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Biomedical subjects

R Baron

Publications and source records attributed to R Baron.

At least 19 recordsLinked to original sources

Performance characteristics according to playing position in elite soccer.

The paper provides a large-scale study into the motion characteristics of top class soccer players, during match play, according to playing position. Three hundred top-class outfield soccer players were monitored during 20 Spanish Premier League and 10 Champions League games using a computerized match analysis system (Amisco Pro, Nice, France). Total distance covered in five selected categories of intensity, and the mean percentage of playing time spent in each activity were analyzed according to playing position. Midfield players covered a significantly greater total distance (p < 0.0001) than the groups of defenders and forwards did. Analyzing the different work rates showed significant differences (p < 0.5 - 0.0001) between the different playing positions. There were no significant differences between halves in the total distance covered, or in distances covered at submaximal and maximal intensities. However, significantly more distance was covered in the first half compared to the second in medium intensities (11.1 - 19 km/h). The current findings provide a detailed description of the demands placed on elite soccer players, according to their positional role at different work intensities, which may be helpful in the development of individualized training programs.

Humans↗

Endothelial dysfunction in cold type complex regional pain syndrome.

The authors examined endothelial function in cold type chronic complex regional pain syndrome (CRPS) I using acetylcholine- and sodium nitroprusside-induced vasodilation combined with laser Doppler flowmetry in 14 patients and 10 controls. On the affected side, acetylcholine-induced vasodilation was significantly reduced in comparison to controls and the unaffected extremity. No significant differences were found after application of sodium nitroprusside. The results demonstrate impaired endothelial function in chronic CRPS I.

Acetylcholine↗

Quantitative sensory testing in the German Research Network on Neuropathic Pain (DFNS): standardized protocol and reference values.

The nationwide multicenter trials of the German Research Network on Neuropathic Pain (DFNS) aim to characterize the somatosensory phenotype of patients with neuropathic pain. For this purpose, we have implemented a standardized quantitative sensory testing (QST) protocol giving a complete profile for one region within 30 min. To judge plus or minus signs in patients we have now established age- and gender-matched absolute and relative QST reference values from 180 healthy subjects, assessed bilaterally over face, hand and foot. We determined thermal detection and pain thresholds including a test for paradoxical heat sensations, mechanical detection thresholds to von Frey filaments and a 64 Hz tuning fork, mechanical pain thresholds to pinprick stimuli and blunt pressure, stimulus/response-functions for pinprick and dynamic mechanical allodynia, and pain summation (wind-up ratio). QST parameters were region specific and age dependent. Pain thresholds were significantly lower in women than men. Detection thresholds were generally independent of gender. Reference data were normalized to the specific group means and variances (region, age, gender) by calculating z-scores. Due to confidence limits close to the respective limits of the possible data range, heat hypoalgesia, cold hypoalgesia, and mechanical hyperesthesia can hardly be diagnosed. Nevertheless, these parameters can be used for group comparisons. Sensitivity is enhanced by side-to-side comparisons by a factor ranging from 1.1 to 2.5. Relative comparisons across body regions do not offer advantages over absolute reference values. Application of this standardized QST protocol in patients and human surrogate models will allow to infer underlying mechanisms from somatosensory phenotypes.

Adolescent↗

[Neuropathic pain].

Arises after an injury to nociceptive systems. Examples of the most common causes are polyneuropathies, acute zoster neuralgia, and postherpetic neuralgia. The differential diagnosis and management are discussed.

Aged↗

[Consumption of hand-hygiene products in health establishments in the west of France].

OBJECTIVES: The study had for aim to investigate hand hygiene product use in French hospitals between 2000 and 2003. DESIGN: A questionnaire was sent in 2002 and 2 more in 2003 and 2004 (for 2000 to 2003) requiring data on type of hospital, number of beds, staff members, admissions and patient-day, litres of mild soap, antiseptic soap and alcohol-based rub used and price per litre. Indices were calculated accordingly. RESULTS: 574 hospitals answered over the 4 year period (average 143 per year) representing an average of 50 000 beds/year, 80 000 full-time staff positions, 1.2 million admissions and 16 millions patient-days. The median consumption of mild soap was 3.8 l per bed, 2.7 l per staff member, 2.4 l per 100 admissions, and 10.6 ml per patient-day. The median consumption of antiseptic soap was 1 l per bed, 0.8 l per staff member, 4.8 l per 100 admissions, and 3.2 ml per patient-day. The median consumption of alcohol-based rub (HAS) was 0.3 l per bed, 0.3 l per staff-member, 1.5 l per admission, and 0.9 l per patient-day. Between 2000 and 2003, HAS use significantly increased from 69 to 88% (a relative increase of 31%) and the median consumption increased from 0.5 ml to 1.5 ml per patient-day. 370 fully completed grids gave a number of 7 opportunities per patient-day with less than 1 for HAS. CONCLUSION: The best indicator for an infection control practitioners is the quantity of alcohol-based solution in ml/patient-day and HAS per patient-day is the reference.

Alcohols↗

Farnesylated RhoB inhibits radiation-induced mitotic cell death and controls radiation-induced centrosome overduplication.

Our previous results demonstrated that expressing the GTPase ras homolog gene family, member B (RhoB) in radiosensitive NIH3T3 cells increases their survival following 2 Gy irradiation (SF2). We have first demonstrated here that RhoB expression inhibits radiation-induced mitotic cell death. RhoB is present in both a farnesylated and a geranylgeranylated form in vivo. By expressing RhoB mutants encoding for farnesylated (RhoB-F cells), geranylgeranylated or the CAAX deleted form of RhoB, we have then shown that only RhoB-F expression was able to increase the SF2 value by reducing the sensitivity of these cells to radiation-induced mitotic cell death. Moreover, RhoB-F cells showed an increased G2 arrest and an inhibition of centrosome overduplication following irradiation mediated by the Rho-kinase, strongly suggesting that RhoB-F may control centrosome overduplication during the G2 arrest after irradiation. Overall, our results for the first time clearly implicate farnesylated RhoB as a crucial protein in mediating cellular resistance to radiation-induced nonapoptotic cell death.

Animals↗

Platelet activation and platelet-leucocyte interaction in patients with migraine. Subtype differences and influence of triptans.

As migraine is the result of an inflammatory mechanism with serotonergic signalling, leucocyte function, platelet function and intercellular communication between those cells is likely to be connected to the final pathway of the disease. We examined P-selectin expression on platelets (platelet activation) and leucocyte-platelet aggregate formation in 72 migraine patients during their attack-free interval and controls using a flow cytometric assay. Patients suffering from migraine without aura had a significantly increased platelet activation and leucocyte-platelet aggregation compared with the control group, unlike the migraine patients with aura. Patients who had taken a triptan within 3 days prior to the investigation showed platelet activation values similar to the control group. The variations in platelet activation patterns of migraine subgroups could indicate different pathomechanisms. Even outside an attack, migraine patients, particularly those without aura, show an increased level of platelet activation which seems to be down-regulated by triptans. This mechanism may account for the triptan-induced increases in headache frequency. The involvement of proinflammatory platelet-leucocyte cross-talk suggests a possible therapeutic strategy using anti-inflammatory drugs.

Female↗

[How neuropathic is sciatica? The mixed pain concept].

Different pathophysiological mechanisms are thought to operate in chronic sciatica. Nociceptive and neuropathic pain components can be distinguished. Neuropathic pain may be caused by lesions of nociceptive sprouts within the degenerated disc (local neuropathic), mechanical compression of the nerve root (mechanical neuropathic root pain), or by action of inflammatory mediators (inflammatory neuropathic root pain) originating from the degenerative disc even without any mechanical compression. Since different pain-generating mechanisms possibly underlie sciatic pain, the term mixed pain syndrome was established. The incidence of each pain component in chronic sciatica as well as validated diagnostic tools to identify them remain unknown. Current analgesic therapeutic first-line strategies for chronic sciatica rely on NSAIDs that are known to relieve nociceptive pain only. In neuropathic pain, different therapeutic approaches are effective, i.e., antidepressants such as amitriptyline and anticonvulsants such as gabapentin, carbamazepine, and pregabalin. Therefore, the combination of these analgesic compounds with NSAID could be useful in patients with sciatic pain who do not respond to NSAID.

Analgesics↗

A new selective estrogen receptor modulator HMR-3339 fully corrects bone alterations induced by ovariectomy in adult rats.

The selective estrogen receptor modulator (SERM) raloxifene has been shown to reduce the risk of vertebral fracture, but without significant effect on nonvertebral fractures. However, there is a need for SERMs capable of improving mechanical competence and reducing the risk of fractures at multiple skeletal sites, with minimal side effects. We investigated the effects of a new steroidal SERM, HMR-3339, compared to raloxifene, on bone strength and its determinants (BMD, microarchitecture, dimensions) at various skeletal sites (lumbar spine, tibia, and femur) of adult ovariectomized rats in both prevention and intervention protocols. In a prevention study, HMR-3339 and raloxifene treatments fully prevented alterations of bone strength. In an intervention protocol, where treatment was started 8 weeks after ovariectomy, HMR-3339 fully restored mechanical properties by influencing both areal BMD and outer diameter. This effect was observed at skeletal sites formed of cancellous and cortical bone or of cortical bone only. In contrast, raloxifene positively influenced structures containing mainly cancellous bone. In HMR-3339-treated rats, IGF-I plasma levels were higher than in ovariectomized controls; this was not observed with raloxifene. In conclusion, these results indicate that HMR-3339 increased not only bone mineral mass, but also restored bone mechanical strength at multiple sites in adult osteoporotic rats. In contrast to raloxifene, HMR-3339 also influenced skeletal sites predominantly formed of cortical bone.

Animals↗

[Outbreak of Enterobacter aerogenes in paediatric unit].

Within the framework of breast milk control the hygiene laboratory of Brest hospital isolates, on 3 January 1996 a strain of Enterobacter aerogenes secretory of cephalosporinase in the breast milk of a mother whose child was hospitalized in neonatalogy. On 15 April 1996 a new strain of E. aerogenes is isolated from another mother's breast milk. Until 18 August 1997, 21 samples of breast milk were tested positive to this bacteria. During the same period, E. aerogenes was isolated in 26 children under 1 year of age, 11 of which were infected and 15 colonized. The breast milk did not correspond to those of the mothers of the infected or colonized children. All the strains presented the same antibioresistance. The pulsed-field gel electrophoresis showed that the children's strains, those colonized or infected as well as those isolated in breast milk had the same restriction profile. The epidemiological study concerned the biberonnery-lactarium. The biberonnery's staff is the same as the staff of the lactarium. A portage was searched for among the members of the staff of these units, but without success. The search for E. aerogenes in the environment and in baby-food, others than breast milk was negative. Finally, we did not find any source for these contagions. The only hypothesis we have retained is that of a common source from the biberonnery-lactarium, but without being able to bring any proof to it. Following this epidemic, we have revised all the working modalities and practices with the staff of the biberonnery-lactarium.

Disease Outbreaks↗

Interaction between histamine-induced itch and experimental muscle pain.

Itch sensation can be inhibited by simultaneously applied cutaneous pain at the same skin site via a central mechanism. Deep muscle pain is often associated with sensory changes in the corresponding dermatome. We investigated whether experimentally induced muscle pain has any influence on histamine-induced itch and vice versa in a double blind placebo-controlled study. Experiments were performed in 18 healthy subjects. In nine individuals control iontophoresis of histamine into the forearm produced a distinct itch sensation. Another nine individuals participated in an additional experiment in which histamine and saline were iontophoresed on the forearm in a randomized double-blinded two-way crossover design after intramuscular injection of capsaicin into the ipsilateral brachioradial muscle. Capsaicin-induced muscle pain reduced itch sensation significantly. In contrast, capsaicin-induced muscle pain increased significantly after cutaneous histamine application compared to muscle pain after iontophoresis of saline (placebo). These novel data indicate that muscle pain inhibits itch and histamine increases muscle pain. A bi-directional interaction between cutaneous histamine-sensitive afferents and nociceptive muscle afferents via central mechanisms is suggested.

Adult↗

Post-herpetic neuralgia case study: optimizing pain control.

Post-herpetic neuralgia (PHN) is a chronic pain syndrome associated with the reactivation of a primary infection with varicella zoster virus (chicken pox), which leads to a chronic infection of the dorsal root ganglia. Under various clinical circumstances, including immunosuppressive diseases or treatments and certain cancers, reactivation of the infection can occur in adults as shingles. Other factors such as psychological distress and stressful life events also appear to play a role in the onset of shingles and the development of PHN. The most common risk factor for shingles and its potential sequela, PHN, is advanced age. For a significant number of patients, the pain following healing of shingles can persist for months to years; this pain is classified as PHN if it persists longer than 3 months. PHN often leads to depression, disrupted sleep, decreased functioning and increased healthcare utilization. Prompt use of antiviral therapy appears to reduce the period of pain following an episode of shingles by about half and may possibly reduce the overall incidence of PHN. Damage to a variety of neurologic pathways as a result of herpes zoster reactivation suggests that intervention with multiple agents having divergent mechanisms of action is an appropriate treatment approach. Current treatment options aimed at relieving the symptoms of PHN include antidepressants, opioids, anticonvulsants and topical analgesics. It is important for the clinician to establish a baseline pain intensity and character as well as quality of life measures against which to judge the effectiveness of any treatment. This review article features a case study of a patient with PHN to illustrate current diagnostic and treatment approaches.

Acetates↗

Platelet-leukocyte interaction and platelet activation in migraine: a link to ischemic stroke?

OBJECTIVES: Migraine has been identified as an independent risk factor for ischemic stroke. Both neurogenic inflammation and platelet activation have been linked to the pathophysiology of migraine. Increased platelet activation results in up-regulation of specific binding to leukocytes which promotes pro-inflammatory leukocyte secretion and their tethering to endothelium, a mechanism that has been demonstrated in stroke and which could provide a link to migraine. We aimed to determine whether platelet-leukocyte aggregation is increased in migraine patients outside an acute attack. METHODS: Seventy two patients with migraine according to IHS criteria were compared to a control group (n = 72). Whole blood flow cytometry was used to quantify the activation dependent P selectin on the platelet, and to assess the fraction of platelets bound to the different leukocyte subsets. RESULTS: Migraine patients showed significantly more platelet-leukocyte aggregates compared to the control subjects (p = 0.003). This effect was driven by an increased polymorphonuclear cell-platelet aggregation (p = 0.003) whereas platelet aggregation with monocytes and lymphocytes was not. Platelet activation was also increased (p = 0.001). CONCLUSIONS: In migraine pro-inflammatory platelet adhesion to leukocytes occurs during the headache free interval similar to that seen in acute coronary and cerebrovascular syndromes. This may suggest a link between migraine and stroke on a cellular level.

Acute Disease↗

[Recent trends in understanding and therapy of complex regional pain syndromes].

Since the term "complex regional pain syndromes" (CRPS) was introduced based on a revised taxonomy for disorders previously called reflex sympathetic dystrophy and causalgia in 1995, much knowledge grew up on the understanding and therapy of the disease. This review gives an overview on the clinical characteristics, pathophysiology, diagnostic tools and therapeutic options in CRPS. It will especially focus on recent findings on the role of the sympathetic nervous system, the central nervous system and peripheral inflammatory processes as underlying mechanisms. Although there is no diagnostic gold standard, careful clinical evaluation and additional apparative test procedures are very helpful for the diagnosis. An early and interdisciplinary approach is the basis for an optimal and successful treatment.

Causalgia↗

[Complex regional pain syndrome. Sympathetic reflex dystrophy and causalgia].

Complex regional pain syndromes (CRPS) occur as the inadequate response to painful trauma in a distal extremity. With CRPS I (sympathetic reflex dystrophy), no lesion of the nerve is present. Aside from sensory disturbances, burning deep spontaneous pain and mechanical allodynia are characteristic. Disturbances in the skin blood circulation,sweating,edema,and trophic disturbances of the skin, joints, and bones are typical. Reduction in muscle strength, tremor, and late dystonic changes comprise the motor disturbances. All symptoms are distributed in the distal extremity and not limited to the region of the peripheral nerves. Complex regional pain syndrome II (causalgia),develops following a partial peripheral nerve lesion. The distally generalized symptoms are identical. Successful therapy depends on an early start of interdisciplinary treatment. In addition to the pain therapy,physiotherapy plays a decisive role in rehabilitation. During the acute phase, freedom from pain at rest and retrogression of the edema must be achieved. With slight spontaneous pain, a conservative therapeutic method may be applied (analgesics, rest, raised position). In case of insufficient improvement and in difficult cases, the effect of intervention (sympathetic blockade) should be tested and possibly a blockade series performed. After reduced spontaneous pain,physiotherapy should be increased stepwise.

Analgesics↗

[The symptom sympathetic maintained pain].

Sympathetically maintained pain is a symptom which occurs in neuropathic pain syndromes of different etiologies. From animal experiments it is known that nociceptive afferents after partial nerve lesions develop adrenergic sensitivity at the site of the injury. In addition, a sympathetic-afferent coupling takes place in the dorsal root ganglia. It is still controversial if these pathophysiological mechanisms are responsible for the developing of SMP in humans. Clinical studies support the idea that also in humans the application of adrenergic substances in pharmacological doses is capable to influence nociception, but a direct interaction between the sympathetic system and the nociceptive system had not been demonstrated so far. By using a thermal suit for whole body cooling and warming, which produces low and high activity of sympathetic vasoconstrictor neurons, it was possible for the first time to demonstrate an interaction between physiological changes in sympathetic activity and nociception.

Afferent Pathways↗