Release of IL-4 and IL-5 from human peripheral blood mononuclear cells co-cultured with Japanese cedar pollen antigen in vitro.

The Japanese cedar pollen (JCP) is a major allergen with respect to pollinosis in Japan. It is believed that interleukin-4 (IL-4) and interleukin-5 (IL-5) derived from lymphocytes and other cells play a pivotal role in allergic reactions. We investigated whether the JCP antigen stimulates the release of these cytokines by peripheral blood mononuclear cells (PBMCs). PBMCs from eight adults (five adults with JCP pollinosis and three adults without JCP pollinosis) were co-incubated with purified JCP antigens. IL-4 was released in response to JCP antigens in six of the eight subjects at 24 h and in three subjects at 48 h. IL-4 release at 24 h occurred in all five subjects with JCP pollinosis but in only one of the three subjects without pollinosis. IL-5 was released in response to the JCP antigen in five of the eight subjects at 24 h and 48 h, including four of the five subjects with JCP pollinosis and one of the three subjects without pollinosis. These results suggest that PBMCs were more likely to release IL-4 and IL-5 in the presence of JCP pollinosis.

Holoprosencephaly: an analysis of callosal formation and its relation to development of the interhemispheric fissure.

PURPOSE: To correlate the degree of hemispheric fusion in holoprosencephaly with degree of callosal formation, with degree of thalamic and basal ganglia fusion, and with presence or absence of dorsal cyst. METHODS: MR, CT, and ultrasonography from 19 patients with holoprosencephaly was retrospectively reviewed. The imaging studies were graded according to extent of the hemispheric fusion, thalamic fusion, corpus striatum fusion, callosal formation, and the presence or absence of a dorsal cyst. These factors were statistically correlated with each other using Kendall rank correlation coefficient. RESULTS: There were significant correlations between hemispheric fusion and failure of corpus callosum formation, presence of dorsal cyst and failure of corpus callosum formation, and hemispheric fusion and presence of dorsal cyst. Additional correlations were noted between thalamic fusion and corpus striatum fusion. CONCLUSIONS: Our results suggest that the presence of an interhemispheric fissure is necessary for callosal formation, and the presence of a dorsal cyst may interfere with callosal formation in holoprosencephaly.

Amyotrophic lateral sclerosis: T2 shortening in motor cortex at MR imaging.

PURPOSE: To determine whether decreased signal intensity of the motor cortex (T2 shortening) at magnetic resonance (MR) imaging is a useful finding for supporting the diagnosis of amyotrophic lateral sclerosis (ALS). MATERIALS AND METHODS: High-field-strength (1.5-T) MR images of 15 patients (seven men and eight women, aged 28-80 years) and 49 neurologically normal age-matched control patients were examined for T2 shortening in the motor cortex. In addition, brains of patients with ALS were examined at autopsy. RESULTS: The MR images of 14 of the 15 patients showed T2 shortening in precentral cortices, while the images of all but one of the control patients showed no such finding. In three of eight brains at autopsy, sections from the precentral cortex showed sparsely distributed, intensely stained astrocytes and macrophages. CONCLUSION: Abnormal iron deposition associated with the degenerative process could be the source of T2 shortening, which is a useful MR imaging finding in the diagnosis of ALS.

[MR imaging of amyotrophic lateral sclerosis].

Magnetic resonance imaging (MR imaging) provides a sensitive method for mapping the normal and pathological distribution of iron in the brain. High field strength MR imaging (1.5 T) was used to evaluate eight patients with amyotrophic lateral sclerosis (ALS) and 49 neurological normal control patients. All eight ALS patients showed decreased signal intensity in the motor cortex on T2-weighted images, while only one of the normal control patients showed this finding. The results suggested that the decreased signal intensity in the motor cortex in ALS was caused by the deposition of iron in this area.