m‐carboxycinnamic acid bishydroxamide improves developmental competence,reduces apoptosis and alters epigenetic status and gene expression pattern in cloned buffalo (Bubalus bubalis) embryos

Incomplete or aberrant reprogramming of nuclear genome is one of the major problems in somatic cell nuclear transfer. In this study, we studied the effect of histone deacetylase inhibitor m‐carboxycinnamic acid bishydroxamide (CBHA) on in vitro development of buffalo embryos produced by Hand‐made cloning. Cloned embryos were treated with CBHA (0, 5, 10, 20 or 50 μM) for 10 hr from the start of reconstruction till activation. At 10 μM, but not at other concentrations examined, CBHA increased (p < .05) the blastocyst rate (63.77 ± 3.97% vs 48.63 ± 3.55%) and reduced (p < .05) the apoptotic index of the cloned blastocysts (8.91 ± 1.94 vs 4.36 ± 1.08) compared to untreated controls, to levels similar to those in IVF blastocysts (4.78 ± 0.74). CBHA treatment, at all the concentrations examined, increased (p < .05) the global level of H3K9ac in cloned blastocysts than in untreated controls to that observed in IVF blastocysts. Treatment with CBHA (10 μM) decreased (p < .05) the global level of H3K27me3 in cloned blastocysts than in untreated controls but it was still higher (p < .05) than in IVF blastocysts. CBHA (10 μM) treatment increased (p < .05) the relative expression level of pluripotency‐related genes OCT‐4 and NANOG, and anti‐apoptotic gene BCL‐XL, and decreased (p < .05) that of pro‐apoptotic gene BAX than in untreated controls but did not affect the relative expression level of apoptosis‐related genes p53 and CASPASE3 and epigenetics‐related genes DNMT1, DNMT3a and HDAC1. These results suggest that treatment of cloned embryos with 10 μM CBHA improves the blastocyst rate, reduces the level of apoptosis and alters the epigenetic status and gene expression pattern.     

Gold nanoelectrodes of varied size: transition to molecule-like charging

A transition from metal-like double-layer capacitive charging to redox-like charging was observed in electrochemical ensemble Coulomb staircase experiments on solutions of gold nanoparticles of varied core size. The monodisperse gold nanoparticles are stabilized by short-chain alkanethiolate monolayers and have 8 to 38 kilodaltons core mass (1.1 to 1.9 nanometers in diameter). Larger cores display Coulomb staircase responses consistent with double-layer charging of metal-electrolyte interfaces, whereas smaller core nanoparticles exhibit redox chemical character, including a large central gap. The change in behavior is consistent with new near-infrared spectroscopic data showing an emerging gap between the highest occupied and lowest unoccupied orbitals of 0.4 to 0.9 electron volt.     

Effect of training location and time period on racehorse performance in New Zealand. 1. Descriptive analysis

AIM: To describe characteristics of Thoroughbred training stables in Matamata and in all other locations in New Zealand combined, over two 19-month time periods in 1996–1997 and 1998–1999, representing equal length periods immediately prior to and after the construction of a new training surface at the Matamata Racing Club.

METHODS: Retrospective records covering all horses training and racing in New Zealand during two 19-month time periods (1996–1997 and 1998–1999), covering 161 locations, were obtained from New Zealand Thoroughbred Racing (NZTR). Outcome variables included whether a horse was raced again in the 6 months following any start in the first 13 months of either time period, number of race starts for every horse, and finishing position. Summary measures with confidence intervals (CI) and unadjusted odds ratios (OR), measuring strength of associations for various factors, were computed.

RESULTS: The datasets contained information on 45,446 horses, 11,336 races, 5,110 trials and a total of 110,643 race starts. Horses trained at Matamata represented 8% (3,715) of the total horse datasets, and accounted for 11,977 race starts (10.8%). They were more likely to start in a race or trial in either time period and were 1.4 and 1.3 times as likely to finish first, second or third compared with horses trained at other locations in 1996–1997 and 1998–1999, respectively. A 6-month no-race period occurred for 9,306/12,584 (74%) horses that started at least once in the first 13 months of either time period. Horses trained at Matamata were less likely to have a 6-month no-race period than horses trained at other locations in both time periods. There was no effect of time period within each location on the probability of either a horse having a 6-month no-race period or of a race start being followed by a 6-month no-race period, but there was an overall effect of time and more 6-month no-race periods were observed in 1998–1999 relative to 1996–1997.

CONCLUSION: Summary statistics are presented for Thoroughbred racing in New Zealand over two 19-month time periods. Differences between the populations of horses trained in Matamata compared with those trained at other locations were attributed, in part, to the fact that many of the more successful racehorse trainers in the country have stables at Matamata. As a result, the population of horses in Matamata may not be representative of the racehorse population in New Zealand. Although more likely to win or place in both time periods, the magnitude of the advantage to horses in Matamata was reduced in 1998–1999 relative to 1996–1997, and this could be due, in part, to effects of the new track surface at Matamata. There was no evidence of a rise in risk of a 6-month no-race period following any race start in those horses trained in Matamata in 1998–1999 relative to either horses trained at other locations or to horses trained in Matamata during the earlier time period.     

Risk factors for injury to the superficial digital flexor tendon and suspensory apparatus in Thoroughbred racehorses in New Zealand

AIM: To investigate risk factors for injury to the superficial digital flexor tendon (SDFT) and suspensory apparatus (SA) of the forelimbs in Thoroughbred racehorses in New Zealand.

METHODS: Poisson and negative binomial regression, with exposure time represented by cumulative training days for each horse, were used to relate explanatory variables to the incidence rate (IR) of cases of inflammation of the SDFT (n=51), and injuries involving the SA (n=48) in a population of 1,571 commercially-trained racehorses over 554,745 study days. Only the first occurrence of an injury for any one horse was eligible for inclusion. Separate analyses were run for data from horses in training regardless of whether they had started in a trial or race, and using a subset of these data restricted to those preparations associated with at least one start in a trial or race. Results were reported as incidence rate ratios (IRR) and 95% confidence intervals (CI).

RESULTS: Male horses had a higher risk of injury to the SA (IRR 2.57; p=0.005) and tended to have a higher risk of injury to the SDFT (IRR 1.74; p=0.09) than female horses. Increasing age was associated with increased risk of injury. Horses aged 4 and ≥5 years were 6.76 (p<0.001) and 15.26 (p<0.001) times more likely to incur injury to the SDFT, and 2.91 (p=0.02) and 3.54 (p=0.005) times more likely to incur injury to the SA, respectively, than 2-year-olds. Horses were more likely to suffer an injury to the SDFT or SA in a training preparation that was not associated with any starts in official trials or races compared with those preparations that were associated with more than one start (p<0.001), and more likely to injure the SA compared with preparations containing one start (p=0.03). The IR of injury to the SDFT tended to be lower between November–January (IRR 0.78; p=0.08) and February-April (IRR 0.75; p=0.08) compared with August–October. Incidence of injury to the SDFT or SA was not associated with the cumulative distance raced in the last 30 days of a training preparation.

CONCLUSION: This study identified risk factors for injury to the SDFT and SA in Thoroughbred racehorses in New Zealand. Injuries were more likely in males, older horses and in horses in training preparations without any starts. There was no evidence of association between injury and cumulative high-speed exercise.     

Cerebral infarction and meningoencephalitis following hot-iron disbudding of goat kids

CASE HISTORY: Twelve of 150 goat kids, 4–10 days old, died 3 days after disbudding with a hot iron. Another 18 kids had been ill the previous day but survived following antibiotic therapy. Five of the dead kids were necropsied.

PATHOLOGICAL FINDINGS: There was necrosis and haemorrhage of the skin, subcutaneous tissues and frontal bone at disbudding sites in all five kids examined post mortem. Beneath disbudding sites in 4/5 kids there were bilateral, dark red, often cavitated areas of necrosis extending deep into the frontal cortex of the brain. Histologically, these areas consisted of coagulation necrosis, haemorrhage, vascular thrombosis and suppurative inflammation. Numerous bacteria, predominantly large Grampositive rods, were present in the necrotic brain tissue. In the remaining kid, bilateral areas of yellow discolouration and flattening of gyri in frontal lobes corresponded histologically to extensive polioencephalomalacia. A mixed growth of aerobes and anaerobes was cultured from the brain of one kid with suppurative lesions.

CLINICAL RELEVANCE: Thermal disbudding of neonatal kids is widely practised in dairy goat herds and is considered the method of choice for disbudding in New Zealand. However, the skull of goat kids is much thinner than that of calves and the safety margin for thermal injury to the brain is markedly reduced. This report highlights the risks associated with the technique and its potential as a welfare issue.