Nutrition for acute renal failure patients on continuous hemofiltration.
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Biomedical subjects
Publications and source records attributed to D J Goldstein.
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Ratio developmental quotients (DQs) from Bayley Scales administered after age 30 months were compared to Stanford-Binet IQs secured later. Means from two testings of 42 mentally retarded children were almost identical. The DQs and IQs correlated .81, p less than .001. These findings justify the use of Bayley ratio quotients to determine intellectual level of children who are too old for the Bayley norms but too retarded to earn a basal level on the Stanford-Binet.
CGP 6085 A, a specific 5-hydroxytryptamine (5-HT), serotonin uptake inhibitor, is also a potent hypotensive agent. Its depressor effect in the spontaneously hypertensive (SH) rats correlates well with its ability to inhibit serotonin uptake. Here we report that the effects of CGP 6085 A on arterial blood pressure were greatly reduced in rats pretreated with p-chlorophenylalanine (pCl-Phe), a specific depletor of serotonin. Moreover, in rats pretreated with the serotonin antagonist, methysergide, CGP 6085 A did not produce significant hypotension. We also found that centrally administered naloxone reverses the hypotensive effect of CGP 6085 A. These results provide further evidence for the existence of an important serotonin-opioid interaction in the mechanisms of arterial blood regulation in the rat.
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Since 1963, 11 cases have been reported in which both the acardiac twin and the "normal" co-twin were studied cytogenetically. Aneuploidy or polyploidy was clearly identified in the acardiac twin in 7 cases and in the co-twin in 1 case. We report on 2 additional twin pairs in which aneuploidy was associated with acephalus-acardia. In both cases the "normal" co-twin had a Klinefelter (47,XXY) karyotype. Chromosome analysis in the 2 acardiac twins documented a 47,XXY constitution in one and 94,XXXXYY anomaly in the other. One of the "normal" co-twins also had the VATER association. Given these data we would recommend chromosome analysis of both members of a twin pair when one has acephalus-acardia.
Several HSV-1 proteins including the major capsid protein (VP5), two minor capsid proteins (VP11-12 and VP18.8), the alkaline nuclease and glycoprotein gH have been reported to be encoded by the left-most one-third of HSV-1 UL DNA. In this paper, we present physical mapping data and phenotypic analysis of six ts mutants whose mutations lie within this region and which collectively represent four functional complementation groups (1-6, 1-7, 1-10, and 1-26). In this study, mutants in complementation group 1-10 were found to be defective in the synthesis of viral DNA, late viral polypeptides, and the formation of mature capsid-like structures--properties characteristic of other ts mutants defective in functions required for viral DNA synthesis. Two DNA-positive mutants in complementation group 1-7 fail to induce capsid formation and probably possess mutations in coding sequences for VP5. Mutants in two other complementation groups (1-6 and 1-26) synthesize significant levels of viral DNA, late polypeptides, and capsids. The functions of the gene products represented by these mutants remain to be determined.
Two affected first cousins with duplication of 15(q22.3----qter) are reported. This resulted from a familial t(8;15)(p23.3;q22.3) translocation. The findings in these patients are compared with each other and with six other published cases. Anthropometric and dermatoglyphic findings are summarised.
Urea kinetic modeling is a hemodialysis prescription technique that includes calculation of patients' protein catabolic rate (grams per kilogram body weight per day). This study compared the use of current guidelines alone with the integration of the urea kinetic modeling-derived protein catabolic rate and current guidelines for the nutrition assessment and management of 27 chronic renal failure patients on hemodialysis. In phase 1, subjects were counseled according to current renal nutrition guidelines. In phase 2, subjects were kinetically modeled and counseled with incorporation of the urea kinetic modeling-derived protein catabolic rate value. Thirteen subjects received a 1-month follow-up. Food records and time length of counseling sessions were recorded in phases 1 and 2. Significant changes seen in the mean blood urea nitrogen value during phase 2 (no. = 22, p less than or equal to .05) and follow-up phase (no. = 13, p less than or equal to 0.05) reflected an improved protein intake from phase 1 for the majority of subjects. Dietary intake and time length of counseling sessions in both phases were not significantly different. The following correlations were noted: reported protein intake and protein catabolic rate: r = .685, p less than or equal to .001; protein catabolic rate and blood urea nitrogen: r = .799, p less than or equal to .001; blood urea nitrogen and serum albumin: r = .485, p less than or equal to .05. Results suggest that the urea kinetic modeling-derived protein catabolic rate value positively affects patient adherence to diet recommendations.(ABSTRACT TRUNCATED AT 250 WORDS)
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This is the first report of necropsy findings associated with diploid-triploid mosaicism. The important pathological findings are presented and compared to those of pure triploidy and those noted in noninvasive studies of diploid-triploid mosaics. The clinical findings in this patient are compared with those of other reported cases.
A high noise/signal ratio in microdensitometry, owing, for example, to the use of a very small measuring spot or light at an extreme of the spectrum, decreases the precision (increases the variability) of results. This can be compensated for by making more measurements, but under some circumstances random signal variations can also cause systematic errors that are not so easily corrected. The present article explains how such errors can arise when measuring either very pale or very dense objects and suggests methods to detect and avoid them. The principles described are applicable to many types of microdensitometer, not only the Vickers flying-spot instruments used in this investigation.
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Enzymatic and immunologic methods were used to study amylase expression in amniotic fluid and human pancreatic tissue from fetuses of various gestational ages. A starch-coated slide assay was used to quantitate amylase activity in amniotic fluids, and samples with activity were studied by electrophoresis to determine the presence of salivary amylase (Amy1) and pancreatic amylase (Amy2) isozymes. Immunohistochemical studies were performed with both a rabbit anti-human Amy1 antibody and a murine anti-human Amy2 antibody (Amy2/SP2/1). Amy2/SP2/1 was used to discriminate between Amy1 and Amy2. Both Amy1 and Amy2 activities were present in amniotic fluid from 14 weeks' gestation, and immunologic activity was present in pancreatic tissue sections from 15.9 weeks' gestation.
Beta-galactosidase conjugated to erythrocyte vesicles was measured by enzymatic and immunologic methods. The immunoassay used a monoclonal antibody and an anti-mouse IgG antibody conjugated to alkaline phosphatase in an adaptation of the enzyme-linked immunosorbent assay. The beta-galactosidase and alkaline phosphatase activities were compared by correlation. The significant correlation indicates that this method is satisfactory for relative quantitation of membrane-associated antigens with exposed epitopes.
A competition enzyme-linked immunosorbant assay (CELIA) can be used to determine the amount of antigen needed to immunoabsorb an antiserum. This is demonstrated using both polyclonal and monoclonal antibodies against human amylase. This method is of especial value when the tissue is particularly difficult to obtain, and especially valuable when CELIA has already been completed.
Quantitative alkaline phosphatase (ALP; EC 3.1.3.1) expression varies among various tissues and among inbred mouse strains. There is about a 20-fold difference in ALP activity in lungs from CBA/J and C57L/J inbred strains and this difference is inherited additively with a heritability of 0.84. Studies of thermostability at 56 and 65 degrees C and sensitivity toward inhibitors (L-phenylalanine, L-homoarginine, L-phenylalanylglycylglycine, and levamisole) do not demonstrate differences in the ALP from lungs or liver of the CBA/J and C57L/J strains. The ALP activity in intestine expressed by the intestinal locus varies over 100-fold between A/J and DBA/1J strains. Further studies of the mechanisms resulting in this difference in ALP activity should help elucidate the mechanisms for aberrant expression of ALP in malignancy and for manipulation of low ALP activity in hypophosphatasia.
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Diphtheria toxin was modified at one or both of its cysteine disulfide bridges by iodoacetamide, methylmethanethiosulfonate, and atomic mercury. The products of these reactions were characterized and tested for toxicity in vitro and in vivo. All were toxic in vitro, but had lost almost all cytotoxic activity toward HeLa cells. It was possible to show from in vivo protection experiments that modification of the cysteine disulfide in the B-chain interfered with cell surface binding, while modification of the cysteine disulfide linking the A and B domains inhibits a step subsequent to binding in the intoxication process. The latter finding supports a functional role for this interdomain cysteine disulfide in the membrane transport process.