Bee diseases as factors in the life and behavior of the honeybee Colony

Summary The honeybee has prospered through the years of recorded history by following a plan of life that contributes to the survival of the colony rather than to the individual. The colony is capable of air-conditioning its hive to meet changing weather and to store up food sources for adverse periods. Since it contributes to the production of fruits, seeds, vegetables and pasture crops, and produces honey, a delectable natural sweet, man has been interested in its production and care.The honeybee is subject to many diseases which affect both the adults and the developing young. Several of the diseases have caused the death or destruction of thousands of colonies annually. Fortunately, none of these diseases are transmitted to other animals. Through the natural laws of survival, certain strains of bees have developed resistance to some of the diseases and man has assisted in this by selective breeding and cultivation of the hardier strains.The most noteworthy contribution to the control of bee diseases has been the use of sulfathiazole, terramycin and other therapeutics in the food of bees in the spring and fall. By their use, at least one disease which had been considered as incurable for centuries can be prevented or controlled without the destruction of colonies or valuable equipment. The use of chemicals and antibiotics as therapeutic agents in disease control has measurably strengthened the position of the honeybee in our general economy and will save the beekeeping industry many thousands of dollars annually.     

Studies on column fractionation of immune cells. VI. Separation of thymus-derived lymphocytes by means of protein beads coated with antigen-antibody complexes.

Calf serum beads coated with antigen-antibody complexes were used as cellular immuno-adsorbents to separate mouse T-lymphocytes with a purity of more than 90%. The beads coated by means of glutaraldehyde could be used at least three times without loss of cell-binding capacity.     

Exploratory studies of some drug charge transfer interactions

Conductivity and capacitance titrations yield minima for the chlorpromazine hydrochloride-heparin interaction, confirming clinical suspicions of its occurrence. The effective dosage of heparin thus is reduced if administered in conjunction with chlorpromazine. The interaction is interpreted as charge transfer complex formation, occurring as an (electrode) surface reaction. It is suggested that the charge transfer complexing capability of heparin preparations, as evidenced by conductance and/or capacitance changes, evaluated against a well defined donor such as chlorpromazine hydrochloride, may be adapted as a more precise method of measuring heparin activity than coagulation time determinations. Phenytoin and chlorpromazine likewise yield conductance and capacitance minima; voltammetry indicates new peaks at +250mV and −300mV vers.SCE supporting the suggestions that an uncharged 1∶1 complex is being formed, again in a type of surface reaction. Phenytoin and lignocain form a precipitate at 0.002 equimolar; in conductance and capacitance titrations phenytoin behaves as a weak electron donor against iodine though as a weak acceptor against lignocain. Lignocain and chlorpromazine conductance and capacitance titrations using gold electrodes fail to show any evidence for their previously reported interaction on Pt/Pt electrodes. Voltammetry on Pt/Pt electrodes indicates 2 new peaks at zero and at −750mV vers.SCE. It is thought that these two compounds interact only on catalytically highly active surfaces, where they form a weak surface charge transfer complex. Adrenalin, in conductance and capacitance titrations, behaves amphoteric, i.e. as an electron acceptor against the strong donor chlorpromazine and as a donor against the strong acceptor tetramethyl-p-phenylenediamine. Voltammograms of the above listed interactions are interpreted as of the ECE type exhibiting mainly irreversible behaviour.     

Cross-polarization optical coherence tomographic assessment of in situ simulated erosive tooth wear

This clinical study tested cross-polarization optical coherence tomography (CP-OCT) monitoring of erosive tooth wear (ETW). Twenty participants completed a 14-day/arm, 3-arm crossover study simulating different ETW severities. Participants received two enamel specimens (per arm) and were randomized to: severe (s-ETW, lemon juice/pH:2.5/4.25%wt/vol citric acid), moderate (m-ETW, grapefruit juice/pH:3.5/1.03%wt/vol citric acid), and non-ETW (water). Enamel thickness was measured with CP-OCT (day[D] 0, 7, 14) and micro-computed tomography (μ-CT; D14). Enamel surface loss was determined with CP-OCT and optical profilometry (OP; D7, D14). CP-OCT showed higher enamel surface loss for D14 than D7 for m-ETW (P = .009) and s-ETW (P = .040) and differentiated severity at D14 (s-ETW > non-ETW, P = .027). OP was able to differentiate surface loss between days (D7 < D14, P < .001) for m-ETW and s-ETW, and ETW severity effect after 7 and 14 days (non-ETW < m-ETW < s-ETW, P < .001). At D14, CP-OCT and μ-CT were positively correlated (r = .87, ICC = .62). CP-OCT showed potential as a tool for clinical ETW monitoring.     

Non-B DNA: a major contributor to small- and large-scale variation in nucleotide substitution frequencies across the genome

Approximately 13% of the human genome can fold into non-canonical (non-B) DNA structures (e.g. G-quadruplexes, Z-DNA, etc.), which have been implicated in vital cellular processes. Non-B DNA also hinders replication, increasing errors and facilitating mutagenesis, yet its contribution to genome-wide variation in mutation rates remains unexplored. Here, we conducted a comprehensive analysis of nucleotide substitution frequencies at non-B DNA loci within noncoding, non-repetitive genome regions, their ±2 kb flanking regions, and 1-Megabase windows, using human-orangutan divergence and human single-nucleotide polymorphisms. Functional data analysis at single-base resolution demonstrated that substitution frequencies are usually elevated at non-B DNA, with patterns specific to each non-B DNA type. Mirror, direct and inverted repeats have higher substitution frequencies in spacers than in repeat arms, whereas G-quadruplexes, particularly stable ones, have higher substitution frequencies in loops than in stems. Several non-B DNA types also affect substitution frequencies in their flanking regions. Finally, non-B DNA explains more variation than any other predictor in multiple regression models for diversity or divergence at 1-Megabase scale. Thus, non-B DNA substantially contributes to variation in substitution frequencies at small and large scales. Our results highlight the role of non-B DNA in germline mutagenesis with implications to evolution and genetic diseases.