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991.
Expression of mRNA for c-kit receptors and their ligands was examined in the cerebellum of mice by in situ hybridization technique. The c-kit receptors were expressed in the molecular layer of the cerebellum and the ligands for the c-kit receptors were detected at the boundary of molecular and granular layers. The expression of the c-kit ligands was not detectable in the cerebellum of lurcher (Lc/+) mutant mice that lack Purkinje cells, indicating the cells expressing the c-kit ligands were Purkinje cells. The cells expressing c-kit receptors decreased but were present in the cerebellum of Lc/+ mice. The c-kit mRNA-positive cells appeared to represent basket cells and stellate cells from their appearance and location. Since neurons in the molecular layer construct suppressive neurojunctions with Purkinje cells, the present result suggests that c-kit receptors and their ligands may play an important role for the construction of their junctions.  相似文献   
992.
A 74 year-old woman, who had been diagnosed as AML (M3) in poor condition, was treated with Retinol Palmitate (Chocola-A, 150,000 unit/m2 per os, after informed consent. An increase of white blood cells (neutrophil) counts was observed after 7 days. After 4 weeks, WBC counts were increased to 20,700/microliters (neutrophil counts 6,400/microliters) Maturation tendency of leukemic cells was also proved in the bone marrow. In vitro studies showed that morphological differentiation was recognizable in cultured leukemic cells treated with 10(-6)M all-trans retinoic acid after 6 days, but not in controls. Responses in the NBT reduction test were slightly less than in the clinical study. The administration of Retinol Palmitate may be a new regimen to treat AML (M3) in aged patients in poor condition.  相似文献   
993.
From the brain slices of normal mice (ddY strain, subcloned from dd strain in National Institute of Health in Japan), N-methyl-D-aspartic acid (NMDA) at 0.01-1 mM evoked [3H]acetylcholine (ACh) release in a concentration dependent manner. [3H]ACh release evoked by 1 mM NMDA was significantly inhibited by 2-amino-5-phosphonovaleric acid (APV), phencyclidine (PCP) and 5-methyl-10,11-dihydroxy-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801). The effects of NMDA were not seen in the Ca2+ free medium and were inhibited by physiological concentration (0.83 mM) of Mg2+. NMDA seems to cause ACh release from nerve terminals through the receptor-ion channel mediated mechanism in the mouse brain. Based upon these results, we determined the activity of a high K(+)- or NMDA-evoked [3H]ACh release using prone/8 strain of senescence-accelerated mouse (SAM-P/8) (a murine model of accelerated aging and memory dysfunction) and SAM-resistance/1 strain (SAM-R/1) (normal aging mice as the control) and these release activities were compared between both strains and during aging. [3H]ACh release evoked by 30 mM KCl was significantly lower than that of age-matched SAM-R/1 at 9 and 12 months. NMDA evoked the [3H]ACh release at 2, 6, 10 and 14 months in R/1 mice. In SAM-P/8 mice the activity of NMDA-evoked release was seen at 2 months, but markedly decreased afterwards. Nonsignificant difference was observed on the uptake of [3H]choline and on the spontaneous release of [3H]ACh between SAM-P/8 and SAM-R/1 strains, and during aging.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   
994.
As a complication of atopic dermatitis (AD), the incidence of hypoproteinemia is increasing among infants with severe AD in Japan. It can be a life‐threatening condition owing to hypovolemic shock as a result of hypoproteinemia and vascular infarction as a result of thrombocythemia. However, the pathophysiology of this condition remains unclear. The objectives of the present study were two‐fold. The first objective was to determine the main route of protein loss, i.e. through the damaged skin or the gastrointestinal tract, or as a result of insufficient food intake. The second objective was to identify whether allergy or infection was the cause of severe skin inflammation. Fifteen patients with AD were enrolled who had serum protein levels of 3.2–5.8 g/dl. Specific immunoglobulin E (IgE) and skin test to allergens, stool eosinophils, α1‐antitrypsin clearance, skin Staphylococcus aureus colonization and superantigens (SAgs) produced by the organism, serum SAg‐specific IgE antibodies, serum interleukin (IL)‐5, IL‐6, IL‐12, and interferon‐γ (IFN‐γ) were evaluated. Prominent serous skin discharge was seen in all of the patients and was found to have almost the same protein concentration as serum. Marked thrombocytosis, with a maximum of 1,060 × 103/ml, was seen. Skin culture revealed S. aureus colonization in all patients. SAg‐producing S. aureus were found in 84.6% of the patients. The concentration of serum IL‐5 was significantly increased and correlated well with the blood eosinophil count. Hence, the main route of protein loss was believed to be through damaged skin. The cause of severe inflammation was thought to be a combination of allergic inflammation and skin colonization by SAg‐producing S. aureus. Serum cytokines showed a T helper 2 (Th2) T‐cell‐mediated pattern. To prevent hypovolemic shock, vascular occlusion, and growth retardation, it is of vital importance to diagnose hypoproteinemia at an early stage and start appropriate therapy.  相似文献   
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997.
A 46-year-old female with primary cervical carcinoid is reported. She was well with no recurrence for more than 5 years after surgery and radiation therapy. Pathologically, the tumor was composed of solid nests including rosette-like structures and tubular formations. Multiple argyrophil granules and a few argentaffin granules were revealed histochemically and serotonin was demonstrated by formalin-induced fluorescence.  相似文献   
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(Received for publication on Apr. 7, 1997; accepted on Nov. 6, 1997)  相似文献   
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