SummaryWe report nine cases of suspected pentastomiasis from China, and propose that diagnosis of this rare parasitic disease should be made aetio-pathologically, subaetio-pathologically, and presumptively. In none of our cases' lesions we could ®nd either a whole or part of an embedded nymph; hence, no aetiopathologic diagnosis of pentastomid infection was established. In three cases, subaetio-pathologic diagnoses of pentastomiasis were made upon the discovery of a peculiar set of relics from lesions, namely two pairs of circumoral hooks of pentastomid from lesions. In one of these three cases, an extra scissorslike image indicating a longitudinal section of a hook of the embedded pentastomid nymph, probably Linguatula serrata, was found. In the other six cases, none of the relics of the aetiological agents were found, and our diagnoses were made presumptively by a series of relatively speci®c pathologic features, i.e. pearly lesions over the peritoneal surface of the abdominal cavity under the serosa of the intestinal wall or under the capsules of liver and spleen. They tend to be uniquely protuberant, sometimes linked by a short thin stalk to the surface. The hyalinization and calci®cation of these centrally caseated granulomatous nodules tend to be concentric and targetoid in appearance. Tuberculosis, the most easily confused condition, was easily ruled out pathohistologically. We believe that there is a need for presumptive pathologic diagnosis of human pentastomid infection not only in China, but worldwide.keywords aetio-pathologic diagnosis of pentastomiasis, pathologic diagnosis of pentastomiasis, pentastomiasis, pentastomid myocarditis, presumptive pathologic diagnosis of pentastomiasis, subaetio-pathologic diagnosis of pentastomiasis correspondence Dr K. C.

This study compared the relationships of the development of both Alzheimer I & II cells to reactive astrogliosis and also their distributional patterns in the demyelinated and non-demyelinated lesions in 6 cases of Wilson's disease by the use of PAP immunohistochemical technique for glial fibrillary acidic protein (GFAP). The development of GFAP positive Alzheimer I (A-I) cells was found to be directly proportional to the capability of reactive astrogliosis, and inversely proportional to the severity of Alzheimer II (A-II) change. The GFAP negative A-II cells could be identified morphologically into 2 subtypes: one with well-developed nuclei, the other with "shrunken" nuclei. They were believed to stand for the "compensatory" and "decompensatory" stages of this dynamic astrogliotic process respectively. The distribution patterns of these 2 types of astrogliosis were different: A-I cells were found only in the regions of demyelination with intensive reactive astrogliosis, while A-II cells were found diffusely in both the grey and white matter, affecting both the protoplasmic and fibrous astrocytes without special predilection.

This study was designed to compare the degree of reactive astrogliosis occurring around a puncture wound in the brain of normal rats and at different intervals after a similar puncture wound in rats with a portocaval anastomosis. The gliosis was evaluated by the number of astrocytes, the thickness of their processes and the intensity of the glial fibrillary acidic protein immunoreactivity. After the puncture wound in the brain of rats with a portocaval anastomosis, the gliosis varied at different intervals being: (1) decreased at 10 days, (2) markedly increased at 5 weeks and (3) significantly decreased at 8, 12, and 16 weeks. These findings suggest that 5 weeks after portocaval anastomosis, an active proliferation of the metabolically altered astrocytes occurs with heightened synthesis of glial fibrillary acidic protein in the period of adaptive compensation, the so-called compensatory 'rebound'. At 8 weeks or more after portocaval anastomosis, these altered astrocytes were considered to be in the phase of decompensation and incapable of maintaining the reactive response which occurred in normal rats. The compensatory rebound and decompensatory 'decline' illustrate the dynamic plasticity of the reactive astrogliosis.