Suppression of the drug-induced morphine withdrawal syndrome by cyproheptadine.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to I Reimann.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Rabbit haemorrhagic disease (RHD) is usually peracute to acute, while subacute to chronic disease is rare. This paper describes gross and histopathological findings in four out of 20 rabbits aged 14 weeks, experimentally infected with one of two German field isolates of RHD virus. Eight rabbits survived the infection for 10 days and were killed after four of them, infected with 100 to 10 000 haemagglutination units, had started to develop progressive jaundice. Histopathologically, icteric livers showed severe subacute centrilobular bridging necrosis with calcification, and proliferation of periportal hepatocytes and bile ducts. Positive-strand RHDV RNA was detected by in-situ hybridization, mainly in periportal macrophages. Loss of the normal hepatic architecture, reparation (fibrosis) and hepatocellular regeneration, together with moderate inflammatory reaction, are signs of liver cirrhosis. These signs, observed in young rabbits given small doses of RHD virus, are interpreted as an unusual outcome of experimental inoculation.
Explore the source record for details and available documents.
The pathogenesis of metatarsus varus was investigated by a series of dissections of 14 normal feet of stillborn or infants who died during the perinatal period. The deformity could not be produced without the surgical incisions described below. A valgus position of the hindfoot was produced by maximal dorsiflexion of the foot. The deformity of the fore part of the foot could not be produced even by extreme traction on the tibialis anterior tendon even after capsulotomy of the first tarsometatarsal joint. Only extensive capsulotomies in the tarsometatarsal joints distal to the joint of Chopart made it possible to displace the bones into the position analogous to metatarsus varus. It is suggested that metatarsus varus may be a deformity which occurs on a maximally dorsiflexed foot and that the primary mechanism of the forefoot deformity is a subluxation in the fore part of the foot. Secondary contractures of the soft tissues, and adaptive bone changes offer a possible explanation for lack of spontaneous recovery as well as the difficulties encountered in treating late cases.
The ratios of synovial fluid concentration to serum concentration (SF/S) for 4 nonimmunoglobulin proteins were higher in osteoarthritic synovia than in normal. The difference increased with increasing molecular weight and was highly significant for the largest molecules. An almost inverse linear relationship was observed between SF/S ratios of the proteins and their molecular weight. As only slight signs of inflammation were found in the osteoarthritic synovium, no correlation could be demonstrated between ratio and the degree of synovial inflammation as assessed by histologic methods. Two types of synovitis were encountered in patients with osteoarthritis: an early "proliferative" stage, characterized by synovial edema and large numbers of dilated venules and capillaries and a later "fibrous" stage characterized by scarring of the synovium. The highest ratios corresponded to the proliferative type. The abnormal protein pattern in osteoarthritic synovia is a result of increased capillary permeability in the synovial membrane owing to capillary dilation and stasis.