Biomedical subjects
Publications and source records attributed to J C Allen.
The excluded fraction from Sephadex G-25 separation of human seminal plasma has been found to suppress lymphocyte transformation and DNA synthesis [7]. We have shown that most of its in vitro activity is due to contamination by spermine which binds tenaciously to, and co-elutes with the protein.
The extinction coefficients, quantum yields and reactivities of the triplet states of 8-methoxypsoralen and 4,5',8-trimethylpsoralen in methanolic solution have been determined using laser flash photolysis techniques. The second-order rate constants for the quenching of these triplet states by pyrimidine and purine bases were found to be several orders of magnitude lower than those found for other furocoumarin derivatives. This may suggest, therefore, that the skin photosensitising ability of such compounds does not necessarily correlate with in vitro triplet state reactivity. Preliminary experiments on the reactivity of the psoralen triplet state with DNA itself indicate that no transient absorptions due to psoralen excited states can be observed when a photon is absorbed by the psoralen-DNA complex.
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Currently, antibiotic efficacy in acute bacterial meningitis is evaluated in several stages. First, animals are used to assess antibiotic penetration into cerebrospinal fluid (CSF) in the absence and presence of an inflammatory stimulus. Second, concentrations of drug are correlated to in vitro killing studies. Third, clinical evaluations compare the new drugs to currently available antimicrobic--but drug failures nevertheless occur, e.g. the experiences with cephalosporins and aminoglycosides. We propose that brain tissue levels of antibiotics are an additional parameter to be monitored. Drugs that penetrate the brain substance should yield higher ventricular concentrations than drugs that penetrate the choroid plexus alone. A protective benefit may also be afforded to brain tissue per se. Experience with chloramphenicol, which penetrates the blood-brain barrier, supports these concepts; so also, do the failures with cephalosporins and aminoglycosides which, despite high CSF concentrations of these agents, afford evidence that currently monitored parameters are inadequate predictors of therapeutic efficacy.
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Linear drift of X-ray attenuation coefficients must be corrected if quantitative comparisons are to be made between computed tomography (CT) brain scans of the same individual performed at different times. Such a correction is accomplished by comparing the low (cerebrospinal fluid) end of the attenuation coefficient frequency histograms using a percentile--percentile plot. A "drift correction" permits serial quantitative assessments of the progression or regression of white matter hypodensity, such as occurs in drug induced leukoencephalopathy.
Several previous authors have examined the association between infection and acute leukemia, especially at the time of death, but none has assessed this problem at the time of diagnosis and initial hospitalization. We have undertaken a retrospective review of cases of acute leukemia diagnosed at the affiliated hospitals of the State University of New York at Buffalo. Results suggest that bacteriologic findings in this population initially resemble those in the general outpatient population. Gram-negative bacilli, especially Pseudomonas aeruginosa, appear as important pathogens after the first week of hospitalization. A statistically significant association with prolonged granulocytopenia and use of antibiotics develops during this course. As a consequence of these data, we recommend careful culture and clinical delineation of the early infection, choosing the narrowest spectrum of antibiotic coverage appropriate to the infection present as data evolve.
Spermine and spermidine in vitro are potent inhibitors of proliferation of phytohaemagglutinin-stimulated rat thymic lymphocytes, lymphoma cells and human lymphoblastic leukaemia cells, but only in media supplemented by foetal calf serum. This inhibition is shown to be due to a bovine plasma polyamine oxidase, with a high specificity for these polyamines. Spontaneously dividing lymphocytes are not subject to this inhibition. This, plus direct evidence from synchronous cultures of EB2 cells demonstrates that the inhibition is expressed in the late G1 or G1/S interface of the cell cycle. Putrescine was not an inhibitor in the presence of foetal calf serum but became so in the presence of human pregnancy serum, possibly due to the action of diamine oxidase.
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The effects of the ionophore, RO 2-2985 (X537A, RO) were studied on isolated coronary, renal and femoral arteries in two types of experiments: (1) the effect of RO as a modulator of various contractile effects of KCl and phenylephrine (PE), and (2) the effect of RO itself as a contractile agonist. The effect of the ionophore A23187 was observed in similar experiments to help determine the nature of the RO response. In the first type of experiment, RO was found to have a differential effect upon the arteries contracted with KCl. The coronary arteries relaxed upon addition of the ionophore, whereas, the femoral and renal arteries did not. A23187 had only a transient effect on KCl-contracted coronary arteries. RO relaxed femoral and renal arteries contracted with PE, and A23187 had only a transient effect. RO attenuated ED50 values and maximum tension developments to both KCl and PE, and A23187 had no effect on these parameters. In the second type of experiment, RO (only at 10-5 M) was found to contract femoral and coronary arteries, but had no effect on renal arteries. Experiments with alpha-blocking agents and calculations using association constants of RO for catecholamines suggest that RO is not acting via catecholamine chelation. The dissimilarity between the effects of RO and A23187 suggest that RO may not be working through a specific effect on Ca++. These differential responses to RO suggest variations in intervessel regulation of PE- AND KCl-induced contradictions and can explain, in part, the in vivo effects of RO on regional blood flow.
Intracarotid (i.c.) hyperosmolar mannitol enhances central nervous system (CNS) penetration of intravenous (i.v.) methotrexate (MTX) in normal adult rats. A fivefold augmentation in the CSF:serum and ipsilateral brain:serum MTX concentration ratios was observed 1 hour after drug administration. Intravenous mannitol had no such effect. Rats with meningeal carcinomatosis have a partial defect in blood-brain barrier function, and the CSF:serum MTX concentration ratio was 4.6 times higher in these animals than in normal rats prior to mannitol therapy. Intracarotid hyperosmolar mannitol further augmented the blood-brain barrier permeability to intravenous MTX. Intracarotid mannitol increased the therapeutic effect of MTX, since rats with meningeal carcinomatosis that received i.v. MTX and i.c. mannitol experienced a slight enhancement in survival.
Potassium chloride and sodium chloride were infused into the reticulorumen of male Holstein calves, approximately 6 mo of age and 260 kg, at .29, .58, 1.15, 1.73, 2.31, or 2.88 g potassium per kilogram body weight or 1.35, 2.12, or 2.16 g sodium per kilogram in equal volumes of water. Paired controls were infused with water. Calves were monitored for physiological changes for 6 h at 15, 30, or 60-min intervals. Potassium and total solids of plasma and packed cell volume were increased at potassium doses greater than .29 g of potassium per kilogram body weight within 1 h after dosing. At the higher doses of potassium, sodium content of plasma increased about 1 h after the increase in plasma potassium. Respiration rates within a potassium treatment varied with respect to time after dosing, but generally they increased, and associated variables of carbon dioxide pressure, pH, and bicarbonate in blood were decreased accordingly. Clinical toxicity signs, including excess salivation, muscular tremors of legs, and excitability were observed with potassium doses greater than .58 g of potassium per kilogram body weight. Three of five calves given 1.73 g of potassium per kilogram, three of four calves given 2.31 g of potassium per kilogram, and one calf given 2.88 g of potassium per kilogram body weight died. With a small number of calves, oral sodium infusions increased plasma sodium in proportion to the dose, but plasma potassium remained relatively constant. Sodium infusions of 2.12 and 2.16 g of sodium per kilogram body weight were fatal.
Young male Holstein calves were fed either a control (.5% chloride) or a low-chloride (.038% chloride) practical diet for 7 wk. Both groups received low-chloride (.00038% chloride) well water. Feeding the low-chloride diet did not produce definite clinical symptoms of chloride deficiency. Neither body weight gains, feed intake, feed digestibility, nor body retention of chloride, sodium, potassium, or nitrogen were effected adversely. Although the chloride intake of the low-chloride calves was only one-sixteenth that of controls, body chloride retention was similar for the two groups. The similar retention of body chloride was due to effective homeostatic mechanisms in which urinary chloride excretion was reduced by 95% in the low-chloride calves. Low-chloride calves consumed more water and excreted more urine than control calves. Although the exact minimum chloride requirement for growth in calves was not established, .038% chloride was adequate for normal growth for the 7 wk.
The cerebrospinal fluid (CSF) and serum of six patients with histologically verified intracranial germ-cell tumors were assayed serially for the presence of alphafetoprotein (AFP) and the beta subunit of human chorionic gonadotropin (HCG). Two patients had embryonal carcinomas, two had choriocarcinomas, and two had dysgerminomas. The marker profile for a given tumor in either CSF or serum correlated with the histological diagnosis; that is, embryonal carcinoma produced AFP and HCG, choriocarcinoma produced HCG, and dysgerminoma produced no markers. The marker levels in serum and CSF declined with therapy and rose usually prior to the development of overt clinical symptoms if the patient's tumor recurred. A CSF-to-serum gradient of the marker levels was present in three of four patients, and the serum levels were often normal when the CSF values were elevated. Ventricular marker levels were lower than the lumbar levels in two of two patients. The assay of these biological markers is a sensitive indicator of the success of therapy, and the presence of a CSF-to-serum gradient suggests that the major portion of the neoplasm rests within the central nervous system. A histological diagnosis can be inferred without the necessity of surgery in appropriate clinical contexts.
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