Laser heating of YBa2Cu3O7 films in Raman experiments.
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Biomedical subjects
Publications and source records attributed to A Bock.
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The data concerning the value of duplex sonography in diagnosing parenchymatous renal allograft dysfunction are controversial. Most early studies did not take into consideration the many factors influencing resistance parameters. We therefore performed a prospective, biopsy-controlled study with exclusion of all known sources of error regarding resistance parameters. Furthermore we investigated the value of a new resistance parameter, the systolic deceleration percentage. Forty-seven duplex sonographic studies were performed on 43 patients (30 male, 13 female, median age 47 years, range 7-70). Fourteen studies were done on normally functioning grafts (control group) an average of 33 days after transplantation. Thirty-three studies were performed on dysfunctional grafts immediately prior to biopsy. Grafts which had been transplanted more than a year previously or with vascular findings or any other clinical or sonographic pathology probably explaining function deterioration were excluded. In all patients, the resistive index (RI), pulsatility index (PI) and systolic deceleration percentage (DP) were calculated in the main renal artery and in the interlobar artery. Of the 33 grafts with dysfunction, nine had vascular rejection (VR), 11 interstitial rejection (IR), 11 cyclosporin A toxicity (CAT) and two other histologies (OR). The mean RI in normal grafts (NO) was 0.71 +/- 0.06 in the main artery and 0.68 +/- 0.06 in the interlobar artery, in VR 0.86 +/- 0.12 and 0.80 +/- 0.18, in IR 0.72 +/- 0.05 and 0.70 +/- 0.07, in CAT 0.67 +/- 0.06 and 0.65 +/- 0.07 and in OR 0.64 +/- 0.07 and 0.60 +/- 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)
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PURPOSE: To evaluate a fast three-dimensional (3D) sequence that permits the acquisition of 16 T2-weighted images within a 29-second breath hold for magnetic resonance (MR) imaging of the liver. MATERIALS AND METHODS: Eighty-seven patients with focal liver lesions were examined at 1.5 T by using a 3D reversed fast imaging with steady-state precession (PSIF) sequence at flip angles of 15 degrees, 30 degrees, and 70 degrees and a T2-weighted spin-echo (SE) sequence. Quantitative and qualitative image analysis was performed. RESULTS: Contrast and signal difference-to-noise ratios were 56% and 33% (liver-spleen) and 76% and 68% (liver-tumor), respectively, with the 3D-PSIF sequence compared with the T2-weighted SE sequence. With 3D-PSIF, overall image quality was poorer than that of the T2-weighted SE sequence at flip angles of 15 degrees but was similar at 30 degrees and 70 degrees. At low flip angles (15 degrees and 30 degrees) all lesion types were hyperintense. At a flip angle of 70 degrees, it was predominantly cysts and hemangiomas that showed high signal intensity. With the 3D-PSIF sequence, intrahepatic vessels are void of signal and can be better distinguished from small liver lesions compared with the flow-compensated T2-weighted SE sequence. CONCLUSION: The fast 3D-PSIF sequence is a valuable addition to MR imaging of the liver.
We tested the hypothesis that the fludrocortisone in doses sufficient to elevate blood pressure (BP) in normal subjects would increase platelet cytosolic calcium. Eight normal volunteers were given 0.8 mg fludrocortisone daily for 7 days (short protocol). Eight other normal volunteers ingested the drug for 6 weeks (long protocol). In the short protocol, fludrocortisone increased platelet cytosolic calcium and body weight by day 3, while BP was increased by day 7. In the long protocol, platelet cytosolic calcium was increased after 1 week, returned to basal values by 3 weeks and remained at that level for the rest of the study. Stimulation of the subjects' platelets ex vivo with thrombin and vasopressin led to a significant increase in intracellular free calcium concentration; however, fludrocortisone treatment did not alter the calcium response to either agonist. Fludrocortisone decreased serum potassium, plasma renin activity, plasma noradrenaline concentration and serum ionised calcium. These changes, as well as the BP increase, reverted to basal values when the drug was discontinued. We next incubated human platelets with fludrocortisone (1.4 nmol/l) and found a significant increase in cytosolic calcium by 30 min. The data suggest that a blood pressure-raising dose of mineralocorticoid leads to a transient (days to weeks) increase in platelet cytosolic calcium. Platelet cytosolic calcium and blood pressure are dissociated in that cytosolic calcium increases before the BP increase and later decreases to lower values, while the BP increase is sustained. Mineralocorticoid also has a direct effect on platelet cytosolic calcium in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
For early diagnosis of cytomegalovirus (CMV) infection after renal transplantation, 18 patients were monitored within the first 3 months. Blood leukocytes were assayed weekly for the presence of the CMV matrix protein p65 (antigenemia assay) and CMV DNA by the polymerase chain reaction (PCR). In 12 out of 18 patients, 70 (37.8%) of 185 blood samples were positive by antigenemia assay or by PCR. 49 and 115 samples concurrently were positive and negative by both tests. 8 blood samples were positive only by the antigenemia assay and 13 only by PCR. Therefore, the relative sensitivity of PCR and of antigenemia assay was 88.6% and 81.4% respectively. In 9 of 10 patients who were pre-transplant CMV seropositive and in 4 of 7 patients who were pre-transplant CMV seronegative and received a graft from a seropositive donor, CMV infection was detected by positive antigenemia and/or PCR. Four of these patients developed CMV disease. In all these patients, antigenemia assay and PCR were positive 7 to 16 days prior to onset of clinical symptoms. Antigenemia and PCR are rapid and sensitive methods for the detection of CMV infection 1 to 2 weeks prior to disease. In addition, the semi-quantitative assay of antigenemia enables monitoring of the efficacy of antiviral therapy.
The heterologous expression of cDNAs encoding the alkaloid biosynthetic enzymes, strictosidine synthase [EC 4.3.3.2] from Rauvolfia serpentina and the berberine bridge enzyme [(S)-reticuline: oxygen oxidoreductase (methylene-bridge-forming), EC 1.5.3.9] from Eschscholtzia californica, has been achieved in a cell culture (Sf9) of the fall army worm, Spodoptera frugiperda, using a baculovirus-based expression system. The expression resulted in the overproduction of each plant enzyme in a catalytically active form. The maximal production attained was 4 mg purified, active enzyme per litre cell culture for both the strictosidine synthase and berberine bridge enzymes.
The neuropeptides thyrotropin-releasing hormone (TRH) and corticotropin-releasing hormone (CRH) have been found to be potent stimulators of the autonomic nervous system in both experimental animals and humans. We studied the effects of different doses of CRH and TRH given intracerebroventricularly in the urethane-anesthetized rat and a single dose of CRH in the chloral hydrate-anesthetized rat to elucidate the effects of these peptides in the unconscious state. All TRH doses studied enhanced blood pressure and noradrenaline and adrenaline secretion. Surprisingly, there were no blood pressure increases following administration of 0.4, 1.3 and 1.7 nmol CRH. In general, there was a tendency for blood pressure to decrease with the largest drop observed after 1.7 nmol CRH. Our data suggest that only TRH clearly augments blood pressure and catecholamine secretion in the anesthetized animal, while CRH does not exert major effects under the two anesthetic conditions employed.
To evaluate long-term benefits and risks of CyA therapy in renal transplantation, we analyzed the 10-year experience with all 59 patients who had received a first cadaveric renal graft until August 1983 and were immunosuppressed with CyA. We compared their actual graft survival with that of all 213 patients who had received a first cadaveric graft from 1967 until August 1983, but were immunosuppressed initially with azathioprine and prednisone (AzaP). For comparison of p-creatinine, proteinuria, blood pressure, lipids, uric acid and skin malignancies we evaluated the patients staying unchanged on initial therapy for 10 years (CyA = 12, AzaP = 53). RESULTS. (1) Actual graft survival at 10 years was 34% (20/59) with CyA and 27% (58/213) in AzaP treated patients (intention to treat) (P = .09 = ns). At 1 to 5 years, graft survival was 15% superior with CyA, but after 7 years the survival curve of the CyA-group has closely joined the chronic decline seen in the AzaP group. This behaviour could neither be explained by chronic CyA-nephrotoxicity nor by chronic rejection after switching from CyA to AzaP. (2) P-creatinine at 10 years was significantly (P < .03), but mildly elevated under CyA (130 +/- 52; AzaP = 109 +/- 65). (3) Proteinuria (g/d) at 10 years was not significantly different (CyA = 0.41 +/- 0.58, versus AzaP = 0.83 +/- 1.61). (4) Systolic blood pressure was higher at 10 years under CyA (152 +/- 19) than under AzaP (136 +/-) (P < .02), but diastolic pressure was not (89 +/- 10 versus 84 +/- 12; ns). Antihypertensive drug/patient was twice as high under CyA (1.25 versus 0.64 P < .02). (5) Cholesterol, triglyceride, HDL were not different. 75% of the CyA-patients were steroid free at 10 years, none of the AzaP-patients. (6) P-uric acid was not significantly different in both groups (494 +/- 192 vs 400 +/- 124), but 42% of CyA-patients were on uric acid lowering drug (given after at least one gout attack) as compared to 9% under AzaP (P < .006). (7) Seventeen percent of patients under CyA for 10 years had at least one skin cancer, not different from 15% of AzaP-patients. CONCLUSIONS. The main benefit of CyA was the better graft survival up to 5 years and the chance to stay free of steroids. The main risks of CyA were nephrotoxicity, hypertension and symptomatic hyperuricemia. No difference was found for hyperlipidemia and skin-malignancies.
In clinical practice p-creatinine is used to estimate changes of GFR. Generally, it is believed that recovery of p-creatinine within 10% of initial baseline allows exclusion of relevant nephrotoxic changes. We evaluated whether recovery of GFR after discontinuation of CyA therapy can be adequately predicted by measuring p-creatinine alone. Fifty-four allogenic BMT patients were followed up by p-creatinine and classical inulin clearance (GFR) before BMT and 1, 3, 6, 12, 18, 24 months after BMT. A total of 10 patients fulfilled following three criteria: (1) 24 months total follow-up time; (2) at least 12 months follow-up after discontinuation of CyA therapy (3) no trimethoprim or cimetidine comedication at time of clearance measurement. Time after CyA withdrawal varied between 13 and 21 months (mean +/- standard deviation, 17 +/- 2 months); mean duration of CyA therapy was 8 +/- 2 months (minimum: 3 months, maximum: 11 months). After at least 12 months of CyA stop mean p-creatinine returned to baseline values. In contrast, mean GFR remained about 20% below baseline (paired sample Wilcoxon-test P < .02). Neither creatinine excretion nor body weight nor creatinine clearance changed significantly between baseline and 24 months after BMT. Follow-up of p-creatinine after CyA stop can overestimate the recovery of GFR. A 20% loss of GFR may remain unrecognized. We speculate that this phenomenon is due to tubular hypertrophy in the recovery phase.
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In the near future several new immunosuppressive substances will be available: Cyclosporin G, IMM125 (both are new derivates of Cyclosporin A), FK506, Rapamycin, Leflunomid, Mycophenolic acid (RS-61443), Bredinin (Mizorinin), Brequinar, Deoxyspergualin and several new monoclonal antibodies (anti-CD4, anti-II-2-Receptor, anti-CD8, anti-CD45, anti-ICAM1 and others). Side-effects of immunosuppressants are classified in 1) relative drug-specific or 2) unspecific effects of over-immunosuppression (infections and malignancies). Nephrotoxicity of Cyclosporin A and guidelines for its prevention are covered in more detail. The authors fear, that the proliferation of new immunosuppressive drugs will make it more difficult, to carefully evaluate their side-effects.
The aim of the present study was to evaluate whether lactate can maintain the energy metabolism and electrical activity of isolated perfused rat brain in the absence of glucose. To exhaust cerebral glucose stores and simultaneously raise endogenous lactate, complete ischemia was induced. After ischemia, when a glucose-free perfusate was supplied, restoration of interstitial potassium (Ke+), cortical discontinuous current (DC) potential, electroencephalogram (EEG) activity, and ATP and phosphocreatine (PCr) was not significantly different from postischemic recovery findings when a glucose-containing perfusate was used. In the group receiving glucose-free perfusate, postischemic application of 1 mM iodoacetic acid did not inhibit the recovery of electrical activity, Ke+, or DC potential. After recovery of Ke+ in glucose-free reperfusion, a 20-30-Hz EEG pattern appeared and was maintained for about 20 min followed by disappearance of spontaneous electrical activity. An abrupt increase of Ke+, a steep negative DC shift, and a substantial decrease of ATP and PCr occurred after about 22 min of reperfusion. During the first 5 min of glucose-free reperfusion, consumption of lactate was significantly higher (0.89 mumol/g wet weight/min) than during reperfusion with medium containing glucose (0.41 mumol/g ww/min). Increasing amounts of tissue lactate prolonged maintenance of electrical function in glucose-free reperfusion. This correlation could not be found for free fatty acids. In conclusion, after a few minutes of ischemia, the brain is able to recover cellular ion transport and electrical activity without a supply of glucose, preferentially by combustion of lactate accumulated in brain tissue. This mechanism is only useful during a limited time period until the lactate accumulated during ischemia is combusted.
Human calcitonin (hCT) injected into the lumen of the descending colon of normal human subjects was absorbed within minutes and could be recognized intact in plasma as shown by RIA in combination with reverse-phase HPLC. The absorption was low and variable, with bioavailabilities ranging from 0.01% to 2.7% relative to intravenously administered hCT (area under the concentration-time curve). With intravenous hCT serum calcium was lowered and the fractional urinary excretion of calcium, phosphorus, sodium and chloride was significantly stimulated. With the intracolonic hCT, the fractional urinary excretions of calcium, sodium and chloride were also marginally stimulated relative to intracolonic vehicle (placebo). In conclusion, hCT is absorbed intact from the colon, but the bioavailability is low and highly variable.
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The purpose of this study was to characterize breast carcinomas by cell kinetic parameters. Mitotic rate (MR) and flow cytometrically (FCM) measured cell cycle distribution as well as chromatin testing in situ employing heparin for determination of activated chromatin, provided the following results: MR counted in 73 unselected carcinomas showed an increase up to a tumor size of 4.2 cm (p less than 0.05); beyond this diameter, the MR was found to decrease. In T1-T2 carcinomas, cell cycle stage analysis yielded higher percentages of cells in S and G2M phase for ductal (13% and 12%, N = 22) than for lobular (8% and 7%, N = 8) node-negative carcinomas (p less than 0.002). In ductal carcinomas, lymph node involvement was reflected by higher % G2M values (15%, N = 26) compared with negative cases (12%, N = 22) (p less than 0.05). Ductal node-positive T3-T4 carcinomas (N = 10) revealed a higher % S value (16%) than their T1-T2 counterparts. A correlation between MR and % G2M was established only up to a tumor size of 4.2 cm (r = 0.39, p less than 0.05). A highly sensitive ('H') and a poorly sensitive ('P') subgroup of carcinomas with respect to heparin-induced changes in fluorescence intensity of the G1/0 peak of the DNA aneuploid cell line were identified, as previously shown. These subgroups were here updated with a larger number of carcinomas and were limited to T1-T2 cancers (N = 57). Group 'H' included more younger patients (p less than 0.005), less cases with nodal involvement in ductal carcinomas (p less than 0.05), and lower % G2M values in lobular node-negative cases (p less than 0.05), than group 'P'. DNA diploid cells always existing in DNA aneuploid carcinomas are more sensitive than their aneuploid counterparts (p less than 0.01); however, they strengthen the stratification to 'H' and 'P'. We suggest 'H' carcinomas to be less aggressive than 'P' carcinomas. Small breast carcinomas are recommended to cell kinetic investigations for individualizing adjuvant therapy.
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