This study was conducted on the left Achilles tendon in five clinically normal dogs. The Achilles tendon was surgically exposed and severed 3-4 cm proximal to the point of its insertion. Tenorrhaphy was undertaken by the application of three sutures on the various tendon units of the Achilles tendon using single locking-loop sutures with polyamide no. 1-0. The superficial digital flexor tendon was sutured with catgut using two horizontal mattress sutures. No ultrasound therapy was used in the animals of group I (control). Ultrasound therapy was given to the animals of group II (treated) starting from the third day post-operatively at 0.5 W/cm2 for 10 min daily for 10 days. A cortical screw was used for immobilization of the tibiotarsal joint which was removed 4 weeks after tenorrhaphy. Post-operatively, healing of the Achilles tendon was monitored using clinical observations, ultrasonography, gross and histomorphological observations at various intervals up to 120 days in both groups. Clinically, the dogs showed significant lameness for the first 4-5 days, which disappeared earlier in the ultrasound-treated (group II) animals than the controls (group I). Extension and flexion of the hock joint were found to be near normal at 6 weeks after the repair of the Achilles tendon. Ultrasonography showed anechoic to hypo-echoic echo-texture on days 3 and 7 after repair. By day 40, the echo-texture started to improve to hypo-echoic in group II, but in group I anechoic areas were still observed. However, the tendon showed near normal mottled hypo- to hyper-echoic texture in both groups by day 120. Gross observations suggested that the Achilles tendon in group II showed comparatively fewer adhesions than in group I animals. Histologically, in group II (treated), on day 40, the union was comparatively better without any inflammatory reaction. Bundle formation had begun in the ultrasound-treated animals which was not observed in the control animals. By day 90, more compact parallel bundle formation had taken place with minimum cellularity. Bundle formation was in its advanced stage in the treated animals. By day 120, the tendon tissue was comparatively acellular and looking like a normal tendon. The use of the cortical screw provided good immobilization and ultrasound therapy at 0.5 W/cm2 enhanced the Achilles tendon healing in dogs.

When the culture from the urine obtained by cystocentesis is negative, cultures of urinary bladder mucosal biopsy and urolith are recommended in dogs with urolithiasis in order to accurately assess the microbiological status of the urinary tract.

Alzheimer disease (AD) is characterized by dementia that begins as mild short term memory deficit and culminates in total loss of cognitive and executive functions. The present study was conducted to evaluate the neuroprotective potential of Bacopa monnieri (BM), an Indian traditional medicinal plant effective against cognitive impairment, in colchicine-induced dementia. Intracerebroventricular administration of colchicine (15 μg/5 μl) induced cognitive impairment in rats as assessed by elevated plus maze. This was accompanied by a significant increase in oxidative stress in term of enhanced levels of lipid peroxidation and protein carbonyls. Concomitantly, decrease in activity of antioxidant enzymes was observed in colchicine treated animals. BM (50 mg/kg body weight) supplementation reversed memory impairment observed in the colchicine treated rats. BM administration attenuated oxidative damage, as evident by decreased LPO and protein carbonyl levels and restoration in activities of the antioxidant enzymes. The activity of membrane bound enzymes (Na(+)K(+) ATPase and AChE) was altered in colchicine treated brain regions and BM supplementation was able to restore the activity of enzymes to comparable values observed in controls. The results suggest therapeutic potential of BM in the treatment of AD associated cognitive decline.

As the major hub of metabolic activity and an organelle sequestering pro-apoptogenic intermediates, mitochondria lie at the crossroads of cellular decisions of death and survival. Intracellular calcium is a key regulator of these outcomes with rapid, uncontrolled uptake into mitochondria, activating pro-apoptotic cascades that trigger cell death. Here, we show that calcium uptake and mitochondrial metabolism in murine T-regulatory cells (Tregs) is tuned by Notch1 activity. Based on analysis of Tregs and the HEK cell line, we present evidence that modulation of cellular calcium dynamics underpins Notch1 regulation of mitochondrial homeostasis and consequently anti-apoptotic activity. Targeted siRNA-mediated ablations reveal dependency on molecules controlling calcium release from the endoplasmic reticulum (ER) and the chaperone, glucose-regulated protein 75 (Grp75), the associated protein Voltage Dependent Anion Channel (VDAC)1 and the Mitochondrial Calcium Uniporter (MCU), which together facilitate ER calcium transfer and uptake into the mitochondria. Endogenous Notch1 is detected in immune-complexes with Grp75 and VDAC1. Deficits in mitochondrial oxidative and survival in Notch1 deficient Tregs, were corrected by the expression of recombinant Notch1 intracellular domain, and in part by recombinant Grp75. Thus, the modulation of calcium dynamics and consequently mitochondrial metabolism underlies Treg survival in conditions of nutrient stress. This work positions a key role for Notch1 activity in these outcomes.