Androgen administration protects against musculoskeletal deficits in models of sex-steroid deficiency and injury/disuse. It remains unknown, however, whether testosterone prevents bone loss accompanying spinal cord injury (SCI), a condition that results in a near universal occurrence of osteoporosis. Our primary purpose was to determine whether testosterone-enanthate (TE) attenuates hindlimb bone loss in a rodent moderate/severe contusion SCI model. Forty (n=10/group), 14 week old male Sprague-Dawley rats were randomized to receive: (1) Sham surgery (T9 laminectomy), (2) moderate/severe (250 kdyne) SCI, (3) SCI+Low-dose TE (2.0 mg/week), or (4) SCI+High-dose TE (7.0 mg/week). Twenty-one days post-injury, SCI animals exhibited a 77-85% reduction in hindlimb cancellous bone volume at the distal femur (measured via μCT) and proximal tibia (measured via histomorphometry), characterized by a >70% reduction in trabecular number, 13-27% reduction in trabecular thickness, and increased trabecular separation. A 57% reduction in cancellous volumetric bone mineral density (vBMD) at the distal femur and a 20% reduction in vBMD at the femoral neck were also observed. TE dose dependently prevented hindlimb bone loss after SCI, with high-dose TE fully preserving cancellous bone structural characteristics and vBMD at all skeletal sites examined. Animals receiving SCI also exhibited a 35% reduction in hindlimb weight bearing (triceps surae) muscle mass and a 22% reduction in sublesional non-weight bearing (levator ani/bulbocavernosus [LABC]) muscle mass, and reduced prostate mass. Both TE doses fully preserved LABC mass, while only high-dose TE ameliorated hindlimb muscle losses. TE also dose dependently increased prostate mass. Our findings provide the first evidence indicating that high-dose TE fully prevents hindlimb cancellous bone loss and concomitantly ameliorates muscle loss after SCI, while low-dose TE produces much less profound musculoskeletal benefit. Testosterone-induced prostate enlargement, however, represents a potential barrier to the clinical implementation of high-dose TE as a means of preserving musculoskeletal tissue after SCI.

BackgroundExamination of bile could be useful to diagnose Platynosomum spp.‐induced cholangitis in cats. Obtaining bile via percutaneous ultrasound‐guided cholecystocentesis (PUC) is possible but raises safety concerns in cats with severe cholecystitis.ObjectivesThe objectives of this study were to investigate the use of PUC to collect bile samples from cats with known platynosomosis and to determine if bile analysis could be a diagnostic test.AnimalsTwenty‐seven free‐roaming cats positive for Platynosomum spp. eggs via fecal examination.MethodsIn this prospective study, fecal egg counts were performed by double centrifugation with Sheather's solution. Bile was collected using PUC from anesthetized cats. Egg counts in bile were performed with a stereoscope. Euthanasia and postmortem examination were performed immediately after PUC.ResultsAll cats had ultrasound (US) evidence of cholangitis or cholecystitis. Thirty‐nine PUCs were performed with 14 cats having 2 PUCs 12 or 24 days apart. Postmortem examinations showed no overt gallbladder damage or leakage but fresh blood was noted in the gallbladder lumen of 3 cats. Median Platynosomum spp. egg counts were higher in bile (1450 eggs/mL; IQR, 400; 5138 eggs/mL) as compared to feces (46 eggs/mL; IQR, 10; 107 eggs/mL) (P < .001).Conclusion and Clinical ImportanceBile egg count analysis is an alternative method with higher egg counts as compared to fecal egg count analysis for the diagnosis of platynosomosis. Obtaining bile via US guidance is technically feasible and safe in cats with cholangitis/cholecystitis. Cholecystocentesis and bile analysis are especially relevant for those cats with chronic cholangitis/cholecystitis and negative fecal egg counts for Platynosomum.

Objective To characterize in rice rats: (a) periodontitis (PD) progress with feeding of standard laboratory rat chow (STD) during ages 4–80 weeks; and (b) PD progress with feeding of a high sucrose-casein (H-SC) diet during young adulthood. Methods One group (N = 12) was euthanized at age 4 weeks (Baseline). Four groups (N = 8–16) consumed a STD diet from baseline and were necropsied at ages 22, 30, 52, and 80 weeks. Three groups (N= 10–16) consumed an H-SC diet from baseline. Two were necropsied at ages 22 and 30 weeks, respectively. The third switched to the STD diet at age 22 weeks and was necropsied at age 30 weeks. All mandibles/maxillae were assessed by histometry for degree of periodontal inflammation (PD Score), alveolar crest height (ACH, mm), and horizontal alveolar bone height (hABH, mm2). Results In STD diet rats aged ≥30 weeks, all endpoints were worse (P < 0.05) than at Baseline. In H-SC diet rats aged ≥22 weeks, all endpoints were worse than at Baseline (P < 0.05). At age 22 weeks, all endpoints were worse in the H-SC group than in the STD group (P < 0.05). By age 30 weeks, the STD and H-SC groups did not differ. Conclusions 1) STD diet fed rice rats develop moderate/severe PD by age 30 weeks; 2) an H-SC diet accelerates moderate/severe PD development; and 3) switching to a STD diet does not halt/reverse PD that was accelerated by an H-SC diet. These data further clarify use of the rice rat as a PD model.

Treatments for Platynosomum fastosum—the liver fluke of cats—have been developed based on fecal egg counts. Post mortem fluke counts are required to understand true efficacy. In this study, two praziquantel treatment regimens were evaluated using post mortem fluke counts: a high-dose treatment (HT) of 20 mg/kg body weight (BW) administered intramuscularly (IM) once a day for three consecutive days and a low-dose treatment (LT) of 5 mg/kg BW administered once (IM) and repeated 14 days later. A continual enrolment study design was used with 16 naturally infected cats randomly allocated in blocks of four to the HT (eight cats) or LT (eight cats) group. Treatment success, defined as absence of live flukes post mortem, was determined 10 days after the last treatment. Pre- and post-treatment fecal egg counts (centrifugation with Sheather’s sugar flotation solution) and bile egg counts (obtained via percutaneous ultrasound guided cholecystocentesis) were evaluated as supportive efficacy data. Twelve cats completed the study with two cats withdrawn from each group. Neither treatment was 100% effective. In the HT group, three of six cats had live flukes, albeit low numbers, at post mortem, while all six LT group cats had live flukes. While fecal and bile egg counts were reduced in both group, they were not reflective of the true infection status of the cats post mortem.

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Our objective was to determine if testosterone enanthate (TE) attenuates bone loss in a rodent mid‐thoracic contusion spinal cord injury (SCI) model. Three month old male Sprague Dawley rats received Sham surgery (T8 laminectomy) + vehicle (V), 150 kdyne SCI + V (SCI 150), 250 kdyne SCI + V (SCI 250), SCI 250 + Low TE (2mg/week), or SCI 250 + High TE (7mg/week). SCI was induced via Infinite Horizons Impactor. Animals were sacrificed 3 weeks after injury. Bone structural parameters were assessed via histomorphometry at the proximal tibial metaphysis. SCI induced intensity‐dependent structural deficits, which were prevented by TE in a dose‐dependent manner. TE may provide treatment for SCI‐induced bone loss, thereby reducing the risk of fragility fractures. Sham (a) SCI 150 (b) SCI 250 (c) SCI 250 + Low T (d) SCI 250 + High T (e) Cancellous Bone Volume (%) 4.6 ± 0.9 c* 2.3 ± 0.3 0.8 ± 0.2 a*,e* 3.5 ± 0.5 4.6 ± 0.9 c* Trabecular Width (μm) 14.6 ± 1.1 c 11.8 ± 1.1 10.7 ± 1.1 a 12.5 ± 0.4 13.0 ± 0.5 Trabecular Number (#/mm) 3.7 ± 0.6 c* 2.4 ± 0.2 0.9 ± 0.2 a*,d,e* 3.3 ± 0.4 c 4.1 ± 0.7 c* Trabecular Separation (μm) 463 ± 189 c* 419 ± 36 c 1520 ± 322 a*,b,d*,e* 384 ± 106 c* 322 ± 75 c* Values are Means ± SE of n = 4–9/group. Letters a‐e indicate differences from respectively labeled groups at p < 0.05 or * p < 0.01. Work was supported by Veterans Department CDA‐2 to JFY.