Combinations of romifidine and butorphanol were used to sedate 55 horses for a variety of surgical, therapeutic and diagnostic procedures. Eighteen of the horses were given the drugs separately, romifidine first followed by butorphanol four minutes later, and 37 were given the drugs together. The levels of sedation and ataxia were assessed and graded, and there were no statistically significant differences between the two methods of administration. The side effects were typical of the alpha-2 agonists, including bradycardia, heart block and some sweating. Box-walking was observed in one horse. The procedure attempted was successfully completed in 54 of the horses, and the combination of drugs was judged to be a safe and effective sedative for horses.

No abstract

This study draws on decision analysis to estimate the utility of seminal variables in predicting pregnancy. The infertile couples selected (n = 709) excluded those who had donor insemination or known female factors (history of pelvic infection, ovulatory disorders, endometriosis, and tubal disease). Diagnostic test properties were calculated with respect to pregnancy for two variables derived from the semen analysis report: sperm density, and the total number of motile sperm in the ejaculate (TMS). Receiver-operating characteristic (ROC) curves based on sensitivity and specificity revealed that none of the proposed thresholds for sperm density or TMS is clearly a best choice. The highest positive predictive values for sperm density (75%) and TMS (75%) were associated with cutoff points at five million sperm per milliliter and five million motile sperm per ejaculate, respectively. The false positive rates when these cutoff points were used were 4.3% (sperm density) and 5.6% (TMS). ROC analysis provides visual and numeric evidence of the quality of a diagnostic test and constitutes a set of procedures for incorporating information from new tests of male gamete function into the diagnostic assessment of infertility.

No abstract

Huntington disease (HD) is an autosomal dominant neurological disorder that is caused by a CAG repeat expansion, translated into polyglutamine, in the huntingtin (HTT) gene. Although the length of this repeat polymorphism is inversely correlated with age of onset (AOO), it does not fully explain the variability in AOO. Genomic studies have provided evidence for the involvement of DNA repair in modifying this trait, potentially through somatic repeat instability. We therefore assessed genetic variants within the 12bp interrupting sequence between the pathogenic CAG repeat and the polymorphic proline (CCG) tract in the HTT gene and identified variants that result in complete loss of interruption (LOI) between the adjacent CAG/CCG repeats.Analysis of multiple HD pedigrees showed that this variant is associated with dramatically earlier AOO and is particularly relevant to HD patients with reduced penetrance alleles. On average AOO of HD is hastened by an average of 25 years in LOI carriers. This finding indicates that the number of uninterrupted CAG repeats is the most significant contributor to AOO of HD and is more impactful than polyglutamine length, which is not altered in these patients. We show that the LOI variant is associated with increases in both somatic and germline repeat instability, demonstrating a potential mechanism for this effect. Screening individuals from the general population (n=2,674 alleles) suggests that the variant occurs only in expanded CAG repeat alleles. Identification of this modifier has important clinical implications for disease management of HD families, especially for those in the reduced penetrance ranges.3