Electrical low-frequency stimulation induces central neuroplastic changes of pain processing in man.

Electrical low-frequency stimulation (LFS) inhibits pain perception and nociceptive processing as shown by psychophysical and electrophysiological means (long-term depression, LTD). Information regarding central mechanisms involved in LTD induction and maintenance are still missing. This study hypothesizes that electrical LFS induces changes in activation pattern of pain-related brain areas. Thirty-two electrophysiological and psychophysical experiments were performed in 16 healthy volunteers. Painful electrical test stimulation (0.125 Hz, 60 pulses) and conditioning LFS (1 Hz, 1200 pulses) were applied by a concentric electrode to the right hand. Test stimulation series were performed before (Pre) and after LFS (Post) or no stimulation period (Control). Volunteers rated pain perception according to a verbal rating scale (0-100). Somatosensory evoked cortical potentials were recorded with 64-channel electroencephalography. Individual dipole source modeling using CURRY software (Compumedics, Hamburg, Germany) yielded information about dipole location and strength. The strongest decrease in LFS-induced pain perception was shown after LFS (p < 0.01). Topographic distribution of cortical potentials revealed reproducible negative (N1, N2) and positive (P2) components. Dipole magnitude analysis showed a significant difference between Post LFS and Post Control for P2 (p < 0.01). P2 dipole location analysis yielded a significant posterior (p < 0.05) shift following LTD induction. Thus, data reveal central changes of pain processing after LTD induction. These experiments may help judging the potency of LTD as model for electrostimulation in future analgesic therapy.

The Mad side of the Max network: antagonizing the function of Myc and more.

A significant body of evidence has been accumulated that demonstrates decisive roles of members of the Myc/Max/Mad network in the control of various aspects of cell behavior, including proliferation, differentiation, and apoptosis. The components of this network serve as transcriptional regulators. Mad family members, including Mad1, Mxi1, Mad3, Mad4, Mnt, and Mga, function in part as antagonists of Myc oncoproteins. At the molecular level this antagonism is reflected by the different cofactor/chromatin remodeling complexes that are recruited by Myc and Mad family members. One important function of the latter is their ability to repress gene transcription. In this review we summarize the current view of how this repression is achieved and what the consequences of Mad action are for cell behavior. In addition, we point out some of the many aspects that have not been clarified and thus leave us with a rather incomplete picture of the functions, both molecular and at the cellular level, of Mad family members.

Inhibition of proliferation and apoptosis by the transcriptional repressor Mad1. Repression of Fas-induced caspase-8 activation.

Mad1 is a member of the Myc/Max/Mad network of transcriptional regulators that play a central role in the control of cellular behavior. Mad proteins are thought to antagonize Myc functions at least in part by repressing gene transcription. To systematically examine the function of Mad1 in growth control and during apoptosis, we have generated U2OS cell clones that express Mad1 under a tetracyline-regulatable promoter (UTA-Mad1). Mad1 was induced rapidly and efficiently, localized to the nucleus, and bound to DNA as a heterodimer with Max. The induction of Mad1 reduced cellular growth and, more profoundly, inhibited colony formation of UTA-Mad1 cells. Conditioned medium neutralized this inhibitory effect implying that Mad1 function is regulated by extracellular signals. In addition Mad1 interfered with Fas-, TRAIL-, and UV-induced apoptosis, which coincided with a reduced activation of caspase-8 during Fas-mediated apoptosis in response to Mad1 expression. Furthermore, microinjection of Mad1-expressing plasmids into fibroblasts inhibited apoptosis induced by the oncoproteins c-Myc and E1A. Thus, Mad1 not only interferes with cellular proliferation but also with apoptosis, which defines a novel aspect of Mad1 function.

Phallus-inflammation of ganders: clinical observations and comparative bacteriological examinations of healthy and altered organs.

The examination of acute or chronically altered phallus-tissues of ganders revealed microorganisms belonging to the genera Mycoplasma, Bacteroides, Clostridium, Streptococcus, Micrococcus, Staphylococcus, Lactobacillus, Corynebacterium, Escherichia, Campylobacter, Proteus, Pseudomonas and Candida and to the family Pasteurellaceae, isolated in different frequencies. Bacteriologic examinations of the phallus-tissues and cloacal mucous membranes of healthy juvenile ganders showed microorganisms of the same genera or family, except Mycoplasma and Candida spp. Pathogenesis and possibilities of treating phallus-inflammations in ganders are discussed.

Studies in vivo on the efficacy of enrofloxacin against Mycoplasma gallisepticum.

After a 5-day medication with drinking water containing 50 ppm enrofloxacin, Mycoplasma gallisepticum (MG) was culturally reisolated in only one of 80 broiler chicks and specific antibodies to MG were detected in none of the 40 birds tested. Medication with 50 ppm for 3 days and 25 ppm for 5 days was only slightly less effective. A significant decline in efficacy was observed, however, when enrofloxacin was added to the drinking water at 50 ppm for 1 day or 12.5 ppm for 5 days. Tiamulin was also significantly effective (250 ppm, 3 days). However, measured by the cultural reisolation of the pathogen and the presence of antibodies to MG. enrofloxacin (50 ppm, 3 days) proved to be more effective. Treatment with tylosin (50 ppm. 5 days) conferred no significant protection.

[Salmonella gallinarum field isolates of the biovars pullorum and gallinarum]. / Uber Salmonella gallinarum-Feldisolate der Biovare Pullorum und Gallinarum.

In 40 cases salmonellae of the serovar Salmonella (S.) gallinarum were culturally isolated from domesticated gallinaceous birds submitted for diagnostic purposes in the period of 1979-1989. On the basis of the cultural and biochemical features found 35 of them could be assigned to the biovar Pullorum and 5 to the biovar Gallinarum. Of 35 isolates of the biovar Pullorum, 29 were isolated from pure bred chickens of small fancy-exhibition type flocks, 4 from floor-housed adult brown hybrid laying hens and one each from broiler chicks and pheasant chicks (Phasianus colchicus). Acute to subacute courses of the pullorum disease were observed in the 4 flocks of brown hybrid hens. Of 5 isolates of the biovar Gallinarum, 4 were isolated from adult brown hybrid laying hens kept in battery cages and one from floor-housed brown hybrid pullets of the laying type. First cases of fowl typhoid occurred early in the summer of 1988. The disease was characterized by a peracute course in the 4 flocks of brown laying hens and by a more acute course in the pullet flock. The primary source of the fowl typhoid producing organisms was not elucidated.