Validation of the synthetic model for the imaging heavy ion beam probe at the ASDEX Upgrade tokamak (invited).

Recent experiments at the ASDEX Upgrade tokamak have provided the first ever measurements from the imaging heavy-ion beam probe. In this work, we show that the developed simulation framework can reproduce qualitatively the measurement's observed shape and position. Quantitatively, we demonstrate that the model reproduces, within the experimental uncertainties, the observed signal levels. A detailed explanation of the synthetic model is presented, along with the calibration of the optical setup that reproduces the measurements.

First measurements of an imaging heavy ion beam probe at the ASDEX Upgrade tokamak.

The imaging heavy ion beam probe (i-HIBP) diagnostic has been successfully commissioned at ASDEX Upgrade. The i-HIBP injects a primary neutral beam into the plasma, where it is ionized, leading to a fan of secondary (charged) beams. These are deflected by the magnetic field of the tokamak and collected by a scintillator detector, generating a strike-line light pattern that encodes information on the density, electrostatic potential, and magnetic field of the plasma edge. The first measurements have been made, demonstrating the proof-of-principle of this diagnostic technique. A primary beam of 85/87Rb has been used with energies ranging between 60 and 72 keV and extracted currents up to 1.5 mA. The first signals have been obtained in experiments covering a wide range of parameter spaces, with plasma currents (Ip) between 0.2 and 0.8 MA and on-axis toroidal magnetic field (Bt) between 1.9 and 2.7 T. Low densities appear to be critical for the performance of the diagnostic, as signals are typically observed only when the line integrated density is below 2.0-3.0 × 1019 m-2 in the central interferometer chord, depending on the plasma shape. The strike line moves as expected when Ip is ramped, indicating that current measurements are possible. Additionally, clear dynamics in the intensity of the strike line are often observed, which might be linked to changes in the edge profile structure. However, the signal-to-background ratio of the signals is hampered by stray light, and the image guide degradation is due to neutron irradiation. Finally, simulations have been carried out to investigate the sensitivity of the expected signals to plasma density and temperature. The results are in qualitative agreement with the experimental observations, suggesting that the diagnostic is almost insensitive to fluctuations in the temperature profile, while the signal level is highly determined by the density profile due to the beam attenuation.

Expression of hepatitis B virus surface antigen gene in Escherichia coli.

Direct expression of hepatitis B virus (HBV) surface antigen (HBsAg) gene under the control of the Escherichia coli tryptophan operon (trp) promoter has been achieved. Synthesis of HBsAg (both complete and lacking its N-terminal segment) as a part of hybrid proteins with the N-terminal portion coded by genes cat, kan or bla is controlled by the appropriate promoters, as well as by the trp promoter. The highest levels of expression, including those for direct synthesis of HBsAg, provide the accumulation of about 10(5) polypeptide molecules per bacterial cell.

Cytomegalovirus infection: a quantitative prospective study of three hundred twenty consecutive renal transplants.

The quantitative effects of cytomegalovirus (CMV) infection on morbidity and mortality rates were examined in 320 renal transplant cases. With the use of virus cultures and CMV antibody measurements, all patients were studied, regardless of symptoms, from a time before transplantation to at least 1 year, 11 months after transplantation for a maximum of 5 years, 9 months. The posttransplant risk factors of CMV infection--patient age, type of donor (living-related or cadaver), antigen match between donor and recipient, presence of diabetes, and the presence of pretransplant CMV antibody--were evaluated for their relative effects on patient survival, graft survival, fever, and leukopenia. CMV infection was a significant risk factor for these four events. CMV infection occurred in 181 patients after transplantation and accounted for 25% of the deaths, 20% of the graft failures, 30% of the occurrences of fever, and 35% of the occurrences of leukopenia. Unexpectedly, female recipients were at higher risk than men for the adverse effects of CMV infection. Young patients and those receiving their second transplant were at higher risk of graft loss if they had associated CMV infection. CMV infection was most reliably predicted by the presence of pretransplant antibody, indicating that reactivation of endogenous virus was responsible for most infections. The presence of pretransplant antibody offered a small amount of protection against fever, but no protection against death, graft failure, or leukopenia. Simultaneous episodes of CMV infection and transplant rejection, both common posttransplant events, most often occurred by chance.

Epstein-Barr virus antibody responses and clinical illness in renal transplant recipients.

Among 88 renal transplant recipients evaluated for a change in Epstein-Barr virus (EBV) antibody status in the period after transplant, 22 showed a 4-fold rise and eight showed an 8-fold or greater rise in EBV antibody. Among the patients with an 8-fold or greater EBV ANTIBODY RISE, THE OCCURRENCE OF FEVER WAS FREQUENT, ONE PATIENT DEVELOPED A LYMPHOPROLIFERATIVE reaction, and one died with a malignant EBV infection. Patients without pretransplant antibody showed a longer mean time to antibody rise (104 +/- 23 days) than did those patients with pretransplant antibody (19 +/- 7 days). The longer incubation period in patients without pretransplant antibody was in the expected range for primary EBV infections. Both primary and secondary (reactivation) EBV infections occur in renal transplant patients. These infections may be assoicated with prolonged fever, and in unusual circumstances, may cause dramatic lymphoproliferative disease.

Viral infections in renal transplant donors and their recipients: a prospective study.

The majority of renal allograft recipients develop viral infections, usually with cytomegalovirus (CMV). Their source if virus has not been defined clearly; one possibility if the transplanted kidney itself. To explore this, prospective viral studies were performed on 28 living related donor-recipient pairs. Donors did not have clinical illnesses and viruses were not recovered from throat, urine, or renal tissue, but five (18%) had fourfold rises in antibody titers to herpes group viruses. During the 6 months after transplantation, 24 recipients (86%) had viral infections, 18 of which were associated with CMV. There was no correlation between specific titer rises in the donors and infections in the recipients. Recipients with dual viral infections had more severe clinical courses than those with single infections or with no infection. Recipients with complement-fixing (CF) antibodies to CMV pretransplant had a higher incidence of CMV infections than recipients without pretransplant antibody. Three of seven recipients who lacked CF antibody to CMV and whose donors were seropositive developed clinical illnesses associated with CMV. Latent virus might have been transmitted with the transplanted kidney in these instances, but since lack of CF antibody does not rule out previous CMV infection, the CMV could have been of recipient origin. We conclude that the donor organ is a source of virus for few renal transplant recipients.

Thermoregulation during prolonged exercise in heat: alterations with beta-adrenergic blockade.

Thermoregulation and cardiovascular drift were studied under conditions of prolonged exercise in a warm environment (dry bulb temperature 31.7 +/- 0.3 degrees C, rh 44.7 +/- 4.7%) during beta-adrenergic blockade. Fourteen subjects performed 90-min rides on a cycle ergometer at a work rate equivalent to 40% of their control maximal O2 uptake under each of three treatments provided in a randomized double-blind manner: atenolol (100 mg/day), propranolol (160 mg/day), and a placebo. Exercise during the propranolol trial resulted in significantly higher forearm vascular resistance values and significantly lower forearm blood flows (FBF) compared with the placebo trial. However, the significantly lower FBF during propranolol did not significantly alter the rectal temperature (Tre) response to prolonged exercise. In addition, both beta-blockers produced lower FBF for any given Tre, suggesting that beta-adrenergic blockade affects FBF through nonthermal factors. The slight differences in Tre, despite the large differences in FBF between the various treatments, are apparently the result of an enhanced sweat loss and a lower mean skin temperature during exercise with beta-blockade. The uncoupling of FBF and sweat loss provides evidence of independent regulation. The reduction in FBF at any given Tre was concomitant to lower blood pressure values during beta-blockade and suggests that baroreflexes provide significant input to the control of skin blood flow when both pressure and temperature maintenance are simultaneously challenged.

Beta-blockade reduces tidal volume during heavy exercise in trained and untrained men.

The effects of beta-blockade on tidal volume (VT), breath cycle timing, and respiratory drive were evaluated in 14 endurance-trained [maximum O2 uptake (VO2max) approximately 65 ml X kg-1 X min-1] and 14 untrained (VO2max approximately 50 ml X kg-1 X min-1) male subjects at 45, 60, and 75% of unblocked VO2max and at VO2max. Propranolol (PROP, 80 mg twice daily), atenolol (ATEN, 100 mg once a day) and placebo (PLAC) were administered in a randomized double-blind design. In both subject groups both drugs attenuated the increases in VT associated with increasing work rate. CO2 production (VCO2) was not changed by either drug during submaximal exercise but was reduced in both subject groups by both drugs during maximal exercise. The relationship between minute ventilation (VE) and VCO2 was unaltered by either drug in both subject groups due to increases in breathing frequency. In trained subjects VT was reduced during maximal exercise from 2.58 l/breath on PLAC to 2.21 l/breath on PROP and to 2.44 l/breath on ATEN. In untrained subjects VT at maximal exercise was reduced from 2.30 l/breath on PLAC to 1.99 on PROP and 2.12 on ATEN. These observations indicate that 1) since VE vs. VCO2 was not altered by beta-adrenergic blockade, the changes in VT and f did not result from a general blunting of the ventilatory response to exercise during beta-adrenergic blockade; and 2) blockade of beta 1- and beta 2-receptors with PROP caused larger reductions in VT compared with blockade of beta 1-receptors only (ATEN), suggesting that beta 2-mediated bronchodilation plays a role in the VT response to heavy exercise.

Effect of beta-blockade on the drift in O2 consumption during prolonged exercise.

The effect of beta-adrenergic blockade on the drift in O2 consumption (VO2 drift) typically observed during prolonged constant-rate exercise was studied in 14 healthy males in moderate heat at 40% of maximal O2 consumption (VO2max). After an initial maximum cycle ergometer test to determine the subjects' control VO2max, subjects were administered each of three medications: placebo, atenolol (100 mg once daily), and propranolol (80 mg twice daily), in a randomized double-blind fashion. Each medication period was 5 days in length and was followed by a 4-day washout period. On the 3rd day of each medication period, subjects performed a maximal cycle ergometer test. On the final day of each medication period, subjects exercised at 40% of their control VO2max for 90 min on a cycle ergometer in a warm (31.7 +/- 0.3 degrees C) moderately humid (44.7 +/- 4.7%) environment. beta-Blockade caused significant (P less than 0.05) reductions in VO2max, maximal minute ventilation (VEmax), maximal heart rate (HRmax), and maximal exercise time. Significantly greater decreases in VO2max, VEmax, and HRmax were associated with the propranolol compared with the atenolol treatment. During the 90-min submaximal rides, beta-blockade significantly reduced heart rate. Substantially lower values for O2 consumption (VO2) and minute ventilation (VE) were observed with propranolol compared with atenolol or placebo. Furthermore, VO2 drift and HR drift were observed under atenolol and placebo conditions but not with propranolol. Respiratory exchange ratio decreased significantly over time during the placebo and atenolol trials but did not change during the propranolol trial.(ABSTRACT TRUNCATED AT 250 WORDS)

Maximal exercise responses to acute and chronic beta-adrenergic blockade in healthy male subjects.

Conflicting data on the alterations in the maximal exercise response to beta blockade (BB) may be the result of differences in the length of time the subject has been on medication, i.e., hours vs days. The purpose of this study was to examine maximal exercise responses during acute and chronic administration of BB. Twenty-eight healthy males, 14 untrained (UT) and 14 involved in a personal training regimen (TR), performed maximal treadmill tests after 1 d and 9 d under three double-blind, randomized conditions: a placebo (PLAC), propranolol (PROP) 80 mg b.i.d., and atenolol (ATEN) 100 mg o.d. Maximal heart rate (HR), oxygen consumption (VO2), ventilation (VE), and treadmill time were significantly reduced by PROP and ATEN after an acute and chronic dose when compared to PLAC (P less than 0.05) in both groups of subjects. Maximal HR was decreased more after 1 d of BB than after 9 d of BB with both PROP and ATEN in the UT subjects and with PROP only in the TR group. VO2max, VEmax, and treadmill time were also less attenuated after 9 d of BB; however, this trend did not reach statistical significance. The nonselective beta blocker, PROP, caused greater reductions in VO2max compared to the selective beta blocker, ATEN, in both groups of subjects. These data indicate that, other than a small change in maximal HR, there is no difference in the exercise response to acute and chronic BB in normal and highly conditioned individuals.

Serological diagnosis of California (La Crosse) encephalitis by immunofluorescence.

A method of indirect immunofluorescence was developed and examined retrospectively as a serological test for the laboratory diagnosis of California encephalitis (CE). LaCrosse virus immunofluorescence immunoglobulin (Ig) G and IgM studies were done on paired sera from 50 patients with acute central nervous system infections. CE had been documented in 25 patients by hemagglutination inhibition, neutralizing, complement fixing, and/or precipitin tests. Five (20%) of the acute and 16 (64%) of the convalescent sera from CE patients had La Crosse IgM antibodies. Seven (28%) of the acute and all of the convalescent CE specimens had La Crosse IgG antibodies. Titers ranged from less than 4 to 256. IgG antibodies were present in all 11 sera collected 1 to 2 years after CE, but IgM antibodies were absent. The 25 serum pairs from patients who did not have CE were negative for IgM and IgG antibodies. This study indicated that La Crosse immunofluorescence antibody tests were as sensitive and specific for CE as conventional hemagglutination-inhibition tests, and would detect at least 20% of patients during their acute illness.

Measles (rubeola) susceptibility among elementary schoolchildren.

Measles (rubeola) immunity among 479 elementary schoolchildren from suburban Minneapolis was serologically surveyed in December 1971. Of the 479 children, 25 (5.2%) had hemagglutination-inhibition (HI) titers less than 2. These children were considered susceptible to measles. For the 233 immunized children with no measles history, 13 (5.6%) had rubeola HI titers less than 2 while 5 (5.1%) of the 98 youngsters with a history of clinical measles had rubeola HI titers less than 2. Of the 454 immune children, 73 (16%) had measles HI titers between 2 and 8. These findings confirm durable immunity and a low rate of vaccine failure following live attenuated measles vaccination but demonstrate the importance of testing sera beginning at a dilution of 2 in order to detect children with low antibody levels. This survey also suggests that maternal antibody interferes with the active immune response in youngsters immunized when less than 1 year of age because this group of children had significantly lower geometric mean titers and significantly more susceptibles than the children immunized when greater than or minus 2 years.

Cytomegalovirus: Clinical virological correlations in renal transplant recipients.

One-hundred thirty-two renal transplant recipients were systematically screened for viral infections and the findings correlated with the clinical course. One-hundred ten patients showed evidence of infection with herpesviruses and 89 patients showed laboratory evidence of infection with cytomegalovirus (CMV) uncomplicated by bacterial infections or technical complications. Patients without viral infections were usually asymptomatic. After recovery and development of anti-viral antibodies, most patients were asymptomatic despite the persistence of viral excretion in the urine. In contrast, the onset of viral infections were almost always accompanied by a significant clinical illness characterized by fever, leukopenia, and renal malfunction. Of 89 patients with cytomegalovirus infections, 83 survived at least three months. In these patients, the fever appeared to be self-limited and resolution of the fever was accompanied by increases in anti-CMV antibody. Renal biopsies demonstrated typical rejection reactions in all the biopsied patients and renal malfunction usually responded to anti-rejection treatment. Six of the 89 patients with CMV infections died within a month of viral isolation. These patients could be distinguished from those who recovered by a decreased or absent antibody response to the virus, suppressed lymphocyte responses to mitogen in autochthonous blood, and absent histologic evidence of rejection in the renal allografts. Thus, two paradoxical responses to CMV infections are seen in transplant patients: In the relatively immunocompetent patient, the infection is associated with renal allograft rejection, a prompt antibody response to the virus, and recovery. The severely immunosuppressed patient cannot make an antibody response, does not exhibit allograft rejection as a cause of renal malfunction, he may be further immunosuppressed by the viral infection, and is susceptible to sequential opportunistic infections leading to death.

Specific cell-mediated immune defect in active cytomegalovirus infection of young children and their mothers.

4 young children with active cytomegalovirus (C.M.V.) infection were found, by an in-vitro lymphocyte-proliferation assay, to have a C.M.V.-specific cell-mediated immune defect. These children had antibodies to C.M.V. and were actively shedding C.M.V. in the urine when studied. Their general cellular immune responses were intact, with normal numbers of T lymphocytes and normal in-vitro responses to mitogens and at least one antigen. 3 of the 4 mothers studied shortly after delivery had decreased cell-mediated immunity to C.M.V. These findings suggest that an antigen-specific immune defect facilitates transmission of virus from mother to infant and permits persistence of viral replication in the offspring.

Prevention or modification of varicella using zoster immune plasma.

Zoster immune plasma (ZIP) was given to 31 susceptible immunocompromised children one to seven days (median, two days) following household, playmate, or hospital exposures to varicella. The average amount of ZIP transfused was 7 ml/kg. Twenty-one children did not develop varicella or persistent antibodies to varicella-zoster virus (VZV). Eight (26%) of the 31 contracted clinical varicella. Seven cases were mild, but in one child, who was given ZIP seven days after exposure, visceral disease developed and the child died. Two children had subclinical varicella that was documented by persistence of VZV antibodies for at least ten months after passive immunization. Because none of the 30 children given ZIP one to six days following exposure had severe varicella, we conclude that ZIP is effective in preventing or modifying varicella in immunocompromised patients if given shortly after exposure.