Current status of the study on the kinetics of β-sheet formation of homopolypeptides is reviewed. A reasonable estimate is presented of the folding time of polypeptide chains into the β -sheet, which is much shorter than the time required for the folding of many globular proteins. The folding rate increases with the stability of the β-sheets as found from the effects of pH, temperature, and denaturants. A simple model is introduced to account for strong dependence of the folding rate on the linear charge density of polypeptide chains. Finkelstein's model is briefly discussed in this context.
Following infection to a host, some pathogens repeatedly alter their antigen expression to escape the immune defense (antigenic drift/switching). Assuming that most mutations are deleterious but a minor fraction of which can alter the antigenic property of the pathogen, I examine the evolutionarily stable mutation rate, μESS, of pathogens which maximizes the stationary pathogen density in a host. The model reveals that: (1) If the mutation rate is higher than a threshold μc, pathogens cannot maintain themselves because too much progenies are lost by lethal mutations. (2) If the mutaiton rate lies between zero and μc, the system converges to a traveling wave of antigen variants with a constant wave speed. (3) The μESS is unexpectedly high: more than 0.25 per genome per replication even if most mutations are lethal. I also examine the optimal schedule of pathogen growth in a host.
The sugar receptor of the fly has at least two functionally separated sugar receptor sites, the P and the F sites. By affinity electrophoresis with starch which is a competitive inhibitor for the P site, a P site candidate protein was detected and characterized, being compared with the electrophysiological data.
Synaptic connections in the brain are functionally and morphologically changed depending on environmental stimuli. A "tracing circuit" model is proposed that a "tracing circuit" of neurons corresponding to human descriptive memory is established by synaptic competition and kept by the following sprouting and increase of the number of synapses in the circuit. The physiological roles of adenosine derivatives are considered to be agonists of two mechanisms of synaptic competition: lateral inhibition and central facilitation. Released ATP can facilitate novel synapse formation through ecto-protein kinase. A new hypothesis is proposed that the occurance of long-term potentiation (LTP) or of long-term depression (LTD) depends on the frequency of conditional stimulation and can be induced by different presynaptic adenosine receptors.