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The effect of maternal alcohol consumption during pregnancy as well as the neonatal period on allometric growth of skeletal muscles of fore and himdlimbs was studied in 252 rats (126 males and 126 females). At the inception of the study the dams of alcohol-exposed groups received 10% ethanol (v/v) in water for 2 weeks and 20% ethanol (v/v) for another 3 weeks. They were then bred overnight by introducing 1 male per 4 females into the cage. Following diagnosis of pregnancy, the two alcohol-exposed groups received 30% ethanol (v/v) till delivery. Neonatally the pre- and postnatal alcohol-exposed group continued to receive alcohol till weaning at 21 days of age. The offspring randomly selected (7 males and 7 females) from each group were killed at 3, 5, 7, 9, 11 and 14 weeks of age. The body weights, muscle weights and percentage of body weights contributed by each muscle were significantly smaller in the offspring of the alcohol-exposed groups as compared to the controls. These parameters were significantly higher in the group exposed to alcohol only prenatally as compared to those exposed both pre- and postnatally up to the 7th week of age, and thereafter were similar in the subsequent weeks. Although the alcohol-exposed groups grew faster than the controls from 9 to 14 weeks of age, they were, however, not able to catch up. This demonstrated that allometric growth of muscles of fetal and neonatal rats was adversely affected by maternal consumption of alcohol during pregnancy and neonatally.

The effect of prenatal exposure to phenobarbital on muscle development was determined in 4 muscles (biceps brachii, triceps brachii, soleus and cranial tibial) of 34 mice (16 males, 18 females) at 12 weeks of age. The control group received unadulterated food ad libitum throughout the period of study. The phenobarbital-exposed group received 3 g of phenobarbital per kilogram of food from gestation day 7 to 18 as the only source of food. Outside this period they received unadulterated food and water ad libitum. Each mouse was killed at 12 weeks of age. The muscle mass of control mice was significantly larger than that of the phenobarbital-exposed group in both sexes. The smaller muscle mass of the phenobarbital-exposed group as observed from the analysis of the soleus muscle was due to a smaller number of muscle fibres being present than in the control group, since the muscle fibre sizes were similar in both groups. This indicated that prenatal administration of phenobarbital inhibits normal hyperplasia of muscle fibres.

Effects of cassava (Manihot esculenta Crantz)-borne organic cyanide and inorganic cyanide in the form of sodium cyanide on bone and muscle development were investigated in eighteen dogs of Nigerian breed. After 16 weeks of stabilization in the laboratory from the time of purchase when the dogs were fed on the same diet, they were randomly assigned to three experimental groups of six dogs each. The control group was fed on rice while the other two groups were fed on either cassava (gari) or rice plus cyanide. The three diets were made isoenergetic and isonitrogenous by varying the quantity of meat incorporated into them. The results obtained after 14 weeks of feeding the respective diets indicated that there was retardation of muscle development in the gari-fed dogs. This may have resulted from gluconeogenesis from muscle protein associated with suppression of production of insulin by the pancreas in this group. The results indicated also that the effects of inorganic dietary cyanides on muscle development were different. Both forms of dietary cyanides, however, had no adverse effect on bone development.

The effect of castration on the development of muscle mass of postural and non-postural muscles was studied in 18 male mice (9 castrated, 9 uncastrated). Results obtained indicated that the castrated males grew faster and were bigger in body size and weight at maturity than the intact males. The bigger body size of castrated males was not due to larger muscle mass but was probably due to increased subcutaneous fat deposition. Atrophy of muscles usually observed following castration was significantly greater in the non-postural (biceps brachii) muscle of the forelimb as compared to the postural (triceps brachii) muscle of the forelimb. Conversely, the amount of reduction in muscle mass was similar in both postural (soleus) and non-postural (tibialis cranialis) muscles of the hindlimb.

The role of nerve impulses and neurogenic factors in the decrease in muscle mass following tenotomy was investigated in 30 adult (15 males, 15 females) guinea pigs. Unilateral tenotomy, neurectomy and simultaneous tenotomy and neurectomy of slow and fast hindlimb muscles were performed in 3 groups respectively. Each group comprised 10 guinea pigs. The unoperated hindlimb of each animal in each group served as control. The weight loss occurred in both slow and fast muscles but was greater in the slow soleus muscle as compared to the fast gastrocnemius muscle. In each muscle the weight loss was least in the tenotomized group. This was followed by the weight loss in the neurectomized group. The greatest weight loss was observed in the simultaneously tenotomized and neurectomized group. These observations agree with the suggestion of other workers that a possible neurogenic factor flowing from the nerves to the muscles was very significant in maintenance of muscle fibre stability. It indicated also that simultaneous neurectomy and tenotomy did not prevent degenerative changes in slow and fast muscles and that it was not nerve impulses reaching the tenotomized muscles that were responsible for degenerative changes observed but that other factors were responsible.

The effect of maternal alcohol consumption during pregnancy on muscle development of the offspring was investigated in 28 mice (14 males, 14 females) at 12 weeks of age. Both the control and alcohol-fed groups received food ad-libitum throughout the period of study. The control group received water ad-libitum also throughout the period of study. The alcohol-fed group, on the other hand, received only water up to six weeks of age. Subsequently, between 6 and 8 weeks of age they received 10% ethanol (v/v) in water and 20% ethanol (v/v) from 8 to 11 weeks age. Both groups were bred at 11 weeks of age. Following diagnosis of pregnancy, the alcohol-fed group received 30% ethanol (v/v) till delivery. The off-spring of both groups were fed water and food ad-libitum throughout the period of study. Each of the off-spring was killed at 12 weeks of age. Body weight, as well as weights of soleus, biceps brachii, long digital extensor and cranial tibial muscles were significantly smaller in off-spring of the alcohol-fed group indicating that maternal consumption of alcohol during pregnancy retards growth, as well as "catch-up growth" in both body weights and muscle mass. The smaller muscle mass, as observed from analyses of soleus muscle, resulted from retardation of muscle growth pre-natally by suppression of normal hyperplasia of muscle fibres during myogenesis and postnatally by suppression of normal hypertrophy of muscle fibres.

The mechanism by which oestrogen inhibits development of muscle mass was investigated in the soleus muscle of 20 sexually immature female mice. Half of the population were injected weekly (from one to nine weeks old) with a physiological dose of 0.01 mg stilboestrol dipropionate (synthetic oestrogen). After each mouse was killed at 10 weeks old, the weight and muscle index was determined for each muscle. The number of muscle fibres was counted in each soleus muscle. The muscle fibre size for each muscle was determined by measuring the greatest diameter of at least 100 fibres. The number of muscle fibres was similar in both normal and oestrogen treated animals but the individual muscle fibre sizes were significantly smaller in oestrogen treated animals. These observations indicated, therefore, that oestrogen inhibits development of muscle mass in females by limiting the size of individual muscle fibres and not by inhibiting the multiplication of muscle fibres.

The total number of fibres, as well as, the number of fibres per fibre type were determined by the indirect fibre-counting method in 32 pectineus muscles from 16 dogs of mixed sexes. Eight pairs of muscles from 8 dogs were judged to be hypotrophic, while the other 8 pairs from another 8 dogs were judged to be normal. The hypotrophic muscles had extremely small muscle fibres, particularly type II fibres. They also had apparently higher percentages of type II muscle fibres within a section. The apparently higher percentage of type II fibres usually observed in the hitsochemical examination of the sections of hypotrophic pectineus muscles did not result from failure of type II fibres to transform to type I fibres. It was rather due to too few type I fibres being present in these muscles as compared to the normal muscles. It was not because there were more type II fibres present in them than in the normal muscles. The fewer type I fibres resulted most likely from loss of already differentiated type I fibres. The loss may be of neural origin.

The effect of early postnatal protein malnutrition on the development of soleus muscle was investigated in 26 mice (13 males, 13 females). The control group received a balanced diet containing 18% lactalbumin while the protein-malnourished group received protein deficient diet containing 0.5% lactalbumin. The body weight was determined both at 3 weeks (weaning age) and 12 weeks of age. The soleus muscle weight, total number and sizes of muscle fibres were also determined at 12 weeks of age for each mouse. There was considerable retardation of body weight and soleus muscle weight. The smaller soleus muscle of protein-malnourished mice resulted from loss of muscle fibres and hypotrophy of the remaining fibres. Permanent retardation of body weight after recovery from early postnatal protein malnutrition may be as a result of loss of muscle fibres during that period.

The total number of muscle fibres, as well as the numbers of Type I, Type II and intermediate muscle fibre types, in transverse sections of the pectineus muscles of dogs of 2 and 12 months of age was determined by an indirect fibre counting method. The total nubmers of fibres in all muscles decreased very significantly (by about 32%) in both sexes between 2 and 12 months of age. The decrease resulted from loss of about 20% of the Type I, 39% of the Type II and 73% of the intermediate muscle fibres.

The effect of oestrogen on muscle development was determined in 8 muscles (biceps brachii, triceps brachii, common digital extensor, soleus, superficial digital flexor, cranial tibialis, gastrocnemius and long digital extensor muscles of sexually immature male and female mice. Each mouse was killed at a mature age of 16 weeks. The muscle development as determined by increase in muscle weight was significantly smaller in muscles of oestrogen-treated male and oestrogen-treated female mice as compared to the muscles of normal male and normal female mice. The muscles of normal male mice were very significantly larger than those of normal female mice. There was, on the other hand, no significant difference between the muscle mass of oestrogen-treated male and oestrogen-treated female mice. This indicated that the smaller mass of normal female mice when compared to normal male mice was connected with inhibitory effect of oestrogen on the muscle development of female mice.

The value of administration of hyperimmune serum in the control of peste des petits ruminants was investigated in goats at different stages of the disease. A group of the goats was given hyperimmune serum intravenously at the fever stage of temperature of 40.5 degrees C or above; another group showing no elevation of temperature but with other clinical signs of the disease were also given hyperimmune serum. Results indicated that hyperimmune serum was very effective in reversing the process of the disease if administered at the fever stage but not in animals that had progressed past the fever stage. The goats given the hyperimmune serum survived for 10 days before showing evidence of reinfection.

The causative agent of stomatitis pneumoenteritis complex was isolated in domesticated goats and Vero cell culture. It was identified immunologically and morphologically as identical with the "Peste des Petits Ruminants" virus. There were cross reactions between stomatitis pneumoenteritis complex virus isolate and rinderpest virus by immunodiffusion and complement fixation tests but no cross neutralization. Goats recovered from stomatitis pneumoenteritis complex were protected against a challenge with rinderpest virus that was lethal to control goats. Ultrastructural morphology revealed intracytoplasmic and intranuclear inclusions made up of random arrays of fibrillar strands. Pleomorphic particles budded from the plasma membrane of infected cells and enveloped virions were seen extracellularly. Specific ferritin tagging was demonstrated in the stomatitis pneumoenteritis complex virus infected cells treated with homologous and peste des petits ruminants viral antibody systems but little, if any, tagging in the heterologous rinderpest system.