Entrainment, stopping, and transmission of microwave solitons of self-induced transparency in counter-propagating magnetized electron beam.

Based on numerical simulations of a boundary problem, we study various scenarios of microwave soliton formation in the process of cyclotron resonance interaction of a short electromagnetic pulse with a counter-propagating initially rectilinear electron beam taking into account the relativistic dependence of the cyclotron frequency on the electrons' energy. When a certain threshold in the pulse energy is exceeded, the incident pulse can propagate without damping in the absorbing beam, similar to the effect of self-induced transparency in optics. However, mutual motion of the wave and electrons can lead to some novel effects. For relatively small energy of the incident pulse, the microwave soliton is entrained by the electron beam opposite to the direction of the wave's group velocity. With an increase in the pulse energy, soliton stopping occurs. This regime is characterized by the close-to-zero pulse velocity and can be interpreted as a variety of the "light stopping." High-energy microwave solitons propagate in the direction of the unperturbed group velocity. Their amplitude may exceed the amplitude of the incident pulse, i.e., nonlinear self-compression takes place. A further increase in the incident energy leads to the formation of additional high-order solitons whose behavior is similar to that of the first-order ones. The characteristics of each soliton (its amplitude and duration) correspond to analytical two-parametric soliton solutions that are to be found from consideration of the unbounded problem.

Pulsed magnetic field generation system for laser-plasma research.

An up to 15 T pulsed magnetic field generator in a volume of a few cubic centimeters has been developed for experiments with magnetized laser plasma. The magnetic field is created by a pair of coils placed in a sealed reservoir with liquid nitrogen, installed in a vacuum chamber with a laser target. The bearing body provides the mechanical strength of the system both in the case of co-directional and oppositely connected coils. The configuration of the housing allows laser radiation to be introduced into the working area between the coils in a wide range of directions and focusing angles, places targets away from the symmetry axis of the magnetic system, and irradiates several targets simultaneously.

Generation of Rogue Waves in Gyrotrons Operating in the Regime of Developed Turbulence.

Within the framework of the average approach and direct 3D PIC (particle-in-cell) simulations, we demonstrate that the gyrotrons operating in the regime of developed turbulence can sporadically emit "giant" spikes with intensities a factor of 100-150 greater than the average radiation power and a factor of 6-9 exceeding the power of the driving electron beams. Together with the statistical features such as a long-tail probability distribution, this allows the interpretation of generated spikes as microwave rogue waves. The mechanism of spikes formation is related to the simultaneous cyclotron interaction of a gyrating electron beam with forward and backward waves near the waveguide cutoff frequency as well as with the longitudinal deceleration of electrons.

Risk factors for the development of delayed graft function in deceased donor renal transplants.

INTRODUCTION: Delayed renal graft function (DGF) is associated with various factors and with a higher complication rate in the posttransplant period. Determination of center-specific risk factors may help to reduce the incidence of DGF and improve transplantation results. The aim of this study was to define risk factors for the development of DGF after renal transplantation. PATIENTS AND METHODS: This study included 290 consecutive deceased donor renal transplantations performed in a single center between January 1, 2004, and November 30, 2007. All cases were examined for the presence of DGF, defined as the need for at least 1 dialysis during the first posttransplant week. The subjects were divided into 2 groups: immediate graft function and DGF. Both groups were compared for donor and recipient transplantation factors as well as early posttransplant results. RESULTS: DGF was observed in 61 cases (21%). Our analysis revealed associations of DGF with recipient age (P = .011), female gender (P = .028), donor age (P = .033), body mass index (P = .007), severe hemodynamic disturbances (P = .005) preexistent glomerular or interstitial sclerosis (P = .002 or P = .028, respectively); and cold ischemia time (CIT; P = .019). Trends toward significance were observed with recipient weight > 100 kg (P = .078), and diabetes mellitus (P = .109). Recipients who experienced DGF showed on higher rate of acute rejection, a longer hospital stay, and an higher level serum creatinine at discharge (P < .001 for all). CONCLUSION: DGF had deleterious effects in the early posttransplant period. Careful allocation and reduction of CIT may improve transplantation results.

Reactivation of BK Virus in the Early Period After Kidney Transplantation.

BACKGROUND: Typically, polyoma BK virus (BKV) remains latent in the urogenital tract after primary infection. Reactivation of BKV in recipients of kidney allografts can cause progressive graft dysfunction known as BK virus nephropathy (BKVN). The cornerstone of treatment for BKVN is prevention; therefore, it is important to detect BKV reactivation early and reduce immunosuppression. We sought to identify the BKV reactivation rate and associated factors in a prospective study. MATERIALS AND METHODS: We studied 37 consecutive unselected adult recipients who underwent deceased donor kidney transplantation in 2007 and completed at least 3 months of observation. Qualitative nested polymerase chain reaction (PCR) testing was performed to detect BKV DNA in urine and plasma specimens. RESULTS: In all cases, BK viremia or viruria was not detected on the postoperative day or 2 weeks thereafter. At 3 months, BKV reactivation developed in 6 (16%) of 37 recipients. Simultaneous viremia and viruria were present on 5 patients and viremia only in 1 patient. Significant risk factors for BK viremia were body mass index >30 kg/m(2) (P = .02), retransplantation (P =.04), and use of tacrolimus (P = .02). Serum creatinine values at 3 months after transplantation were significantly higher among patients with active BKV infection (P = .008). CONCLUSIONS: Early BKV reactivation is associated with worse graft function as early as 3 months after transplantation. Obesity, retransplantation, and use of tacrolimus were factors promoting early development of BKV viremia.

Donation and transplantation in Latvia--2006.

The 75 kidney transplant operations (32.6 per million population per year) and 2 heart transplant operations were performed in 2006 in Latvia. This represents a slight decrease of 3% compared to 2005. 86 kidneys were procured from 43 deceased donors. There were 46% donors with brain death and 54% non-heart-beating donors among them. During last decade the donor rate increased from 10.9 per million population in 1996 to 18.7 per million population in 2006. In our center patient survival was 93.2% at 1 year and 87.4% at 5 years, and graft survival was 84.5% at 1 year and 72.3% at 5 years. Such transplantation activity ensures mean waiting time of 6-7 months for patients accepted for kidney transplantation.

Vascular access outcomes as a predictor of development of chronic allograft nephropathy.

INTRODUCTION: The vascular condition influences the outcomes of arteriovenous fistula (AVF) surgery. However, it has not been established how it influences the outcomes of renal transplantation and the development of chronic allograft nephropathy (CAN). The aim of this study was to define the relationship between AVF failure in the pretransplant period and the development of CAN. PATIENTS AND METHODS: In this study we included all patients who underwent AVF surgery and then first kidney allotransplantations from January 1, 1999 to December 31, 2002. Patients were divided into two groups according to the AVF surgery outcomes: group 1 (n = 45, mean age 50 +/- 13 years, male/female ratio 27/18) had no vascular access complications and were dialysed through a native AVF. Group 2 (n = 39, mean age 51 +/- 11 years, male/female ratio 17/22) had additional interventions due to AVF failure. We analyzed the incidence of CAN in both groups. RESULTS: During the follow-up period CAN was observed in five patients in group 1 and 11 patients in group 2 (11,1% vs 28,2%, P < .05). There was a statistically significant relationship between CAN and acute rejection episodes (P < .005) and diabetes mellitus (P < .05). CONCLUSION: Failures of arteriovenous fistulas in hemodialysis patients were associated with an increased incidence of CAN in the posttransplant period.

Organ donors: deceased or alive? Quo vadis?

Irrespectively of universal shortage of donor organs there is a tendency of increasing the number of transplantations from living and deceased donors. Each of these two methods has positive and negative features. The main obstacles using living donors are health hazard, necessity to solve certain donor's social and psychological problems, possibility of organ trade and moving. The main problems connected with organ retrieval from deceased donors are possible conflicts with public opinion: difficulties in interpretation of brain death, legislation, obtaining of informed consent from donor's relatives, etc. Future progress in organ transplantation may take place through activation of organ retrieval from deceased donors. The most perspective ways are change to presumed consent in all countries, establishing of centralized system of donor detection and registration, intensification of transplant coordination, active contacts with mass-media, etc. It is necessary to increase (enhance) participation of the members of the public in organ donation process, to develop solidarity among the public members and to involve public authorities to deal with this problem. Bioethical standards should be put in accordance with common progress and some ethical traditions should be changed.

Human and mouse microglia express connexin36, and functional gap junctions are formed between rodent microglia and neurons.

Microglia, the tissue macrophages of the central nervous system (CNS), intimately interact with neurons physically and through soluble factors that can affect microglial activation state and neuronal survival and physiology. We report here a new mechanism of interaction between these cells, provided by the formation of gap junctions composed of connexin (Cx) 36. Among eight Cxs tested, expression of Cx36 mRNA and protein was found in microglial cultures prepared from human and mouse, and Cx45 mRNA was found in mouse microglial cultures. Electrophysiological measurements found coupling between one-third of human or mouse microglial pairs that averaged below 30 pico-Siemens and displayed electrical properties consistent with Cx36 gap junctions. Importantly, similar frequency of low-strength electrical coupling was also obtained between microglia and neurons in cocultures prepared from neocortical or hippocampal rodent tissue. Lucifer yellow dye coupling between neurons and microglia was observed in 4% of pairs tested, consistent with the low strength and incidence of electrical coupling. Cx36 expression level and/or the degree of coupling between microglia did not significantly change in the presence of activating agents, including lipopolysaccharide, granulocyte-macrophage colony-stimulating factor, interferon-gamma, and tumor necrosis factor-alpha, except for some reduction of Cx36 protein when exposed to the latter two agents. Our findings that intercellular coupling occurs between neuronal and microglial populations through Cx36 gap junctions have potentially important implications for normal neural physiology and microglial responses in neuronopathology in the mammalian CNS.

Hypoxic rise in cytosolic calcium and renal proximal tubule injury mediated by a nickel-sensitive pathway.

In the kidney, cell injury resulting from ischemia and hypoxia is thought to be due, in part, to increased cytosolic Ca(2+) levels, [Ca(2+)]i, leading to activation of lytic enzymes, cell dysfunction, and necrosis. We report evidence of a progressive and exponential increase in [Ca(2+)]i (from 245 +/- 10 to 975 +/- 100 nM at 45 mins), cell permeabilization and propidium iodide (PI) staining of the nucleus, and partial loss of cell transport functions such as Na(+)-gradient-dependent uptakes of (14)C-alpha-methylglucopyranoside and inorganic phosphate ((32)Pi) in proximal convoluted tubules of adult rabbits subjected to hypoxia. The rise in [Ca(2+)]i depended on the presence of extracellular [Ca(2+)] and could be blocked by 50 microM Ni(2+)but not by verapamil (100 microM). Presence of 50 microM Ni(2+) also reduced the hypoxia-induced morphological and functional injuries. We also used HEK 293 cells, a kidney cell line, incubated in media without glucose and exposed for 3.5 hrs to 1% O(2)-5% CO(2) and then returned to glucose-containing media for another 3.5 hrs in an air-5% CO(2) atmosphere and finally exposed for 1 min to media containing 1 microM PI. NiCl(2) (50 microM) or pentobarbital (300 microM) more than phenobarbital (1.5 mM), when present in the incubation medium during both the hypoxic and the reoxygenation periods, induced significant (P < 0.001) reductions in the number of cell nuclei stained with PI, similar to their relative potency as inhibitors of T channels. Our findings indicate that hypoxia-induced alterations in calcium level and subsequent cell injury in the proximal convoluted tubule and in HEK cells involve a nickel-sensitive and dihydropyridine insensitive pathway or channel.

Sodium butyrate induces apoptosis in MSN neuroblastoma cells in a calcium independent pathway.

Sodium butyrate (NaBt), a histone deacetylase inhibitor, can cause apoptosis in a number of cancer cells. However, the mechanism of this action is poorly understood. Increased intracellular [Ca(2+)] level has been suggested as a likely mechanism, but there is little corroborating data. In this report we provide evidence that NaBt-treated MSN neuroblastoma cells undergo massive apoptosis in the presence of serum and regardless of external or internal [Ca(2+)] levels. Presented data suggest that apoptotic effect of NaBt is both time- and dose-dependent (LD50 1 mM); and that, presence of serum or cAMP, a second messenger molecule that modulates the apoptotic program in a wide variety of cells could not circumvent the apoptotic effect of NaBt. Our findings suggest that NaBt-induced apoptosis in MSN neuroblastoma cells occurs via a pathway that is independent of Ca(2+) flux, intracellular [Ca(2+)] or cAMP levels. Further, we also present data that exclude a role for PKC or histones acetylation.

Renal morphology in connexin43 knockout mice.

Connexins (Cx) are a family of proteins that constitute the intercellular membrane channels of gap junctions. These junctions permit intercellular movement of ions and other molecules between cells, a property vital to organogenesis. Cx43 is a member of the family of channel-forming proteins that are essential for cell-cell communication of developmental signals. Studies demonstrate that Cx43 is observed in mesenchymal cells of 12-day gestation mouse kidney, a crucial period of renal development. In order to study the significance of Cx43 on renal developmental morphology, we evaluated the kidneys of embryos lacking the gene encoding for Cx43. Polymerase chain reaction (PCR) from tail specimens identified wild-type (WT), heterozygote (HT) and knockout (KO) progeny. In situ RT-PCR displayed abundant Cx43 staining in glomeruli, vasculature, and tubules in kidneys obtained from WT progeny. In contrast, Cx43 expression was completely absent in kidneys isolated from the KO. Renal histology in all three groups displayed no significant differences. Renal size was similar and there was no evidence of dysplasia or cyst formation in the KO. Our results indicate that absence of Cx43, heretofore considered essential for renal development, does not affect early renal morphological development.

Gap junction-mediated bidirectional signaling between human fetal hippocampal neurons and astrocytes.

Gap junctions are clusters of intercellular channels that connect the interiors of coupled cells. In the brain, gap junctions function as electrotonic synapses between neurons and as pathways for the exchange of metabolites and second-messenger molecules between glial cells. Astrocytes, the most abundant glial cell type coupled by gap junctions, are intimately involved in the active control of neuronal activity including synaptic transmission and plasticity. Previous studies have suggested that astrocytic-neuronal signaling may involve gap junction-mediated intercellular connections; this issue remains unresolved. In this study, we demonstrate that second-trimester human fetal hippocampal neurons and astrocytes in culture are coupled by gap junctions bidirectionally; we show that human fetal neurons and astrocytes express both the same and different connexin subtypes. The formation of functional homotypic and heterotypic gap junction channels between neurons and astrocytes may add versatility to the signaling between these cell types during human hippocampal ontogeny; disruption of such signaling may contribute to CNS dysfunction during pregnancy.

Gap junctions in the nervous system.

Synapses are classically defined as close connections between two nerve cells or between a neuronal cell and a muscle or gland cell across which a chemical signal (i.e., a neurotransmitter) and/or an electrical signal (i.e., current-carrying ions) can pass. The definition of synapse was developed by Charles Sherrington and by Ramon y Cajal at the beginning of this century and refined by John Eccles and Bernard Katz 50 years later; in this collection of papers, the definition of synapses is discussed further in the chapter by Mike Bennett. who provided the first functional demonstration of electrical transmission via gap junction channels between vertebrate neurons. As is evidenced by the range of topics covered in this issue, research dealing with gap junctions in the nervous system has expanded enormously in the past decade, major findings being that specific cell types in the brain expresses specific types of connexins and that expression patterns coincide with tissue compartmentalization and function and that these compartments change during development.

Gap junctions in the cardiovascular and immune systems.

Gap junctions are clusters of intercellular channels directly connecting the cytoplasm of adjacent cells. These channels are formed by proteins named connexins and are present in all metazoan organisms where they serve diverse functions ranging from control of cell growth and differentiation to electric conduction in excitable tissues. In this overview we describe the presence of connexins in the cardiovascular and lympho-hematopoietic systems giving the reader a summary of the topics to be covered throughout this edition and a historical perspective of the discovery of gap junctions in the immune system.