Our previous study showed that mice fed on a soft diet after weaning had reduced levels of brain-derived neurotrophic factor (BDNF) protein in the hippocampus after 3 months of age compared with mice fed on a hard diet. BDNF is one of the most effective promoters of neurogenesis in the hippocampus, and enhancement of BDNF production has been shown to enhance neural precursor cell proliferation in the dentate gyrus. We hypothesized that soft-diet feeding during development would reduce the proliferation rate of precursor cells, resulting in lower production of new neurons in the hippocampus. Male C57BL/6 mice pups were fed either a solid (hard-diet group) or powdered (softdiet group) diet starting at weaning. Three and six months after birth, mice of each group received intraperitoneal injections of bromodeoxyuridine (BrdU, 50 mg/kg body weight), twice a day for 3 consecutive days. After survival time of 1 day, 1 week, or 4 weeks, the mice were anesthetized and perfused transcardially. Newborn cells in the dentate gyrus were examined by immunohistochemistry using anti-BrdU antibody. In addition, phenotypically neuronal cells among the newborn cells were detected by immunofluorescent double labeling for BrdU and mature neuron-specific nuclear protein (NeuN) using anti-BrdU and anti-NeuN antibodies. Total number of BrdU-positive cells in the dentate gyrus was fewer in the 6-month-old mice than in the 3-month-old mice at any survival time investigated, and fewer in the soft-diet group than in the hard-diet group at 3 and 6 months of age. Neither soft-diet feeding nor aging affected ratio of phenotypically neuronal cells among newborn cells. These results indicate that insufficient mastication activity during development as well as aging restrains hippocampal neurogenesis in adulthood.
Liver disease is associated with an abnormal elevation of the plasma concentrations of the aromatic amino acids phenylalanine and tyrosine. The liver is the main site of aromatic amino acid metabolism, particularly the hydroxylation of phenylalanine to tyrosine and further tyrosine degradation. In the present study, we have examined the usefulness of the L-[1-
Our previous study showed that mice fed a soft diet after weaning had reduced synaptic connections in the hippocampal formation and impaired spatial learning ability after 3 months of age. We hypothesized that soft-diet feeding during development reduced levels of brain-derived neurotrophic factor (BDNF) protein in the hippocampus, resulting in lower synaptic densities in this region. Male pups of C57BL/6 mice were fed either a solid (hard-diet group) or powdered diet (soft-diet group), starting at weaning. Expression of BDNF protein in the hippocampus and cerebral cortex was evaluated quantitatively with enzyme-linked immunosorbent assay (ELISA) at 1, 3 and 6 months of age. Reduction in BDNF protein levels due to soft diet was detected markedly in the hippocampus of 3-and 6-month-old mice. On the other hand, a soft diet showed no significant effect on BDNF content in the cerebral cortex throughout the ages investigated. Immunohistochemistry of hippocampal formation in 3-month-old mice revealed that intensities of BDNF immunoreactivity in the dentate gyrus granule cell layer and CA1 and CA3 pyramidal cell layers appeared diminished in mice fed the soft diet compared with mice fed the hard diet. These results indicate that insufficient mastication activity during development reduces BDNF protein levels in the hippocampus and influences synaptic plasticity in this region.
A 37-year-old male, a poorly-controlled insulin-dependent diabetic patient, was admitted to our hospital with complaints of high fever and confusion. Laboratory data showed hyper glycemia, positive inflammatory reaction and liver dysfunction. Blood culture demonstrated Yersinia enterocolitica. Liver CT scan showed multiple low density areas. These data were consistent with a diagnosis of liver abscess secondary to Yersinia enterocolitica. He died of disseminated intravascular coagulation; subsequent autopsy confirmed the clinical diagnosis. Liver abscess secondary to Yersinia enterocolitica with septicemia is rare, but has been reported in compromised hosts. In the mechanism of this disease, the alimentary tract has been suggested to be the port of entry in most cases. (Internal Medicine 31: 1125-1127, 1992 Key words: sepsis, diabetes mellitus, serotype 03 antibody, hepatic encephalopathy Intr oductionWe treated a case of sepsis and multiple liver ab scesses due to Yersinia enterocolitica (Y.E) in an insulin dependent diabetes mellitus patient. In Japan, it is rare to find severe infection caused by Y.E., especially in adult patients. Case ReportA 37-year-old diabetic man was treated with insulin for ten years, but his diabetic condition was not well controlled. On September 27, 1986, he began to suffer from high fever and diarrhea; nausea, vomiting and mild disturbance of consciousness later developed, and he was admitted to our hospital on November 7, 1986. On admission, BP was 94/70 mmHg, body temperature was 37.4°C, and consciousness was confused. The patient's skin was dry; there were no other abnormal findings on physical examination.Laboratory data showed WBC 5800/mm3 (Band 3, Seg (Fig. 1) showed multiple round low density areas (2-5cm in diameter) in the bilateral lobes of the liver. Ultrasound also showed multiple clear margins around hypoechoic lesions. These data suggested liver abscesses secondary to Y.E. with septicemia. Chemo therapy was started with ceftizoxime (CZX) 6g/day; piperacillin (PIPC) 4 g/day was later added. Neurological signs (flapping tremor, confusion and dyscalculia) were thought to be caused by hepatic encephalopathy. Lactulose and aminoleban were administrated, and the patient's serum ammonia level decreased, but the disturbance of consciousness did not show any improvement. Spike fever continued and serum albumin decreased to 0.9 g/dl.Generalized edema, pulmonary effusion, ascites and jaundice developed. Diuretics and frozen fresh plasma were administered, but hypoalbuminemia, generalized edema, and pulmonary effusion failed to improve. On the 17th day after admission, gastrointestinal bleeding occured. He died of disseminated intravascular coagu lation (DIC) and pulmonary edema on the 29th day after admission.
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