The bias due to incomplete matching

Observational studies comparing groups of treated and control units are often used to estimate the effects caused by treatments. Matching is a method for sampling a large reservoir of potential controls to produce a control group of modest size that is ostensibly similar to the treated group. In practice, there is a trade-off between the desires to find matches for all treated units and to obtain matched treated-control pairs that are extremely similar to each other. We derive expressions for the bias in the average matched pair difference due to the failure to match all treated units--incomplete matching, and the failure to obtain exact matches--inexact matching. A practical example shows that the bias due to incomplete matching can be severe, and moreover, can be avoided entirely by using an appropriate multivariate nearest available matching algorithm, which, in the example, leaves only a small residual bias due to inexact matching.     

Negative-Staining of Protozoa with Nigrosin

The use of nigrosin in a rapid but accurate method for the demonstration of cilia bands, vacuoles and cytoplasmic inclusions in infusorians is discussed. The general effects of the dye as well as its staining action are presented together with a brief explanation of the physics of the action. The technic proposed involves mixing a drop of infusion on the slide with a drop of 10% aqueous nigrosin; excess stain is drained off, the specimen dried and mounted.     

Glutamic acid modification of vincristine toxicity

The principal limiting feature of the antitumor agent, vincristine, in the clinic has been neurotoxicity; there are no known agents which can routinely prevent or decrease this side effect. Glutamic acid in laboratory and clinical investigations in the early 1960s was found to antagonize vinblastine, another clinically useful vinca alkaloid. Glutamic acid 250 mg/kg/d i.p. was given to normal mice treated with repetitive doses of vincristine 1.5 mg/kg every other day. When glutamic acid was given both before and during vincristine administration, it produced a 49-79% increase in survival compared to control mice receiving vincristine only (p less than 0.01). Other schedules of glutamic acid administration were ineffective. Also, there appeared to be a delay in development of neurotoxic manifestations (toe-walking gait) but the results were not as consistent as the improvement in survival. Glutamic acid given to tumor-bearing mice (P-388 and P-1534 murine leukemia) did not inhibit the antitumor effect of vincristine-induced host toxicity in a schedule-dependent fashion without inhibition of the antitumor effect of vincristine.     

Chlamydomonas alpha-tubulin is posttranslationally modified by acetylation on the epsilon-amino group of a lysine

Previous work has shown that the principal alpha-tubulin within Chlamydomonas reinhardtii flagellar axonemes differs from the major alpha-tubulin in the cell body. These two variants of alpha-tubulin are related to one another since posttranslational modification of the cell body form converts it to the axonemal form. When flagella are induced to assemble in the absence of de novo protein synthesis, tritiated acetate can be used to posttranslationally label alpha-tubulin in vivo, and under these conditions, no other flagellar polypeptides exhibit detectable labeling [L'Hernault, S. W., & Rosenbaum, J. L. (1983) J. Cell Biol. 97, 258-263]. In the present report, this labeling method has been used to provide material for chemical analysis of the tritiated moiety that is posttranslationally added to flagellar alpha-tubulin. This radioactivity was volatile after acid hydrolysis, suggesting that the posttranslational modification is the addition of neither an amino acid nor carbohydrate. Treatment of posttranslationally 3H-labeled alpha-tubulin with hydrazine yields radioactive acetylhydrazine, indicating that the moiety involved in posttranslational modification is an acetyl group. Analysis of complete proteolytic digests by thin-layer chromatography has revealed that this acetyl group is located on the epsilon-amino group of a flagellar alpha-tubulin lysine residue.     

Rethinking trophic niches: Speed and body mass colimit prey space of mammalian predators

1. Realized trophic niches of predators are often characterized along a one‐dimensional range in predator–prey body mass ratios. This prey range is constrained by an “energy limit” and a “subdue limit” toward small and large prey, respectively. Besides these body mass ratios, maximum speed is an additional key component in most predator–prey interactions.
2. Here, we extend the concept of a one‐dimensional prey range to a two‐dimensional prey space by incorporating a hump‐shaped speed‐body mass relation. This new “speed limit” additionally constrains trophic niches of predators toward fast prey.
3. To test this concept of two‐dimensional prey spaces for different hunting strategies (pursuit, group, and ambush predation), we synthesized data on 63 terrestrial mammalian predator–prey interactions, their body masses, and maximum speeds.
4. We found that pursuit predators hunt smaller and slower prey, whereas group hunters focus on larger but mostly slower prey and ambushers are more flexible. Group hunters and ambushers have evolved different strategies to occupy a similar trophic niche that avoids competition with pursuit predators. Moreover, our concept suggests energetic optima of these hunting strategies along a body mass axis and thereby provides mechanistic explanations for why there are no small group hunters (referred to as “micro‐lions”) or mega‐carnivores (referred to as “mega‐cheetahs”).
5. Our results demonstrate that advancing the concept of prey ranges to prey spaces by adding the new dimension of speed will foster a new and mechanistic understanding of predator trophic niches and improve our predictions of predator–prey interactions, food web structure, and ecosystem functions.

     

Identification of Tumor Antigens in the HLA Peptidome of Patient-derived Xenograft Tumors in Mouse

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Highlights

• •Sufficient tumor tissues are often unavailable large HLA peptidome discovery.
• •Using patient derived xenograft (PDX) tumors can overcome this limitation.
• •The large PDX HLA peptidomes expand significantly those of the original biopsies.
• •The HLA peptidomes of the PDX tumors included many tumor antigens.