No abstract

Based on the available data, we speculated that changes in brain iron metabolism induced by L-DOPA might be associated with the neurotoxicity of L-DOPA. To investigate this possibility, the effects of L-DOPA on the expression of iron influx proteins [transferrin receptor (TfR) and divalent metal transporter 1 (DMT1)], iron efflux protein (ferroportin 1), and iron uptake in C6 glioma cells were determined in this study using Northern blot and Western blot analysis and the calcein method. The findings showed that treatment of C6 cells with different concentrations of L-DOPA (0 -100 M) did not affect the expression of mRNA and protein of TfR and DMT1 with iron-responsive element (ϩIRE) and protein of ferroportin 1. However, a significant increase in the expression of DMT1(ϪIRE) mRNA and protein was found in cells treated, respectively, with 10 and 30 M L-DOPA (mRNA) and 1, 5, 10 and 30 M L-DOPA (protein). The increase in DMT(ϪIRE) protein induced by L-DOPA treatment was in parallel with the increase in DMT(ϪIRE) mRNA. The levels of DMT1(ϪIRE) mRNA and protein peaked in the cells treated with 10 M L-DOPA and then decreased progressively with increasing concentrations of L-DOPA. Further study demonstrated that treatment of the cells with 10 M L-DOPA induced a significant increase in ferrous uptake by C6 glioma cells. The findings suggested that the increased DMT1(ϪIRE) expression might be partly associated with the neurotoxicity of L-DOPA. Clinical relevance of the findings needs to be investigated further.Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized mainly by degeneration of dopamine-containing neurons. The affected sections of the brain are therefore deprived of adequate amounts of the neurotransmitter dopamine (Foley, 2000). Because dopamine itself cannot access the brain directly, its natural precursor, L-DOPA, is used in clinical treatment of patients with PD. L-DOPA remains the most effective treatment for the symptomatic control of PD (Dunnett and Björklund, 1999;LeWitt and Nyholm, 2004). However, it was reported that long-term administration of high oral doses could cause drug-induced involuntary movements, on-off fluctuation of efficacy, and dyskinesias (Jenner and Brin, 1998;Foster and Hoffer, 2004).The causes of the long-term side effects caused by L-DOPA treatment of PD are not yet completely known. Based on available data, we speculated that changes in brain iron metabolism induced by L-DOPA might be associated with neurotoxicity or side effects of L-DOPA. First, it has been suggested that changes in trace metal concentrations in the brain may be related to the long-term toxicity of L-DOPA (Weiner et al., 1978). Second, a clinical study (Boll et al., 1999) demonstrated that L-DOPA can significantly affect brain ceruloplasmin, a major factor in the regulation of regional brain iron content and that cerebrospinal fluid ferroxidase (CP) in L-DOPA-treated patients with PD was significantly higher than that in patients with PD who were not This work was supported ...

Allergic anaphylactic (type I) reactions to corticosteroid medications are uncommon; however, a number of well-documented cases have been reported. We present a review of the literature, and report on two patients who suffered anaphylaxis after injections of corticosteroids. The first patient, a registered nurse, was finally found to be sensitive to all corticosteroid preparations containing carboxymethylcellulose, as well as the pure carboxymethylcellulose. The second patient had positive skin tests to hydrocortisone, hydrocortisone sodium succinate, methylprednisolone sodium succinate, and suxamethonium. Both patients were tested on two occasions; four normal subjects were tested in parallel, and did not elicit any positive skin reaction. In patients with systemic severe reactions to injectable corticosteroids, we recommend careful and comprehensive skin testing with most available corticosteroids, as well as the components of the injectables.

No abstract

It has been difficult to confirm that a given building is responsible for allergic symptomatology, exacerbation of asthma, or immunological dysfunction. In fact, in most studies, few objective immunological parameters have been studied and only rarely has there been any quantitation of IgE or secondary mediators. Furthermore, although many studies deal with rhinitis or respiratory tract irritation, there is a misconception that all such symptoms are allergic in nature, and studies attempting to prove that allergies are caused by buildings frequently neglect to prove that these are indeed true allergic responses. In addition, many of the symptoms that people attribute to sick building syndrome (SBS) or building-related illness, such as headaches, dizziness, fatigue, nausea, cough, and eye irritation, are subjective, and studies often fail to take into account other possible causes that may be inherent in the subjects, such as sinusitis, hyperventilation syndrome, or psychosomatic illness. Unfortunately, most clinical studies on SBS pay little attention to the preexisting conditions that a subject may have and discount the possibility that the inciting agent does not cause symptoms, but merely exacerbates a preexisting condition. Moreover, they offer no information about the nature of the mechanisms of action or pathophysiological relationships. Clearly, further studies are necessary to further explain the complexity of complaints that currently exist. Indeed, SBS might properly be paraphrased as "what is it?--if it is!"