Both acid pH (4.0) and fusicoccin (FC) strongly stimulate root elongation in intact lentil (Lens culinaris Med.) seedlings. FC-induced elongation is apparently mediated by FC-enhanced H(+) secretion since the toxin induces massive secretion of H(+) in these roots after a latent period of less than 5 min. Auxin (indole-3-acetic acid) strongly inhibits elongation in control roots as well as acid-induced and FC-induced root elongation. Treatment of apical root segments with auxin causes only a slight apparent uptake of H(+) and has no inhibitory effect on FC-induced H(+) secretion, whether the hormone is given before or after the toxin. Auxin induces ethylene production in excised roots of lentil but the latent period is at least 30 min while inhibition of root elongation by IAA is maximal within 30 min. It is concluded that the inhibitory action of auxin on acid-and fusicoccin-induced root elongation is a direct effect, independent of auxin-induced ethylene production or auxin-mediated modification of cell-wall pH.

Background Reduced pelvic limb reflexes in dogs with spinal cord injury typically suggests a lesion of the L4‐S3 spinal cord segments. However, pelvic limb reflexes might also be reduced in dogs with a T3‐L3 myelopathy and concurrent spinal shock. Hypothesis/Objectives We hypothesized that statistical models could be used to identify clinical variables associated with spinal shock in dogs with spinal cord injuries. Animals Cohort of 59 dogs with T3‐L3 myelopathies and spinal shock and 13 dogs with L4‐S3 myelopathies. Methods Data used for this study were prospectively entered by partner institutions into the International Canine Spinal Cord Injury observational registry between October 2016 and July 2019. Univariable logistic regression analyses were performed to assess the association between independent variables and the presence of spinal shock. Independent variables were selected for inclusion in a multivariable logistic regression model if they had a significant effect (P ≤ .1) on the odds of spinal shock in univariable logistic regression. Results The final multivariable model included the natural log of weight (kg), the natural log of duration of clinical signs (hours), severity (paresis vs paraplegia), and pelvic limb tone (normal vs decreased/absent). The odds of spinal shock decreased with increasing weight (odds ratio [OR] = 0.28, P = .09; confidence interval [CI] 0.07‐1.2), increasing duration (OR = 0.44, P = .02; CI 0.21‐0.9), decreased pelvic limb tone (OR = 0.04, P = .003; CI 0.01‐0.36), and increased in the presence of paraplegia (OR = 7.87, P = .04; CI 1.1‐56.62). Conclusions and Clinical Importance A formula, as developed by the present study and after external validation, could be useful for assisting clinicians in determining the likelihood of spinal shock in various clinical scenarios and aid in diagnostic planning.

A 12-year old male castrated Siamese cat was evaluated for a one-day history of mild obtundation and decerebellate rigidity. Neurological examination findings were consistent with multifocal disease including lesions within the right cerebellum and right brainstem. Investigations included hematology, biochemistry, urinalysis, and urine culture. A definitive diagnosis was not achieved clinically and differential diagnoses included vascular disease, neoplasia, and infectious disease. About nine hours after admission, the cat had an episode where it became rigid and then limp. The cat became agonal and went into cardiopulmonary arrest and attempts of resuscitation were unsuccessful. Post-mortem examination revealed evidence of multiple fibrocartilaginous emboli (FCE) within the cerebellum and within meningeal vessels on the ventral aspect of the brainstem. This is the first reported case of fibrocartilaginous embolism causing an encephalopathy in a cat. While this is a rare disease, it is an important differential diagnosis that should be considered in cases of acute encephalopathies in cats.

Cummings on our recent paper reporting the development of a clinical predictive model for spinal shock. We thank the author for his thorough review of the literature related to clinical predictive models (CPMs) and agree with his assertion that CPMs must be externally validated before they can be widely deployed for prognostication in the clinical setting. This is a future direction for our group, and a limitation