Isolation and characterization by conventional methods and genetic transformation of Psychrobacter and Acinetobacter from fresh and spoiled meat, milk and cheese.

Of 126 samples of fresh and spoiled meat and dairy products, 40% were positive for the presence of Moraxella-like bacteria and 64% of Acinetobacter; 279 and 466 strains, respectively, were isolated and a part of these were tested by biochemical methods and DNA transformation assays. In some cases, the Moraxellaceae in the samples examined reached considerable quantitative levels, but their percentage in the microflora was generally low. Moraxella-like bacteria were predominant in fresh meat, Acinetobacter in spoiled meat and milk. Most acinetobacters belonged to biotype lwoffii (sensu lato) and all 90 strains tested were positive for DNA transformation with an auxotrophic Acinetobacter. Moraxella-like bacteria were identified as Psychrobacter immobilis in 96% of 103 transformation assays. Moraxellaceae show lipolytic activity but they are considered of low incidence in food spoilage. Only 3.7% of acinetobacters from dairy sources was able to produce ropy milk. Unlike strains from clinical isolates, psychrobacters and acinetobacters isolated from food often do not grow at 37 degrees C.     

Chronic inhibition of NOS does not prevent plasticity of rat somatosensory (S1) cortex following deafferentation

Nitric oxide (NO) has been proposed as an intercellular messenger mediating postsynaptic to presynaptic information transfer in the induction of long-term potentiation. A number of studies support the possible involvement of NO in synaptic plasticity. NO may have a role in synaptogenesis and synaptic plasticity in developing rat brain and may play a fundamental part in the process of regeneration, plasticity, and retargeting of axons following injury. We examined the possible role of NO on plasticity in the rat first somatosensory cortex with [14C]2-deoxyglucose (2-DG) autoradiography in rats treated daily with l-nitroarginine (l-NA) following neonatal unilateral vibrissae deafferentation. After 6 weeks of l-NA treatment, the local cerebral glucose utilization (LCGU) and the spatial extent of the metabolic activation following stimulation of the spared whisker was measured. NOS catalytic activity exhibited significant inhibition throughout the treatment period. Vibrissae deafferentation produced a small but not statistically significant increase of LCGU in the vibrissa activated C3 barrel, and l-NA treatment did not alter the activation of LCGU in the deafferented cortex following whisker stimulation. Additionally, l-NA treatment did not alter the area of metabolic activation on either the non-deafferented side or the deafferented side. Deafferentation produced a 298% increase in the metabolic representation of the spared C3 barrel following stimulation in the saline treated animals, a 257% increase in the chronically l-NA treated animals, and a 256% increase in the short-term treated animals, all with respect to the response in the non-deafferented cortex. Metabolic plasticity in the barrel cortex was not attenuated by l-NA treatment. These results show that nitric oxide does not play a major role on developmental cortical plasticity induced by vibrissae deafferentation in the rat.     

Ionic mechanisms of action of neurotensin in acutely dissociated neurons from the diagonal band of Broca of the rat

Whole cell recordings were performed on acutely dissociated neurons from the horizontal limb of the diagonal band of Broca (hDBB) from rats to elucidate the ionic mechanisms of action of neurotensin. Neurotensin caused a decrease in whole cell voltage-activated outward currents and failed to elicit a response when Ca2+ influx was blocked by changing the external solution to the one containing 0 mM Ca2+ and 50 microM Cd2+, suggesting the involvement of Ca2+-dependent conductances. Charybdotoxin, a specific blocker of voltage-sensitive calcium-activated K+ channels (IC), caused a decrease in outward currents comparable with that caused by blocking calcium influx and occluded the neurotensin-induced decrease in outward currents. Similarly, 50 microM tetraethylammonium ions also blocked the neurotensin response. Also neurotensin reduced whole cell barium currents (IBa) and calcium currents (ICa). Amiloride and omega-conotoxin GVIA, but not nimodipine, were able to eliminate the neurotensin-induced decrease in IBa. Thus T- and N- but not L-type calcium channels are subject to modulation by neurotensin, and this may account for its effects on IC. The predicted changes in action potential as a result of the blockade of currents through calcium channels culminating into changes in IC were confirmed in the bridge current-clamp recordings. Specifically, neurotensin application led to depolarization of the resting membrane potential, broadening of spike and a decrease in afterhyperpolarization and accommodation. These alterations in action potential characteristics that resulted in increased firing rate and excitability of the hDBB neurons also were produced by application of charybdotoxin. Neurotensin effects on these properties were occluded by 2 - [(1 - 7 - chloro - 4 - quinolinyl) - 5 - (2, 6 - di - methoxyphenyl) pyrazol-3-yl) carbonylamino] tricyclo (3.3.1.1.)decan-2-carboxylic acid, a nonpeptide high-affinity neurotensin receptor antagonist. Neurotensin blockade of IC, possibly through ICa, is a potential physiological mechanism whereby this peptide may evoke alterations in the cortical arousal, sleep-wake cycle, and theta rhythm.     

Early hormonal and surgical treatment of cryptorchidism

PURPOSE: We investigated the efficacy of early gonadotropin treatment of cryptorchidism for promoting testicular descent and ameliorating testicular histology. MATERIALS AND METHODS: We treated 319 cryptorchid testes in 281 boys 4 months to 3 years old with luteinizing hormone-releasing hormone and human chorionic gonadotropin sequential therapy. Surgery was done on the 207 testes that did not respond to medical treatment. Microscopic biopsies were performed in 134 of these 207 testes. Histological findings were compared to those of 30 cryptorchid testes in boys younger than 1 year who underwent surgery without previous hormonal treatment. RESULTS: Combined luteinizing hormone-releasing hormone and human chorionic gonadotropin treatment induced scrotal descent of a percentage of cryptorchid testes depending on clinical position. Therapeutic success was greater when testes were in a lower position and results were not age dependent. Hormonal treatment of cryptorchidism during the first year of life stimulated spermatogonia maturation. CONCLUSIONS: When administered at the end of age 6 months, hormonal treatment can be considered an effective and timely substitution for gonadotropin and testosterone insufficiency in cryptorchid infants. Therefore, we recommend this therapeutic procedure combined with surgery in the first year of life.