BackgroundSeveral factors may influence kinetic data measurements, including body conformation and body mass. In addition, gender differences in gait pattern have been observed in healthy humans. Therefore, the aim of this study was to compare the kinetic and temporospatial parameters in clinically healthy male and female cats using a pressure-sensitive walkway. Eighteen crossbreed adult cats were divided into two groups: G1 had ten male cats (nine neutered) aged from 1 to 4 years and body mass 3.1-6.8 kg; G2 had eight spayed female cats, aged from 1 to 6 years and body mass 3.3-4.75 kg. The data from the first five valid trials were collected for each cat. A trial was considered valid if the cat maintained a velocity between 0.54-0.74 m/s and acceleration from -0.20 to 0.20 m/s2. The peak vertical force (PVF), vertical impulse (VI), gait cycle time, stance time, swing time, stride length, and percentage body weight distribution among the four limbs were determined. In addition, the lengths of each forelimb and each hind limb were measured using a tape with the animal standing.ResultsNo significant differences were observed in each group in either the forelimbs or the hind limbs or between the left and right sides for any of the variables. For both groups, the PVF (%BW), the VI, and the percentage body weight distribution were higher at the forelimbs than the hind limbs. The stride length was larger for males; however, the other kinetic and temporospatial variables did not show any statistically significant differences between the groups. The lengths of the forelimbs and hind limbs were larger in the male cats. There was a significant moderate positive correlation between the stride length and the length of the limbs.ConclusionsIn conclusion, the only difference observed between male and female cats was the stride length, and this was due to the greater body size of male cats. This difference did not affect other temporospatial or kinetics variables.

While gap junctions mediate intercellular communication and support liver homeostasis, connexin hemichannels are preferentially opened by pathological stimuli, including inflammation and oxidative stress. The latter are essential features of non-alcoholic steatohepatitis. In this study, it was investigated whether connexin32 and connexin43 hemichannels play a role in non-alcoholic steatohepatitis. Mice were fed a choline-deficient high-fat diet or normal diet for 8 weeks. Thereafter, TAT-Gap24 or TAT-Gap19, specific inhibitors of hemichannels composed of connexin32 and connexin43, respectively, were administered for 2 weeks. Subsequently, histopathological examination was carried out and various indicators of inflammation, liver damage and oxidative stress were tested. In addition, whole transcriptome microarray analysis of liver tissue was performed. Channel specificity of TAT-Gap24 and TAT-Gap19 was examined in vitro by fluorescence recovery after photobleaching analysis and measurement of extracellular release of adenosine triphosphate. TAT-Gap24 and TAT-Gap19 were shown to be hemichannel-specific in cultured primary hepatocytes. Diet-fed animals treated with TAT-Gap24 or TAT-Gap19 displayed decreased amounts of liver lipids and inflammatory markers, and augmented levels of superoxide dismutase, which was supported by the microarray results. These findings show the involvement of connexin32 and connexin43 hemichannels in non-alcoholic steatohepatitis and, simultaneously, suggest a role as potential drug targets in non-alcoholic steatohepatitis.

SummaryObjectives: The aim of this study was to evaluate angle-of-motion values for the forelimb and hindlimb in clinically healthy adult Santa Ines sheep by means of a standard goniometer.Methods: Twenty female Santa Ines sheep, ranging in age between three- to six-yearsold, and weighing 32–45 kg (mean ± standard deviation [SD]: 30.4 ± 3.7) were used. A standard transparent plastic goniometer was used to measure passive maximum flexion, maximum extension, and range-of-motion (ROM) of the shoulder, elbow, carpal, hip, stifle, and tarsal joints in the right and left limbs. The goniometric measurements were done with the sheep awake and in a standing position. The measurements were made in triplicate by two independent investigators.Results: In all evaluated joints, there was no significant difference either between the means of the two sides or between measurements performed by the two investigators. The mean ± SD values of the measurements (degrees) were as follows: 20 ± 1 (flexion), 170 ± 2 (extension), and 150 ± 2 (ROM) for the carpal joint; 34 ± 4 (flexion), 145 ± 6 (extension), and 110 ± 4 (ROM) for the elbow joint; 88 ± 2 (flexion), 144 ± 6 (extension), and 56 ± 5 (ROM) for shoulder joint; 35 ± 4 (flexion), 163 ± 3 (extension), and 129 ± 4 (ROM) for tarsal joint; 46 ± 4 (flexion), 146 ± 6 (extension), and 100 ± 4 (ROM) for the stifle joint; 54 ± 3 (flexion), 143 ± 7 (extension), and 89 ± 5 (ROM) for the hip joint.Clinical significance: The data obtained provide useful and objective information on the joints. More studies are necessary using other sheep breeds.

Histological grading systems remain cornerstones in the prognosis of canine cutaneous mast cell tumours (MCTs), but the distinct biological behaviour of each tumour often necessitates the use of complementary markers. Although a plethora of immunohistochemical markers have been proposed as prognostic factors, few are presently applied in routine diagnosis. This systematic review and meta‐analysis was designed to establish which immunohistochemical markers have verifiable prognostic value for cutaneous MCTs in dogs. A Boolean search of five databases identified 200 articles for screening, of which 73 were selected for full‐text assessment and 24 ultimately included in the systematic review. Odds Ratio (OR) was adopted as the summary measure for subsequent meta‐analysis but only 15 articles, relating to the immunomarkers Ki‐67 (9), KIT (5), and BAX (2), provided either a value for OR or sufficient data to calculate this statistic. Meta‐analysis verified that canine cutaneous MCTs with elevated expression of Ki‐67 or BAX, as well aberrant immuno‐expression of KIT, showed an increased odds of death, with respective OR values of 11.2 (95% CI 6.3‐20.0; p < .01), 9.9 (95% CI 1.3‐73.6; p = .03), and 4.1 (95% CI 1.1‐15.3; p = .03). Despite KIT, Ki67, and BAX arise as suitable prognostic factor for canine MCTs, this study highlighted the lack of important clinical and statistical data in many published articles, rendering it impossible to complete the meta‐analysis of several potentially valuable immunohistochemical markers.

Pannexins are transmembrane proteins that form communication channels connecting the cytosol of an individual cell with its extracellular environment. A number of studies have documented the presence of pannexin1 in liver as well as its involvement in inflammatory responses. In this study, it was investigated whether pannexin1 plays a role in acute liver failure and non-alcoholic steatohepatitis, being prototypical acute and chronic liver pathologies, respectively, both featured by liver damage, oxidative stress and inflammation. To this end, wild-type and pannexin1 mice were overdosed with acetaminophen for 1, 6, 24 or 48h or were fed a choline-deficient high-fat diet for 8weeks. Evaluation of the effects of genetic pannexin1 deletion was based on a number of clinically relevant read-outs, including markers of liver damage, histopathological analysis, lipid accumulation, protein adduct formation, oxidative stress and inflammation. In parallel, in order to elucidate molecular pathways affected by pannexin1 deletion as well as to mechanistically anchor the clinical observations, whole transcriptome analysis of liver tissue was performed. The results of this study show that pannexin1 diseased mice present less liver damage and oxidative stress, while inflammation was only decreased in pannexin1 mice in which non-alcoholic steatohepatitis was induced. A multitude of genes related to inflammation, oxidative stress and xenobiotic metabolism were differentially modulated in both liver disease models in wild-type and in pannexin1 mice. Overall, the results of this study suggest that pannexin1 may play a role in the pathogenesis of liver disease.