46 research outputs found

    A reliable Differentiation of Mucor from Aspergillus in Tissue Sections with Ultraviolet Illumination

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    In tissue, hyphae of mucor are characteristically broad and infrequently septate. However, it may be difficult to distinguish mucor from aspergillus in tissue sections occasionally, because sometimes aspergillus septa are not detected with hematoxylin-eosin (HE), periodic acid Schiff (PAS ), and Grocott\u27s methenamine silver (GMS). In a case, aspergillus septa can be seen under ultraviolet light. Specifically, structures of these septum were clear cut differences in the histological finding between mucor and aspergillus with ultraviolet illumination. Therefore, we developed a new procedure for rapid and useful differentiation of mucor from aspergillus

    A Case of Primary Trabecular Carcinoid of the Ovary

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    A case of trabecular carcinoid originating in the left overy is presented. Clinically, no signs of carcinoid syndrome were noted. Various examinations including X-ray and CT, especially of gastrointestinal tracts and pelvic organs, revealed that the tumor mass is originated from the left ovary. Histologically, the resected tumor exhibited trabecular pattern of tumor cells, which contained numerous argentaffin and argyrophic granules. Immunostaining of NSE and calcitonin was strongly demonstrated in tumor cells. On ultrastructural examination, tumor cells had uniformly round shape granules, which were interpreted as neurosecretory granules. These findings clearly indicate that this neoplasm is primary trabecular carcinoid of the ovary

    Pathogenesis of Metastatic Calcification due to Hypercalcemia in Adult T-cell Leukemia-Lymphoma

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    Two cases of metastatic calcification due to hypercalcemia in adult T-cell leukemia-lymphoma (ATLL)associated with osteolytic change for activation of osteoclasts are reported. These cases of serum calcium were at a high level, 16.2 and 19.4mg/dl (normal range 8.4-10.4mg/dl). In our cases, metastatic calcification was detected in the tubules of kidneys, in the pulmonary alveolar septa of lungs, in the myocardium, in the muscular layer of stomach, in the lower portion of media of aorta, in the mucosa of stomach, in the tubules of testis, and in the liver by von Kossa\u27s silver nitrate method for calcium. Scattered osteoclasts were seen around the cortex of the bone. Roentgenograms showed osteolytic change in the skull, in the bilateral ulna, in the radius, in the humerus, in the tibia, and in the fibula. Therefore, hypercalcemia in ATLL may be caused by bone resorption-stimulating factors which promote the differeniation of osteocalast cells, resulting in calcium increases in the serum

    A local anesthetic, ropivacaine, suppresses activated microglia via a nerve growth factor-dependent mechanism and astrocytes via a nerve growth factor-independent mechanism in neuropathic pain

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    <p>Abstract</p> <p>Background</p> <p>Local anesthetics alleviate neuropathic pain in some cases in clinical practice, and exhibit longer durations of action than those predicted on the basis of the pharmacokinetics of their blocking effects on voltage-dependent sodium channels. Therefore, local anesthetics may contribute to additional mechanisms for reversal of the sensitization of nociceptive pathways that occurs in the neuropathic pain state. In recent years, spinal glial cells, microglia and astrocytes, have been shown to play critical roles in neuropathic pain, but their participation in the analgesic effects of local anesthetics remains largely unknown.</p> <p>Results</p> <p>Repetitive epidural administration of ropivacaine reduced the hyperalgesia induced by chronic constrictive injury of the sciatic nerve. Concomitantly with this analgesia, ropivacaine suppressed the increases in the immunoreactivities of CD11b and glial fibrillary acidic protein in the dorsal spinal cord, as markers of activated microglia and astrocytes, respectively. In addition, epidural administration of a TrkA-IgG fusion protein that blocks the action of nerve growth factor (NGF), which was upregulated by ropivacaine in the dorsal root ganglion, prevented the inhibitory effect of ropivacaine on microglia, but not astrocytes. The blockade of NGF action also abolished the analgesic effect of ropivacaine on neuropathic pain.</p> <p>Conclusions</p> <p>Ropivacaine provides prolonged analgesia possibly by suppressing microglial activation in an NGF-dependent manner and astrocyte activation in an NGF-independent manner in the dorsal spinal cord. Local anesthetics, including ropivacaine, may represent a new approach for glial cell inhibition and, therefore, therapeutic strategies for neuropathic pain.</p

    Late presented congenital myasthenic syndrome with novel compound heterozygous CHRNE mutations mimicking seronegative myasthenia gravis

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    We found a late presented congenital myasthenic syndrome (CMS) patient with novel CHRNE gene mutations. Although our patient has shown blepharoptosis since youth, fatigable muscle weakness began at age 71. Genetic analysis revealed novel compound heterozygous CHRNE mutations (c.1032+2T>G, c.1306_1307 delGA). His myasthenic symptoms were well managed by oral anti‐cholinesterase drug until he died at 82‐year‐old. The present case showed mild myasthenic symptoms with very late presentation and slow progression. Late presented CMS is often underdiagnosed; therefore, genetic testing is important to distinguish it from other myasthenic disease

    Spectrum of color gene deletions and phenotype in patients with blue cone monochromacy

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    Blue cone monochromacy (BCM) is an X-linked ocular disease characterized by poor visual acuity, nystagmus, and photodysphoria in males with severely reduced color discrimination. Deletions, rearrangements and point mutations in the red and green pigment genes have been implicated in causing BCM. We assessed the spectrum of genetic alterations in ten families with BCM by Southern blot, polymerase chain reaction, and sequencing analysis, and the phenotype was characterized by ophthalmoscopy, fluorescein angiography, and a battery of tests to assess color vision in addition to routine ophthalmological examination. All families showed clinical features associated with BCM. Acuities were reduced in all affected males, and photopic b-wave was reduced by more than 90% in seven families. In three families, however, the photopic b-wave response showed uncharacteristic relative preservation of 30–80% (of the clinical low-normal value). The color vision was unusually preserved in two affected males, but this was not correlated with photopic electroretinography retention. Progressive macular atrophy was observed in affected members of two BCM families while the rest of the families presented with normal fundus. In nine families deletions were identified in the gene encoding the red-sensitive photopigment and/or in the region up to 17.8 kb upstream of the red gene which contains the locus control region and other regulatory sequences. In the same nine families the red pigment gene showed a range of deletions from the loss of a single exon to loss of the complete red gene. In one family no mutation was found in the exons of the red gene or the locus control region but showed loss of the complete green gene. No association was observed between the phenotypes and genotypes in these families.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42266/1/439-107-1-75_s004390000338.pd
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