Decreased serum levels of epidermal growth factor in adult subjects with high-functioning autism.

BACKGROUND: The neurobiological basis for autism remains poorly understood. Given the role of growth factors in brain development, we hypothesized that epidermal growth factor (EGF) may play a role in the pathophysiology of autism. In this study, we examined whether serum levels of EGF are altered in adult subjects with high-functioning autism. METHODS: We measured serum levels of EGF in the 17 male subjects with high-functioning autism and 18 age-matched healthy male subjects. RESULTS: The serum levels of EGF in the subjects with high-functioning autism (72.4 +/- 102.8 pg/mL [mean +/- SD]) were significantly lower (Mann-Whitney U = 22.0, p < .001) than those of normal control subjects (322.3 +/- 122.0 pg/mL [mean +/- SD]). However, there were no correlations between serum EGF levels and clinical variables in the subjects with autism. CONCLUSIONS: This study suggests that decreased levels of EGF might be implicated in the pathophysiology of high-functioning autism.     

Quantitative evaluation of extracellular glutamate concentration in postischemic glutamate re-uptake, dependent on brain temperature, in the rat following severe global brain ischemia

Changes in brain temperature are known to modulate the marked neuronal damage caused by an approximately 10-min intra-ischemic period. Numerous studies have suggested that the extracellular glutamate concentration ([Glu](e)) in the intra-ischemic period and the initial postischemia period is strongly implicated in such damage. In this study, the effects of intra-ischemic brain temperature (32, 37, 39 degrees C) on [Glu](e) were investigated utilizing a dialysis electrode combined with ferrocene bovine serum albumin (BSA), which allows oxygen-independent real-time measurement of [Glu](e). This system allowed separate quantitative evaluation of intra-ischemic biphasic glutamate release from the neurotransmitter and metabolic pools, and of postischemic glutamate re-uptake in ischemia-reperfusion models. The biphasic [Glu](e) elevation in the intra-ischemic period did not differ markedly among intra-ischemic brain temperatures ranging from 32 to 39 degrees C. Intra-ischemic normothermia (37 degrees C) and mild hyperthermia (39 degrees C) markedly inhibited [Glu](e) re-uptake during the postischemic period, although the intra-ischemic [Glu](e) elevation did not differ from that during intra-ischemic hypothermia (32 degrees C). It was assumed that normothermia or mild hyperthermia in the intra-ischemic period influences intracellular functional abnormalities other than the intra-ischemic [Glu](e) elevation, thereby inhibiting glutamate re-uptake after reperfusion rather than directly modulating intra-ischemic [Glu](e) dynamics.     

An imported case of primary pulmonary coccidioidomycosis

Coccidioides immitis is a causative agent of coccidioidomycosis, which is one of the most dreadful mycosis because of its infectious and pathogenic nature. The endemic areas are in the southwestern parts of the United States and other semi-arid regions throughout the Western Hemisphere. During the early 1990s, the incidence of coccidioidomycosis in California increased dramatically, resulting in recognition for this mycosis as a reemerging infectious disease in the United States. The patients included a large number of non-informed visitors from non-endemic countries. Our report is on an imported case of primary pulmonary coccidioidomycosis. A 35-year-old Japanese male, after living in the United States for nine months, suffered from a combination of headache and fever. He was given a serological examination, and a chest radiograph in Phoenix, Arizona in the United States and was diagnosed as coccidioidomycosis. A daily dosage of 400 mg of fluconazole was administered and he returned to Japan. His headache and skin rash persisted and he was admitted to our hospital to evaluate the severity of his disease. There were no fungi cultured from neither bronchoalveolar nor cerebrospinal fluid and he was discharged. The patient had been treated with fluconazole and his symptoms, high-resolution CT and serological antibody titer were monitored. After 18 months, his clinical and radiological evolution was favorable and his serological IgM titer was below its sensitivity medication was stopped and there were no relapses.     

High correlation between results of the [1-13C]-phenylalanine breath test and phenylalanine hydroxylase (EC 1.14.16.1) activity of the liver in rats

BACKGROUND: (13)CO(2) is decreased in patients with end-stage liver disease by the [1-(13)C]-phenylalanine breath test. Decreased (13)CO(2) is supposed to be caused by the decreased ability of the liver to oxidize phenylalanine. However, no direct evidence has been reported. METHODS: The [1-(13)C]-phenylalanine breath test was performed in galactosamine hepatitis rats (n = 14) and control rats (n = 8). Plasma phenylalanine concentration before intravenous administration of [1-(13)C]-phenylalanine, the elimination rate of phenylalanine and the phenylalanine hydroxylase (PAH; EC 1.14.16.1) activity of the whole liver were examined. RESULTS: Increase of (13)CO(2) in the breath [Delta(13)CO(2) ( per thousand)] of galactosamine hepatitis rats 2 min after administration of [1-(13)C]-phenylalanine was only 1/5 of that in control rats. The concentration of plasma phenylalanine and the elimination rate of plasma phenylalanine in hepatitis rats did not show significant differences compared to control rats. On the other hand, a clear difference in the activity of PAH was observed between hepatitis rats and control rats. Delta(13)CO(2) ( per thousand) 2 min after administration of [1-(13)C]-phenylalanine was highly correlated to the PAH activity of the whole liver (r = 0.917). CONCLUSION: It was strongly indicated that decreased Delta(13)CO(2 ) in hepatitis rats was the result of decreased activity of PAH.     

Quantitative analysis of the Epstein-Barr virus-inducing properties of short-chain fatty acids present in the culture fluids of oral bacteria

Summary The culture fluids of various anaerobic bacteria induced the synthesis of early antigens (EA) in Epstein-Barr virus (EBV) carrying lymphoblastoid cells. The culture fluids ofCorynebacterium butyricum andFusobacterium nucleatum were the effective inducer on EA. The inducing activity was, to some extent, dependent on theirn-butyric acid content, but appeared to be regulated by yet unidentified materials.     

The utility of cerebrospinal fluid for the molecular diagnosis of toxoplasmic encephalitis

The aim of this study was to assess the efficacy of nested polymerase chain reaction (PCR) and the loop-mediated isothermal amplification (LAMP) assay, which were developed to detect and identify toxoplasma parasites in human cerebrospinal fluid (CSF). Nested PCR was performed using primers generated by Dr. L.D. Sibley to target the 18S rDNA instead of the conventionally used primers which target the B1 gene. We also designed Toxoplasma gondii–specific LAMP primers targeting both genes. In vitro detection sensitivity was evaluated using 10-fold serially diluted genomic DNA purified from RH tachyzoites, and clinical sensitivity and specificity were evaluated using clinical CSF samples from 16 patients with toxoplasmic encephalitis (TE) and from 12 patients with other diseases. The 18S rDNA nested PCR showed the highest detection sensitivity limit with a minimum of 1.0 × 10⁻⁸ ng/μL. However, sensitivity and specificity of nested PCR with clinical specimens were 50% and 100%, respectively. The sensitivity of molecular diagnosis of TE is not sufficient; therefore, patients clinically suspected of having TE should be treated promptly. Our molecular diagnostic tool would restrictively facilitate a definitive diagnosis of TE at an early stage in approximately 50% of patients.     

Ventricular septal defect with right pulmonary agenesis and left bronchial stenosis

We report a case of ventricular septal defect (VSD) with right pulmonary agenesis and left bronchial stenosis. Delivery of a male infant was uneventful. Birth weight was 3,050g. At 12 days of age, he presented himself with tachypnea and wheezing. Dextrocardia was noted on a chest X-ray. Computed tomography (CT) of the chest showed right pulmonary agenesis and severe narrowing of the left main bronchus. An echocardiogram showed VSD, patent ductus arteriosus (PDA) and pulmonary hypertension (PH). At 22 days of age, he was put on ventilator. At 1 month of age, pulmonary artery banding and division of PDA were performed through median sternotomy. At 5 months of age, weighing 5.0 kg, the VSD was closed with a Dacron patch through median sternotomy. At 6 months of age, tracheostomy was necessitated. At 1-year-old, he became free from ventilator.