Erratum

The ordinate of Fig. 1A in the report by R. Berezny and D. S. Coffey (25 July, page 292) should read "103 count/min per 100 microg of DNA" rather than "per microg of DNA"     

Correction

In the report "Motor neuron degeneration in mice that express a human Cu, Zn super-oxide dismutase mutation" by M. E. Gurney et al. (17 June 1994, p. 1772)(1), a systematic, 10-fold error was made in calculating the dilutions of brain extract used for determinations of total brain superoxide dismutase (SOD) activity shown in column 6 of table 1 (p. 1774). Each value reported should have been reduced by that factor, for example, the total SOD activity reported for the G1 line should have been 4.26 +/- 0.2 SOD (U)/total protein (microg), not 42.6 +/- 2.1 U/microg, and so forth.     

Erratum

In the report "Aflatoxin production by a variant of Apergillus oryzae (NRRL strain 1988) on cowpeas (Vigna sinensis)" by N. El-Hag and R. E. Morse [192, 1345 (1976)], the third sentence in the legend to Table 1 should read "This strain produced aflatoxin on rice (expressed as micrograms per kilogram ...)." Also, the heading for columns 2 and 3 of Table 1 should read "Aflatoxin (microg/kg) from A. oryzae."     

Erratum

In the report "DNA amplification for direction detection of HIV-1 in DNA of peripheral blood mononuclear cells " Chin-Yih Ou et al. (15 Jan., p. 295), the fourth sentence of reference 21 (p. 297) should have read, "The PCR reaction mixture contained 1 microg of PBMC DNA, 100 pmol each of primers (Table 2), 200 microM each of four deoxyribonucleoside triphosphates, 10 microM tris-HC1, pH 8.3, 50 mM KC1, 2.5 mM MgCl(2), 0.01% gelatin and 0.6 unit of thermoresistant DNA polymerase of Thermus aquaticus."     

Chloramphenicol-specific antibody

Antibody to the antibiotic chloramphenicol was obtained by immunizing rabbits with a chloramphenicol derivative coupled to bovine gamma globulin. Production of antibody was demonstrated by the precipitin and complement fixation reactions with "reduced chloramphenicol" coupled to rabbit serum albumin as the test antigen. Specificity of the antibody was confirmed in that crystalline chloramphenicol completely inhibited complement fixation and precipitin reactions. "reduced chloramphenicol" coupled to human serum albumin provides an antigen for the detection of antibody to chloramphenicol, if it occurs in human serum in dyscrasias. With quantitative complement fixation, as little as 10(-5) microg (4 x 10(-14) mole) of chloramphenicol was detectable by the inhibition assay.     

CORTISOL FROM HUMAN NERVE

Cortisol was found in myelinated nerve fibers of the lumbo-sacral plexus (2.0 to 6.0 microg per gram of tissue) and in the sympathetic chain with dorsal root ganglia (0.2 to 0.4 microg per gram of tissue).     

NOREPINEPHRINE AND 3,4DIHYDROXYPHENETHYLAMINE TURNOVER IN GUINEA PIG BRAIN IN VIVO

By administering C(14)-la-beled tyrosine or H(3)-labeled 3,4-dihy-droxyphenylalanine to guinea pigs it has been possible to achieve sufficient labeling of the norepinephrine and dopamine in the brain to permit measurement of their turnover rates. The half-life of brain dopamine was about 2.5 hours. The half-life of norepinephrine was about 4 hours, suggesting a rate of synthesis of at least 0.03 to 0.04, microg/g per hr or 2.4 microg/day for the whole guinea pig brain.     

Erratum

In the report by L. D. Fetcher and Z. Annau [197, 680 (1977)], the values for whole brain dopamine levels in 1-day-old rats were given as 5.47 +/- 1.62 and 3.01 +/- 0.81, microg/g (wet weight) in air and CO subjects injected with L-dopa. The correct values are 5.47 +/- 0.38 and 3.01 +/- 0.20 microg/g. The difference between the groups is significant at P < .01 as reported.     

Erratum

In the report "Mutagenicity of fly ash particles in Paramecium" by J. Smith-Sonneborn et al. (9 Jan., p. 180), Tables 1 and 2 are printed incorrectly. Significance lines are missing from both tables and "uninduced" should read "induced" in the sixth, eighth, and ninth entries of the first column in Table 1. The tables are reprinted below as they should have appeared. Table 1. Mutagenic effect of fly ash and heat-treated fly ash in Paramecium. Values not connected by the same line are significantly different from each other (Wilcoxon matched-pairs signed-ranks test, alpha = .05). The data from six experiments were pooled since the control values for autogamous progeny were not significantly different. Cerophyl is the ryegrass extract used for cultivation of Paramecium. Induced S-9 is the Ames liver microsome fraction from rats receiving Arochlor 1254 (polychlorinated biphenyl) to activate the enzymes for conversion of promutagens to mutagenic form; uninduced S-9 is from rats receiving corn oil only (the vehicle for the Arochlor). Glass beads (1 to 3 ,microm) suspended in either induced or uninduced S-9 were used as a negative control for nonnutritive particles. Kaolinite was also used in one experiment, and the results were the same as those for the glass beads. Benzo[a]pyrene was the positive control for mutagenicity requiring induced S-9. The initial concentration of suspended fly ash was 535 ,microg/ml. The average number of affected progeny from treated parent cells was 20 percent higher than the average number of affected control progeny. Since one mutation would theoretically yield only 4 affected progeny in 16 autogamous progeny from a treated parent cell (6), the percentages, though low, reflect significant damage. [See table in the PDF file] Table 2. Mutagenicity of heat-treated fly ash extracted with HCl or DMSO. Values not connected by the same line are significantly different from each other (pairwise comparisons of proportions, P < .05). The concentration of fly ash particles suspended in uninduced S-9 was 1068 ,ug/ml. The higher than usual value for mutagenicity in the controls can be attributed to the considerable age of the clone used here [micronuclear damage increases with age (12)]. [See table in the PDF file].     

Erratum

In the report by A. Persechini and D. J. Hartshorne (18 Sept., p. 1383), the abscissa of the insert in Fig. 2 is labeled incorrectly. It should read "(32)P incorporation/kinase (microg/ml)."     

An immunological investigation of human pituitary growth hormone

Growth hormone isolated from human pituitaries has been demonstrated to be a good antigen in the rabbit. With the rabbit antiserum to human somatotropin, it is possible to detect as little as 0.1 microg of the hormone by precipitin test. The antiserum was also capable of neutralizing the growth-promoting activity of human somatotropin.     

Abscisin II, an Abscission-Accelerating Substance from Young Cotton Fruit

Crystalline abscisin II, with a tentative molecular formula of C(15)H(20)O(4), has been isolated from young cotton fruit. It accelerates abscission when applied in amounts as low as 0.01 microg per abscission zone. It inhibits indoleacetic acid-induced straight growth of Avena coleoptiles but has no gibberellin activity on dwarf maize.     

A Technique for Aeration of Sterile Liquid Culture Medium

Streptomycin held in solution in concentrations of 100 and 1,000 microg./ml. at 10 degrees C. is stable at pH 6.0, 7.0, and 8.0 for a period of three months. The depressor effect observed in the turbidimetric assay appears to be the result of two factors, buffer salt concentration and pH, and is most marked at pH 6.0. Almost normal activity reappears at pH 8.0 even in the presence of the greater concentration of phosphates.     

Suppressive effects of 2-thiouracil on differentiation and flowering in Cannabis sativa

The pyrimidine, 2-thiouracil, partly annuls the effect of photoperiodic induction in the short-day plant, Cannabis sativa L., when it is supplied at the onset of the dark period in quantities of 15-30 microg per plant. This treatment also produces aberrations in cellular differentiation in the leaves. Tracer studies show that 2-thiouracil becomes bound in cellular ribonucleic acid, which suggests that the effects on morphogenesis are due to interference with nucleic acid metabolism.     

Mitosis and Differentiation in Roots Treated with Actinomycin

In the presence of actinomycin D (90 microg/ml), mitosis in root meristem of Allium cepa L. ceases after a delay of 36 hours. The block occurs at interphase. Differentiation of prevascular tissue is suppressed, and the evidence suggests it begins to fail before mitosis stops. Autoradiograms of roots treated with tritiated uracil show that synthesis of ribonucleic acid is blocked after mitosis fails. The effects of the antibiotic are reversible.     

LSD and genetic damage

Of nine studies in vitro, six have indicated some degree of induced chromosomal breakage after exposure to LSD; three failed to confirm these results. The damage, when found, was generally of the chromatid type, arising during or after DNA synthesis. This damage, with one exception, was the result of concentrations of drug and durations of exposure which could not be achieved in humans with reasonable dosages. There did not appear to be a dose-response relation. The magnitude of damage, when found, was in the range encompassing the effects of many commonly used substances. The absence in vitro of excretory and detoxifying systems present in vivo, as well as several negative reports, cast doubt on the relevance of in vitro results. In 21 chromosomal studies in vivo, 310 subjects were examined. Of these, 126 were treated with pure LSD; the other 184 were exposed to illicit, "alleged" LSD. A maximum of only 18 of 126 (14.29 percent) of the subjects in the group exposed to pure LSD showed higher frequency of chromosome aberration than the controls. In contrast, a maximum of 90 of 184 (48.91 percent) of the subjects taking illicit LSD showed an increase in frequency of aberrations. Of all the subjects reported to have chromosome damage, only 18 of the 108 (16.67 percent) were exposed to pure LSD. The frequency of individuals with chromosomal damage reported among illicit drug users was more than triple that associated with the use of pharmacologically pure LSD. We conclude that chromosome damage, when found, was related to the effects of drug abuse in general and not, as initially reported, to LSD alone. We believe that pure LSD ingested in moderate dosages does not produce chromosome damage detectable by available methods. No significant work on carcinogenic potential of LSD has been reported so far. No cause-and-effect relation and no increase in the incidence of neoplasia among LSD users have been demonstrated. Case reports (three in 4.0 years) of leukemia and other neoplasia in this population are rare. The results of early chromosome studies suggested that true genetic damage might be a consequence of LSD exposure. The comprehensive evidence from studies on drosophila indicates no mutagenic effect from 0.28 to 500 microg of LSD per milliliter and a definite mutagenic effect from 2,000 to 10,000 microg/ml; this is consistent with a threshold response or a sigmoid dose-effect relation. We believe that LSD is, in fact, a weak mutagen, effective only in extremely high doses; it is unlikely to be mutagenic in any concentration used by human subjects. Circular dichroism experiments suggested that the specific mechanism of action of LSD on DNA may be a direct interaction resulting in conformational changes in the DNA helix. These changes are unlikely to result in a decrease of internal stability sufficient to cause breakage of chromosomes, but they may be the physical basis of the weak mutagenicity. Early chromosomal studies implicated LSD as a potential cause of congenital malformations, fetal wastage, and germinal chromosome damage. First reports of a teratogenic effect in hamsters and rats have not been confirmed. A review of 15 rodent studies indicated a wide range of individual, strain, and species susceptibility to the effects of LSD. The applicability of such investigations to man is doubtful. In a study of human pregnancies, those exposed to illicit LSD had an elevated rate of spontaneous abortions. There is no reported instance of a malformed child born to a woman who ingested pure LSD; there are six cases of malformation associated with exposure to illicit LSD, four of which have similar limb defects. Given, however, the high frequency of unexplained "spontaneous" birth defects, the rare occurrence of malformed infants born to women who used illicit LSD may be coincidental. While there is no evidence that pure LSD is teratogenic in man, the use of any drug during pregnancy requires that its potential benefits significantly outweigh its potential hazards. From our own work and from a review of the literature, we believe that pure LSD ingested in moderate doses does not damage chromosomes in vivo, does not cause detectable genetic damage, and is not a teratogen or a carcinogen in man. Within these bounds, therefore, we suggest that, other than during pregnancy, there is no present contraindication to the continued controlled experimental use of pure LSD. Note added in proof: A brief review has been brought to our attention. Although based on a sample of only 15 studies the author reached conclusions similar to our own (92).     

Genetic analysis of a high-level vancomycin-resistant isolate of Staphylococcus aureus

Vancomycin is usually reserved for treatment of serious infections, including those caused by multidrug-resistant Staphylococcus aureus. A clinical isolate of S. aureus with high-level resistance to vancomycin (minimal inhibitory concentration = 1024 microg/ml) was isolated in June 2002. This isolate harbored a 57.9-kilobase multiresistance conjugative plasmid within which Tn1546 (vanA) was integrated. Additional elements on the plasmid encoded resistance to trimethoprim (dfrA), beta-lactams (blaZ), aminoglycosides (aacA-aphD), and disinfectants (qacC). Genetic analyses suggest that the long-anticipated transfer of vancomycin resistance to a methicillin-resistant S. aureus occurred in vivo by interspecies transfer of Tn1546 from a co-isolate of Enterococcus faecalis.     

Specific tropism of HIV-1 for microglial cells in primary human brain cultures

Human immunodeficiency virus (HIV) frequently causes neurological dysfunction and is abundantly expressed in the central nervous system (CNS) of acquired immunodeficiency syndrome (AIDS) patients with HIV encephalitis or myelopathy. The virus is found mostly in cells of the monocyte-macrophage lineage within the CNS, but the possibility of infection of other glial cells has been raised. Therefore, the effects of different HIV-1 and HIV-2 strains were studied in primary cultures of adult human brain containing microglial cells, the resident CNS macrophages, and astrocytes. These cultures could be productively infected with macrophage-adapted HIV-1 isolates but not with T lymphocyte-adapted HIV-1 isolates or two HIV-2 isolates. As determined with a triple-label procedure, primary astrocytes did not express HIV gag antigens and remained normal throughout the 3-week course of infection. In contrast, virus replicated in neighboring microglial cells, often leading to their cell fusion and death. The death of microglial cells, which normally serve immune functions in the CNS, may be a key factor in the pathogenesis of AIDS encephalitis or myelopathy.     

大红甜橙和冰糖橙果实发育过程中有机酸和氨基酸含量变化研究

以冰糖橙和大红甜橙为材料,研究两个品种果实发育过程中有机酸和氨基酸含量的变化。结果表明,果实发育过程中大红甜橙果实柠檬酸含量、总氨基酸含量均显著高于冰糖橙;大红甜橙和冰糖橙成熟果实中氨基酸总量分别为5.06 g/100g DW和3.46 g/100g DW,以天冬氨酸、谷氨酸和半胱氨酸含量较高。果实发育过程中,谷氨酸族氨基酸在大红甜橙果实中无明显变化,而在冰糖橙果实中逐渐降低;果实发育前期天冬氨酸族氨基酸含量在大红甜橙果实中高于冰糖橙,而果实成熟期两品种无明显差异;鲜味和甜味氨基酸在大红甜橙果实中含量均高于冰糖橙,且均伴随果实成熟而降低。