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At least 325 records · Page 18Linked to original sources

Flower color variation: a model for the experimental study of evolution.

We review the study of flower color polymorphisms in the morning glory as a model for the analysis of adaptation. The pathway involved in the determination of flower color phenotype is traced from the molecular and genetic levels to the phenotypic level. Many of the genes that determine the enzymatic components of flavonoid biosynthesis are redundant, but, despite this complexity, it is possible to associate discrete floral phenotypes with individual genes. An important finding is that almost all of the mutations that determine phenotypic differences are the result of transposon insertions. Thus, the flower color diversity seized on by early human domesticators of this plant is a consequence of the rich variety of mobile elements that reside in the morning glory genome. We then consider a long history of research aimed at uncovering the ecological fate of these various flower phenotypes in the southeastern U.S. A large body of work has shown that insect pollinators discriminate against white phenotypes when white flowers are rare in populations. Because the plant is self-compatible, pollinator bias causes an increase in self-fertilization in white maternal plants, which should lead to an increase in the frequency of white genes, according to modifier gene theory. Studies of geographical distributions indicate other, as yet undiscovered, disadvantages associated with the white phenotype. The ultimate goal of connecting ecology to molecular genetics through the medium of phenotype is yet to be attained, but this approach may represent a model for analyzing the translation between these two levels of biological organization.

Journal Article↗

The evolution of an experimental distal motor axonopathy. Physiological studies of changes in neuromuscular transmission caused by cycloleucine, an inhibitor of methionine adenosyltransferase.

Cycloleucine (CL), a synthetic amino acid is known to cause degeneration of motor nerve terminals. This paper describes the changes in neuromuscular transmission, the morphology of motor end-plates and the responses of muscle spindles after a single dose of CL was administered to weanling and adult mice. Animals were allowed to survive for between 12 h and 7 days. Twitch and tetanic responses of muscles stimulated through their nerves fell dramatically within 24 h in both young and adult mice and intracellular recordings revealed that a large proportion of end-plates in calf muscles became denervated, whilst at other end-plates intermittent failure of transmission and end-plate potentials (EPPs) with prolonged latency were demonstrated. End-plates with an abnormally high frequency of miniature end-plate potentials (mEPPs) were found in young mice at 12 h, and in the adult mice at 24 h. Morphological abnormalities in intramuscular nerves and nerve terminals included areas of electron lucent axoplasm, swollen degenerative mitochondria and loss of synaptic vesicles. Over the next 2-3 days further reductions occurred in the number of end-plates at which mEPPs or EPPs could be demonstrated. At 7 days a limited recovery of function occurred in distal muscles but proximal muscles, hitherto unaffected, now began to show abnormalities of transmission. Muscle spindles were found to be both functionally and structurally intact. It is suggested that this acute distal motor axonopathy is due to abnormalities in phospholipid composition of the axolemma of motor nerve terminals resulting from the failure of methyl-transfer pathways. These abnormalities in phospholipid composition might cause an increase in microviscosity of the axolemma and hence a decrease in efficiency of ion channels and pumps responsible for maintaining electrochemical gradients, essential for the structural and functional integrity of the neuromuscular junction.

Animals↗

Experimental brain abscess evolution: computed tomographic and neuropathologic correlation.

Brain abscess evolution was studied in dogs by correlating the CT appearance with the neuropathologic findings. The abscess, produced by direct inoculation, progressed from an area of cerebritis to a well encapsulated abscess over 14 days. Ring enhancement was seen in the cerebritis stage prior to capsule formation. The ring reached its maximum size at this stage and correlated best with the area of cerebritis surrounding the developing necrotic center; the rim of this ring increased in thickness, resulting in progressive diminution of the central lucent area on scans delayed up to 60 min. The diameter of the ring decreased as cerebritis receded. Once the capsule had formed, the central lucent area was similar and no longer filled in on delayed scans.

Animals↗

HSV1 strain sensitivity in experimental rabbit keratitis: evolution under repeated topical IDU administrations.

The effects of repeated topical idoxuridine (IDU) administration of HSV1 strain sensitivity were investigated during 6 serial passages (P1 to P6) in the rabbit. By comparison to placebo treated rabbits, a delay in ulcer cicatrization appeared at P2 and clinical resistance was completed at P3. Clinical cross resistance to acyclovir (ACV) was also tested and demonstrated at P7. In vitro, a plaque reduction test on Vero cells using directly the tear film HSV populations allowed the prediction of the resistance by an early rise in the effective dose 90% (ED 90) value anticipating that in ED 50%. An ED 50 determination by dye-uptake assay on P6 HSV isolate demonstrated a cross resistance to viral thymidine kinase (TK) dependent drugs without any change in Ara-A and PFA sensitivity, according to a 23% TK activity at P6. At the last passage the HSV drug resistant population had an unrestricted corneal pathogenicity. A return to IDU and ACV in vitro sensitivity was demonstrated in group control animals at P2 but not at P4 or P6.

Acyclovir↗

[Experimental equine fascioliasis: evolution of serologic, enzymatic and parasitic parameters].

Three, four, and one horses were respectively infected with 100, 1,000, and 5,000 metacercariae of Fasciola hepatica. Six of them were reinfected 38 weeks later with 1,000 metacercariae each. Specific antibodies assayed by counter-electrophoresis, passive hemagglutination and ELISA tests appeared three to six weeks post-infection and peaked 10 to 17 weeks post-infection. Horses infected by 1,000 metacercariae and more showed 17.6% of positive samples by counter-electrophoresis, 49.2% by ELISA, and 75.6% by passive hemagglutination. Plasma glutamate dehydrogenase and gamma-glutamyltransferase levels increased significantly 3 to 5 months post-infection in the most infected animals. Eggs of Fasciola hepatica were only observed in 2 of the 8 horses, 14 and 15 weeks post-infection. This last observation indicates the limits of fecal examination in the diagnosis of fascioliasis in horses.

Animals↗

[Complement: a sign of infestation of sheep by Trypanosoma brucei brucei in an experimental model: its evolution following treatment].

Broad variations in complement levels are seen during the course of many infectious diseases, particularly human and animal african trypanosomiasis. In this study, sheep complement is measured by means of its haemolytic activity expressed in 50% haemolytic complement units per ml (HCU50/ml). In healthy sheep, the average value is 23.3 HCU50/ml. Complement levels dramatically decrease five days after subcutaneous inoculation of Trypanosoma brucei brucei and remain undetectable until death of non treated infected animals. Eight infected sheep are treated with graded dosages of melarsoprol when central nervous system involvement appeared. Complement levels rapidly recover normal values after efficient treatment (0.9 and 1.8 mg/kg/d).

Animals↗