71 research outputs found
Development of the springbok skin — colour pattern, hair slope and horn rudiments in Antidorcas marsupialis
Get PDFIn the foetal springbok skin, identifiable melanocytes are present before colour patterns are established. These pigment cells fail to appear in the pouch and belly areas, indicating that these zones are piebald and not albinotic. Areas of regional colour differences are sharply separated. Their distinctiveness is caused by a discontinuous change in brightness of the hairy coat. This is due to a stepwise shift in the average quanta of melanin in the hairs. The pigment itself does not alter its colour from one colour-zone to another, but the density of the pigment particles merely changes. It is suggested that the steps could correspond to a discontinuous difference in tissue dosage, resulting perhaps from differing activation among multiple melanizing genes. Anatomical peculiarities of the pouch area and horn rudiment are described. A proposal is made that hair slope is brought about by traction from mobile superficial fibroblasts. These cells travel preferentially in the direction of the greatest tissue strain. By dragging the papillary layer components along behind them, such as the hair buds and arrector pili muscles, the hair streams could arise. The tips of the hair shafts will then point away from each direction of greatest internal expansion, which the fibroblasts strive to cover
Book Reviews
Get PDFBook Review 1Book Title: Early Life Histories of Fishes: New Developmental, Ecological and Evolutionary PerspectivesBook Author:Â Edited by E.K. BalonDr W. Junk, Dordrecht. 280 pp.Book Review 2Book Title: Comparative Aspects of Extracellular Acid-base BalanceBook Author:Â J.P. TruchotSpringer, 1987. 248 pp. 51 figures.Book Review 3Book Title:Â Insect Flight: Dispersal and MigrationBook Author:Â Edited by W. DanthanarayanaSpringer-Verlag, Berlin, 1986. 289 pp.Book Review 4Book Title: Â The Mammalian Herbivore Stomach. Comparative Anatomy, Function and EvolutionBook Author:Â Peter LangerGustav Fischer, Stuttgart, 1988. 557 pages, 246 figures and 72 tablesBook Review 5Book Title: Â Biology of the Integument. Vol. 2: VertebratesBook Authors: Edited by J. Bereiter-Hahn, A.G. Matoltsy & K.S. RichardsSpringer, Berlin, 1986. 855 pp.Book Review 6Book Title: Â Advances in the Biology of Turbellarians and related PlatyhelminthesBook Author:Â Edited by Seth TylerDr. W. Junk Publishers, 1986. 357 pages; 253 figuresBook Review 7Book Title:Â Evolutionary Physiological EcologyBook Author:Â Edited by P. CalowCambridge University Press, Cambridge. 239 pp.Book Review 8Book Title:Â DragonfliesBook Author:Â Peter L. MillerCambridge University Press, Cambridge, New York and Melbourne, 1987. 84 pp
Whole-genome sequencing reveals host factors underlying critical COVID-19
Get PDFCritical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
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