Evidence for the First Excited State of

The ^{7}H system was populated in the ^{2}H(^{8}He,^{3}He)^{7}H reaction with a 26 AMeV ^{8}He beam. The ^{7}H missing mass energy spectrum, the ^{3}H energy and angular distributions in the ^{7}H decay frame were reconstructed. The ^{7}H missing mass spectrum shows a peak, which can be interpreted either as unresolved 5/2^{+} and 3/2^{+} doublet or one of these states at 6.5(5) MeV. The data also provide indications of the 1/2^{+} ground state of ^{7}H located at 1.8(5) MeV with quite a low population cross section of ∼25 µb/sr within angular range θ_{c.m.}≃(17°-27°).

Coexistence of Reflection Asymmetric and Symmetric Shapes in

Level structures in the neutron-rich ^{144}Ba nucleus have been reinvestigated by measuring prompt γ rays in the spontaneous fission of ^{252}Cf. The previous s=+1 octupole band structure with reflection asymmetric shape has been expanded, and a side quadrupole band structure based on a 3^{+} state with reflection symmetric shape is identified. Thus, the results show the coexistence of reflection asymmetric and symmetric shapes in ^{144}Ba. This is a first identification of such a shape coexistence structure in a nuclear structure. The other structural characteristics are discussed.

Exercise modifies α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor expression in striatopallidal neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned mouse.

The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic-acid-type glutamate receptor (AMPAR) plays a critical role in modulating experience-dependent neuroplasticity, and alterations in AMPAR expression may underlie synaptic dysfunction and disease pathophysiology. Using the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of dopamine (DA) depletion, our previous work showed exercise increases total GluA2 subunit expression and the contribution of GluA2-containing channels in MPTP mice. The purpose of this study was to determine whether exercise-dependent changes in AMPAR expression after MPTP are specific to the striatopallidal (D2 R) or striatonigral (D1 R) medium spiny neuron (MSN) striatal projection pathways. Drd2 -eGFP-BAC transgenic mice were used to delineate differences in AMPAR expression between striatal D2 R-MSNs and D1 R-MSNs. Striatal AMPAR expression was assessed by immunohistochemical (IHC) staining, Western immunoblotting (WB) of preparations enriched for postsynaptic density (PSD), and alterations in the current-voltage relationship of MSNs. We found DA depletion results in the emergence of GluA2-lacking AMPARs selectively in striatopallidal D2 R-MSNs and that exercise reverses this effect in MPTP mice. Exercise-induced changes in AMPAR channels observed after DA depletion were associated with alterations in GluA1 and GluA2 subunit expression in postsynaptic protein, D2 R-MSN cell surface expression, and restoration of corticostriatal plasticity. Mechanisms regulating experience-dependent changes in AMPAR expression may provide innovative therapeutic targets to increase the efficacy of treatments for basal ganglia disorders, including Parkinson's disease.

Structure of 10He low-lying states uncovered by correlations.

The 0+ ground state of the 10He nucleus produced in the 3H(8He,p)10He reaction was found at about 2.1±0.2 MeV (Γ∼2 MeV) above the three-body ^{8}He+n+n breakup threshold. Angular correlations observed for ^{10}He decay products show prominent interference patterns allowing us to draw conclusions about the structure of low-energy excited states. We interpret the observed correlations as a coherent superposition of a broad 1- state having a maximum at energy 4-6 MeV and a 2+ state above 6 MeV, setting both on top of the 0+ state "tail." This anomalous level ordering indicates that the breakdown of the N=8 shell known in 12Be thus extends also to the ^{10}He system.

Brief mitochondrial inhibition causes lasting changes in motor behavior and corticostriatal synaptic physiology in the Fischer 344 rat.

The striatum is particularly vulnerable to mitochondrial dysfunction and this problem is linked to pathology created by environmental neurotoxins, stimulants like amphetamine, and metabolic disease and ischemia. We studied the course of recovery following a single systemic injection of the mitochondrial complex II inhibitor 3-nitropropionic acid (3-NP) and found 3-NP caused lasting changes in motor behavior that were associated with altered activity-dependent plasticity at corticostriatal synapses in Fischer 344 rats. The changes in synapse behavior varied with the time after exposure to the 3-NP injection. The earliest time point studied, 24h after 3-NP, revealed 3-NP-induced an exaggeration of D1 Dopamine (DA) receptor dependent long-term potentiation (LTP) that reversed to normal by 48 h post-3-NP exposure. Thereafter, the likelihood and degree of inducing D2 DA receptor dependent long-term depression (LTD) gradually increased, relative to saline controls, peaking at 1 month after the 3-NP exposure. NMDA receptor binding did not change over the same post 3-NP time points. These data indicate even brief exposure to 3-NP can have lasting behavioral effects mediated by changes in the way DA and glutamate synapses interact.

[Regularities of endogenous lipid metabolites formation in phorbol 12-miristate 13-acetate-stimulated peripheral blood lymphocytes at leukemia].

Regularities of biologically active lipid metabolites formation in dynamics (5, 10, 30, 60 s) by phorbol 12-miristate 13-acetate stimulation in [14C]palmitic acid have been investigated in normal and leukemia peripheral blood lymphocytes prelabeled with [14C]palmitate. In normal cells there was two-phase formation of 1,2-diacylglycerol (5, 30 s), lysophosphatidylcholine (10, 60 s), as well as free palmitic acid at 10 s of stimulation. Under the identical experimental conditions there was inhibition of investigated lipid release processes at early (5 and 10 s) stages of stimulation of leukemic lymphocytes. At later (30, 60 s) terms of these lymphocytes the activation, basically, similar to norm changes in the formation of palmitic acid-containing metabolites except free palmitic acid (the level of which raised only at 60 second of the post-stimulation) was found. Various protein kinases C are involved in the regulation of investigated lipid levels at certain stages of signal transduction both in norm, and in blast cells. Short-term (5, 10 s) activations of healthy donors lymphocytes are coupled to functioning of Ca2+-independent isoforms of protein kinase C. The inhibition of this protein kinase C in leukemic cells leads to normalization of the investigated lipid release. The data obtained suggests disorders of early membrane-bound reactions in agonist - and a protein kinase C-mediated processes of formation palmitic acid-containing lipid metabolites in the leukemic cells in comparison with the norm.

[Pathogenesis of enteral insufficiency in patients with postoperative peritonitis].

Enteral insufficiency is considered to trigger the syndrome of endogenous intoxication and, further, multiple organ failure. Enteral insufficiency often accompanies postoperative septic complications, such as peritonitis. Morphologic changes of the intestinal wall by septic peritonitis consisted of edema, fibrinous degradation of muscular layer and dystrophy of local nervous pathways. Microbiologic analysis of intestinal and gastric contents, peritoneal fluid and blood samples demonstrated a broad spectrum of pathogenic flora. Besides, enterotoxin allocated from blood and intestinal contents coincided in all cases. Adequate algorithm of detoxication, including extracorporal methods, had been worked out.

Reliable long-lasting depression interacts with variable short-term facilitation to determine corticostriatal paired-pulse plasticity in young rats.

Synaptic plasticity at corticostraital synapses is proposed to fine tune movment and improve motor skills. We found paired-pulse plasticity at corticostriatal synapses reflected variably expressed short-term facilitation blended with a consistent background of longer-lasting depression. Presynaptic modulation via neuotransmitter receptor activation was ruled out as a mechanism for long-lasting paired-pulse depression by examining the effect of selective receptor antagonists. EPSC amplitude and paired-pulse plasticity, however, was influenced by block of D2 dopamine receptors. Block of glutamate transport with l-transdicarboxylic acid (PDC) reduced EPSCs, possibly through a mechanism of AMPA receptor desensitization. Removal of AMPA receptor desensitization with cyclothiazide reduced the paired-pulse depression at long-duration interstimulus intervals (ISIs), indicating that AMPA receptor desensitization participates in corticostriatal paired-pulse plasticity. The low-affinity glutamate receptor antagonist cis-2,3-piperidine dicarboxylic acid (PDA) increased paired-pulse depression, suggesting that a presynaptic component also exists for long-lasting paired-pulse depression. Low Ca(2+)-high Mg(2+) or BAPTA-AM dramatically reduced the amplitude of corticostriatal EPSCs and both manipulations increased the expression of facilitation and, to a lesser extent, they reduced long-lasting paired-pulse depression. EGTA-AM produced a smaller reduction in EPSC amplitude and it did not alter paired-pulse facilitation, but in contrast to low Ca(2+) and BAPTA-AM, EGTA-AM increased long-lasting paired-pulse depression. These experiments suggest that facilitation and depression are sensitive to vesicle depletion, which is dependent upon changes in peak Ca(2+) (i.e. low Ca(2+)-high Mg(2+) or BAPTA-AM). In addition, the action of EGTA-AM suggests that basal Ca(2+) regulates the recovery from long-lasting paired-pulse depression, possibly thourgh a Ca(2+)-sensitive process of vesicle delivery.

[Comparative evaluation of empirical antibacterial therapy for ventilator-associated pneumonia].

The problem of nosocomial pneumonias remains most urgent for intensive care units so far. Particular emphasis is placed on clinical and diagnostic monitoring and therapy for ventilation-induced nosocomial pneumonias (VINP) in intensive care patients on ventilation. This is accounted for by not only the high incidence of this pathology, but also by its severity and mortality rates. In the pattern of nosocomial complications, pneumonia ranks second-third in its prevalence, which accounts for about 10-15%, and first in mortality rates (30%); it afflicts 50% of the elderly patients on ventilation. Antibacterial therapy plays a great role in ventilation therapy. The study deals with the comparative characteristics of empirical antibacterial therapy for VINP.

Pre- and postsynaptic contributions to age-related alterations in corticostriatal synaptic plasticity.

Aging creates deficits in motor performance related to changes in striatal processing of cortical information. This study describes age-related changes in corticostriatal snaptic plasticity and associated mechanisms, which may contribute to declines in motor behavior. Intracellular recordings revealed an age-related decrease in the expression of paired-pulse, posttetanic, and long-term potentiation (LTP). The age-related difference in LTP was associated with reduced sensitivity to block of N-methyl-D-aspartate (NMDA) receptors in the aged population. These age-related changes could not be explained by increased L-type Ca(2+)channel activity, since block of L-type Ca(2+) channels with nifedipine increased rather than decreased the age-related difference in long-term plasticity. Age-related increases in reactive oxygen species (ROS) modulation were also ruled out, since application of H(2)O(2) produced changes in synaptic function that were opposite to trends seen in aging, and addition of the antioxidant Trolox-C had a larger effect on long-term plasticity in young rats than in older rats. A robust age-related difference in long-term synaptic plasticity was found by studying synaptic plasticity following the blocking of D2 receptors with l-sulpiride, which may involve age-difference in NMDA receptor function. l-sulpiride consistently enabled a slow development of LTP at young (but not aged) corticostriatal synapses. However, No age differences were found in the sensitivity to the addition of the D2 receptor agonist quinpirole. These findings provide evidence for age-induced changes in the release properties of cortical terminals and in the functioning of postsynaptic striatal NMDA receptors, which may contribute to age-related deficits in striatum control of movement.

[Modulation of endotoxin-induced respiratory splash of granulocytes and monocytes in patients with Familial Mediterranean Fever by iodine-lithium-alpha-dextrin and sodium thiosulfate].

The effect of an endotoxin--E. coli liposaccharide (LPS) of serotype 026:B6--on the respiratory splash (RS) of neutrophils and monocytes in peripheral blood of patients with Familial Mediterranean Fever (FMF) was studied. It is shown that FMF patients have a periodic increase (during an attack) and a decrease (in the period of remission) in endotoxin-induced RS of neutrophils and monocytes. LPS stimulates chemotoxis-induced RS of neutrophils and monocytes in patients both in the period of remission and during the attack equally effectively. Iodine-lithium-alpha-dextrin and sodium thiosulfate have a marked anti-endotoxic effect which manifests with quick neutralization of endotoxin activity on RS of monocytes and neutrophils in FMF patients both during the attack and remission.

[Study of volatile fatty acids in the blood of patients with periodic disease].

Microecological "failures" are an important pathogenetic factor of different diseases and, in the authors' opinion, periodic disease (PD) is one of them. PD is a recessive disease characterized by fever attacks and neutrophil-mediated serous inflammation. A genetic factor has been established to be responsible for half the cases of PD, the influence of non-hereditary factors, particularly a role of the host automicroflora in the genesis of an inflammatory process, has been little studied. The authors' early studies indicate that there are changes in the qualitative and quantitative composition of microbial molecules in the blood of patients with PD. The anaerobic bacterial metabolites that are volatile fatty acids (VFAs) represent biologically active substances that affect the growth of the microflora, on the one hand, and the host's immunological responsiveness, on the other. Out of VFAs, only is acetic acid detectable in small quantities in the blood of healthy individuals. The other VFAs, namely propionic, valeric, butyric, and caproic acids and their isomers, are absent. Gas chromatography was used for qualiitative and quantitative determination of the metabolites of anaerobic microorganisms in the blood of patients with PD (n = 13) during an attack and remission and in that of healthy volunteers (Armenians) (n = 5) of a control group from one Yerevan region. The blood samples from all the patients with PD displayed a significantly higher concentration of caproic acid while the latter was absent in the blood of the controls. This finding suggests that there is a specific shift in the structure of the microbiocenosis in patients with PD. It is conceivable that caproic acid plays a certain role in the pathogenesis of the disease under study. Further studies will deal with the association of some microbial molecules with the manifestation of an attack of PD, which may provide the key to the goal-oriented regulation of detected homeostatic disorders and to the management of the frequency of its attacks.

[Spontaneous and inducible respiratory burst of monocytes and neutrophils in periodic autoinflammatory fever].

We investigated spontaneous, chemotaxis-, phagocytosis- and proteinkinase C-dependent respiratory burst of neutrophils and monocytes in the whole blood of patients with familial Mediterranean fever (FMF). We also analysed transient activation of neutrophils and monocytes on the level of a single cell using flow cytofluorimetry. It is shown that compared to healthy donors, the respiratory burst of monocytes and neutrophils in the patients is characterized by an increase in both spontaneous and inducible production of free radicals. In FMF patients probability of transient activation of chemotaxis- and phagocytosis-dependent respiratory burst is higher. This has an important influence rather on production of free radical by activated cells than on their number.

[A phytogenic drug kanefron H in patients with chronic cystitis and urolithiasis].

To evaluate efficacy of kanefron H (KH) in combined therapy of chronic cystitis and urolithiasis (after extracorporeal shock-wave lithotripsy-ESWL), we examined 48 women suffering from chronic cystitis. The patients were divided into two groups by the presence of pyuria: 20 patients of group 1 had pyuria, 28 patients of group 2 had no pyuria. Each group was subdivided into two groups in relation to KH. Subgroup 1a received phosphomycin as monotherapy, subgroup 1b--phosphomycin with KH (2 pellets 3 times a day for 30 days). Subgroup 2a was initially treated with anti-inflammatory drugs, local medication physiotherapy, circulation improving drugs for 10 days. Then the patients were followed up for a months without any treatment. Subgroup 2b received the same initial course but it was followed for 30 days with KH. 79 patients with urolithiasis (uroliths and ureteroliths) have undergone ESWL. 45 entered KH group (2 pellets 3 times a day), 34--the control group (spasmolytic and anti-inflammatory therapy). KH in combined treatment of chronic cystitis raises efficacy of the initial therapy (antibacterial or combined, made in the absence of pyuria), promotes achievement of longer disease remission, elimination of concrement fragments from the urinary tract. Long-term administration of KH induce no side effects. Thus, KH can be recommended in chronic cystitis and urolithiasis in patients exposed to ESWL as an effective and safe drug.

Increased susceptibility of glutathione peroxidase-1 transgenic mice to kainic acid-related seizure activity and hippocampal neuronal cell death.

Glutathione peroxidase (GSHPx) has been demonstrated in several in vivo studies to reduce both the risk and severity of oxidatively-induced tissue damage. The seizure-inducing neurotoxin kainic acid (KA) has been suggested to elicit its toxic effects in part via generation of oxidative stress. In this study, we report that expression of elevated levels of murine GSHPx-1 in transgenic mice surprisingly results in increased rather than decreased KA susceptibility including increased seizure activity and neuronal hippocampal damage. Isolated transgenic primary hippocampal culture neurons also display increased susceptibility to KA treatment compared with those from wildtype animals. This could be due to alterations in the redox state of the glutathione system resulting in elevated glutathione disulfide (GSSG) levels which, in turn, may directly activate NMDA receptors or enhanced response of the NMDA receptor.

[A respiratory splash of monocytes and neutrophils in familial Mediterranean fever].

AIM: To study spontaneous chemotaxis-, phagocytosis-, and proteinkinase C-mediated respiratory splash (RS) of neutrophils and monocytes in colchicin-untreated patients with familial Mediterranean fever (FMF). MATERIAL AND METHODS: Of 17 FMF patients, 8 ones were examined during the attack, 9 patients--in fever-free period. Spontaneous and induced RS of peripheral blood neutrophils and monocytes was investigated with quantitative flow-cytofluorimetric method. RESULTS: Compared to healthy donors, RS is characterized with activation of both spontaneous and induced production of free radicals. The activity and intensity of the RS in FMF was low in the attack vs in the attack-free period but monocytes population has a stable high activity of the RS. CONCLUSION: Activation of neutrophilic RS in FMF patients is characterized by periodicity the direction of which is opposite to induced monocyte activation in the attack and in attack-free interval.

Observation of excited states in 5H.

The 5H system was produced in the 3H(t,p)5H reaction studied with a 58 MeV tritium beam at small c.m. angles. High statistics data were used to reconstruct the energy and angular correlations between the 5H decay fragments. A broad structure in the 5H missing mass spectrum showing up above 2.5 MeV was identified as a mixture of the 3/2+ and 5/2+ states. The data also present evidence that the 1/2+ ground state of 5H is located at about 2 MeV.

Experimental evidence for the existence of 7H and for a specific structure of 8He.

Experimental search for the superheavy 7H isotope was performed in the reaction p(8He,pp)7H with the 8He beam at 61.3A MeV. The evidence for existence of the 7H state near the t+4n threshold was obtained. In the same experiment, the p(8He,t) reaction populating the ground and excited 2(+) state of 6He was investigated. The obtained results argue on a specific structure of the 8He ground state containing the 6He subsystem in the excited 2(+) state with a large weight.

Superheavy hydrogen (5)H.

Experimental search for (5)H using a secondary beam of (6)He has been performed. The transfer reaction (1)H((6)He,(2)He)(5)H was studied by detecting two protons emitted from the decay of (2)He. A peak consistent with a (5)H resonance at 1.7+/-0.3 MeV above the n+n+t threshold was observed, with a width of 1.9+/-0.4 MeV. The angular distribution of the (1)H((6)He,(2)He)(5)H reaction was measured as well as the energy correlation of the two protons.

Regional differences in the expression of corticostriatal synaptic plasticity.

Field recordings of responses to activation of corticostriatal afferents were made in coronally sectioned rat brain slices. Each recording site was categorized according to its medial to lateral and rostral to caudal position to investigate anatomical differences in synaptic plasticity. Individual responses were highly variable exhibiting extremes of tetanus induced depression and potentiation. Consequently, averaging masked the capacity of these synapses to express long-term forms of plasticity. Block of GABA(A) inhibition and elimination of dopaminergic input with 6-hydroxydopamine lesions both acted to increase the expression of potentiation, but again considerable variability was observed. Separation of recordings into medial and lateral groups revealed clear anatomical trends which contributed to the variability observed in the total sample. Paired-pulse, post-tetanic and long-term potentiation was greater in medial than in lateral groups in normal artificial cerebral spinal fluid. Similar tendencies were seen after block of GABA(A) receptors with bicuculline. 6-Hydroxydopamine lesions in combination with bicuculline treatment reduced medial to lateral differences. Factoring in medial to lateral trends revealed block of GABA(A) receptor mediated inhibition had its greatest effect on medial corticostriatal responses and 6-hydroxydopamine lesions had their greatest effect on lateral responses. From these data we suggest anatomical variation in striatal circuitry may underlie regional differences in synaptic plasticity evoked by corticostriatal activation.