Effect of probiotic Bifidobacterium longum BB536 [corrected] in relieving clinical symptoms and modulating plasma cytokine levels of Japanese cedar pollinosis during the pollen season. A randomized double-blind, placebo-controlled trial.

Probiotic microorganisms have been shown to be effective in the treatment of allergic inflammation and food allergy, but their efficacy remains controversial. This study tested the effect of a yogurt supplemented with a probiotic strain Bifidobacterium longum BB536 in the treatment of Japanese cedar pollinosis (JCPsis). Forty subjects with a clinical history of JCPsis were given yoghurt either containing BB536 (BB536 yoghurt) or without BB536 (placebo yoghurt) at 2 X 100 g per day for 14 weeks, in a randomized, double-blind, placebo-controlled trial. Subjective symptoms and self-care measures were recorded daily and blood samples were taken before and during the intervention (at weeks 4, 9, and 14) to measure the blood parameter levels related to JCPsis. Yoghurt supplemented with BB536 significantly alleviated eye symptoms compared with placebo yoghurt (odds ratio 0.31; 95% confidence interval 0.10-0.97; p = 0.044). Although no statistically significant differences were detected, nasal symptoms such as itching, rhinorrhea, and blockage, as well as throat symptoms tended to be relieved with the BB536 yoghurt. BB536 tended to suppress the decreasing blood levels of interferon-gamma (IFN-y) and the increasing blood eosinophil rates; a significantly higher IFN-gamma level was observed for the difference from baseline at week 4. A decreased trend in the difference from baseline levels of JCP-specific IgE levels was also observed at week 4 in the BB536 group compared with the placebo group. In conclusion, these results suggest that intake of BB536-supplemented yoghurt may relieve JCPsis symptoms, probably through a modulating effect on Th balance.

Licorice-induced hypokalemic myopathy and hypokalemic renal tubular damage in anorexia nervosa.

A patient with a history of anorexia nervosa developed licorice-induced hypokalemic myopathy. With potassium replacement, high CPK blood level and myopathic signs returned to normal. However, the patient manifested persistent hypokalemia and impaired renal function to concentrate and acidify the urine. Renal biopsy demonstrated intense degeneration and vacuolation of tubules with a normal glomerus which was consistent with hypokalemic nephropathy. Prolonged hypokalemia in anorexia nervosa is sometimes attributed to surreptitious purging or taking diuretics, but it is necessary to check the urine pH, the urine-specific gravity, and the urine potassium level in order to find underlying renal damage even after hypokalemic myopathy is treated successfully.

[Guidelines of drug therapies for Parkinson's disease].

Treatment of Parkinson's disease has progressed steadily for the last decades after introduction of levodopa. For recovery of striatal dysfunction caused by loss of projecting nigral cells, supplementation of neurotransmitter dopamine (DA), facilitation of neural transmission by DA agonists and amantadine, suppression of acetyl-choline neurons, having antagonistic action to DA cells, are all effective especially at the early to middle stages of illness. As prevention of neuronal cell death in parkinsonian brain has not yet been succeeded, difficulties in treatment with symptom fluctuation and CNS side effects such as dyskinesia or psychic symptoms develop inevitably in the long course of evodopa treatment. Proper choice of drugs for parkinsonian core and accompanying symptoms and selection of methods of medication for maintenance of natural daily life activities are necessary for attainment of good QOL for whole time course of the disease.

A mutation in the ceruloplasmin gene is associated with systemic hemosiderosis in humans.

We identified a mutation in the ceruloplasmin (Cp) gene in a Japanese family with aceruloplasminemia, some of whose members showed extrapyramidal disorders, cerebellar ataxia, and diabetes mellitus. A post-mortem study of the proband revealed excessive iron deposition mainly in the brain, liver and pancreas. The G to A transition at the splice acceptor site introduces a premature termination codon at the amino acid position 991 by defective splicing, thereby truncating the carboxyl terminus of Cp in affected individuals. We conclude that the mutation in the Cp gene is associated with systemic hemosiderosis in humans.

[A case of midbrain and thalamic infarction showing Collier's sign in one side and blepharoptosis in the other side].

A 68-year-old man was admitted to the hospital complaining of aphasia and right hemiparesis. Neurological examination revealed aphasia, right hemiparesis and ataxia in the left upper extremity. He showed striking ocular symptoms: intense retraction of the right eyelid (Collier's sign), complete ptosis of the left eyelid which might conceal Collier's sign, marked upward gaze palsy and slight downward gaze palsy. Vertebral angiography and MRI revealed an infarction in the left medial area and the left crus cerebri in the upper midbrain, the left subthalamic area inferomedially extending from the adjacent area to the posterior commissure and the medial area in the left thalamus resulting from occlusion of the left mesencephalic artery. From these MRI findings and the reports on pathological findings of patients with Collier's sign, we suggest that damage in the posterior commissure or its adjacent area may be responsible for the sign. Upward gaze palsy is often associated with Collier's sign because fibers mediating upward gaze may decussate in the posterior commissure. Third nerve palsy is also associated with the Collier's sign in some patients. The mechanism creating Collier's sign may be a disturbance of inhibitory fibers leading to the motoneuron pool of the levator muscle in the posterior commissure or its adjacent area.

In vitro degradation of amyloid material by four proteases in tissue of a patient with familial amyloidotic polyneuropathy.

The effects of 4 proteolytic enzymes, alpha-chymotrypsin, bromeline, collagenase, and lysozyme on amyloid tissue sections from a patient with familial amyloidotic polyneuropathy (FAP) were evaluated. Degradation of amyloid fibrils was significant with alpha-chymotrypsin, moderate with bromeline and collagenase, and slight with lysozyme. All of these proteases except collagenase are used as oral mucolytics in humans. The possibility of their clinical usefulness in the treatment or prevention of the development of FAP is discussed.

Double encephalitis with herpes simplex virus and cytomegalovirus in an adult.

A 51-year-old housewife developed symptoms of a cold followed by high fever, delirium, coma, rigidity of extremity muscles, positive Babinski sign and generalized convulsions, while complement-fixing antibody titre to herpes simplex virus in the sera raised over 128 X and declined to 8 X in the course. She finally expired of bronchopneumonia following status epilepticus after 94 days of illness. Severe necrosis with extensive hemorrhage in the white matter was predominant in the temporal, insular and orbitofrontal cortex, thalamus and globus pallidus. Focal rarefaction of the cerebral cortex with a very few eosinophilic intranuclear inclusions in the oligodendroglia and nerve cells, nerve cell destruction in the substantia nigra with glial nodules and perivascular inflammatory cell cuffs were observed. Abundant cytomegalic inclusion cells, originating from hypertrophic astrocytes, were present in the necrotic areas of cerebrum as well as in the rarefied tissue in the subependymal layers of the brainstem and cerebellum. Electron-microscopic study of the cytomegalic cells demonstrated the presence of numerous virions in both nucleus and cytoplasm. Fortuitour infection of the brain by cytomegalovirus with necrotizing encephalitis by herpes simplex virus is unique. The cause of double viral infections and severe lesions by less virulent strains is discussed.