Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.36 (hyaluronidase)
 4,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An explanation is proposed as to how the total amount of cells normally are in a cellular equilibrium which results from an energetic equilibrium. When a group of cells is damaged the body can restore this disturbance by the fight and flight reaction-a mechanism in which the circulating body energy is redistributed and in which all body cells are involved cooperatively. An unfavourable side-effect of this mechanism is a diminished uptake of nutrients from the gastro-intestinal tract. Therefore in chronic irritation, cachexia and a decreased resistance to all forms of insult occurs. The energetic equilibrium becomes severely disturbed. Differentiation from a morula cell to a ripe cell is proposed to be an expression of a decreased nutrient supply to the morula. The predominant mechanism for cellular survival is a change from a demand on nutrient supply to a demand on the specialisation of the cell function. The role of the nutrient supply - regulated by hyaluronidase synthesis - then becomes subsidiary to this specific function. It is proposed that cancer originates because of chronic irritation. As a result of the secondary chronic redistribution of body energy in the direction of the irritated area, these cells are chronically hypernourished and then dedifferentiate again in the direction of the morula cell. As a consequence of the reactive mechanism, the cachexia which is so typical of cancer, then occurs. From theoretical considerations, it is predictable that cancer may be effectively treated by two basic manipulations of the energetic equilibrium: firstly by chronically decreasing the nutrient supply to the cancer cells, thereby stimulating differentiation again, and secondly by restoring the energetic equilibrium. In practice this involves supplementation of hyaluronidase together with hyperalimentation.
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PMID:Hyaluronidase, from wound healing to cancer. 728 25

The patient had been employed in an asbestos factory for four years from the age of 16. Five years ago, she complained of sputum and cough, and she was treated for chronic bronchitis. From March, 1977, when she was 53 years old, hydrothorax and ascites increased, her weight decreased and she was hospitalized for cachexia. The clinical diagnosis of malignant diffuse mesothelioma was made on the presence of atypical cells in the effusions. Atypical cells showed a positive colloidal iron staining test and positive hyaluronidase digestion test. Asbestos bodies were found in the sputum. The patient died on February 1978. Postmortem confirmed asbestosia and mesothelioma which was scattered over the pleura, pericardial sac, diaphragma, peritoneum and pancreas. In addition, bronchiolo-alveolar cell type lung cancer was found localized in the lower lobe of the left lung. The electron beam diffraction disclosed the asbestos as amosite (brown asbestos).
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PMID:Mesothelioma with lung cancer complicating asbestosis. 741 39

A variant of gelatinous transformation of marrow was described in leukemic patients post-chemotherapy. This lesion was found in 8 out of 1833 post-chemotherapy bone marrows from 429 patients with leukemia. Histologically, this variant form was identical to the classical gelatinous transformation except for the absence of fat atrophy. In marrow smears, mucoid strands were seen between marrow particles and oriented along the direction of spread. In clot and trephine sections, an eosinophilic ground substance was widespread, filling out spaces around the fat cells, which occupied the normal proportion of marrow space. At high magnification, this ground substance appeared granular and fibrillary, a non-specific feature which could also be seen in fibrin clot commonly found in marrow sections. This eosinophilic ground substance, however, can be distinguished from fibrin clots by positive staining with Alcian Blue (pH 2.3) and inhibition of the staining after treatment with hyaluronidase. Clinically, in contrast to the classical form, this variant form of gelatinous transformation was acute in onset, transient, and associated with chemotherapy but not with cachexia.
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PMID:A variant of gelatinous transformation of marrow in leukemic patients post-chemotherapy. 826 50