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Biomedical subjects

L Lenzi

Publications and source records attributed to L Lenzi.

At least 37 records · Page 2Linked to original sources
PubMed1981

[Complement. Evaluation of some complement fractions in patients affected by neoplasia undergoing chemotherapy (author's transl)].

Serum complement levels (UE50, C3, C4, act. C3, C1q) were determined in 75 healthy subjects and 130 cancer patients undergoing treatment. The results were correlated with statistical analysis. The patients were divided into the following groups: a) with local tumor; b) with tumor in complete remission; c) with tumor in incomplete remission; d) stationary. Three blood samples were obtained over a period of about two months. All cancer patients had decreased UE50 levels and increased act. C3 levels compared to normal values, while C3, C4, and C1q were normal. C4 levels were not significant in any group of cancer patients, but act. C3 levels were significantly increased (as compared to those of the healthy subjects). UE50 levels appeared significantly decreased only in the group with complete remission, C3 levels were increased in incomplete remission patients and were variable in stationary patients. C1q values were always increased except in the complete remission group. The variability of complement levels was dependent on the stage of the disease and on the therapy: our results provide considerable support for this hypothesis. We found that complement activity was triggered through classic or alternative means caused by antigen-antibody complexes or inflammatory processes, according to the increase or decrease of the tumor mass.

Adult↗
PubMed1981

Defective Aspergillus killing by neutrophil leucocytes in a case of systemic aspergillosis.

A persistent defect of Aspergillus killing was observed in the neutrophils of a 6-year-old patient with a systemic A. fumigatus infection which was highly refractory to anti-mycotic therapy. Aspergillus phagocytosis in vitro was normal, but nearly 80% of the ingested organisms (versus 30% in the controls) survived intracellularly during the 2-hr assay period. The patient's neutrophils showed a subnormal frequency of nitroblue tetrazolium reduction and a subnormal hexose monophosphate shunt activation in response to phagocytosis. The metabolic responsiveness, however, was clearly superior to that of chronic granulomatous disease neutrophils tested for comparison. The immune status of the patient and the following properties of his neutrophils were found to be normal: random and chemotactic motility, killing of S. aureus and C. albicans, and the contents of several granula enzymes. Our findings suggest the existence of neutrophil factors or functions which are required for killing Aspergillus, but not S. aureus and C. albicans.

Aspergillosis↗
PubMed1979

Biochemical and structural abnormalities of the connective tissue in Larsen's syndrome.

Skin, iliac crest cartilage and tendon of a patient affected with Larsen's syndrome were subjected to biochemical and ultrastructural investigation. A substantial increase in the ratio of glucosamine to galactosamine was found both in skin and cartilage. Ultrastructural abnormalities of collagen fibres and proteoglycan filaments were also found in Larsen's tissues. The significance of these findings are discussed.

Cartilage↗
PubMed1977

Osteogenesis imperfecta: morphological, histochemical and biochemical aspects. Modifications induced by (+)-catechin.

Two patients affected with two different forms of Osteogenesis Imperfecta were examined in order to study collagen and glycosaminoglycans (GAGs) in skin and iliac crest cartilage. A sharp decrease of the galactosamine to glucosamine ratio due to a reduced content of chondroitin sulfate was evidenced in both patients. Moreover the structure of proteoglycans appeared altered, this being more evident in the severe form of the disease. Morphological examination in light and electron microscopy of cartilage of the less severely diseased patient showed that GAGs in the extracellular matrix did not present regular connection with collagen fibers. Chondrocytes, elongated and disorderly scattered, showed large lipidic inclusions and, on histochemical basis, were devoid of UDPG dehydrogenase activity. Treatment with (+)-catechin produced an improvement, in both patients, of the biochemical pattern of collagen and GAGs. Similarly a shift of the cellular activity and of the matrix morphology towards normality was observed in the investigated cartilage of the less severely affected patient.

Adolescent↗
PubMed1977

Experimental arthrosis from intra-articular vitamin A injection in the rabbit. Morphological and biochemical study: considerations on the pathogenesis of human arthrosis in relation to the experimental model.

The key to the pathogenesis of arthrosis lies in the mechanism responsible for the initial lesions. In this experimental work the possibility of producing arthrosic changes is demonstrated by activating lysosomal chondrocytic enzymes by the intra-articular injection of Vitamin A in rabbits. On the basis of the experimental results the authors discuss the possible role that activation of the lysosomal hydrolytic enzymes might play in producing primary and secondary arthrosis in humans. They advance the hypothesis that this mechanism may be the common final step in the degradation of the articular cartilage, whatever the aetiological factor.

Acid Phosphatase↗