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Biomedical subjects

M F Waters

Publications and source records attributed to M F Waters.

At least 55 records · Page 3Linked to original sources
PubMed1978

Rifampicin for lepromatous leprosy: nine years' experience.

Over 100 patients with lepromatous leprosy were treated with rifampicin in a series of pilot, uncontrolled, and controlled trials in 1968-77. The rapid bactericidal effect of rifampicin on Mycobacterium leprae was confirmed. Clinical improvement became apparent sometimes as early as 14 days after the start of treatment. Nevertheless, a few persisting viable M leprae were detected as long as five years after the start of treatment with rifampicin either by itself or in combination with the bacteriostatic drug thiambutosine. Treatment with rifampicin and dapsone for six months reduced the number of persisting leprosy bacteria more than treatment with dapsone alone. Although rifampicin proved more effective than dapsone, it is unlikely that used by itself if can significantly shorten the length of treatment in lepromatous leprosy. Therefore initial intensive combined treatment with two or more bactericidal drugs (including rifampicin) warrants further investigation in both untreated leprosy and lepromatous leprosy resistant to dapsone.

Animals↗
PubMed1978

Experimental lepromatous leprosy in the white-handed gibbon (Hylobatus lar): successful inoculation with leprosy bacilli of human origin.

Leprosy bacilli of human origin were inoculated into a white-handed gibbon by the i.v. and i.p. routes, and also locally into ears, testis and around an ulnar nerve. The animal was observed closely during a period of nearly 15 years and did not exhibit any clinical evidence of cutaneous or neurological disease. At death, a wide range of tissues was taken for bacterial counts and histological examination, and a disseminated and progressive infection was demonstrated. Acid-fast bacilli were found in many sites; their morphological appearance distribution in nerves, and pattern of multiplication in mouse foot-pads, and also the presence of anti-mycobacterial antibody in the serum and the absence of specific lymphocyte transformation were all in keeping with an infection by Mycobacterium leprae, at an early lepromatous stage. This is probably the first fully documented report of experimental lepromatous infection in a primate. The findings are discussed in relation to the long incubation period of le promatous leprosy and the difficulties of diagnosing the disease at an early stage in man.

Animals↗
PubMed1975

Sulphone resistance in leprosy. A review of one hundred proven clinical cases.

An account is given of the first hundred consecutive proven cases of sulphone resistance in leprosy, detected in Malaysia between 1963 and 1974. Proof of resistance was clinical in eighty patients and was obtained by drug-sensitivity testing in mice in ninety-six patients; 76 cases were proved both clinically and experimentally, and there was no discrepancy between the two methods. Sulphone resistance was confined to patients with lepromatous-type leprosy--i.e., patients with a large bacterial population. Clinical evidence of relapse due to drug resistance appeared 5-24 years after the start of sulphone treatment. Low dosage favoured the appearance of resistance; therefore regular treatment of lepromatous leprosy with dapsone in full dosage is recommended. The attainment of "skin smears negative for leprosy bacilli" is no test of cure of lepromatous leprosy.

Adolescent↗
PubMed1975

Depressive effect of serum from patients with leprosy on mixed lymphocyte reactions. Influence of anti-leprosy treatment.

Mixed leucocyte cultures, from two normal donors, were set up in media containing human serum from one of the following sources: (a) a pool of normal group AB donors; (b) Chinese, Malay or Indian patients with untreated leprosy; (c) the same patients after effective anti-leprosy treatment; (d) control Chinese, Malay or Indian subjects. Transformation was estimated by measuring the incorporation of tritiated thymidine in the last 24 hr of a 7-day culture period. Transformation was impaired in sera from treated lepromatous patients, but was less impaired or not impaired at all in sera from treated lepromatous patients. The loss of depressive activity after treatment was more marked in Chinese and Indian than in Malay patients. Transformation was also impaired, though to a lesser extent, in sera from patients with untreated tuberculoid leprosy; it was still impaired in sera from treated tuberculoid patients. There was no evidence of specificity in impairment of mixed lymphocyte reactivity and lymphocytotoxic antibodies appeared to play no role. The incidences of hepatitis B antigen and antibody and of anti-nuclear factor were not notably high.

Adolescent↗
PubMed1974

Neuraminidase-mediated augmentation of in vitro immune response of patients with solid tumors.

Host blood lymphocytes undergo accentuated blastic transformation when cultured with tumor cells pretreated with neuraminidase. The effect has been observed in 38 patients with such common solid tumors as bronchus carcinoma, skin melanoma, hypernephroma, or adenocarcinoma of the breast, lung, colon, or rectum. Individual response varied but often exceeded response to allogeneic cells. Three patients with glioblastoma of the brain did not respond. Lymphoblastic transformation was not observed in three of four cultures containing benign tumor or in any cultures containing normal tissue analogues of the malignant tumors. A factor in host blood serum inhibiting lymphoblastic transformation correlated to abnormal elevation of serum-bound sialic acid. This blocking factor differed in specificity from enhancing antibody or serum blocking complexes described by other investigators. Blocking effects were observed when the tumor-cell type of a serum donor differed from the cell type of the culture test tumor. Serum with abnormal elevation of bound sialate from a cancerfree human also non-specifically blocked host response to tumor. The blocking effect could be eliminated by partial enzymatic removal of bound sialic acid from serum glycoproteins.

Adenocarcinoma↗