It still remains unclear whether the New World begomoviruses directly evolved from the Old World bipartite begomoviruses because of the sharp environmental change after their transfer to the New World, or whether the Old World bipartite begomoviruses had evolved into the New World bipartite ones before their transmission to the New World. Rybicki (1994) suggested that the absence of the AV2 gene in all the New World begomoviruses could be attributed to its earlier loss after the New World begomoviruses arriving in the New World. These results suggest that the current New World begomoviruses evolved from ancient viruses after transferring to the New World. Ha et al.(2006) speculated that the new identified begomovirus termed Corchorus yellow vein virus (CoYVV) might belong to a New World begomovirus group that previously existed in the Old World, which suggested that the common ancestor of the New World begomovirus might originate from the Old World begomovirus. However, both the New World and Old World begomoviruses had began to evolve and coexisted in this area for a long time before the separation of the continents. In other words, the present New World begomoviruses might have evolved in the Old World, and then moved to the New World by some unknown means (Ha et al., 2006) . Animal models of acute lung injury Acute lung injury in humans is characterized histopathologically by neutrophilic alveolitis, injury of the alveolar epithelium and endothelium, hyaline membrane formation, and microvascular thrombi. Different animal models of experimental lung injury have been used to investigate mechanisms of lung injury. Most are based on reproducing in animals known risk factors for ARDS, such as sepsis, lipid embolism secondary to bone fracture, acid aspiration, ischemia-reperfusion of pulmonary or distal vascular beds, and other clinical risks. However, none of these models fully reproduces the features of human lung injury. The goal of this review is to summarize the strengths and weaknesses of existing models of lung injury. We review the specific features of human ARDS that should be modeled in experimental lung injury and then discuss specific characteristics of animal species that may affect the pulmonary host response to noxious stimuli. We emphasize those models of lung injury that are based on reproducing risk factors for human ARDS in animals and discuss the advantages and disadvantages of each model and the extent to which each model reproduces human ARDS. The present review will help guide investigators in the design and interpretation of animal studies of acute lung injury.  Intrapulmonary administration of recombinant activated factor VII in diffuse alveolar haemorrhage: a report of two case stories BACKGROUND: Diffuse alveolar haemorrhage (DAH) is a serious pulmonary complication characterised by a high mortality rate and the absence of specific treatment. The intrapulmonary administration of activated recombinant factor VII (rFVIIa) in DAH was recently published in six patients by Heslet et al with an efficient hemostatic effect. We describe two cases of DAH treated with intrapulmonary rFVIIa. METHODS: Two cases of DAH were admitted to the ICU after presenting abrupt desaturation, tachypnea, cough and haemoptysis, requiring orotracheal intubation and mechanical ventilation. The diagnosis was achieved by the bloody return during the bronchoalveolar lavage, during the procedure rFVIIa (50 μg/Kg in 50 ml of isotonic saline) was administered via the bronchoscope. RESULTS: Immediate cessation of bleeding was observed. Prior to intrapulmonary administration of rFVIIa, the FiO(2 )was 1, which was reduced to 0.4 24 hours later. Following the procedure, the haemostatic effect made blood transfusion superfluous. No thrombotic complications associated with administration of the drug were observed. After the intervention both cases progressed fast and was discharged from the ICU with no further episodes of bleeding. CONCLUSION: 1. Local intrabronchial deposition of DAH with rFVIIa has been shown to be effective in controlling life-threatening DAH. 2. In the case described above, no thrombotic complications were observed following the intrapulmonary administration of rFVIIa. Conclusion: 1. Local intrabronchial deposition of DAH with rFVIIa has been shown to be effective in controlling life-threatening DAH. 2. In the case described above, no thrombotic complications were observed following the intrapulmonary administration of rFVIIa.