Response of potato tuber yield to stem injury by European corn borer (Lepidoptera: Crambidae) in the Mid-Atlantic United States.

The response of potato, Solanum tuberosum L., tuber yield to stem injury by European corn borer, Ostrinia nubilalis (Hübner), larvae was investigated in the Mid-Atlantic region of the United States for 3 yr. This response was described for 'Superior', 'Atlantic', and 'Snowden' potato, which are early-season, midseason, and late-season maturing cultivars, respectively. To model the yield/injury relationship, a range of corn borer injury levels was established in the field by augmenting the natural infestation with varying densities of laboratory-reared larvae. Linear and nonlinear regression analyses (plateau and second-order polynomial models) were used to describe the relationship between yield of U.S. No. 1 grade tubers and the percentage of stems injured by corn borer larvae. The maturity of the cultivar did not affect the response of potato yield to stem injury. In nine of 14 experiments, potato tolerated high levels of corn borer injury (55-90% of stems injured) without yield loss, suggesting that control of corn borer may not be necessary. Yet, in one of five Superior tests, in two of four Atlantic tests and in two of five Snowden tests, corn borer injury significantly reduced yield. Of the five data sets in which corn borer injury reduced yield, the plateau model fit two data sets and the quadratic model fit one data set. In two of the three cases, these models accounted for nearly identical amounts of total variation in yield as that accounted for by the linear model. The linear model fit four of the five data sets, but the R2 values were low for three of the four tests (0.10, 0.18, and 0.31). The parameter or parameters that interact with corn borer injury to cause tuber yield reduction should be identified before economic injury levels and thresholds are developed.

Compensatory adaptations of skeletal muscle composition to a long-term functional overload.

Compensatory hypertrophy of rat plantaris muscle was induced by ablating the synergistic gastrocnemius muscle. The sham-operated contralateral muscle served as a control. Within 5, 30 and 60 days postoperatively, the wet weight of the hypertrophied plantaris was 40, 64, and 109% greater, respectively, than the contralateral control. Two patterns of changing muscle composition emerged with compensatory hypertrophy: (1) an early (less than or equal to 5 days) increase in DNA content (+190%) which resulted in a sharp decline in the wet weight per nucleus ratio (-50%). This coincided with an increase in sarcoplasmic and stromal proteins and a fall in myofibrillar protein concentration. These changes were followed by (2) a secondary increase (30-60 days postoperatively) in the proportions of myofibrillar proteins with a corresponding decline in sarcoplasmic proteins.

The laboratory rat as a model for hyperthermic syndromes in humans.

To assess the lethal effects of work-induced hyperthermia on exercising animals, untrained rats were run to exhaustion at 5 and 20-26 degrees C or restrained at 41.5 degrees C. An exercise-induced core temperature of 40.4 degrees C represented a base line above which mortalities occurred. With increasing core temperature at exhaustion (between 40.4 and 43 degrees C), mortality increased within 24 h. A dose-respones curve with an LD50 equivalent to a core temperature of 41.5 +/- 0.1 degrees C was calculated. Although differences in body weight loss, core temperature at exhaustion, and cooling rate will clearly distinguish between survivors and fatalities, the severity of heat injury as inferred from survival times is best measured by the time versus intensity of hyperthermia in degree-minutes.