A behavioural finance perspective on trade imbalanceand stock prices

In this thesis I examine, within a behavioural finance framework, the impact on stock prices of order and trade imbalance in three separate but related studies. The first study, chapter two, begins with a question that plagues behavioural finance theories do the investors most likely to be influenced by the behavioural biases described in the literature, i.e., individual investors, affect stock prices? My data enable me to consider the impact of net individual investor trading for the entire market over several years. I find that net individual investor purchasing Granger causes stock price changes. The correlation is negative, however, contradicting common sense by demonstrating that individuals investor buying pressure makes prices go down and selling pressure forces them up. More investigation is required. Chapter three references order imbalance results from experimental finance. I use field data to test a robust laboratory model and my modified versions. My findings suggest that, with appropriate modifications, laboratory results can be applied to real financial markets. Chapter four combines the data from the chapters two and three to revisit the question of individual investor impact on stock prices. Other studies have argued that individual investor influence is strongest in smaller capitalization stocks. Moreover, various theories propose that individual investors are the driving force behind the irrational stock prices of a bubble. I focus on the stocks from chapter three, bubble stocks, and ask whether, in the context of the trading of the entire market, individual investor trades are influential. Once again I find Granger causality, but in the wrong direction. Moreover, the activity and volume of the individual investor category of the holdings data is completely overshadowed by that of the two large investor categories, domestic and foreign institutions. I conclude that individual investor trades are not influential in determining stock prices. This conclusion has important implications for some behavioural finance models of asset pricing. I suggest that emphasis might be better placed on educating individual investors about the errors to which they are prone, rather than on trying to explain market anomalies with those errors

Outbreak of Bovine Herpetic Meningoencephalomyelitis in Southern Brazil

Background: Herpetic meningoencephalitis is an infectious contagious disease worldwide distributed, most often caused by bovine alphaherpesvirus type 5 (BoHV-5), although bovine alphaherpesvirus type 1 (BoHV-1) may occasionally be the causative agent. The disease is characterized by subacute to acute clinical onset, often affecting animals submitted to stressful situations. Clinical signs are mainly neurologic due to meningoencephalitis and cortical necrosis. The involvement of the spinal cord has also been reported, however in BoHV-1 associated disease only. The aim of this report is to describe an outbreak of bovine meningoencephalomyelitis associated to BoHV-5.Case: In August 2017, nine 1-year-old calves died in a beef cattle farm with a flock of approximately 400 bovines. The animals presented neurological clinical signs characterized by excessive salivation, nasal and ocular discharges, incoordination, apathy, head tremors, head pressing, wide-based stance, recumbency followed by convulsions and paddling. According to the owner and referring veterinarian, affected animals displayed severe clinical signs with rapid progression and often leading to death in up to seven days. Four of these calves were submitted for necropsy, and gross lesions were present in the brain, characterized by mild to moderate multifocal hemorrhagic and soft areas. On cut surface, extensive areas of dark brown discoloration and malacia were observed. Histologically, lesions were characterized by extensive areas of liquefactive necrosis in the cerebral cortex grey matter, associated with inflammatory infiltrates composed of neutrophils, lymphocytes, plasma cells and foamy macrophages, as well as multifocal to coalescing areas of hemorrhage and fibrin deposition. Intranuclear eosinophilic inclusion bodies were rarely observed in neurons and astrocytes. On leptomeninges, there was diffuse inflammatory infiltrates of lymphocytes and plasma cells. Inflammation was also seen in a milder degree in the spinal cord, characterized by infiltrate of lymphocytes at grey matter, mainly around vessels. A herpesvirus which induced typical cytopathic effect in cell cultures was recovered from tissues. The isolated virus was typed as BoHV-5 by nucleotide sequencing analysis of the gC coding region.Discussion: The diagnosis of meningoencephalomyelitis associated to BoHV-5 was based on epidemiological, clinical, macroscopical, histological, virological and genomic findings. In the outbreak here reported, the disease occurred in young animals, with low morbidity but high lethality rates. Clinical signs on this case were consistent with previous reports on the literature. Bovines affected by BoHV-5 may display no gross lesions within the CNS; however, inflammatory and degenerative changes are frequently seen, characterized by malacia, leptomeningeal vessels hyperemia, edema and hemorrhages. Histologically, non-suppurative necrotizing meningoencephalitis is seen, with perivascular inflammatory infiltrates and, occasionally, intranuclear eosinophilic inclusion bodies in astrocytes and neurons. Similar but milder lesions were seen in the spinal cords of two of the necropsied calves, a feature which has only been previously associated to BoHV-1 infections. The identification of the implicated agent was accomplished by virus isolation in cell cultures followed by genome typing. Specific treatments for this condition are not currently available, and the number of animals that recover from clinically apparent disease is extremely low. Preventive measures are based on serological testing of herds, and segregation or elimination of seropositive calves. To avoid progression of the disease in seropositive animals, control efforts must be directed to avoid stressful conditions. Vaccination with BoHV-1 and BoHV-5 vaccines is expected to confer protection to clinical disease

Outbreak of bovine herpetic meningoencephalomyelitis in Southern Brazil

Background: Herpetic meningoencephalitis is an infectious contagious disease worldwide distributed, most often caused by bovine alphaherpesvirus type 5 (BoHV-5), although bovine alphaherpesvirus type 1 (BoHV-1) may occasionally be the causative agent. The disease is characterized by subacute to acute clinical onset, often affecting animals submitted to stressful situations. Clinical signs are mainly neurologic due to meningoencephalitis and cortical necrosis. The involvement of the spinal cord has also been reported, however in BoHV-1 associated disease only. The aim of this report is to describe an outbreak of bovine meningoencephalomyelitis associated to BoHV-5. Case: In August 2017, nine 1-year-old calves died in a beef cattle farm with a flock of approximately 400 bovines. The animals presented neurological clinical signs characterized by excessive salivation, nasal and ocular discharges, incoordination, apathy, head tremors, head pressing, wide-based stance, recumbency followed by convulsions and paddling. According to the owner and referring veterinarian, affected animals displayed severe clinical signs with rapid progression and often leading to death in up to seven days. Four of these calves were submitted for necropsy, and gross lesions were present in the brain, characterized by mild to moderate multifocal hemorrhagic and soft areas On cut surface, extensive areas of dark brown discoloration and malacia were observed. Histologically, lesions were characterized by extensive areas of liquefactive necrosis in the cerebral cortex grey matter, associated with inflammatory infiltrates composed of neutrophils, lymphocytes, plasma cells and foamy macrophages, as well as multifocal to coalescing areas of hemorrhage and fibrin deposition. Intranuclear eosinophilic inclusion bodies were rarely observed in neurons and astrocytes. On leptomeninges, there was diffuse inflammatory infiltrates of lymphocytes and plasma cells. Inflammation was also seen in a milder degree in the spinal cord, characterized by infiltrate of lymphocytes at grey matter, mainly around vessels. A herpesvirus which induced typical cytopathic effect in cell cultures was recovered from tissues. The isolated virus was typed as BoHV-5 by nucleotide sequencing analysis of the gC coding region. Discussion: The diagnosis of meningoencephalomyelitis associated to BoHV-5 was based on epidemiological, clinical, macroscopical, histological, virological and genomic findings. In the outbreak here reported, the disease occurred in young animals, with low morbidity but high lethality rates. Clinical signs on this case were consistent with previous reports on the literature Bovines affected by BoHV-5 may display no gross lesions within the CNS; however, inflammatory and degenerative changes are frequently seen, characterized by malacia, leptomeningeal vessels hyperemia, edema and hemorrhages. Histologically, non-suppurative necrotizing meningoencephalitis is seen, with perivascular inflammatory infiltrates and, occasionally, intranuclear eosinophilic inclusion bodies in astrocytes and neurons. Similar but milder lesions were seen in the spinal cords of two of the necropsied calves, a feature which has only been previously associated to BoHV-1 infections. The identification of the implicated agent was accomplished by virus isolation in cell cultures followed by genome typing. Specific treatments for this condition are not currently available, and the number of animals that recover from clinically apparent disease is extremely low. Preventive measures are based on serological testing of herds, and segregation or elimination of seropositive calves. To avoid progression of the disease in seropositive animals, control efforts must be directed to avoid stressful conditions. Vaccination with BoHV-1 and BoHV-5 vaccines is expected to confer protection to clinical disease