scholarly journals Determination of female-biased sexual size dimorphism in moths with a variable instar number: The role of additional instars

2006 ◽  
Vol 103 (3) ◽  
pp. 575-586 ◽  
Author(s):  
Toomas ESPERK ◽  
Toomas TAMMARU
Keyword(s):  
Sexual Size Dimorphism ◽  
Size Dimorphism

scholarly journals Sexual size dimorphism and sexual selection in artiodactyls

2020 ◽  
Vol 31 (3) ◽  
pp. 792-797
Author(s):  
Marcelo H Cassini
Keyword(s):  
Sexual Selection ◽  
Sexual Dimorphism ◽  
Group Size ◽  
Sexual Size Dimorphism ◽  
Alternative Hypothesis ◽  
Mammalian Species ◽  
Generalized Least Squares ◽  
Size Dimorphism ◽  
Selection For

Abstract Sexual size dimorphism is biased toward males in most mammalian species. The most common explanation is precopulatory intramale sexual selection. Large males win fights and mate more frequently. In artiodactyls, previous tests of this hypothesis consisted of interspecific correlations of sexual dimorphism with group size as a surrogate for the intensity of sexual selection (Is). However, group size is not a proper measure of sexual selection for several reasons as is largely recognized in other mammalian taxa. I conducted an interspecific test on the role of sexual selection in the evolution of sexual dimorphism using the variance in genetic paternity as a proxy for the Is. I reviewed the literature and found 17 studies that allowed estimating Is= V/(W2), where V and W are the variance and mean number of offspring per male, respectively. A phylogenetic generalized least squares analysis indicated that dimorphism (Wm/Wf) showed a significant positive regression with the intensity of sexual selection but not group size (multiple r2= 0.40; F3,17= 12.78, P = 0.002). This result suggests that sexual selection may have played a role in the evolution of sexual size dimorphism in Artiodactyla. An alternative hypothesis based on natural selection is discussed.

The role of fecundity and sexual selection in the evolution of size and sexual size dimorphism in New World and Old World voles (Rodentia: Arvicolinae)

Oikos ◽  
2015 ◽  
Vol 125 (9) ◽  
pp. 1250-1260 ◽  
Author(s):  
Vicente García-Navas ◽  
Timothée Bonnet ◽  
Raúl Bonal ◽  
Erik Postma
Keyword(s):  
Sexual Selection ◽  
New World ◽  
Sexual Size Dimorphism ◽  
Old World ◽  
Size Dimorphism

A Molecular Approach to Immunoscintigraphy: A Study of the T-Antigen Conformation on the Surface of Tumors

1987 ◽  
Vol 26 (01) ◽  
pp. 1-6 ◽  
Author(s):  
S. Selvaraj ◽  
M. R. Suresh ◽  
G. McLean ◽  
D. Willans ◽  
C. Turner ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Tumor Cell ◽  
T Antigen ◽  
Human Carcinomas ◽  
Animal Tumor ◽  
Synthetic Antigens

The role of glycoconjugates in tumor cell differentiation has been well documented. We have examined the expression of the two anomers of the Thomsen-Friedenreich antigen on the surface of human, canine and murine tumor cell membranes both in vitro and in vivo. This has been accomplished through the synthesis of the disaccharide terminal residues in both a and ß configuration. Both entities were used to generate murine monoclonal antibodies which recognized the carbohydrate determinants. The determination of fine specificities of these antibodies was effected by means of cellular uptake, immunohistopathology and immunoscintigraphy. Examination of pathological specimens of human and canine tumor tissue indicated that the expressed antigen was in the β configuration. More than 89% of all human carcinomas tested expressed the antigen in the above anomeric form. The combination of synthetic antigens and monoclonal antibodies raised specifically against them provide us with invaluable tools for the study of tumor marker expression in humans and their respective animal tumor models.

On The Mechanism Of Heparin-Induced Potentiation Of Platelet Aggregation

1981 ◽  
Author(s):  
M Yamamoto ◽  
K Watanabe ◽  
Y Ando ◽  
H Iri ◽  
N Fujiyama ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Platelet Activation ◽  
Coagulation Factors ◽  
Marked Enhancement ◽  
Matrix Bound ◽  
Induced Aggregation ◽  
Aggregation Of Platelets ◽  
Plasma Heparin

It has been suggested that heparin caused potentiation of aggregation induced by ADP or epinephrine. The exact mechanism of heparin-induced platelet activation, however, remained unknown. In this paper, we have investigated the role of anti-thrombin III ( AT ) in heparin-induced platelet activation using purified AT and AT depleted plasma. When ADP or epinephrine was added to citrated PRP one minute after addition of heparin ( 1 u/ml, porcine intestinal mucosal heparin, Sigma Co. USA ), marked enhancement of platelet aggregation was observed, compared with the degree of aggregation in the absence of heparin. However, in platelet suspensions prepared in modified Tyrode’s solution, heparin exhibited no potentiating effect on platelet aggregation induced by epinephrine or ADP. Potentiation of epinephrine- or ADP-induced platelet aggregation by heparin was demonstrated when purified AT was added to platelet suspensions at a concentration of 20 μg/ml. AT depleted plasma, which was prepared by immunosorption using matrix-bound antibodies to AT, retained no AT, while determination of α1-antitrypsinα2- macroglobulin and fibrinogen in AT depleted plasma produced values which corresponded to those of the original plasma when dilution factor was taken into account. The activities of coagulation factors were also comparable to those of the original plasma. Heparin exhibited potentiating effect on ADP- or epinephrine-induced aggregation of platelets in original plasma, but no effect in AT depleted plasma. When purified AT was added back to AT depleted plasma at a concentration of 20 μg/ml, potentiation of platelet aggregation by heparin was clearly demonstrated.Our results suggest that effect of heparin on platelet aggregation is also mediated by anti-thrombin III.

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