A. Sullo

Similar histopathological picture in males with Achilles and patellar tendinopathy.

PURPOSE To ascertain whether there are differences in the histopathological appearance of tendinopathic Achilles and patellar tendons. METHODS In males, we studied biopsies from tendinopathic Achilles (N = 28; average age 34.1 yr) and patellar tendons (N = 28; average age 32.1), Achilles tendons (N = 21; average age 61.8 yr) from deceased patients with no known tendon pathology, and patellar tendons (N = 15; average age 28.3) from patients undergoing anterior cruciate ligament reconstruction. Hematoxylineosin stained slides were interpreted using a semiquantitative grading scale (0: normal to 3: maximally abnormal) for fiber structure, fiber arrangement, rounding of the nuclei, regional variations in cellularity, increased vascularity, decreased collagen stainability, and hyalinization. All slides were assessed blindly twice, the agreement between two readings ranging from 0.170 to 0.750 (kappa statistics). RESULTS The highest mean score of tendinopathic Achilles tendons was not significantly different from that of tendinopathic patellar tendons (11.6 +/- 5 and 10.4 +/- 3, respectively). The ability to differentiate between an Achilles tendon and a patellar tendon was low. CONCLUSIONS Tendinopathic Achilles and patellar tendons show a similar histological picture. It was not possible to identify whether a specimen had been harvested from an Achilles or a patellar tendon on the basis of histological examination. The general pattern of degeneration was common to both tendinopathic Achilles and patellar tendons. A common, as yet unidentified, etiopathological mechanism may have acted on both these tendon populations.

Calcific Insertional Achilles Tendinopathy Reattachment With Bone Anchors

Background Recalcitrant calcific insertional Achilles tendinopathy is difficult to treat. Hypothesis Bursectomy, excision of the distal paratenon, disinsertion of the tendon, removal of the calcific deposit, and reinsertion of the Achilles tendon with bone anchors is safe and effective. Study Design Longitudinal study. Methods Twenty-one patients (six women) (21 feet) (average age 46.9 ± 6.4 years) with recalcitrant calcific insertional Achilles tendinopathy were treated surgically with removal of the calcific deposit; the Achilles tendon was reinserted with bone anchors. Results At an average follow-up of 48.4 months, one patient necessitated a further operation. Eleven patients reported an excellent result, and five a good result. The remaining five patients could not return to their normal levels of sporting activity and kept fit by alternative means. The results of the VISA-A questionnaire were markedly improved in all patients, from an average of 62.4% to 88.1%. Conclusions We recommend disinsertion of the Achilles tendon to excise the calcific deposit fully and reinsertion of the Achilles tendon in the calcaneus with suture anchors. No patient experienced a traumatic disinsertion of the reattached tendon. However, five patients were not able to return to their original level of physical activity.

Surgery for chronic achilles tendinopathy yields worse results in nonathletic patients

ObjectiveTo report the outcome of surgery for chronic recalcitrant Achilles tendinopathy in nonathletic and athletic subjects. DesignCase-control study. SettingUniversity teaching hospitals. PatientsWe matched each of the 61 nonathletic patients with a diagnosis of tendinopathy of the Achilles tendon with an athletic patient with tendinopathy of the main body of the Achilles tendon of the same sex and age (±2 years). A match was possible for 56 patients (23 males and 33 females). Forty-eight nonathletic subjects and 45 athletic subjects agreed to participate. InterventionsOpen surgery for Achilles tendinopathy. Main Outcome MeasureOutcome of surgery, return to sport, complication rate. ResultsNonathletic patients were shorter and heavier than athletic patients. They had greater body mass index, calf circumference, side-to-side calf circumference differences, and subcutaneous body fat than athletic patients. Of the 48 nonathletic patients, 9 underwent further surgery during the study period, and only 25 reported an excellent or good result. Of the 45 athletic subjects, 4 underwent further surgery during the study period, and 36 reported an excellent or good result. The remaining patients could not return to their normal levels of activity. In all of them, pain significantly interfered with daily activities. ConclusionsNonathletic subjects experience more prolonged recovery, more complications, and a greater risk of further surgery than athletic subjects with recalcitrant Achilles tendinopathy.

Posterior hypothalamic activity and cortical control during the PGE1 hyperthermia.

THE firing rate of the posterior hypothalamic neurones, and interscapular brown adipose tissue, and colonic temperatures (TIBAT, and TC) were monitored in 36 urethane-anaesthetized male Sprague-Dawley rats before, and after an intracerebroventricular (i.c.v.) injection of 400 ng prostaglandin E1 (PGE1) or saline. The i.c.v. injection was preceded by functional decortication in half of each group. The results show an increase of firing rate, TIBAT, and TC after PGE, injection in the rats without decortication. Functional decortication significantly reduced these enhancements. These findings demonstrate that the posterior hypothalamus plays a significant role in the hyperthermia induced by PGE, and that the cerebral cortex is involved in the control of posterior hypothalamic activity.

Injection of muscimol in the posterior hypothalamus reduces the PGE1-hyperthermia in the rat.

The firing rate of the nerves innervating interscapular brown adipose tissue (IBAT), IBAT and colonic temperatures (TIBAT and Tc), heart rate, and oxygen (O2) consumption were monitored in urethane-anesthetized male Sprague-Dawley rats. These variables were measured for 40 min before (baseline values) and 40 min after a 56 ng muscimol injection in the posterior hypothalamus and an intracerebroventricular administration of 500 ng prostaglandin E1 (PGE1). The same variables were monitored in other rats with muscimol injection or PGE1 administration alone. No drug was injected in control rats. The results show that muscimol injection reduces the increases in firing rate, TIBAT, Tc, heart rate, O2 consumption induced by PGE1. These findings suggest that GABAergic tone in the posterior hypothalamus is important in the control of thermogenic changes induced by PGE1.

Aspartic and glutamic acids increase in the frontal cortex during prostaglandin E1 hyperthermia

The aim of the present experiment was to evaluate the role played by aspartic acid and glutamic acid of frontal cerebral cortex during the hyperthermia induced by prostaglandin E1. Two groups of six Sprague Dawley male rats were anaesthetized with ethyl-urethane. The frontal cortical concentrations of aspartic and glutamic acids, the firing rate of the sympathetic nerves to the interscapular brown adipose tissue, the colonic and interscapular brown adipose tissue temperatures were monitored both before and after an intracerebroventricular injection of prostaglandin E1 (500 ng) or saline. Aspartic and glutamic acids were collected using a microdialysis probe placed in the frontal cortex. Concentrations of aspartic and glutamic acids were measured by high-pressure liquid chromatography with fluorescence detector. Prostaglandin E1 induced an increase in the concentrations of aspartic and glutamic acids, in the firing rate of sympathetic nerves and in the colonic and interscapular brown adipose tissue temperatures. The findings of the present experiment indicate that an intracerebroventricular injection of prostaglandin E1 causes release of aspartic and glutamic acids in the frontal cortex.

Nitric oxide reduces body temperature and sympathetic input to brown adipose tissue during PGE1-hyperthermia

The firing rate of the nerves innervating interscapular brown adipose tissue (IBAT) and IBAT and colonic temperatures (TIBAT and TC were monitored in urethane-anaesthetized male Sprague-Dawley rats. These variables were measured for 40 min before (baseline values) and 40 min after a 4 micromoles L-arginine (L-arg) or 400 nmoles nitroprusside (NP) injection in a lateral cerebral ventricle and an intracerebroventricular administration of 500 ng prostaglandin E1 (PGE1). The same variables were monitored in other rats with L-arg or NP or PGE1 administration alone. No drug was injected in control rats. The results show that L-arg or NP injection reduces the increases in firing rate, TIBAT, Tc induced by PGE1. These findings suggest that nitric oxide is important in the control of thermogenic changes during the PGE1 hyperthermia.

Lesions of the Ventromedial Hypothalamus Reduce Postingestional Thermogenesis

The aim of this experiment was to evaluate the effects of ventromedial hypothalamus lesions on the thermogenic changes that follow food intake. Four groups of six Sprague-Dawley male rats were used. Under anesthesia with pentobarbital, the animals in the first and second groups received lesions at the ventromedial hypothalamus, and animals in the third and fourth groups received sham lesions. Body weight and food intake were monitored daily until the experimental procedure began. Twenty days after lesion, oxygen consumption, firing rate of sympathetic nerves to interscapular brown adipose tissue (IBAT), and IBAT temperature were monitored for 45 min both before and after 5 g food intake in 24 h fasted rats from the first and third groups. The same variables were measured in the animals of the second and fourth groups 50 days after receiving the lesions. Lesion placements were histologically verified. The results showed that lesions produced hyperphagia and obesity. Firing rate of nerves to IBAT, IBAT temperature, and oxygen consumption increased after food intake in sham-lesioned rats. This increase was significantly reduced by the lesion at both the 20- and 50-day time points. These findings indicate that the ventromedial hypothalamus controls postingestional activation of sympathetic discharge to IBAT. The reduction of postingestional thermogenesis could be involved in the development of obesity induced by lesion of the ventromedial hypothalamus.

Neuroprotective Effects of Physical Activity: Evidence from Human and Animal Studies

In the present article, we provide a review of current knowledge regarding the role played by physical activity (PA) in preventing age-related cognitive decline and reducing risk of dementia. The cognitive benefits of PA are highlighted by epidemiological, neuroimaging and behavioral studies. Epidemiological studies identified PA as an influential lifestyle factor in predicting rates of cognitive decline. Individuals physically active from midlife show a reduced later risk of cognitive impairment. Neuroimaging studies documented attenuation of age-related brain atrophy, and also increase of gray matter and white matter of brain areas, including frontal and temporal lobes. These structural changes are often associated with improved cognitive performance. Importantly, the brain regions that benefit from PA are also those regions that are often reported to be severely affected in dementia. Animal model studies provided significant information about biomechanisms that support exercise-enhanced neuroplasticity, such as angiogenesis and upregulation of growth factors. Among the growth factors, the brain-derived neurotrophic factor seems to play a significant role. Another putative factor that might contribute to beneficial effects of exercise is the neuropeptide orexin-A. The beneficial effects of PA may represent an important resource to hinder the cognitive decline associated with aging.

LATERAL HYPOTHALAMIC LESION INDUCES SYMPATHETIC STIMULATION AND HYPERTHERMIA BY ACTIVATING SYNTHESIS OF CEREBRAL PROSTAGLANDINS

This experiment tests the effect of intracerebroventricular (icv) injection of lysine acetylsalicylate on the sympathetic and thermogenic changes induced by lesion of the lateral hypothalamus (LH). The firing rate of the nerves innervating interscapular brown adipose tissue (IBAT), along with IBAT and colonic temperatures (TIBAT and Tc) were monitored in urethane-anaesthetized male Sprague-Dawley rats lesioned in the LH. These variables were measured before and after an icv injection of 1mg lysine acetylsalicylate. The same variables were also monitored in: a) lesioned rats with icv administration of saline; b) sham-lesioned animals with icv injection of lysine acetylsalicylate; c) sham-lesioned rats with icv injection of saline. In an additional experiment, the same variables were monitored after an icv injection of lysine acetylsalicylate or saline in rats with LH lesion performed 48 h before the icv injection. The results show that lysine acetylsalicylate injection reduces the increases in firing rate, TIBAT and Tc induced by LH lesion. These findings suggest that cerebral prostaglandin synthesis plays a key role in the sympathetic and thermogenic changes following LH lesion.