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Heparin was prepared and purified by two methods. Rf value, elemental and chemical analyses of our isolate coincided with the clinically used heparin. Heparin stimulated mitotic activities in Escherichia coli B and Aspergillus ochraceus. This was evident from the increase in DNA, RNA, and protein synthesis. The mechanism of growth stimulation by heparin probably takes place as follows: Heparin associates with nuclear protein, releasing DNA from DNP and thus stimulates DNA synthesis. Heparin was taken up by the cells of A. flavus, A. niger, and A. ochraceus. The uptake of heparin increased with time and was affected by several factors, such as pH, different salts, and heparin concentration.

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An investigation on the mechanism of action of bilharcid and tartar-emetic produced the following results. Deoxyribonucleic acid (DNA) synthesis by cell of E. coli B from either the maximum stationary phase or the exponential phase are inhibited by 3.62 mM of bilharcid or 16.81 mM of tartar-emetic immediately upon addition of the inhibitor. These drugs cause a downshift of the Tm of native DNA. They displace MG from the DNA-MG complex. They increase the specific viscosity of DNA solution. Also the synthesis of constitutive enzyme (alkaline phosphatase) was stopped, as was the induction of the synthesis of new enzyme (beta-galactosidase). Bilharcid and tartar-emetic act primarily on cell membrane and cause the release of 260 mM absorbing substances from E. coli B. Moreover, they lyse not only protoplasts of B. subtilis, but also spheroplasts of E. coli B.

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Leucine aminopeptidase (LAP) activity and creatinine concentration was estimated in serum of twenty five normal adult subjects, twenty four cases with active urinary bilharziasis, eleven cases with active intestinal bilharziasis, ten cases with mixed bilharzial infection (urinary and intestinal), fourteen bilharzial cases with clinical hepato-splenomegaly of bilharzial etiology, thirteen bilharzial cases with clinical hepatosplenomegaly and ascites, and twelve cases with cancer bladder of bilharzial etiology. Significant elevation in the serum enzyme level was found in all bilharzial cases which generally ran parallel to the course of the disease, being more marked in hepatosplenomegalic cases than in cases which showed no clinical signs of liver or spleen involvement. However, it was observed that the enzyme level was lower ascitic than in nonascitic cases. For serum creatinine concentration, no significant variation from normal value was observed in the group of patients with active urinary, active intestinal, mixed infections of bilharziasis and bilharzial hepatosplenomegalic cases. However, a very highly significant decrease in serum creatinine concentration was observed in the group of patients with bilharzial hepatosplenomegaly and ascites. Serum LAP activity and creatinine concentration in the group of patients with cancer bladder of bilharzial etiology showed no statistical variation from normal values.

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Leucine aminopeptidase activity and total protein concentration was estimated in the fresh early morning sample of urine of twenty five normal adult subjects, twenty four cases with active urinary bilharziasis, eleven cases with active intestinal bilharziasis, ten cases with mixed bilharzial infection (urinary and intestinal), fourteen bilharzial cases with clinical hepatosplenomegaly of bilharzial etiology, thirteen bilharzial cases with clinical hepatosplenomegaly and ascites, and twelve cases with cancer bladder of bilharzial etiology. It was found that there is a significant increase in LAP activity in the urine of all groups of patients studied. Again this increase ran parallel to the course of the disease in bilharzial cases. Urine protein concentration was found to be increased significantly in all groups of bilharzial cases studied with the highest value in urine of patients with cancer bladder of bilharzial etiology. However no direct correlation was found between urinary LAP level and protein concentration either within the individual cases or within the different groups.

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Arylsulfatase A and B in urine have been estimated in 18 normal subjects and 50 bilharziasis patients. The bilharziasis patients were divided into two groups according to the type of infeciton. Those with bilharziasis haematobian type of infection and those with the bilharziasis mansoni type. Each group was further subdivided into subgroups according to the severity and progress of the disease. The activities of arylsulfatase A and B were significantly elevated in all the groups of patients studied and it is evident that there is a progressive increase with the progress of the disease in both types of bilharziasis infections (the haematobian and mansoni types). Liver dysfunction consequent of bilharzial infestation appears to take part in the mechanism of induction of the bilharzial bladder cancer.

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