[Newcastle disease in southern Chad: peak epidemic periods and the impact of vaccination]. / La maladie de Newcastle au sud du Tchad: périodes de pic épidémique et impact de la vaccination.

In spite of its universally acknowledged importance, backyard chicken production is still being hampered by Newcastle disease in some parts of the world. In Chad, the disease has been reported almost everywhere in the country and confirmed in several regions, but there are no control measures in place. A survey was conducted at three sites in south-eastern Chad in July and August 2001, based on face-to-face interviews with 20% of the peasant farmers keeping chickens at these sites. The aim was to collect information on peak epidemic periods and on ways in which the infection spreads. The survey revealed that the peak epidemic periods for Newcastle disease are April, during the mango harvesting and selling period, and December, when trade increases for the seasonal festivities. The survey also showed that peasant farmers attach great importance to chicken farming. The survey was followed by a vaccination trial in November 2001 and February 2002, using the La Sota strain administered ocularly. All of the birds vaccinated during the trial were successfully protected from the disease and both chicken production and the income of the villagers increased. The authors conclude that in order to sustain poultry farming and maximise production in the southern zone, vaccination programmes must be urgently introduced, campaigns to raise awareness of Newcastle disease should be carried out and financial support to pay for vaccines should be provided. Efforts to combat other causes of poultry mortality must also be undertaken.

Acidic fibroblast growth factor (aFGF) injection stimulates cartilage enlargement and inhibits cartilage gene expression in rat fracture healing.

The effect of the administration of acidic fibroblast growth factor (aFGF) on normal fracture healing was examined in a rat fracture model. One microgram of aFGF was injected into the fracture site between the first and the ninth day after fracture either every other day or every day. aFGF-injected calluses were significantly larger than control calluses, although this does not imply an increased mechanical strength of the callus. Histology showed a marked increase in the size of the cartilaginous soft callus. Total DNA and collagen content in the cartilaginous portion of the aFGF-injected calluses were greater than those of controls, although the collagen content/DNA content ratio was not different between the aFGF-injected and control calluses. Fracture calluses injected with aFGF remained larger than controls until 4 weeks after fracture. The enlarged cartilaginous portion of the aFGF-injected calluses seen at 10 days after fracture was replaced by trabecular bone at 3 and 4 weeks. Northern blot analysis of total cellular RNA extracted separately from the cartilaginous soft callus and the bony hard callus showed decreased expression of type II procollagen and proteoglycan core protein mRNA in the aFGF-injected calluses when compared with controls. A slight decrease in types I and III procollagen mRNA expression was also observed. We concluded that aFGF injections induced cartilage enlargement and decreased mRNA expression for type II procollagen and proteoglycan core protein.

Defects of early fracture-healing in experimental diabetes.

Diabetes has been implicated as a cause of impaired fracture-healing. To test this hypothesis, we tested the tensile strength of femora from normal rats and from untreated and insulin-treated diabetic rats two weeks after the production of a closed fracture. One week before the fracture, diabetes was induced by administration of streptozotocin (sixty-five milligrams per kilogram of body weight). The concentration of serum glucose increased from 6.1 +/- 0.3 millimoles per liter (110 +/- 5 milligrams per deciliter) in the control animals to 31.1 +/- 0.8 millimoles per liter (560 +/- 15 milligrams per deciliter) in the untreated diabetic animals. After two weeks of healing, fracture callus from the untreated diabetic animals had a 29 per cent decrease in tensile strength and a 50 per cent decrease in stiffness compared with the controls. Treatment of the diabetic animals with insulin resulted in a mean concentration of serum glucose of 14.4 +/- 0.6 millimoles per liter (260 +/- 10 milligrams per deciliter) and restored the tensile strength and stiffness of the callus to a value that was not statistically different from that of the controls. Between the fourth and eleventh days of healing, there was a 50 to 55 per cent decrease in the collagen content of the callus of the untreated diabetic animals compared with the controls. In addition, on the fourth day of healing, DNA content, an indicator of cellularity of the callus, was decreased 40 per cent in the untreated diabetic group. Between the fourth and eleventh days of healing, the collagen-to-DNA ratio, which was determined as an indicator of net collagen synthesis per cell, was decreased 15 to 50 per cent in callus from the untreated diabetic animals.