Calcium oxalate crystal deposition in a patient with Aspergilloma due to Aspergillus niger

Discrimination between aspergilloma and chronic necrotizing pulmonary aspergillosis (CNPA) based on radiological findings can difficult. We describe a patient with aspergilloma and organizing pneumonia that was possibly caused by Aspergillus niger infection and radiologically mimicked CNPA. A postmortem histological analysis showed diffuse alveolar damage that had originated in peri-cavitary lung parenchyma. Calcium oxalate or Aspergillus niger was located inside, but not outside the cavity in the right upper lobe. Calcium oxalate or other unknown hyphal bioactive components might provoke severe lung inflammation not only adjacent to the cavity, but also on the contralateral side.KEY WORDS : Calcium oxalate crystal deposition, aspergilloma, black deposits, Aspergillus niger     

High neuron-specific enolase level of cerebrospinal fluid in the early stage of Creutzfeldt-Jakob disease

Summary The measurement of neuron-specific enolase level in serum and cerebrospinal fluid was conducted time-sequentially in an autopsy confirmed patient with Creutzfeld-Jakob disease. The level was markedly high in the early stage of the disease at which time the brain CT showed no or minimal abnormalities, while falling into the normal range in the advanced stage. This is the first report of the elevated level of neuron-specific enolase in Creutzfeldt-Jakob disease.Abbreviations CT Computed tomography - CSF Cerebrospinal fluid - CJD Creutzfeldt-Jakob disease - NSE Neuronspecific enolase - CEA Carcinoembryonic antigen - PSD Periodic synchronous discharge - PET Positron emission tomography     

Adrenomedullin protects against oxidative stress-induced podocyte injury as an endogenous antioxidant.

BACKGROUND: We previously reported that puromycin aminonucleoside (PAN) increased adrenomedullin (AM) secretion and AM mRNA expression in podocytes, through overproduction of oxidative stress. To clarify the cytoprotective role of AM as antioxidative and antiapoptotic substance in podocytes, we investigated the effect of exogenous AM and AM antagonist on PAN-induced apoptosis in conditionally immortalized murine podocytes. METHODS: The expression of AM, RAMP 2 and RAMP 3 was investigated using real-time PCR, western blotting analysis and immunofluorescence microscopy. Reactive oxygen species (ROS) production was measured by CM-H(2)DCFDA fluorescence intensity method. The percentage of apoptotic cells was measured by Hoechst 33342 staining. RESULTS: PAN (100 microg/ml) significantly (P < 0.01) increased ROS production, associated with an increase in apoptosis; the percentage of apoptotic cells is 5.3% + 0.05% (P < 0.01) with 36 h treatment of PAN compared to 0.24 + 0.16% with no treatment. Several antioxidants could markedly reduce PAN-induced apoptosis in cultured podocytes, suggesting that PAN-induced apoptosis might be attributable to the overproduction of ROS. Accordingly, the administration of exogenous AM (10(-6) M) could significantly reduce not only ROS production via a PKA-dependent pathway, but also the resultant apoptosis induced by PAN. AM antagonists, CGRP8-37, augmented PAN-induced apoptosis, associated with increased ROS production, 2.2- and 2.3-Fold, respectively. RAMP 2 and RAMP 3 could be detected in podocytes and glomeruli. CONCLUSIONS: This suggests that ROS-induced up-regulation of AM with PAN could counteract ROS-induced apoptosis, by the suppression of ROS production. Therefore, AM might have the endogenous antioxidant potential to protect against ROS-induced podocyte injury.     

Muscle plasma membrane abnormalities in infants with Duchenne muscular dystrophy

Muscle biopsies from one preclinical case, one early case, four symptomatic cases of Duchenne muscular dystrophy, and six controls were investigated for the presence of delta lesions by phase optics and conventional electronmicroscopy. By phase microscopy the frequency of delta lesions was 4.9% in the preclinical and early cases and 4.0% in the four symptomatic cases. The incidence of delta lesions in the controls was 0.4%. Electronmicroscopic studies of delta lesions revealed similar findings in the preclinical, early, and symptomatic cases. The common denominator of the delta lesions was disruption of the muscle plasma membrane. Plasma membrane lesions occur early in Duchenne muscular dystrophy.     

Application of lectin cytochemistry to the study of human neuromuscular disease

This is a review of the application of cell surface cytochemistry to the study of human neuromuscular disease. The advantages and limitations of the use of lectins coupled to peroxidase are discussed, and the application of this technique is illustrated by a study of the surface of muscle cells in Duchenne muscular dystrophy and polymyositis.     

DIFFERENTIATION OF AMYLOID FIBRIL PROTEINS IN TISSUE SECTIONS Two Simple and Reliable Histological Methods Applied to Fifty-one Cases of Systemic Amyloidosis

The potassium permanganate method and the unlabeled immunoperoxidase (PAP) method were applied for distinguishing different types of amyloid fibril proteins in conventionally fixed, paraffin-embedded tissue sections obtained from fifty-one autopsied cases of systemic amyloidosis and three control cases of well-analysed fibril proteins. All of the eighteen cases "sensitive" to permanganate treatment, whose amyloid deposits lost completely their affinity to Congo red and birefringence under polarized light, were shown to have AA antigenic determinants by the PAP method. Meanwhile, all of the remaining thirty-three "resistant" cases, where Congo red affinity and birefringence were retained at various degree even only in minimal areas, were negative for AA antigenicity. This indicated the feasibility of potassium permanganate method for the identification of AA protein based on this criterion of "sensitivity". Twenty-eight cases were classified as AA, Aγ, A_k or AA+[A_k] the remaining twenty-three cases were unclassified, and there were some discrepancies between the preliminary clinicopathological classification and the protein nature of the amyloid. It is important to differentiate the types of amyloid fibril protein of individual patients because the expedience of selective therapeutic approaches had been suggested. The two methods applied herein are handy and useful for this purpose.