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Characterisation of cervical synovial folds in horses

L. N. Thomsen, L. C. Berg, B. Markussen, P. D. Thomsen

CERVICAL synovial folds have been suggested as a potential cause of neck pain in human beings; however, little is known about the extent and characteristics of cervical synovial folds in horses. The objective of this explorative study was to determine the frequency of synovial folds in equine cervical articular process joints and to provide a characterisation of the size and morphology of the synovial folds.

Folds of the synovial membrane may have a supportive, stabilising, lubricating and protective function in the joint and could potentially prevent direct contact between incongruent and bony structures. Horses are prone to cervical trauma and, because of the extensive range of motion in some of the joints and the load on the cervical articular process joints, synovial folds could become entrapped or disrupted.

Six horses, euthanased for reasons other than cervical joint disease, were used in the study and yielded 50 joints and 85 potential synovial folds for examination. The synovial folds were evaluated in both the cranial and caudal aspect of the cervical articular process joints, and in both sides of the neck.

Synovial folds were identified in 98 per cent of cervical articular joints examined. The folds varied in width (4 to 41 mm) and height (1 to 17.8 mm). They were examined histologically and classed according to type: adipose (38 per cent), fibrous (41 per cent) and mixed type (21 per cent). The side of the neck significantly influenced the size of the synovial folds.

The authors state that characterising the folds provided some interesting insights. They conclude that the size of the synovial folds indicates that they could be damaged by acute injury or chronic disease in the cervical articular process joints, and suggest that they should be considered when diagnosing and treating arthropathies of equine cervical articular process joints.

Equine Veterinary Journal (2012)

doi: 10.1111/j.2042-3306.2012.00687.x

Obese dogs can suffer metabolic syndrome, just like people

A. Tvarijonatviciute, J. J. Ceron, S. L. Holden, D. J. Cuthbertson, V. Biourge, P. J. Morris, A. J. German

OBESE dogs, like people, can experience metabolic syndrome – a combination of health problems that, when occurring together, increase the risk of the development of diabetes and cardiovascular disease.

Although canine obesity is known to cause insulin resistance, mild hypertension and high blood cholesterol levels, researchers at the University of Liverpool carried out a study to see if there were also links to metabolic syndrome, common in obese humans.

Dogs were classified as obese if they had a body fat mass greater than 35 per cent. Of the 35 obese dogs in the study, canine obesity-related metabolic dysfunction (ORMD) was identified in seven dogs (20 per cent) based on the definitions of four parameters (systolic blood pressure [SBP], cholesterol, triglyceride and glucose), as well as body condition score (BCS).

The animals were then put on a weight loss programme: the median body weight before weight loss was 32.9 kg and decreased to 25.6 kg; the median BCS decreased from eight to five. SBP (P = 0.008), cholesterol (P = 0.003), triglyceride (P = 0.018) and fasting insulin (P < 0.001) all decreased after weight loss while plasma total adinopectin increased (P = 0.001). Canine ORMD was not associated with total fat mass but with increased plasma insulin concentrations (P = 0.030) and decreased adiponectin concentrations (P = 0.031).

The authors conclude that defining obese dogs on their metabolic status may have some merit, although further work is required to establish the implications of ORMD in terms of disease risk and outcome. They add that, although ORMD may not be fully understood, it is important to note that metabolic abnormalities improved when the dogs lost weight.

BMC Veterinary Research (2012) 8:147

doi: 10.1186/1746-6148-8-147

Insights into the in vivo response against active tuberculosis

E. F. Castillo, A. Dekonenko, J. Arko-Mensah, M. A. Mandell, N. Dupont, S. Jiang, M. Delgado-Vargas, G. S. Timmins and others

THE role of autophagy as a cell-autonomous defence against Mycobacterium tuberculosis, in vivo, has been further elucidated by researchers in the USA.

The execution of autophagy, a fundamental cellular biological pathway, depends on factors collectively termed Atg proteins, such as Atg5. Recent developments reveal a crucial role for the autophagy pathway and proteins in response to infection, including M tuberculosis.

The role of autophagy in controlling M tuberculosis in vitro has been reported; however, this study demonstrates the role of autophagy, in vivo, in protection against TB.

Gene knockout mice, missing the Atg5 protein and therefore with a deficient autophagy pathway, and autophagy-proficient littermates were infected with M tuberculosis. This resulted in increased bacillary burden and weight loss and in the autophagy-compromised mice. The lung pathology of autophagy-compromised mice showed gross lesions, in contrast to the smaller infected foci of autophagy-proficient animals. Comparison of the cytokine profiles of infected mice with and without a compromised autophagy response, demonstrated significant increases in markers for inflammation for mice lacking the Atg5 protein.

The results lead the authors to conclude that autophagy plays a dual role: it both protects against the microbe and guards against host-inflicted tissue deconstruction and the active disease. In this model, autophagy protects against tissue necrosis and lung pathology, the hallmarks of TB. They add that strategies aimed at the pharmacological manipulation of autophagy could diminish TB spread and prove vital in containing the emergence of increasingly drug-resistant TB strains.

Proceedings of the National Academy of Sciences USA (2012)

doi: 10.1073/pnas.1210500109

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