Demonstration of Semiochemically Induced Aggregation in the Green June Beetle, Cotinis nitida (L.) (Coleoptera: Scarabaeidae)

1988 ◽  
Vol 17 (2) ◽  
pp. 147-149 ◽  
Author(s):  
J. M. Domek ◽  
D. T. Johnson
1987 ◽  
Vol 22 (3) ◽  
pp. 264-267 ◽  
Author(s):  
J. M. Domek ◽  
D. T. Johnson

A trapping study was conducted in an area of heavy green June beetle (GJB), Cotinis nitida (L.) (Coleoptera: Scarabaeidae), emergence to collect evidence in support of the hypothesis that unmated females attract males with a sex pheromone. Yellow-painted baffle and funnel traps, baited with unmated females, mated females, unmated males or no beetles (control), were arranged in a Latin-cube design and randomized daily for four consecutive days. Trap catch was not significantly affected by trap placement (row or column) or time. Significantly more male beetles were caught in traps baited with unmated females than in any other treatments (P = 0.05, Duncan's multiple range test).


Mycologia ◽  
1990 ◽  
Vol 82 (4) ◽  
pp. 471 ◽  
Author(s):  
H. S. Vishniac ◽  
D. T. Johnson

1922 ◽  
Author(s):  
Frank Hurlbut Chittenden ◽  
David Ely Fink

2016 ◽  
Vol 89 (1) ◽  
pp. 45-52
Author(s):  
Cory Creed ◽  
Brian Cowell ◽  
Donn T. Johnson ◽  
Maciej A. Pszczolkowski

Author(s):  
B.A. Shinoda ◽  
M.D. Hardison ◽  
S.F. Mohammad ◽  
H.Y.K. Chuang ◽  
R.G. Mason

The utilization of blood platelets in experimentation frequently requires their separation from blood and subsequent resuspension in media of known composition. Several methods are available for preparation of isolated platelets (1-3) by differential centrifugation or gel filtration, but most methods are tedious and time consuming. Often platelets obtained by use of such methods are in a state different functionally and ultrastructurally from that of platelets in plasma (4).Recently Mohammad, Reddick, and Mason (5) reported a method in which platelets were separated from plasma by ADP-induced aggregation, washed several times, and then incubated in a carefully selected medium that resulted in deaggregation of platelets.


Author(s):  
D.E. Loudy ◽  
J. Sprinkle-Cavallo ◽  
J.T. Yarrington ◽  
F.Y. Thompson ◽  
J.P. Gibson

Previous short term toxicological studies of one to two weeks duration have demonstrated that MDL 19,660 (5-(4-chlorophenyl)-2,4-dihydro-2,4-dimethyl-3Hl, 2,4-triazole-3-thione), an antidepressant drug, causes a dose-related thrombocytopenia in dogs. Platelet counts started to decline after two days of dosing with 30 mg/kg/day and continued to decrease to their lowest levels by 5-7 days. The loss in platelets was primarily of the small discoid subpopulation. In vitro studies have also indicated that MDL 19,660: does not spontaneously aggregate canine platelets and has moderate antiaggregating properties by inhibiting ADP-induced aggregation. The objectives of the present investigation of MDL 19,660 were to evaluate ultrastructurally long term effects on platelet internal architecture and changes in subpopulations of platelets and megakaryocytes.Nine male and nine female beagle dogs were divided equally into three groups and were administered orally 0, 15, or 30 mg/kg/day of MDL 19,660 for three months. Compared to a control platelet range of 353,000- 452,000/μl, a doserelated thrombocytopenia reached a maximum severity of an average of 135,000/μl for the 15 mg/kg/day dogs after two weeks and 81,000/μl for the 30 mg/kg/day dogs after one week.


1994 ◽  
Vol 71 (01) ◽  
pp. 091-094 ◽  
Author(s):  
M Cattaneo ◽  
B Akkawat ◽  
R L Kinlough-Rathbone ◽  
M A Packham ◽  
C Cimminiello ◽  
...  

SummaryNormal human platelets aggregated by thrombin undergo the release reaction and are not readily deaggregated by the combination of inhibitors hirudin, prostaglandin E1 (PGE1) and chymotrypsin. Released adenosine diphosphate (ADP) plays an important role in the stabilization of thrombin-induced human platelet aggregates. Since ticlopidine inhibits the platelet responses to ADP, we studied thrombin-induced aggregation and deaggregation of 14C-serotonin-labeled platelets from 12 patients with cardiovascular disease before and 7 days after the oral administration of ticlopidine, 250 mg b.i.d. Before and after ticlopidine, platelets stimulated with 1 U/ml thrombin aggregated, released about 80–90% 14C-serotinin and did not deaggregate spontaneously within 5 min from stimulation. Before ticlopidine, hirudin (5× the activity of thrombin) and PGE1 (10 μmol/1) plus chymotrypsin (10 U/ml) or plasmin (0.06 U/ml), added at the peak of platelet aggregation, caused slight or no platelet deaggregation. After ticlopidine, the extent of platelet deaggregation caused by the same inhibitors was significantly greater than before ticlopidine. The addition of ADP (10 μmol/1) to platelet suspensions 5 s after thrombin did not prevent the deaggregation of ticlopidine-treated platelets. Thus, ticlopidine facilitates the deaggregation of thrombin-induced human platelet aggregates, most probably because it inhibits the effects of ADP on platelets.


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