Severe Graves' ophthalmopathy accompanied by myasthenia gravis]

We report a 53-year-old woman with severe Graves' ophthalmopathy accompanied by uncontrolled myasthenia gravis. She presented remarkable exophthalmos, chemosis, and restriction of eye movement. Despite plasma exchange, steroid pulse therapy, local injection of steroid, and irradiation, ocular symptoms did not ameliorate. Since optic neuropathy was seen, orbital decompression surgery was performed in the left eye. Bilateral chemosis was improved after the surgery. Five years after surgery, there was no ocular palsy in the operated left eye, but in the contralateral eye. For the good prognosis of the eye movement, orbital decompression might be recommended in the severe Graves' ophthalmopathy accompanied by the optic neuropathy and/or ophthalmoplegia with proptosis.     

Effects of subacute toluene exposure on neuronal and glial marker proteins in rat brain

The behavior of marker proteins of neurons (gamma-enolase) and glial cells (alpha-enolase, beta-S100 protein and creatine kinase-B) was investigated quantitatively by using enzyme immunoassay systems in toluene-exposed rat brains. Three groups of animals were exposed to toluene vapor at 300 ppm, 1000 ppm, and 3000 ppm, respectively, 8 h/day, 6 days/week, for 2 weeks. After subacute repeated solvent exposure, both neuron-specific gamma-enolase and glial marker proteins displayed an overall concentration-dependent increase tendency in separate brain regions. In cerebrum, only the 3000 ppm group showed a significant increase in alpha-enolase by 27% and creatine kinase-B (CK-B) by 26%. alpha-Enolase and gamma-enolase exhibited a pronounced elevation in cerebellum relative to other brain regions, while beta-S100 protein appeared to be the most markedly altered marker in brainstem. The development of gliosis, which is a frequent phenomenon following CNS damage, is presumed to be responsible for the elevation of glial marker content. Energy metabolism disruption in brain tissues may also bring about the compensatory oversynthesis of glycolytic enzymes such as gamma-enolase, alpha-enolase and CK-B. The dose-dependent alteration patterns following toluene exposure suggest the feasibility of using these brain specific markers to evaluate solvent-induced CNS effects.     

Heat shock protein hsp72 induction in cortical and striatal astrocytes and neurons following infarction

Transient global and transient focal ischemia induced the 72 kDa heat shock protein (hsp72) in neurons in cortex, striatum, and other regions known to be injured during transient ischemia. A novel finding was the induction of hsp72 in islands (cylinders in three dimensions) of cells composed of astrocytes around the perimeter and neurons in the interior. Since histology showed pale staining in these regions, it is proposed that these islands represent areas of focal infarction in the distribution of small cortical and lenticulostriate arteries. Although the factors responsible for hsp72 induction during ischemia and infarction are unknown, these results suggest differences in mechanisms of hsp72 induction in astrocytes compared to neurons.     

Germinoma with granulomatous reaction arising from the corona radiata; case report and review of articles]

We report a rare case of germinoma with granulomatous reaction arising from the corona radiata. This 20-year-old man was admitted to our hospital complaining of progressive motor weakness on the right side. CT demonstrated a poorly demarcated high density area in the left corona radiata, which was heterogeneously enhanced after administration of contrast medium. Moreover, the continuity of the mass to the ventricular wall was confirmed on MRI. At the first operation, subtotal removal of the tumor was performed through a fronto-parietal craniotomy. The diagnosis for the specific neoplasm was not established histologically, but granuloma caused by fungal infection was the most likely cause of the lesion. We tried amphotericin B (AmB), and remission of the tumor was obtained. However, during the following 3 months, the size of the tumor gradually enlarged again. AmB was repeatedly administered, but this time the treatment was ineffective. Six months later, on May 21, 1990, the second operation was performed and histological examination revealed typical germinoma consisting of two-cell pattern. Subsequently, the patient underwent focal irradiation of 33 Gy to the tumor site, and the tumor completely disappeared. As intracranial germinomas are observed to be successfully cured by radiotherapy and/or chemotherapy, choice of the therapeutic management must be carefully determined according to the histological diagnosis, especially in young people. A variety of locations of germinomas and the accompanying granulomatous reactions could create some diagnostic confusion, so great care must be taken in the treatment of much intracranial germinomas.     

Transfer of occupational health problems from a developed to a developing country: Lessons from the Japan–South Korea experience

Many corporations move their manufacturing facilities or technologies from developed to developing countries. Stringent regulations have made it costly for industries to operate in developed, industrialized countries. In addition, labor costs are high in these countries, and there is increasing awareness among the general public of the health risks associated with industry. The relocation of hazardous industries to developing countries is driven by economic considerations: high unemployment, a cheaper labor force, lack of regulation, and poor enforcement of any existing regulations make certain countries attractive to business. The transfer of certain industries from Japan to Korea has also brought both documented occupational diseases and a new occupational disease caused by chemicals without established toxicities. Typical examples of documented occupational diseases are carbon disulfide poisoning in the rayon manufacturing industry, bladder cancer in the benzidine industry, and mesothelioma in the asbestos industry. A new occupational disease due to a chemical without established toxicities is 2‐bromopropane poisoning. These examples suggest that counter‐measures are needed to prevent the transfer of occupational health problems from a developed to a developing country. Corporate social responsibility should be emphasized, close inter‐governmental collaboration is necessary and cooperation among non‐governmental organizations is helpful. Am. J. Ind. Med. 52:625–632, 2009. © 2009 Wiley‐Liss, Inc.     

Effects of MEK on kinetics ofn-hexane metabolites in serum

The neurotoxicity ofn-hexane is thought to be caused ultimately by 2,5-hexanedione (2,5-HD), one of then-hexane metabolites. The potentiation ofn-hexane neurotoxicity by co-exposure with MEK, therefore, is suspected to be related to kinetics of 2,5-HD in blood. To clarify the kinetics ofn-hexane metabolites in the mixed exposure ofn-hexane and MEK, rats were exposed to 2000 ppmn-hexane or a mixture of 2000 ppmn-hexane and 2000 ppm MEK, and the time courses of serumn-hexane metabolites were determined. 2,5-HD in serum increased until 2 h after the end of exposure, when serum 2,5-HD concentration reached a peak of 16.35 g/ml in then-hexane-alone group. In contrast, 2,5-HD in the mixed exposure group increased much more slowly during and after exposure than in then-hexane-alone group. It reached a peak of 2.12 g/ml at 8 h after the end of exposure. Serum MBK, a precursor of 2,5-HD in the co-exposure group, was about half in then-hexane-alone group during exposure. However, MBK decreased more slowly in the co-exposure group than in then-hexane-alone group after the end of the exposure. The results suggest that co-exposed MEK might inhibit oxidation ofn-hexane and decrease clearance ofn-hexane metabolites. Co-exposed MEK did not increase serum 2,5-HD, which was considered a main neurotoxic metabolite. Therefore the enhancement of neurotoxicity could not be attributed to increased serum 2,5-HD in the co-exposed group. The mechanism of enhancement of neurotoxicity ofn-hexane by MEK should be studied further.