination of acute brain damage and acute myocardial injury often indicated a poor prognosis.

A new cause of increased serum aspartate aminotransferase activity.

Two healthy young women had an unexplained persistent elevation of aspartate aminotransferase (ASAT) activity. In both cases electrophoresis of serum ASAT isoenzymes displayed an abnormally moving fraction that comprised the whole serum activity, while liver and muscle revealed the normal cytoplasmic and mitochondrial isoenzymes. In the first case serum ASAT was found to be bound by serum IgG, in the second case the binding protein remained unidentified.

Accurate determination of serum ASAT isoenzymes.

An improved electrophoretic modification for measuring aspartate aminotransferase (ASAT) isoenzymes is presented. This method fulfils the clinical requirements for sensitivity and allows the detection of 1 U/l mitochondria ASAT activity at 25 degree C. The procedure is relatively simple, requiring about one hour for a series of 8 determinations. Mitochondrial ASAT activity was found in all patients suffering from acute myocardial infarction pathological activity was observed for several days longer than that of total serum ASAT enzyme. None of the 25 healthy people studied had mitochondrial ASAT in their serum.

Creatine kinase isoenzymes in the confirmation of acute myocardial infarction.

Serum MB isoenzyme of creatine kinase is the most specific and sensitive indicator of myocardial infarction. Despite these virtues, its clinical use is handicapped by rapid normalization after the onset of myocardial injury. In patients suffering brain accidents, the increase of serum CK-MB isoenzymes indicates stimultaneous myocardial damage and means poor prognosis.

Brain-type creatine kinase isoenzyme. Occurrence in serum in acute cerebral disorders.

Acute brain damage-cerebrovascular or cardiovascular, traumatic or infectious-released brain-type isoenzyme of creatine kinase (BB-CK) into the circulation within a few hours in 16 of 62 patients (26%). Occurrence of BB-CK was transient in the serum. BB-CK activity was found in the peripheral blood in 13 of 23 patients with diffuse brain damage compared to three of 39 patients with a local cerebrovascular accident (P less than .0005). The mortality of patients having BB-CK in their serum was 63% compared to 39% of those without BB-CK activity in their serum (P less than .05).

Brain creatine kinase in blood after acute brain injury.

Severe cold injury of the brain increased significantly both total creatine kinase and the corresponding brain isoenzyme (CKBB) activity in confluens sinuum samples. CKBB could be detected also in peripheral blood a few hours after severe brain injury in eight of 12 patients. Finding of CKBB in human plasma may prove a useful indicator of severe brain injury.