A controlled trial for evaluating two live attenuated mumps-measles vaccines (Urabe Am 9-Schwarz and Jeryl Lynn-Moraten) in young children

A prospective, randomised clinical trial was conducted to evaluate the efficacy of two live attenuated mumps-measles vaccines, the Urabe Am 9-Schwarz and the Jeryl Lynn-Moraten vaccine, in 400 young children aged 9 months-4.5 years (median 13.4 months). Antibody responses to both vaccine components were measured by the enzyme-linked immunosorbent assay (ELISA); 96.9% of the seronegative children who received the Urabe Am 9-Schwarz vaccine showed satisfactory mumps antibody responses compared to 90% of the Jeryl Lynn-Moraten vaccine recipients (P less than .01). Similar proportions of both groups, 98.5% and 96.8%, respectively, developed measles virus specific antibodies. Both vaccines were equally well tolerated and clinically acceptable.     

Sensitivity and specificity of the Rey Dot Counting Test in patients with suspect effort and various clinical samples.

The Rey Dot Counting Test was administered to 100 patients with suspect effort drawn from two separate settings (personal injury/disability, n=86; prison hospital, n=14) and to 251 subjects in nine clinical groups (head injury, learning disability, right and left cerebrovascular accident, schizophrenia, older normals, depressed elderly, and mild and moderate dementia). Sensitivity of cut-offs for individual test scores (mean grouped dot counting time, ratio of mean grouped to ungrouped dot counting time, and number of errors) differed markedly across the two suspect effort groups (e.g., 28-100%), indicating that noncredible patients drawn from different settings employ somewhat differing approaches in their fabrication of cognitive symptoms. Use of a cut-off of > or =17 applied to a combination score (mean ungrouped dot counting time+meangrouped dot counting time+number of errors) resulted in 100% sensitivity in the forensic suspect effort group and 75% sensitivity in the civil litigation/disability suspect effort group, while maintaining specificity of > or =90% for the clinical groups combined (excluding moderate dementia).     

Cranial neuropathy associated with primary amyloidosis

We report 6 patients for whom cranial neuropathy was a major manifestation of primary amyloidosis. In 3 of the 6, multiple cranial nerves were involved. All had tissue biopsy documentation of amyloidosis. In 2, nerve biopsy also confirmed amyloidosis. All had renal involvement manifested by proteinuria. Primary systemic amyloidosis must be considered in the differential diagnosis of cranial neuropathy, especially when proteinuria is present.     

Cellular events associated with peripherally induced rejection of mature neural xenografts placed into neonatal rat brains

Various circumstances have brought about a dispute concerning the immunologically priviledged status of the central nervous system (CNS). Using a transplantation paradigm, we have examined the cellular events associated with an experimentally induced focal assault on the CNS by the immune system. Chunks of embryonic mouse cortex were transplanted into neonatal rat brains and allowed to survive for 4 weeks. The adult rats then received a skin graft of donor origin to induce rejection of the transplanted tissue. Animals were sacrificed at various time points and examined histologically and immunocytochemically. Under these circumstances, the transplant is rejected via a first-set rejection response, and astrocytes of donor origin appear to be the primary target of the host immune system. Expression of class I and class II major histocompatibility antigens is noted to correlate with lymphocytic invasion of the transplant.     

Microglia enhance manganese chloride-induced dopaminergic neurodegeneration: Role of free radical generation

Exposure to elevated levels of manganese has been shown to cause neuronal damage in the midbrain and the development of Parkinsonian symptoms. Activation of microglia and release of neurotoxic factors in particular free radicals are known to contribute to neurodegeneration. We have recently reported that manganese chloride (MnCl₂) stimulates microglia to produce reactive oxygen species (ROS). The aim of this study is to determine the role of microglia in the MnCl₂-induced degeneration of dopaminergic (DA) neurons that are particularly vulnerable to oxidative insult. MnCl₂ (10-300 μM; 7 days) was markedly more effective in damaging DA neurons in the rat mesencephalic neuron-glia cultures than the neuron-enriched (microglia-depleted) cultures. In addition, the microglia-enhanced MnCl₂ toxicity was found to be preferential to DA neurons. The microglial enhancement of DA neurotoxicity was further supported by the observation that replenishment of microglia to the neuron-enriched cultures significantly increased the susceptibility of DA neurons to the MnCl₂-induced damage. Analysis of the temporal relationship between microglial activation and DA neurodegeneration revealed that MnCl₂-stimulated microglial activation preceded DA neurodegeneration. Mechanistically, MnCl₂ (10-300 μM) stimulated a concentration- and time-dependent robust production of ROS and moderate production of nitric oxide but no detectable release of tumor necrosis factor-alpha and interleukin-1beta. Application of free radical scavengers including superoxide dismutase/catalase, glutathione, N-acetyl cysteine and an inhibitor of nitric oxide biosynthesis significantly protected DA neurons against the MnCl₂-induced degeneration. These results demonstrate that microglial activation and the production of reactive nitrogen and oxygen free radicals promote the MnCl₂-induced DA neurodegeneration.     

Laryngeal cancer incidence among workers exposed to acid mists (United States)

In 1992, the International Agency for Research on Cancer (IARC) determined that sufficient evidence existed to classify sulfuric acid mists as a human carcinogen, based primarily on six human studies. Possible mechanisms include irritation of epithelial cells in conjunction with cigarette smoking, or a direct genotoxic effect due to a modification of cellular pH. We have followed 1,031 men exposed to acid mists in the steel industry in the United States, via mailed questionnaire and telephone interview, extending by 10 years a prior follow-up of this cohort. These workers averaged 9.2 years of exposure, with an average first year of exposure of 1949. The primary exposure was to sulfuric acid mist, although part of the cohort was exposed to other acid mists. Fourteen laryngeal cancers were observed in the cohort compared with 5.6 expected based on US rates, with follow-up through 1994. A 14 percent upward adjustment in expected cancers due to differences in tobacco and alcohol consumption led to 6.4 laryngeal cancers expected, yielding a rate ratio of 2.2 (95 percent confidence interval=1.2-3.7). Our findings are consistent with previous findings from this cohort and from most other studies, and tend to confirm IARC's classification of acid mists as a human carcinogen. The occupational exposures of this cohort were at least an order of magnitude higher than usual ambient exposures in urban air.