Psychological influences on repetition-induced summation of activity-related pain in patients with chronic low back pain

This study examined the role of pain catastrophizing, fear of movement and depression as determinants of repetition-induced summation of activity-related pain. The sample consisted of 90 (44 women and 46 men) work-disabled individuals with chronic low back pain. Participants were asked to lift a series of 18 canisters that varied according to weight (2.9 kg, 3.4 kg, 3.9 kg) and distance from the body. The canisters were arranged in a 3 × 6 matrix and the weights were distributed such that each ‘column’ of three canisters was equated in terms of physical demands. Participants rated their pain after each lift, and in a separate trial, estimated the weight of each canister. Mean activity-related pain ratings were computed for each Column of the task. An index of repetition-induced summation of pain was derived as the change in pain ratings across the six ‘columns’ of the task. Pain catastrophizing, fear of movement and depression were significantly correlated with condition-related pain (e.g., MPQ) and activity-related pain ratings. Women rated their pain as more intense than men, and estimated weights to be greater than men. A repetition-induced summation of pain effect was observed where pain ratings increased as participants lifted successive canisters. Fear of movement, but not pain catastrophizing or depression, was associated with greater repetition-induced summation of pain. The findings point to possible neurophysiological mechanisms that could help explain why fear of pain is a robust predictor of pain-related disability. Mechanisms of repetition-induced summation of activity-related pain are discussed.     

Pelvic endometriosis with ureteral obstruction. Case report

The authors report 1 clinical case of pelvic endometriosis. The urinary symptoms and the radiological appearance of endometriosis with compression of the ureter are non specific. The diagnosis was established by histological examination of the resection specimen. The authors describe the therapeutic approach based on radical surgery designed to eradicate the endometriosis, while remaining as conservative as possible in order to allow subsequent pregnancy, and the place of urological surgery combined with medical treatment with LHRH analogue.     

Didanosine extended-release matrix tablets: optimization of formulation variables using statistical experimental design

Statistical experimental design was applied to evaluate the influence of some process and formulation variables and possible interactions among such variables, on didanosine release from directly-compressed matrix tablets based on blends of two insoluble polymers, Eudragit RS-PM and Ethocel 100, with the final goal of drug release behavior optimization. The considered responses were the percent of drug released at three determined times, the dissolution efficiency at 6 h and the time to dissolve 10% of drug. Four independent variables were considered: tablet compression force, ratio between the polymers and their particle size, and drug content. The preliminary screening step, carried out by means of a 12-run asymmetric screening matrix according to a D-optimal design strategy, allowed evaluation of the effects of different levels of each variable. The drug content and the polymers ratio had the most important effect on drug release, which, moreover, was favored by greater polymers particle size; on the contrary the compression force did not have a significant effect. The Doehlert design was then applied for a response-surface study, in order to study in depth the effects of the most important variables. The desirability function was used to simultaneously optimize the five considered responses, each having a different target. This procedure allowed selection, in the studied experimental domain, of the best formulation conditions to optimize drug release rate. The experimental values obtained from the optimized formulation highly agreed with the predicted values. The results demonstrated the reliability of the model in the preparation of extended-release matrix tablets with predictable drug release profiles.     

Sustained Ca2+-induced Ca2+-release underlies the post-glutamate lethal Ca2+ plateau in older cultured hippocampal neurons

Several studies have shown that a prolonged Ca(2+) elevation follows a glutamate-mediated excitotoxic insult in cultured neurons, and may be associated with impending cell death. Recently, we showed that the prolonged Ca(2+) elevation that emerges as neurons age in culture is specifically linked to an age-related increase in excitotoxic vulnerability. However, the multiple sources of Ca(2+) that contribute to Ca(2+) elevation during and after glutamate exposure are not well understood. Here, we examined the Ca(2+) sources of the age-related prolonged Ca(2+) elevation in cultured hippocampal neurons. Studies with caffeine showed that the ryanodine receptor-dependent releasable pool of Ca(2+) from intracellular stores was similar in older and younger neurons. Thapsigargin, which inhibits intracellular store refilling, did not mimic the age-related prolonged Ca(2+) elevation and, in fact, partially reduced it. Ryanodine, which blocks Ca(2+)-induced Ca(2+)-release (CICR) from stores, completely blocked the age-related prolonged Ca(2+) elevation following glutamate exposure but did not alter maximal Ca(2+) elevation during the glutamate exposure. Thus, we conclude that sustained CICR plays a selective and key role in generating the lethal, age-related, prolonged Ca(2+) elevation, and is the likely mechanism underlying age-related, enhanced vulnerability to excitotoxicity in neurons.     

Biomechanics and neuropathology of adult and paediatric head injury

The objective of this study was to understand the biomechanics in age-related primary traumatic brain injuries (TBI) causing initial severity and secondary progressive damage and to develop strategy reducing TBI outcome variability using biomechanical reconstruction to identify types of causal mechanisms prior to clinical trials of neuro-protective treatment. The methods included the explanation of TBI biomechanics and physiopathological mechanisms from dual perspectives of neurosurgery and biomechanical engineering. Scaling of tolerances for skull failure and brain injuries in infants, children and adults are developed. Diagnostic assumptions without biomechanical considerations are critiqued. Methods for retrospective TBI reconstruction for prevention are summarized. Mechanisms of TBI are based on the differences between the mechanical properties of the head and neck related to age. Skull fracture levels correlate with increasing cranial bone thickness and in the development of the cranial sutures in infants and in adults. Head injury tolerance levels at three age categories for cerebral concussion, skull fracture and three grades of diffuse axonal injuries (DAI) are presented. Brain mass correlates inversely for TBI caused by angular head motions and locations of injurious stresses are predictable by centripetal theory. Improved quantitative diagnosis of TBI type and severity levels depend primarily on age and biomechanical mechanisms. Reconstruction of the biomechanics is feasible and enables quantitative stratification of TBI severity. Experimental treatment has succeeded in preventing progressive damage in animal TBI models. In humans this has failed, because the animal model received biomechanically controlled TBI and humans did not. Clinical similarities of human TBI patients do not necessarily predict equivalent biomechanics because such trauma can be produced in various ways. We recommend 'reverse engineering' for in-depth reconstruction of the TBI injury mechanism for qualitative diagnoses and reduction of outcome variability.     

Biomechanical comparison of effects of supraspinatus tendon detachments,tendon defects,and muscle retractions

BACKGROUND: Rotator cuff ruptures are frequently associated with loss of strength of the shoulder. However, the characteristics of the rotator cuff tear that are responsible for the loss of force generation and transmission have not yet been identified. The purpose of this study was to compare the effects of supraspinatus tendon detachments, tendon defects, and muscle retractions on in vitro force transmission by the rotator cuff to the humerus. METHODS: The rotator cuff tendons from ten cadaver shoulders were loaded proportionally to the respective cross-sectional areas of their muscles. A fiberglass rod was cemented into the medullary canal of the humerus and connected to a three-component load cell for the measurement of the forces transmitted by the rotator cuff to the humerus. This study was performed with the humerus in a hanging arm position and with various sizes of supraspinatus tendon detachments, tendon defects, and muscle retractions. RESULTS: Detachment or creation of a defect involving one-third or two-thirds of the supraspinatus tendon resulted in a minor reduction in the force transmitted by the rotator cuff (< or =5%), while detachment or creation of a defect involving the whole tendon resulted in a moderate reduction (11% and 17%, respectively). Simulated muscle retraction involving one-third, two-thirds, and the whole tendon resulted in losses of torque measuring 19%, 36%, and 58%, respectively. Side-to-side repair of the one-third and two-thirds defects nearly restored the force transmission capability, whereas a deficit remained after side-to-side repair following complete resection. CONCLUSIONS: Our results support the rotator cable concept and correspond to the clinical observation that patients with a small rupture of the rotator cuff may present without a loss of shoulder strength. Muscle retraction is potentially an important factor responsible for loss of shoulder strength following large rotator cuff ruptures. Clinical Relevance: Supraspinatus muscle retraction diminishes glenohumeral abduction torque significantly more than either a defect in the tendon or a simple detachment of the tendon from the tuberosity. In cases of irreparable defects, side-to-side repair may be worthwhile to restore muscle tension and the integrity of the rotator cable.     

Helicobacter infection in patients with HCV-related chronic hepatitis,cirrhosis, and hepatocellular carcinoma

Chronic hepatitis may progress to cirrhosis and hepatocellular carcinoma (HCC). HCC represents one of the most common human cancers. Incidence rates for this tumor vary widely on a worldwide, suggesting that environmental factors such as infectious microorganisms, carcinogens, or nutrition play a role in its pathogenesis. Several Helicobacter spp. colonize the liver of animals and induce hepatitis. The aim of this study was to determine whether Helicobacter infection was associated with HCV-related liver diseases in humans. Liver tissue samples, including biopsy and surgically excised tissues, were collected from patients positive for hepatitis C viruses (HCV) RNA in the serum. Genomic DNA was extracted from sections of formalin-fixed paraffin-embedded tissues by using the QIAamp Tissue Kit and subjected to polymerase chain reaction (PCR) analysis using two sets of Helicobacter-specific 16S ribosomal RNA primers. To identify positive samples for H. pylori, a set of primers specific for a conserved region in the H. pylori vacA gene were also used. The patients' H. pylori status was determined by ELISA. Forty-one patients (mean age 54.9, range 19–78 years; 24 men) were studied. Thirty patients had chronic viral hepatitis (CH) without (N = 18) or with (N = 12) cirrhosis (CIR), and 11 patients had HCC. Anti-H. pylori IgG was detected in 54%. The expected 422- and 210-bp fragments of Helicobacter 16S rRNA were amplified from 27% of liver samples, including 17% of CH-CIR and 55% of HCC (P = 0.004). The vacA sequence was amplified in 10 of 41(24%) samples (27% of those with HCC).: These data confirm the presence of H. pylori DNA sequences in human liver and suggest an association of Helicobacter spp. with HCV-related chronic liver diseases. Further studies are needed to ascertain whether Helicobacter spp. infection plays a role in the development of HCC.