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K Samson

Publications and source records attributed to K Samson.

5 recordsLinked to original sources
PubMed2001

Capture-recapture method to assess the prevalence of disabled leprosy patients.

The capture-recapture technique was applied in estimating the prevalence of disabled leprosy patients in four States in Northern Nigeria. A two-sample capture-recapture method, using data from hospital admissions during 1997 and 1998 in three leprosy referral hospitals, and from a sample survey on leprosy patients with disabilities in the clinics in 1999. In the sample, 1395 (ex) leprosy patients were found, 393 with a disability. Of these 393 patients, 47 had been admitted during 1997 and 1998 to one of three leprosy referral hospitals. In these hospitals, 151 individuals from the 24 study Local Government Areas (LGA) in four states of Northern Nigeria were admitted in 1997 and 1998. Using the Peterson estimator, we calculated the number of unknown disabled leprosy patients in the studied LGAs to be 1262 (95% confidence interval 991-1533). This was nearly four times greater than the field reported figure. The capture-recapture method can be applied in a leprosy care programme. Limitations of the method are the completeness of reporting after invitation in the field, as well as the probable biased sample of leprosy patients admitted to hospital. Our finding implies that relying on patients to report for prevention of disabilities and rehabilitation to the clinics, causes the real size of the problem to be underestimated by a factor of 3-4. We recommend the use of a special 'care' register for disabled leprosy patients to better address their needs for prevention of disabilities and rehabilitation.

Adolescent↗
PubMed1994

Characterization of illudin S sensitivity in DNA repair-deficient Chinese hamster cells. Unusually high sensitivity of ERCC2 and ERCC3 DNA helicase-deficient mutants in comparison to other chemotherapeutic agents.

Illudins, novel natural products with a structure unrelated to any other known chemical, display potent in vitro and in vivo anti-cancer activity against even multi-drug resistant tumors, and are metabolically activated to an unstable intermediate that binds to DNA. The DNA damage produced by illudins, however, appears to differ from that of other known DNA damaging toxins. The sensitivity pattern of the various UV-sensitive cell lines differs from previously studied DNA cross-linking agents. Normally, the ERCC1- (excision repair cross complementing) and ERCC4-deficient cell lines are most sensitive to DNA cross-linking agents, with ERCC2-, ERCC3- and ERCC5-deficient cell lines having minimal sensitivity. With illudins the pattern is reversed, with ERCC2 and ERCC3 being the most sensitive. The sensitivity to illudins in complementation groups 1 through 3 is due to a deficiency of the ERCC1-3 gene products, as cellular drug accumulation studies revealed no differences in transport capacity or total drug accumulation. Also, a transgenic cell line in which ERCC2 activity was expressed through an expression vector regained its relative resistance to the illudins. The EM9 cell line, which displays sensitivity to monoadduct producing chemicals, was not sensitive. Thus, excision repair is involved in repair of illudin-induced damage and, unlike other anti-cancer agents, the involvement of ERCC2 and ERCC3 helicases is critical for repair to occur. The requirement for ERCC2 and ERCC3, combined with the finding that ERCC1 but not ERCC2 is upregulated in drug-resistant tumors, may explain the efficacy of illudins against drug-resistant tumors. The inhibition of DNA synthesis in cells within minutes after exposure to illudins at nanomolar concentrations may be related to the finding that the ERCC3 gene product is actually the p89 helicase component of the BTF2 (TFII) basic transcription factor and the high sensitivity of ERCC3-deficient cells to illudins.

Animals↗
PubMed1989

Epidemic of "shocks" in telephone operators: lessons for the medical community.

In January 1986 two brief power failures occurring within an hour of each other affected the operation of visual display terminals in a section of the Manitoba Telephone System. After the power failures three operators reported an alarming tingling sensation in their arms and one side of their body, which they called "shocks". Other operators then began to report incidents of numbness and tingling in their limbs, face or head as well as other, diffuse symptoms. During the next 2 weeks 92 such incidents were reported by 55 operators. The media carried alarming headlines, and medical practitioners perpetuated the label of "electric shock". Despite extensive investigation, which revealed no electrical fault, the section was closed by the regulatory authority, and an independent medical panel was convened to review the findings. The panel concluded that there was no immediate hazard to life or health and recommended continued workplace assessment and follow-up of affected operators; however, because the panel lacked electrical engineering expertise, uncertainty persisted as to the cause of the events. The reports of incidents persisted, peaking in association with continued rumours of diagnoses of "nerve damage". In the fall of 1987 a multidisciplinary committee ruled out as causative factors all known hazards other than electrostatic shock and occupational stress. This costly and lengthy investigation underlines the danger in regarding collective stress reaction as a diagnosis of exclusion. It highlights the need to scrutinize objective evidence before validating potentially unfounded concerns and underlines the desirability of considering the psychosocial effects of technology and regimented tasks.

Disease Outbreaks↗
PubMedDate not supplied

Nonresponsiveness of the metastatic human lung carcinoma MV522 xenograft to conventional anticancer agents.

The human lung carcinoma cell line MV522 was previously noted to produce extensive metastasis to the lungs, spleen and lymph nodes after subcutaneous transplantation into athymic nude mice. Animals eventually succumb to these metastases, and not primary tumor growth. The ability to produce extensive metastasis after a simple subcutaneous injection in 100% of animals (> 100 tested to date) would be an advantage when screening compounds for anticancer activity. To validate the utility of this xenograft model for testing anticancer agents, we tested the ability of 10 anticancer drugs to either inhibit primary tumor growth and/or prolong life span of MV522-bearing animals. Among the 10 antitumor conventional agents, only mitomycin C and taxol demonstrated primary tumor growth inhibition. Mitomycin C produced a mild increase in median life span of 41% to 63%, while taxol had inconsistent effects. The metastatic MV522 carcinoma model appears to reflect clinical resistance of primary non-small cell lung cancer to conventional chemotherapeutic agents and should be useful for testing new anti-cancer drugs.

Animals↗