The occurrence and function of humor in biochemistry, and in science in general, is a topic that has been left in the hands of the social scientists for too long. Although some [ 1 Gilbert G.N. Mulkay M. Opening Pandora's Box: a sociological analysis of scientists’ discourse. Cambridge University Press, 1984 Google Scholar ] provide interesting perspectives, too often their epistemology of humor within the scientific milieu is, inevitably, of limited scope. Too often, in the course of deconstructing the semiotic architecture of scientific humor, the signifier has been confused with the signified, thus providing no grounds for expecting that we can subjugate our humanity and write about the way the universe is in any relative, laughter-dependent manner.

In a previous article, I analyzed two 'in-house' journals produced by the Department of Biochemistry in Cambridge and by the Gilbert Laboratory at Harvard in the 1920s and 1970S, respectively.That study showed that humor is important for scientists, but the sample was too small for any statistically significant conclusions to be drawn regarding the general role of humor in scientists' lives. Now, I have extended the study to examine the occurrence of humor in peer-reviewed scientific journals, specialist publications devoted to scientific humor and in formal publications in the healthcare professions.

An abstract is not available for this content so a preview has been provided. As you have access to this content, a full PDF is available via the 'Save PDF' action button.

This article describes the historical background to the demonstration by Hayflick and Moorhead that human diploid cell strains in culture have limited life-spans. I suggest that the recognition of cell aging in vitro is an example from the biological sciences of a Kuhnian scientific revolution.

Cultured skin fibroblasts from patients with Duchenne muscular dystrophy (DMD) are more sensitive than normal cells to prolonged exposure to the ionophore monensin. In a cell spreading assay in which cells were preincubated with monensin and subsequently allowed to adhere to and spread on a glass substratum in serum-free medium for 100 min, the mean transformed cell area of normal and DMD cells was 5.97 +/- 0.11 and 5.29 +/- 0.03, respectively. Cultured fibroblasts from carriers of DMD yielded a value of 5.59 +/- 0.03, which is intermediate between, and significantly different from, the values for both normal and DMD cultures. This result would be predicted on the basis of random X-chromosome inactivation in female carriers of this disorder. However, comparison of DMD carrier cell spreading data with data obtained from pooled and summated measurements taken from separate experiments using either normal or DMD fibroblasts suggest a more complex situation. Examination of the variance of the means of cell area for the true carrier population and the summated normal and DMD population provides evidence suggesting that some form of cellular interaction may occur between the two cell genotypes in culture.

Bivariate fluorescence-activated sorting is a method for obtaining relatively pure fractions of chromosomal DNA. Unfortunately, the yields (<0.25 μg/day) frequently limit the types of molecular analysis that can be performed. The polymerase chain reaction (PCR) is capable of amplifying unique sequences from scant amounts of template DNA. The purpose of this study was to determine whether the sensitivity of the PCR could be used to detect sequences specific to chromosomes discriminated and purified by flow cytometry. Flow-sorted chromosomal DNA was prepared by collecting ∼105 chromosomes onto a nitrocellulose filter and eluting the DNA by boiling. Amplification products were not detected when different amounts of chromosomal DNA were used in a single 30 to 40-cycle PCR assay. However, when the eluted DNA was primed with degenerate 15-bp oligonucleotides and randomly amplified prior to performing the PCR assay, sequence-tagged sites (STSs) were detected after gel electrophoresis and ethidium bromide staining. This random amplification step eliminated the need for both reamplification with nested primers and detection by DNA hybridization. Furthermore, the random amplification scheme provided enough template DNA from a single sort (105 chromosomes) to perform > 1000 PCR assays. Representational analysis of one chromosome type revealed that >74% of 70 STSs were detected. Moreover, the technology could be used to identify and delineate the breakpoint region of a marker chromosome. This amplification scheme should simplify greatly the molecular analysis of normal and aberrant chromosomes.

In order to clarify the possible involvement of the cell surface in the pathogenesis of Duchenne muscular dystrophy, we have examined the behaviour of fibroblasts cultured from Duchenne patients in hydrated collagen lattices. No differences could be found between Duchenne and normal skin fibroblasts, either after initial seeding or following prolonged culture within the collagen gel.

This review continues with studies of protein, lipid, and purine metabolism of Duchenne muscular dystrophy (DMD) cells in vitro and of muscle cells in combined culture with nerve cells. In vitro studies of human metabolic myopathies are tabulated. Results using the hamster, chicken, and mouse (dy 25 , dy, mdg, and mdx) myopathies are discussed. Interesting findings include suggestions of altered collagen synthesis by DMD cells. Analysis of cell proteins by two‐dimensional gel electrophoresis and the use of combined nerve‐muscle cultures remain important areas of development. It is disappointing that so few attempts have been made to repeat significant findings in this field, and when a number of laboratories have examined the same phenomenon, the results are often contradictory. It remains to be shown how these various abnormalities found in cells in vitro are related to each other and to those pathologic features of diseased muscle observed in vivo.

We have previously reported that skin fibroblasts from patients with Duchenne muscular dystrophy (DMD) have a lower intercellular adhesiveness than control cells, and that cells from carriers of DMD have normal adhesiveness instead of the expected intermediate value. We have now cloned skin fibroblasts from a carrier of DMD (subject AS) who is also heterozygous for G6PD B/G6PD Mediterranean and determined the intercellular adhesiveness and G6PD phenotypes of the clones. G6PD activity was determined using the 2d-G6P/G6P ratio method. Normal cells had a percentage utilisation of 7.31% and uncloned cells from AS a value of 25.16%. Of 16 clones, 15 had normal values (mean 8.72%) while one clone was G6PD Med with a value of 57.5%. Mean intercellular adhesiveness of normal and uncloned cells from AS were 2.95 and 2.90 respectively. Of 11 clones tested, nine had normal values of adhesiveness (mean 3.1) and all these clones were G6PD B. The single G6PD Med clone had a value of 0.88, compared with 1.39 for DMD cells. We have no explanation at present for the single clone that was G6PD B but DMD-like on aggregation.

Measurements of aggregation kinetics using couette viscometry show that freshly trypsinized skin fibroblasts from patients with Duchenne muscular dystrophy have values of intercellular adhesiveness approx. 40% those of normal cells. If cells are allowed to recover from the effects of trypsinization (by incubation for 2 h at 37 degrees C in serum-containing medium) the intercellular adhesiveness of both cell types increases, and normal and Duchenne cells aggregate to the same extent. Exposure to the ionophore monensin during the recovery phase leads to suppression of recovery in both cell types, and this effect of the drug is greater in Duchenne fibroblasts. These results are discussed in relation to other data on the reported differential effects of trypsin and monensin on normal and Duchenne fibroblasts.

Developments in neuroscience have provided the opportunity to know unconscious consumer reactions and acknowledge direct measures of cognitive constructs like attention. Given the ever-increasing concern over packaging's contribution to creating a positive first impression, the current research seeks to examine consumers' attention and declarative preferences regarding the three main different packaging attributes as isolated variables: images, texts and colours. The experiment exposed participants (N = 40) to 63 stimuli, which were based on modifications of the three main packaging attributes of three products of three different food categories. This study used electroencephalogram (EEG) and eye-tracking (ET) to measure attention, and a declarative test was employed to examine preference. First, the results presented herein show that the presence of visual elements, either images or texts on packages, increased the participants' level of attention. Second, the results reveal that colour modifications do not have a significant effect on participants' neurophysiological attention levels. Third, the results demonstrated that the neurophysiological effects among the participants do not necessarily coincide with their subjective evaluations of preference. Hence, this study increases awareness of the relevance of combining traditional market research tools that rely on explicit consumer responses with neuroscientific techniques. These findings indicate, first of all, that more research is needed to ascertain the extent to which consumers' neurophysiological outcomes correspond to their declarative preferences and second, that neurophysiological methods should be given more attention in research.

Duchenne muscular dystrophy (DMD) is a severe degenerative disorder of skeletal muscle. It has been suggested that an abnormality of the plasma membrane may be responsible for the pathogenesis of DMD, and a number of cell surface changes have been described in DMD muscle fibres and other cell types. Alterations in cell-to-cell and cell-to-substratum adhesiveness have been reported for DMD cells and we have determined whether these alterations in cell adhesiveness affect migration of cells from DMD muscle explants. DMD cells move more rapidly and spend less time at rest than do normal or DMD carrier cells, although the differences were statistically significant only for the latter cells. An inverse relationship between cell speed and contact with surrounding cells was not observed. All cells tended to persist in their direction of movement, and there were no differences between the types of cells studied. Our results support the view that there may be a cell surface defect in DMD.

Rotation-mediated aggregation of human skin fibroblasts has been studied and the patterns of aggregation compared between cultures obtained from 9 patients with Duchenne muscular dystrophy and from 10 normal controls. The rate of aggregation was dependent on the growth state of the cells, with growing cells aggregating more rapidly than growth-arrested cells. There was considerable variation between individuals in the rate at which cells aggregated but no differences were detected in the aggregation of normal and DMD cells measured by this method. The monovalent cation ionophore monensin, which inhibits the transport of cellular proteins to the extracellular medium, reduced aggregation of all cells. The data suggest that after initial cell-cell contact continued aggregation is dependent on the secretion of materials to the cell surface. The aggregation of normal and DMD cells was affected similarly by this treatment.