Identification and characterization of nuclear matrix protein[s] and assessment of its usefullness for early diagnosis of bladder cancer

The highest incidence rates of bladder cancer are generally found in industrially developed countries, particularly North America and Western Europe, and areas associated with endemic schistosomiasis, including parts of Africa and the Middle East. The appropriate treatment of patients with bladder cancer mandates early detection and regular follow up for recurrences. Currently, cystoscopy is the standard method for diagnosing and monitoring bladder cancer recurrence, but it is an invasive and relatively costly technique, and may sometimes be inconclusive, particularly in cases of cystitis. Western blot and specific immunoglobulin-G antibody were used to identify the urinary NMP marker. Urine samples from 123 patients with bladder cancer and 50 controls were evaluated using the developed SDS-PAGE, Western blot and ELISA. The NMP marker was identified in the urine of patients with bladder cancer at 52 kDa [NMP- 52] by SDS-PAGE, Western blot and ELISA. In addition, the NMP-52 tumor marker was not detected in the urine of patients. Detecting the urinary NMP-52 marker using SDS-PAGE, Western blot and ELISA, would be helpful in the rapid diagnosis of bladder cancer

Impairment of immune response by meprobamate

Previous studies from this laboratory and others showed that perturbations of the central nervous system modulate immune function. This study investigates the effects of meprobamate on the immune response. It leads to low humoral response shown by decreased precipitin titers, and elevated cellular immune response shown by the increased level of B-glucuronidase in both serum and Kupffer cells. However, the response returns to normal levels by the treatment with thiola. These data further substantiate the existence of a link between the brain and the immune response

Cytotoxicity of nonspecific activated macrophages

Partial resistance against Ehrlich ascites tumor [EAT] in Swiss albino mice was nonspecifically induced by single injection of a dead bacterial vaccine [i.p tumor +AD0- 90 ml/ kg body weight] rather than a living bacterial vaccine [i.p. tumor +AD0- 205 ml/ kg body weight] of the Gram- positive cocci of M. luteus, when compared to controls [i. P. tumor +AD0- 387 ml/ kg body weight]. Tumor inhibition was better noted in mice injected 4 and 7 days previously with living or dead bacteria respectively. The observed inhibition was related at least in part to the presence of activated macrophages in the peritoneum after vaccination. There was a proportional relationship between the macrophage of the i.p. tumor and the degree of inhibition+ADs- the more the inhibition the higher the content. Macrophage content was 16, 19 and 22+ACU- of total ascites cells, in mice given dead bacterial vaccine 1, 4 and 7 days previously, and developing ascites tumor measuring 330, 300 and 90 ml/kg body weight [on termination: 2 weeks post i.p. tumor transplantation] respectively. A similar correlation was observed in mice given living vaccine of the same bacteria. Although these findings of the apparent inhibition of i.p. tumor could be explained on the basis of local interaction between the activated macrophages and the ascites tumor cells, the associated inhibition of sc. tumor growth in the same host at challenge the site was encouraging enough to suggest that vaccination might bring activated macrophages in contact with tumor cells at distant sites of the disease +ADs- Sc. tumor measured 3, 9, and 13 cu mm in mice injected with the dead bacterial vaccine compared to 86 cu mm in the untreated controls. Similar inhibition was observed in mice given the living bacterial vaccine

Peritoneal macrophage activation by microbial and nonmicrobial agents

Exposure of peritoneal macrophages to two stimulants [gelatin and typhoid vaccine] was associated with the synthesis of greater quantities of intracellular acid phosphatase [AP- ase] and increased phagocytosis [NBT reduction]. NBT reduction to the insoluble formazan was apparently dependent on the nature of the inflammatory agent [gelatin +AD0- 16.6+ACUAOw- typhoid vaccine +AD0- 21.4+ACU-]+ADs-both chemically elicited and microbially activated macrophages differ in their production of the enzymatic system [s] responsible for reduction of oxygen to toxic molecules [revealed by NBT reduction] in accordance to the nature of the inflammatory agents [whether it is particulate like typhoid vaccine or soluble like gelatin]. On the other hand, though intracellular hydrolases were also synthesized by peritoneal macrophages in response to the inflammatory agents, the magnitude of elevation in the level of AP- ase did not correlate well with the intensity of NBT reduction by these cells when exposed to any of the two agents. Chemically elicited or microbially activated macrophages gave rise to similar elevations nature of the nature of the inflammatory agent [gelatin +AD0- 54.6+ACU-, typhoid vaccine +AD0- 57.0+ACU-]. Lysozymuria observed after exposure to gelatin was not interpretable on basis of macrophage stimulation. False positive and false negative results were not uncommon

Toxicity and antitumour activity of three novel antibiotics in relation to their effects on protein, DNA and RNA syntheses

The antimicrobial activity, toxicity and antitumor activity of three new antibiotics were investigated in conjunction with their effects on protein and nucleic acids synthesis of some bacterial strains. The new antibiotic vinaceomycin, did not show any toxic effect to normal Swiss albino mice at a concentration up to 500 mg/kg body weight, meanwhile it exhibited an in vivo antitumor effect against Ehrlich ascites tumor [33% increase in MST]. Both xanthominomycin and rubrominomycin which act as inhibitors of DNA synthesis, showed a very slight toxicity [10%] to normal Swiss albino mice at a concentration o f450mg/kg body weight but they did not show a significant antitumor effect against Ehrlich ascites tumor

Transplantation immunity and isograft size of spontaneous mammary carcinomata in mice

A method was described for determining the size of palpable mammary tumors in a mice without removing the tumor or killing the host. A formula was worked out and nomographs were made for simple and direct use employing only 2 diameters, bisecting the palpable growth at right angles to each other. Small tumor implants [0.05 to 5 cu mm in size] of C 3H spontaneous mammary carcinomas developed palpable tumors with same growth rates and same times of appearance in young syngeneic hosts of C 3H virgin females irrespective of the initial implant size. On the other hand, large implants [25 and 50 cu mm in size] of same carcinomas underwent necrosis and/or regression after an initial retarded growth and delayed appearance in syngeneic hosts.However, animals with regressing tumors from large implants remained refractory to a second challenge implant [0.5 cu mm in size], those with progressing growing tumors from small implants developed large tumors at challenge site.Resistance to challenge implants apparently immunologic in nature could be passively transferred to normal syngeneic hosts by lymph node cells and peritoneal washing cells