The valuation of malnutrition in the mono-digestion of maize silage by anaerobic batch tests.

Anaerobic digestion is a technology which is used to produce methane from organic solids and energy crops. Especially in recent years, the fermentation of energy crops has become more and more important because of increasing costs for energy and special benefits for renewable energy sources in Germany. Anaerobic bacteria require macro and micro nutrients to grow. Absence of these elements can inhibit the anaerobic process significantly. In particular mono-substrates like maize or certain industrial wastewater often cannot provide all required nutrients. For this reason this research investigates the influence of substrate and trace elements on anaerobic digestion in detail. Different agricultural anaerobic biomasses are analysed with special regard to their trace element content. Based on these results, the influence of three trace elements (iron, cobalt, and nickel) on anaerobic digestion was studied in anaerobic batch tests at different sludge loading rates and for different substrates (maize and acetate). Biogas production was found to be 35% for maize silage and up to 70% higher for acetate with trace element dosage than in the reference reactor.

Energy- and CO2-reduction potentials by anaerobic treatment of wastewater and organic kitchen wastes in consideration of different climatic conditions.

The classical municipal wastewater treatment in Germany consists of an aerobic carbon and nitrogen elimination and mostly an anaerobic sludge treatment. Organic kitchen wastes from separate waste collection as well as yard wastes are converted mostly in composting plants to soil conditioner. With these conventional types of treatment, the energy potential in waste and wastewater is lost due to aerobic material conversion. In this article three scenarios for the treatment of municipal wastewater and waste are compared on the subject of energy efficiency and useable potential: Sc1. the classical wastewater treatment and the composting of the organic waste fraction, Sc2. the anaerobic treatment of wastewater combined with deammonification and the digestion of the organic waste fraction, and Sc3. a mutual anaerobic treatment of wastewater and waste as co-digestion with deammonification. The calculation of energy and CO2-balance considers different climatic conditions. In case of using anaerobic treatment, not only the energy balance will be positive, also the CO2-balance is improved by the substitution of fossil fuels with generated biogas.

Anaerobic treatment of municipal wastewater using the UASB-technology.

The anaerobic treatment of municipal wastewater enables new applications for the reuse of wastewater. The effluent could be used for irrigation as the included nutrients are not affected by the treatment. Much more interesting now are renewable energies and the retrenchment of CO(2) emission. With the anaerobic treatment of municipal wastewater, not only can the CO(2) emission be reduced but "clean" energy supply can be gained by biogas. Most important for the sustainability of this process is the gathering of methane from the liquid effluent of the reactor, because the negative climate-relevant effect from the degassing methane is much higher than the positive effect from saving CO(2) emission. In this study, UASB reactors were used with a flocculent sludge blanket for the biodegradation of the carbon fraction in the wastewater with different temperatures and concentrations. It could be shown that the positive effect is much higher for municipal wastewater with high concentrations in hot climates.

Chemical LTD in the CA1 field of the hippocampus from young and mature rats.

Within the hippocampal formation, two forms of long-lasting synaptic plasticity, long-term potentiation (LTP) and long-term depression (LTD), can be induced which require the activation of NMDA receptors. Interestingly, it has been shown that both LTP and LTD are reduced in adult animals. Recently, a new chemical protocol has been described which elicits LTD in the CA1 field of the hippocampus. Application of 20 microM NMDA for 3 min results in a stable and long-lasting decrease in the evoked synaptic responses. We used this protocol to induce LTD in hippocampal slices from young and adult rats and show that this form of LTD is AP5-sensitive and can be blocked by the protein phosphatase inhibitor cyclosporin A in slices from adult animals. In contrast to electrical LTD (induced by prolonged low frequency stimulation), the extent of chemical LTD was not different between the young and adult rats. These findings indicate that the intracellular signal transduction cascades involved in long-lasting synaptic depression are still intact in adult animals.

Effects of changes in glucose concentration on synaptic plasticity in hippocampal slices.

The effects of a low or high concentration of glucose in the perfusion medium on synaptic activity and plasticity were studied in hippocampal slices from rats. Low-glucose medium depressed the field excitatory post-synaptic potentials (fEPSP) significantly, whereas high-glucose medium had little effect on the fEPSP. Tetanization of the afferent fibres elicited significant potentiation (LTP) of synaptic activity irrespective of the glucose concentration in the medium. This may indicate that LTP induction does not depend on optimal neural transmission. Paired-pulse facilitation (PPF) experiments showed that the medium glucose concentration did not significantly influence potentiation of the second response.

Hippocampal synaptic plasticity in streptozotocin-diabetic rats: impairment of long-term potentiation and facilitation of long-term depression.

Streptozotocin-diabetic rats, an animal model for diabetes mellitus, show learning deficits and impaired long-term potentiation in the CA1-field of the hippocampus. The present study aimed to further characterize the effects of streptozotocin-diabetes on N-methyl-D-aspartate receptor-dependent long-term potentiation in the CA1-field, to extend these findings to N-methyl-D-aspartate receptor-dependent and independent long-term potentiation in other regions of the hippocampus and to examine effects on long-term depression. First, the effect of diabetes duration on long-term potentiation in the CA1-field was determined. A progressive deficit was observed after a diabetes duration of six to eight weeks, which reached a maximum after 12 weeks of diabetes and remained stable thereafter. Next, long-term potentiation was examined in the dentate gyrus and in the CA3-field after 12 weeks of diabetes. Both were found to be impaired compared to controls. Finally, long-term depression was examined in the CA1-field of the hippocampus after 12 weeks of diabetes and found to be enhanced in slices from diabetic rats compared to controls. Changes in synaptic plasticity were observed in hippocampal slices from streptozotocin-diabetic rats. Expression of N-methyl-D-aspartate receptor-dependent long-term potentiation was impaired in the CA1-field and dentate gyrus and expression of N-methyl-D-aspartate receptor-independent long-term potentiation was impaired in the CA3-field. In contrast, expression of long-term depression was facilitated in CA1. It is suggested that this combination of changes in plasticity may reflect alterations in intracellular signalling pathways.

Water maze learning and hippocampal synaptic plasticity in streptozotocin-diabetic rats: effects of insulin treatment.

Streptozotocin-diabetic rats express deficits in water maze learning and hippocampal synaptic plasticity. The present study examined whether these deficits could be prevented and/or reversed with insulin treatment. In addition, the water maze learning deficit in diabetic rats was further characterized. Insulin treatment was commenced at the onset of diabetes in a prevention experiment, and 10 weeks after diabetes induction in a reversal experiment. After 10 weeks of treatment, insulin-treated diabetic rats, untreated diabetic rats and non-diabetic controls were tested in a spatial version of the Morris water maze. Next, hippocampal long-term potentiation (LTP) was measured in vitro. To further characterize the effects of diabetes on water maze learning, a separate group of rats was pre-trained in a non-spatial version of the maze, prior to exposure to the spatial version. Both water maze learning and hippocampal LTP were impaired in diabetic rats. Insulin treatment commenced at the onset of diabetes prevented these impairments. In the reversal experiment, insulin treatment failed to reverse established deficits in maze learning and restored LTP only partially. Non-spatial pre-training abolished the performance deficit of diabetic rats in the spatial version of the maze. It is concluded that insulin treatment may prevent but not reverse deficits in water maze learning and LTP in streptozotocin-diabetic rats. The pre-training experiment suggests that the performance deficit of diabetic rats in the spatial version of the water maze is related to difficulties in learning the procedures of the maze rather than to impairments of spatial learning.

Increasing age reduces expression of long-term depression and dynamic range of transmission plasticity in CA1 field of the rat hippocampus.

Long-term depression, depotentiation and long-term potentiation of field excitatory postsynaptic potentials in the CA1 field of the hippocampus were studied in slices from two-, 12-, 24- and 36-week-old rats. Long-term potentiation was induced by stimulating afferent fibres for 1 s at 100 Hz. Long-term depression was induced either by stimulating the afferent pathways twice for 15 min at 1 Hz (protocol 1), giving in total 1800 pulses, or by stimulating the fibres at 5 min intervals twice at 1 Hz for 5 min followed by 5 min stimulation at 5 Hz (protocol 2), giving in total 2100 pulses. We found significant long-term depression in slices of all groups stimulated with protocol 1; however, the magnitude of long-term depression in slices from 24- and 36-week-old rats was significantly lower than that in slices from two- and 12-week old rats, although there was no such difference in the magnitude of long-term potentiation between slices. Stimulation protocol 2 induced long-term depression only in slices from two- and 12-week-old rats. Comparison of the dynamic range of transmission plasticity in slices from two- and 36-week-old rats, calculated as the difference between the nearly saturated long-term potentiation and nearly saturated depotentiation, revealed a significantly smaller dynamic range in slices from 36-week-old rats in comparison with slices from two-week-old animals. The decrease in the dynamic range in slices from 36-week-old rats was due to a diminished capacity to depotentiate the nearly saturated long-term potentiation and not due to a decreased long-term potentiation expression in these slices. In contrast to long-term depression, in which the slope of the field excitatory postsynaptic potentials consistently and significantly decreased below the baseline level, the nearly saturated depotentiation did not decrease below the original, pre-long potentiation baseline level. The results demonstrate that increasing age reduces expression of long-term depression and the dynamic range of transmission plasticity.

Effects of vasopressin and related peptides on neurons of the rat lateral septum and ventral hippocampus.

The effects of vasopressin (VP), VP fragments and propressophysin glycopeptide on neuronal activities in the septum-hippocampus complex of rats were studied in vitro and in vivo. The frequency of the hippocampus theta rhythm in Brattleboro rats homozygous for diabetes insipidus was significantly slower than that of heterozygous litter mates and normal rats. Intracerebroventricular micro-injection of des-glycine-amide vasopressin corrected for several hours the frequency deficit of the theta rhythm in the homozygous Brattleboro rats and the centrally administered VP slowed down theta rhythm in normal rats. Microinotophoretically administered VP excited single neurons in the lateral septum of ventral hippocampus, and/or facilitated the responses of these neurons to glutamate and to stimulation of the glutamatergic afferent fibers in the fimbria bundle. The excitatory effects of VP vanished within seconds after termination of the peptide administration, however, the peptide-induced enhancement of glutamate and syntatically induced excitations were sustained for up to 60 min after the peptide administration. In vitro, pM concentrations of VP, VP 4-8 and C-terminus glycopeptide of propresophysin facilitated for 30-60 min the glutamate-mediated EPSPs in neurons of the lateral septum or the ventral hippocampus. The EPSPs increase in the lateral septum neurons was not prevented by pretreatment with antagonist of the V1a type of the vasopressin receptor. The resting membrane potential and input resistance were not affected by the peptides. A low-frequency electrical stimulation in the diagonal Band of Broca or in the Bed nucleus of the stria terminals, sources of the vasopressinergic innervation of the septum, facilitated the negative wave of the filed potentials responses evoked in the lateral septum by stimulating the fimbria bundle fibers in control Long-Evans and Brattleboro rats heterozygous for diabetes insipidus. The field potential increase was sustained for several hours after the stimulation, and it was not occluded by long-term potentiation elicited by high frequency stimulation of the fimbria bundle afferent fibers. Brattleboro rats homozygous for diabetes insipidus failed to show the filed potential increase after the diagonal band stimulation. It is suggested that the long-lasting facilitation of glutamate-mediated excitations might be a physiological action of the propressophysin-derived peptides in the septum-hippocampus complex which, in concert with other forms of synaptic plasticity like the long-term potentiation, facilitates the hippocampus-mediated forms of learning and memory. This action is presumably related to the memory enhancing effect of the propressophysin-derived peptides.

[Neurogenic sarcoma of the vagal nerve]. / Nerwiakomiesak (nerilemmona sarcomatosum) nerwu blednego.

A rare case of neurogenic sarcoma of the vagal nerve was presented. Ten cases of such location have been described so far. Neurogenic sarcoma derives from supported elements of peripheral nerves. Its development is asymptomatic and usually the first manifestation is the occurrence of the tumour. This kind of disease is local malignant neoplasm, but it can give metastases, and then the prognosis is significantly worse. The modern treatment is radiotherapy with preceding radical dissection.

Place learning and hippocampal synaptic plasticity in streptozotocin-induced diabetic rats.

Moderate impairment of learning and memory has been recognized as a complication of diabetes. The present study examined behavioral and electrophysiological measures of cerebral function in streptozotocin (STZ)-induced diabetic rats. Behavioral testing consisted of a spatial learning task in a water maze. Electrophysiological testing consisted of in vitro assessment of hippocampal long-term potentiation (LTP), an activity-dependent form of synaptic plasticity, which is believed to be related to the cellular mechanisms of learning and memory. Two experiments were performed: the first with severely hyperglycemic rats and the second with moderately hyperglycemic rats. Rats were tested in the water maze 11 weeks after induction of diabetes. Next, LTP was measured in vitro in trained animals. Both spatial learning and LTP expression in the CA1 field of the hippocampus were impaired in severely hyperglycemic rats as compared with nondiabetic controls. In contrast, spatial learning and hippocampal LTP were unaffected in moderately hyperglycemic rats. The association of alterations in hippocampal LTP with specific learning impairments has previously been reported in conditions other than diabetes. Our findings suggest that changes in LTP-like forms of synaptic plasticity in the hippocampus, and possibly in other cerebral structures, are involved in learning deficits in STZ-induced diabetes. The beneficial effect of moderate glycemic control on both place learning and hippocampal LTP supports the significance of the relation between these two parameters and indicates that the development of the observed deficits may be related to the level of glycemic control.

Pre- and postnatal development of dopaminergic neuron numbers in the male and female mouse midbrain.

Quantitative information about dopaminergic neuron numbers in the mesencephalon is needed to assess the significance of physiological cell death in the regulation of the development of this neural system. Therefore, stereological techniques were applied to determine absolute numbers of mesencephalic neurons immunoreactive to tyrosine hydroxylase during the ontogenetic period between embryonic day (E) 13 and postnatal day (P) 90. Male and female CBA/J mice were examined separately. The most rapid development with a 2.5-fold increase of total counts of immunostained cells per midbrain took place in the prenatal period. Beginning at E21, immunostained cells were counted separately in their three main locations, substantia nigra (SN), ventral tegmental area (VTA), and retrorubral field (RRF). Neuron numbers in RRF and VTA reached adult levels perinatally. In contrast, counts of immunostained cells in SN continued to increase postnatally. The only sign of cell loss was a transient decrease in VTA cell numbers (but not in total numbers of immunostained midbrain neurons) between E21 and P14. There were no statistically significant sex differences in cell numbers at any time point investigated. It is concluded that physiological cell death is not a major factor in the developmental regulation of dopaminergic cell numbers in the mouse midbrain.

Long-lasting enhancement of synaptic excitability of CA1/subiculum neurons of the rat ventral hippocampus by vasopressin and vasopressin(4-8).

Vasopressin (VP) is axonally distributed in many brain structures, including the ventral hippocampus. Picogram quantities of VP injected into the hippocampus improve the passive avoidance response of rats, presumably by enhancing memory processes. Vasopressin is metabolized by the brain tissue into shorter peptides, such as [pGlu4,Cyt6]VP(4-9) and [pGlu4,Cyt6]VP(4-8), which preserve the behavioral activity but lose the peripheral activities of the parent hormone. Using brain slices, we investigated whether VP or VP(4-8) affects excitatory postsynaptic potentials (EPSPs) and/or membrane responses to depolarization in neurons of the CA1/subiculum of the ventral hippocampus. The EPSPs were evoked by stimulating the striatum radiatum of the CA1 field; the membrane responses were elicited by current injections. Exposure of slices for 15 min to 0.1 nM solution of these peptides resulted in an increase in the amplitude and slope of the EPSPs in 21 neurons (67%) tested. No consistent change in either the resting membrane potential or the input resistance of the neurons was observed. The peptide-induced increase in EPSPs reached a maximum 30-45 min after peptide application. In 14 of these neurons (66%), the peptide-induced increase in EPSPs remained throughout the entire 60-120 min washout period. In the remaining 7 neurons (33%), the initial increase in EPSPs amplitude was followed by a gradual decline to the pre-administration level. The increase in EPSP amplitude was often, but not always, associated with a decrease in the threshold and increase in the number of action potentials in response to depolarizing current injection. Suppression of GABAA receptor-mediated inhibition and N-methyl-D-aspartate (NMDA) receptor-mediated excitation did not prevent the effects of VP and VP(4-8) on the EPSP amplitude or the threshold for action potentials. The results demonstrate that 0.1 nM concentrations of these neuropeptides can elicit a long-lasting enhancement of the excitability of CA1/subiculum neurons of the ventral hippocampus to excitatory, glutamatergic synaptic input. This novel action of VP and its metabolite in the ventral hippocampus may be the physiological action, mediating the memory-enhancing effect of these peptides.

Temporal differences in the phosphorylation state of pre- and postsynaptic protein kinase C substrates B-50/GAP-43 and neurogranin during long-term potentiation.

The phosphorylation state of two identified neuralspecific protein kinase C substrates (the presynaptic protein B-50 and the postsynaptic protein neurogranin) was monitored after the induction of long term potentiation in the CA1 field of rat hippocampus slices by quantitative immunoprecipitation following 32Pi labeling in the recording chamber. B-50 phosphorylation was increased from 10 to 60 min, but no longer at 90 min after long term potentiation had been induced, neurogranin phosphorylation only at 60 min. Increased phosphorylation was not found when long term potentiation was blocked with the N-methyl-D-aspartate receptor antagonist D-2-amino-5-phosphonovalerate, when only low frequency stimulation was applied or tetanic stimulation failed to induce long term-potentiation. Our data show that both B-50 and neurogranin phosphorylation are increased following the induction of long term potentiation, thus providing strong evidence for pre- and postsynaptic protein kinase C activation during narrow, partially overlapping, time windows after the induction of long term potentiation.

A long-lasting increase and decrease in synaptic excitability in the rat lateral septum are associated with high and low shuttle box performance, respectively.

In a series of experiments with rats, using evoked field potentials, the influence of massed trial training in 2-way shuttle box avoidance and step-through passive avoidance tasks was studied on the synaptic excitability of the lateral septum (LS) neurons and on the induction of long-term potentiation in the lateral septum in vivo. The majority of rats that attained a high performance level in the shuttle box task exhibited, after the shuttle box training, a long-lasting enhancement of synaptic excitability of lateral septum neurons, whereas most of the rats with low performance in the shuttle box showed a long-lasting depression in the LS synaptic excitability. Both types of excitability changes disappeared within 24 h. Neither the first habituation session in the passive avoidance apparatus nor the subsequent one-trial learning in passive avoidance task had a marked influence on lateral septum synaptic excitability. Both high-performance and low-performance rats exhibited a long-term potentiation (LTP)-like potentiation of synaptic excitability of the lateral septum neurons after high frequency stimulation of the fimbria fibers although the amount of LTP in high performance rats was slightly higher than that in low performance animals.

Long-term potentiation and synaptic protein phosphorylation.

Long-term potentiation (LTP) is a well known experimental model for studying the activity-dependent enhancement of synaptic plasticity, and because of its long duration and its associative properties, it has been proposed as a system to investigate the molecular mechanisms of memory formation. At present, there are several lines of evidence that indicate that pre- and postsynaptic kinases and their specific substrates are involved in molecular mechanisms underlying LTP. Many studies focus on the involvement of protein kinase C (PKC). One way to investigate the role of PKC in long-term potentiation is to determine the degree of phosphorylation of its substrates after in situ phosphorylation in hippocampal slices. Two possible targets are the presynaptic membrane-associated protein B-50 (a.k.a. GAP 43, neuromodulin and F1), which has been implicated in different forms of synaptical plasticity in the brain such as neurite outgrowth, hippocampal LTP and neurotransmitter release, and the postsynaptic protein neurogranin (a.k.a. RC3, BICKS and p17) which function remains to be determined. This review will focus on the protein kinase C activity in pre- and postsynaptic compartment during the early phase of LTP and the possible involvement of its substrates B-50 and neurogranin.

[Gastric carcinoma. Our experience]. / Il carcinoma gastrico. Nostra esperienza.

This study analysed 66 cases of gastric cancer from 1985 to 1992. Twenty-seven patients (41%) has been treated with anti-H2 drug, either medical care or Jerkily "a la demande": 12 patients have been treated several years. Of the 66 patients: 52 (89%) were operated on while the other 16 received medical treatment because of the extension disease and their precarious condition. Long-term 35 (67%) patients (of the 52 operated) died four years later, independently of the stage and PKT of the first and the second level. The 27 patients treated with anti-H2 drug showed the most undifferentiated grading and 88% belong to the third and the fourth stage; moreover 81% underwent first diagnostic endoscopy notwithstanding a clinical and surgical history of gastric ulcer. Is it possible, therefore, that anti-H2 drug delay the diagnosis.

The impaired long-term potentiation in the CA1 field of the hippocampus of cognitive deficient microencephalic rats is restored by D-serine.

Rat embryos exposed on gestational day 15 to methyl-azoxymethanol acetate develop a microencephaly characterized primarily by a hypoplasia of the neocortex and CA fields of the hippocampus that in adulthood is associated with disturbances in learning. In brain slices prepared from microencephalic rats, we have examined the field excitatory postsynaptic potentials and population spike in the CA1 field of the hippocampus evoked by stimulation of the stratum radiatum. These parameters did not differ from those obtained in slices from control rats. High frequency stimulation of the stratum radiatum afferent fibres, which readily induced long-term potentiation of the field excitatory postsynaptic potentials and population spike in the CA1 field of the hippocampus of control rats, failed to induce long-term potentiation in that of microencephalic rats. High frequency stimulation of the perforant path readily elicited long-term potentiation in the dentate gyrus of both control and microencephalic rats. Picrotoxin had no apparent effect on field excitatory postsynaptic potentials and population spike in the CA1 field of the microencephalic rats, indicating that little GABAergic inhibition was present in slices from these rats. D-2-Amino-phosphonovalerate suppressed the field potentials in slices from microencephalic rats by more than 50%, suggesting that N-methyl-D-aspartate receptors contributed markedly to the synaptic responses evoked by single stimuli. D-Serine, but not picrotoxin, restored long-term potentiation in the CA1 field of the microencephalic rats. The D-serine effect was prevented by pretreating the slices with either 7-chloro-kynurenate or D-2-amino-phosphonovalerate. The failure to induce long-term potentiation, if also found in vivo, may be among the factors related to the learning deficits displayed by these rats.

Two actions of vasopressin on neurons in the rat ventral hippocampus: a microiontophoretic study.

Vasopressin (VP), applied by brief iontophoretic pulses on ventral hippocampus neurons in vivo, excited approximately 30% of the neurons tested. Glutamate (Glu) and acetylcholine (ACh) excited nearly all neurons recorded. A selective antagonist of vasopressin V1 receptors suppressed the VP-induced excitation and, in addition, suppressed the excitations induced by Glu but not those by ACh. The specificity of the action in the brain of this VP antagonist must therefore be doubted. Two excitatory amino acid antagonists, D(-)-2-amino-5-phosphonovaleric acid (2APV) and glutamic acid diethyl ester (GDEE), suppressed the responses to Glu and also those to VP. ACh excitations, tested in the same neurons, were little affected by 2APV and GDEE. The remaining 70% of VH neurons were not excitable with VP. However, the responses of these neurons to Glu but not to Ach, increased markedly both while the peptide was released and for tens of minutes thereafter. The increase in Glu responses induced by VP could not be prevented by the VP or excitatory amino acid receptor antagonists applied before the peptide. The possibility that the excitation and the potentiation of Glu responses caused by VP originated from two different actions of the peptide is discussed.