Search PubMed⌕ Search

Biomedical subjects

J Weis

Publications and source records attributed to J Weis.

At least 163 records · Page 9Linked to original sources
PubMed1975

Incidence of Listeria monocytogenes in nature.

During a research project on the occurrence of Listeria monocytogenes 194 strains were isolated in southern West Germany during the years 1972 to 1974:154 from soil and plant samples (20.3%), 16 from feces of deer and stag (15.7%), 9 from old moldy fodder and wildlife feeding grounds (27.2%), and 8 from birds (17.3%). The highest number of isolates was obtained from uncultivated fields. The beta-hemolytic serovars 1/2b and 4b were were predominant; other serovars (some of them identified for the first time), including nonhemolyzing strains, have been encountered frequently. It is suggested that Listeria monocytogenes is a saprophytic organism which lives in a plant-soil environment and therefore can be contracted by humans and animals via many possible routes from many sources.

Animal Feed↗
PubMedDate not supplied

[Pseudoarthrosis in neurofibromatosis type 1].

Neurofibromatosis type 1 (NF1) is the most common neurocutaneous disease. The clinical manifestations are diverse. Some of the skeletal changes are most relevant to the patient. We report on 9 patients with NF1 who presented with typical pseudarthrosis. In 8 of these children the lower extremity was involved. In 2 cases lesions of both tibia and fibula were found, in one case even over long segments with a fully instable leg. One child had a complete pseudarthrosis of the radius and ulna. This report analyses the bony changes, the operations performed and the possible technical improvements to be made. The present study as well as other recent studies suggest that bony lesions should be operated early using microsurgical methods.

Child, Preschool↗
PubMedDate not supplied

Adult polyglucosan body myopathy with subclinical peripheral neuropathy: case report and review of diseases associated with polyglucosan body accumulation.

A 65-year-old female had polyglucosan body myopathy, usually called "polysaccharide storage myopathy" that presented with increasing distal paresis and only slight weakness of the proximal limb girdle musculature. Muscle biopsy revealed dystrophic changes that could have been mistaken for muscular dystrophy, and the characteristic light as well as electron microscopic features of polyglucosan bodies varying in number at the three sites of muscle biopsies studied (deltoid, quadriceps femoris, and anterior tibial muscle). In addition, there were occasional nonspecific paracristalline mitochondrial inclusions. No abnormal polyglucosan deposits were found in the sural nerve biopsy. Morphometric evaluation of nerve fiber cross sectional areas revealed some degree of demyelination and remyelination, and of nerve fiber degeneration and regeneration. Unlike a series of 10 unselected control sural nerves with Renaut bodies, hypomyelinated nerve fibers were more numerous adjacent to Renaut bodies. This is the first case of polyglucosan body myopathy in which the axon/myelin ratio and the axonal circularity factor in the sural nerve is evaluated and in which a definite lack of polyglucosan bodies or other abnormal glycogen storage products in a peripheral nerve is documented.

Aged↗
PubMedDate not supplied

Mitochondrial changes in muscle phosphoglycerate kinase deficiency.

X-linked phosphoglycerate kinase (PGK) deficiency is a rare disorder which affects the glycolytic pathway and leads to reduced ATP production. Clinically, PGK deficiency is often associated with nonspherocytic hemolytic anemia and symptoms caused by disturbances of the central nervous system. In addition, myopathy characterized by weakness, cramps, intolerance to exercise, and myoglobinuria has been described in a few cases. We here report on a 23-year-old man who presented with episodes of muscular weakness, cramps, rhabdomyolysis, and renal failure induced by intensive physical exercise. Biochemical analysis of muscle specimens disclosed markedly reduced PGK activity (11.5% compared to normal controls). A moderate increase of glycogen was seen in numerous muscle fibers. Mitochondria in muscle fibers and endothelial cells showed accumulations of glycogen. In muscle fibers unusually large matrix granules were present in several mitochondria. A sural nerve biopsy disclosed scattered large hypomyelinated axons without evidence of demyelination and remyelination. These findings indicate involvement of mitochondria in this case of symptomatic PGK deficiency.

Adult↗