Botulinum versus tetanus neurotoxins: Why is botulinum neurotoxin but not tetanus neurotoxin a food poison?

Botulinum and tetanus neurotoxins, produced by Clostridium botulinum and Clostridium tetani, respectively, are the most poisonous poisons known to mankind. Although botulinum and tetanus neurotoxins share several characteristics, such as similar mol. wts, similar macrostructure, virtually identical mode of action, and a strong amino acid sequence homology, the two neurotoxins differ in one very significant way; only botulinum neurotoxin is a food poison. Factors responsible for the food poisoning potential of botulinum neurotoxins seem to be a group of complexing proteins that are also produced by C. botulinum, and are known to associate with the neurotoxin. Translation products of nucleotide sequences upstream to the neurotoxin genes of serotypes A, B, C, D, E and F botulinum neurotoxin reveal the location of genes for one of the complexing proteins that could be transcribed as polycistronic mRNA to include neurotoxin sequences. No such protein seems to be present in C. tetani, suggesting that the lack of complexing proteins might be responsible for tetanus not being a food poison.     

Spontaneous regression of extramedullary plasmacytoma--a case report

A case of extramedullary plasmacytoma in the soft tissues of the posterior chest wall of an 80-year old man is reported herein. Immunofluorescence study showed that the tumor cells produced IgG lambda. An M-component was also detected in the patient's serum by paper electrophoresis. Two months following the open biopsy done to establish diagnosis, the tumor underwent spontaneous regression and the M-component in the serum also disappeared. This is the first case report of spontaneous regression of an extramedullary plasmacytoma and the probable reasons for this spontaneous regression are discussed herein.     

Soluble factors released by the target organ enhance the urokinase-type plasminogen activator activity of metastatic tumor cells

The ability of tumor cells to respond to microenvironmental factors present in the target organ may be necessary for successful metastasis. Many studies suggest that urokinase-type plasminogen activator (u-PA) has a significant role in several steps of the metastatic process. In previous work it had been observed that lung conditioned media stimulated the migration and growthin vitro of cells from a murine mammary adenocarcinoma (M3) with moderate lung metastasizing potential. In the same experiments liver conditioned medium exerted a marked cytostatic effect on M3 cells. The aim of the present work to investigate whether conditioned media from lung, kidney or liver, were able to modulate u-PAin vitro secretion by these murine M3 cells. Secreted u-PA measured by fibrinolytic assay, was significantly increased only when M3 primary cultured cells were treated for 24 h with lung conditioned media prepared from normal mice or from mice bearing a small tumor. Exposure to kidney or liver conditioned media did not modify the u-PA secretion pattern already shown by the tumor cells. The activity shown by lung conditioned media seemed to be specific for these syngeneic tumor cells, as no effect was observed on murine embryo cells. These results suggest that soluble factors released by the target organ could specifically induce tumor cellsin vivo to enhance the production of degradative enzymes, thus facilitating the last steps of the metastatic cascade.     

An immediate light microscopic response of neuronal somata,dendrites and axons to contusing concussive head injury in the rat

Summary Thirty-four rats were killed by transcardial perfusion fixation 1 min after a contusing concussive head injury, and 17 rats 1 day later. From the results obtained with a new silver method demonstrating traumatically damaged neuronal somata, dendrites and axons the following conclusions were drawn: (1) outside the contused territories all features of traumatically induced neuronal argyrophilia are similar to those found in non-contusing concussive head injury, as reported in an accompanying paper; (2) within contused territories the neuronal argyrophilia is abolished by some substance released either from damaged blood vessels or from damaged parenchymal cells, while the neuronal damage otherwise underlying the induction of argyrophilia is present; (3) different phenotypes of neurons are vulnerable to different values of the parameters of the intracranial pressure wave generated by the trauma; (4) some of the neurons may recover from the traumatically induced argyrophilic damage; (5) traumatically induced inundation of neurons with extracellular tracers, as reported by other authors, and somato-dendritic argyrophilia may be different manifestations of one and the same phenomenon; and (6) diffuse primary traumatic axonal injury in human neuropathology may be closely correlated to axonal argyrophilia.     

Protection from environmental tobacco smoke in California. The case for a smoke-free workplace.

OBJECTIVE--To determine the extent of exposure of nonsmoking indoor workers to environmental tobacco smoke (ETS) according to type of work-site smoking policy, work area, workplace size, and demographic characteristics. DESIGN AND PARTICIPANTS--Participants included 7162 adult, nonsmoking, indoor workers who were interviewed as part of the 1990 California Tobacco Survey. Respondents were asked whether anyone had smoked in their work area within the past 2 weeks. RESULTS--An estimated 2.2 million California nonsmokers were exposed to tobacco smoke at indoor work sites in 1990. Nonsmoker exposure to ETS was 9.3% for those working in a smoke-free worksite, 23.2% for those working where there was only a work-area restriction, 46.7% for those working where there was a policy that did not include the work area, and 51.4% for those working where there was no work-site smoking policy. After adjustment for type of work area (eg, office, open area), workplace size, and demographic factors, it was determined that nonsmokers working where there was only a work-area ban were 2.8 times more likely to be exposed to ETS than those working in a smoke-free work site. In workplaces with no policy or a policy not covering the work area, nonsmokers were over eight times more likely to be exposed to ETS than those who worked in a smoke-free work site. Nonsmokers who were 18 to 24 years of age, male, or Hispanic, and those with less than a high school education had more exposure to ETS. CONCLUSION--These results indicate that adequate protection of nonsmokers from ETS exposure requires a smoke-free work site.     

Martin-Bell syndrome. Improved possibilities for molecular genetic diagnosis]

In a former molecular segregation analysis of fra x mental retardation in 27 families at risk we had used marker gene probes with a relatively high recombination fraction. Thus, the resulting risk for a false diagnosis was comparatively high. To diminish this risk, all families were reanalyzed with the newly invented and more closely linked gene probes RN1A, VK23B, VK21C and U6.2. Using these probes as molecular markers we performed Southern hybridization experiments. The remaining diagnostic risk due to recombination events could be reduced to 2% up to 20% compared to preanalysis. The portion of informative families (91%) is in good agreement with the expected cumulative heterozygosis frequency of 93.4% for all 4 markers investigated. This high frequency and the very low remaining risk for a false diagnosis therefore enable a far more precise molecular diagnostic of the Martin-Bell-syndrome.