Cuticular lesions from twenty-four market sized lobsters (Homarus americanus) with winter impoundment shell disease were examined. Histological descriptions of cuticular lesions were correlated with the substage of molt for each lobster, because cuticle components and inflammatory mechanisms vary in each. A lesion severity grading system was developed and applied to four specific substages of the five-stage (A-E) molting cycle. Lesions present in substage C4, in which the membranous layer is deposited, and D0 (passive premolt) were divided into five grades, ranging from mild erosions (Grade I) to severe ulceration (Grade V) of the cuticle. Cuticular lesions from lobsters in C4/D0 were compared with cuticular lesions from lobsters in substages C2/C3. Defensive mechanisms exhibited by animals in all substages were epicuticle deposition, melanization, inflammatory cell infiltration, and pseudomembrane formation. In addition, animals in C4 and D0 showed proliferation of the membranous layer in affected foci. The lesion grading scheme presented in this paper can be used to describe and compare both inter- and intraspecies crustacean shell lesions.

Further studies of hereditary patent ductus arteriosus (PDA) in the dog show the defect to have a graded phenotypic expression. A high proportion of offspring of test matings had a fully patent ductus arteriosus, while a smaller proportion had a blind diverticulum of the ductus arteriosus which communicated with the aorta. This is considered to be a forme fruste of PDA, representing incomplete closure. Approximately 50% of pups with fully patent ductus arteriosus developed signs of left heart failure, and about 15% developed severe pulmonary hypertension with right-to-left or bidirectional shunts. Genetic analysis indicated that hereditary PDA in the dog is not a simple mendelian trait. Rather, it resembles a quasi-continuous or threshold trait with a high degree of heritability. Results were analyzed using a polygenic model with two developmental thresholds. Liability to defective closure of the ductus arteriosus increased with the proportion of the genome received from dogs with PDA. Moreover, in pups which had PDA, the incidence of serious sequelae (left heart failure and severe pulmonary hypertension) increased in a parallel fashion, suggesting that an increased liability to PDA was accompanied by an increase in the severitv of the lesion. KEY WORDSductus diverticulum threshold trait heritability quasi-continuous trait left heart failure pulmonary hypertension vascular shunt • Persistent patency of the ductus arteriosus after birth (PDA) is one of the most common cardiovascular anomalies found in man (1, 2) and the dog (3-5). A number of reports of the familial occurrence of PDA have implicated genetic factors in the cause of this defect in man (6-11) but the mode of transmission and pathogenetic mechanisms involved are From the Comparative Cardiovascular Studies Unit and the Section

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