Study on the antidepressant effect of panaxynol through the IκB-α/NF-κB signaling pathway to inhibit the excessive activation of BV-2 microglia.

Panaxynol (PAL) mainly comes from Umbelliferae plants, which has anti-inflammatory and neuroprotective activities. Lipopolysaccharide (LPS)-induced depression in mice was a classic model for studying the effects of drugs on depression in mice. The purpose of this study was to investigate the mechanism and effect of PAL on depression by LPS induced in mice. In the tail suspension test (TST) and forced swimming test (FST) results, PAL significantly reduced the immobility time of mice. In the result of the open field test (OFT) and the elevated plus maze test (EPM), improved their exploration ability. According to the results of ELISA, PAL could significantly reduce the tumor necrosis factor-α (TNF-α) and interleukin- 6 (IL-6) levels in serum. Increase the superoxide dismutase (SDO) level and decrease the malondialdehyde (MDA) level in hippocampus. According to Western blotting analysis results, PAL increased the protein expression of brain-derived neurotrophic factor (BDNF) and tyrosine kinase receptor B (TrkB), decreased the nuclear transport of nuclear factor kappa-Bp65 (NF-κBp65) and phosphorylation of inhibitor of NF-κB (IκB-α). Meanwhile, PAL also inhibited the production of nitric oxide in BV-2 microglia and decreased the level of inflammatory factors. PAL also reduced levels of oxidative stress and inhibited protein expression in the NF-κB/IκB-α inflammatory pathway and increased the protein expression of BDNF/TrkB, thereby inhibiting the over-activation of BV-2 microglia. In conclusion, according to the results of the behavioral text, it is proved that PAL could effectively alleviate LPS induced depression behavior in mice. The mechanism may be that the anti-inflammatory and anti-oxidative stress effects of PAL reduce the release of inflammatory factors in the mouse brain. Meanwhile, PAL could improve brain neurotrophic factors, inhibit the excessive activation of BV-2 microglia, and further inhibit the depressive state of the mice.

[Effects of repeated immobilization stress on hypothalamic-pituitary- ovarian axis in female rats].

Objective: To explore the effects of repeated immobilization stress on hypothalamic-pituitary-ovarian axis in female rats. Methods: Forty female SD rats were randomly divided into two groups: control group (n=20) and experimental group (n=20). One group was fed normally, the other group was subjected to incremental load restraint stress. Brake stress once a day in the retainer (starting at 9: 00 a.m.), braking for 2 hours on the first day, increasing load by 0.5 hours a day for two weeks. Body weight, estrous cycle, sex hormone, organ coefficient, pathology and expression of related genes were detected to explore the harm of hypothalamic-pituitary-ovarian axis. Results: Repeated immobilization stress caused weight loss, prolonged estrous cycle, and changed the organ coefficient and morphology of ovaries and uterus. QPCR technique was used to detect the related genes. It was found that the expressions of gonadotropin releasing hormone, pituitary gonadotropin releasing hormone receptor, follicle stimulating hormone and luteinizing hormone mRNA were decreased significantly, while the expressions of ovarian follicle stimulating hormone and luteinizing hormone receptor mRNA were increased significantly. The expression of estrogen receptor mRNA in ovary and uterus was decreased significantly. Conclusion: Repeated immobilization stress may disrupt the estrous cycle by interfering with the endocrine regulation of the hypothalamic-pituitary-ovarian axis, thus damaging the gonadal and reproductive endocrine function of female animals.

Daily heat treatment maintains mitochondrial function and attenuates atrophy in human skeletal muscle subjected to immobilization.

Skeletal muscle immobilization leads to atrophy, decreased metabolic health, and substantial losses in function. Animal models suggest that heat stress can provide protection against atrophy in skeletal muscle. This study investigated the effects of daily heat therapy on human skeletal muscle subjected to 10 days of immobilization. Muscle biopsies were collected, and MRIs were analyzed from the vastus lateralis of 23 healthy volunteers (11 women, 12 men) before and after either 10 days of immobilization with a daily sham treatment (Imm) or with a targeted, daily 2-h heat treatment using pulsed shortwave diathermy (Imm + H). Diathermy increased intramuscular temperature 4.2 ± 0.29°C (P < 0.0001), with no change during sham treatment. As a result, heat shock protein (HSP)70 and HSP90 increased (P < 0.05) following Imm + H (25 ± 6.6 and 20 ± 7.4%, respectively) but were unaltered with Imm only. Heat treatment prevented the immobilization-induced loss of coupled (-27 ± 5.2% vs. -8 ± 6.0%, P = 0.0041) and uncoupled (-25 ± 7.0% vs. -10 ± 3.9%, P = 0.0302) myofiber respiratory capacity. Likewise, heat treatment prevented the immobilization-induced loss of proteins associated with all five mitochondrial respiratory complexes (P < 0.05). Furthermore, decreases in muscle cross-sectional area following Imm were greater than Imm + H at both the level of the whole muscle (-7.6 ± 0.96% vs. -4.5 ± 1.09%, P = 0.0374) and myofiber (-10.8 ± 1.52% vs. -5.8 ± 1.49%, P = 0.0322). Our findings demonstrate that daily heat treatments, applied during 10 days of immobilization, prevent the loss of mitochondrial function and attenuate atrophy in human skeletal muscle. NEW & NOTEWORTHY Limb immobilization results in substantial decreases in skeletal muscle size, function, and metabolic capacity. To date, there are few, if any, interventions to prevent the deleterious effects of limb immobilization on skeletal muscle health. Heat stress has been shown to elicit a stress response, resulting in increased heat shock protein expression and improved mitochondrial function. We show that during 10 days of lower-limb immobilization in humans, daily exposure to heat stress maintains mitochondrial respiratory capacity and attenuates atrophy in skeletal muscle. Our findings suggest that heat stress may serve as an effective therapeutic strategy to attenuate the decreases of muscle mass and metabolic function that accompany periods of disuse.

The negative effect of unloading exceeds the bone-sparing effect of alkaline supplementation: a bed rest study.

Potassium bicarbonate was administrated to an already alkaline diet in seven male subjects during a 21-day bed rest study and was able to decrease bed rest induced increased calcium excretion but failed to prevent bed rest-induced bone resorption. INTRODUCTION: Supplementation with alkali salts appears to positively influence calcium and bone metabolism and, thus, could be a countermeasure for population groups with an increased risk for bone loss. However, the extent to which alkalization counteracts acid-induced bone resorption or whether it merely has a calcium and bone maintenance effect is still not completely understood. In the present study, we hypothesized that additional alkalization to an already alkaline diet can further counteract bed rest-induced bone loss. METHODS: Seven healthy male subjects completed two parts of a crossover designed 21-day bed rest study: bed rest only (control) and bed rest supplemented with 90 mmol potassium bicarbonate (KHCO3) daily. RESULTS: KHCO3supplementation during bed rest resulted in a more alkaline status compared to the control intervention, demonstrated by the increase in pH and buffer capacity level (pH p = 0.023, HCO3p = 0.02, ABE p = 0.03). Urinary calcium excretion was decreased during KHCO3 supplementation (control 6.05 ± 2.74 mmol/24 h; KHCO3 4.87 ± 2.21 mmol/24 h, p = 0.03); whereas, bone formation was not affected by additional alkalization (bAP p = 0.58; PINP p = 0.60). Bone resorption marker UCTX tended to be lower during alkaline supplementation (UCTX p = 0.16). CONCLUSIONS: The more alkaline acid-base status, achieved by KHCO3 supplementation, reduced renal calcium excretion during bed rest, but was not able to prevent immobilization-induced bone resorption. However, advantages of alkaline salts on bone metabolism may occur under acidic metabolic conditions or with respect to the positive effect of reduced calcium excretion within a longer time frame. TRIAL REGISTRATION: Trial number: NCT01509456.

Phytochemical screening, antioxidant, and in vivo neuropharmacological effect of Monotheca buxifolia (Falc.) barks extract.

Owing to its pharmacological versatility, the current study focuses the evaluation of Monotheca buxifolia (M. buxifolia) bark crude extract and its fractions for phytochemical and pharmacological analysis. Phytochemical investigation of bark extract was carried out through GC-MS, LC-MS and FT-IR. ICP-OES was used for analyzing essential metals in bark extract. Plant samples were further investigated for their in vitro antioxidant and in vivo neuropharmacological activities in mice. Phytochemical analysis of bark extract revealed the presence of various active constituents such as serotonin, α-tocopherol, 3-deoxyestradiol, ascorbyl palmitate and cirsimaritin. Metal analysis showed presence of various metals in diverse concentration. M. buxifolia bark extract and its chloroform fraction showed significant antioxidant activity against DPPH (89.55 ±1.29; 84.80±1.66%), superoxide (82.10 ±1.86; 80.0±1.0%), H2O2 (80.55±2.0; 78.10±2.26%) at 500µg/mL concentration. Similarly, bark extract and its chloroform fraction demonstrated antidepressant activity in mice and improve generalized locomotive behavior. The effective use of M. buxifolia in treatment and management of depression and free radicals based disorders can be safely concluded from the results of present study.

Creatine Loading Does Not Preserve Muscle Mass or Strength During Leg Immobilization in Healthy, Young Males: A Randomized Controlled Trial.

BACKGROUND: A short period of leg immobilization leads to rapid loss of muscle mass and strength. Creatine supplementation has been shown to increase lean body mass in active individuals and can be used to augment gains in muscle mass and strength during prolonged resistance-type exercise training. OBJECTIVE: Our objective was to investigate whether creatine loading can attenuate the loss of muscle mass and strength during short-term leg immobilization. METHODS: Healthy young men (n = 30; aged 23 ± 1 years; body mass index [BMI] 23.3 ± 0.5 kg/m-2) were randomly assigned to either a creatine or a placebo group. Subjects received placebo or creatine supplements (20 g/d) for 5 days before one leg was immobilized by means of a full-leg cast for 7 days. Muscle biopsies were taken before creatine loading, prior to and immediately after leg immobilization, and after 7 days of subsequent recovery. Quadriceps cross-sectional area (CSA) (computed tomography [CT] scan) and leg muscle strength (one-repetition maximum [1-RM] knee extension) were assessed before and immediately after immobilization and after 1 week of recovery. Data were analyzed using repeated measures analysis of variance (ANOVA). Data are presented consistently as mean ± standard error of the mean (SEM). RESULTS: There was a significant overall increase in muscle total creatine content following the 5-day loading phase (p = 0.049), which appeared driven by an increase in the creatine group (from 90 ± 9 to 107 ± 4 mmol/kg-1 dry muscle) with no apparent change in the placebo group (from 88 ± 4 to 90 ± 3 mmol/kg-1; p = 0.066 for time × treatment interaction). Quadriceps muscle CSA had declined by 465 ± 59 and 425 ± 69 mm2 (p < 0.01) in the creatine and placebo group, respectively, with no differences between groups (p = 0.76). Leg muscle strength decreased from 56 ± 4 to 53 ± 4 kg in the creatine and from 59 ± 3 to 53 ± 3 kg in the placebo group, with no differences between groups (p = 0.20). Muscle fiber size did not change significantly over time in either group (p > 0.05). When non-responders to creatine loading were excluded (n = 6), responders (n = 8; total creatine content increasing from 70 to 106 mmol/kg-1) showed similar findings, with no signs of preservation of muscle mass or strength during immobilization. During the subsequent recovery phase, no differences in muscle mass or strength were found between the two groups (p > 0.05). CONCLUSION: Creatine supplementation prior to and during leg immobilization does not prevent or attenuate the loss of muscle mass or strength during short-term muscle disuse. NIH Clinical Trial Registration Number: NCT01894737 ( http://www.clinicaltrials.gov/ ).

CXCR4 antagonist AMD3100 reverses the neurogenesis and behavioral recovery promoted by forced limb-use in stroke rats.

PURPOSE: Forced limb-use can enhance neurogenesis and behavioral recovery as well as increasing the level of stromal cell-derived factor-1 (SDF-1) in stroke rats. We examined whether the SDF-1/CXCR4 pathway is involved in the enhanced neurogenesis and promoted behavioral recovery induced by forced limb-use in the chronic phase of stroke. METHODS: The CXCR4 antagonist, AMD3100, was used to block the SDF-1/CXCR4 pathway in the ischemic rats. Brain ischemia was induced by endothelin-1. One week after ischemia, the unimpaired forelimb of rats was immobilized for 3 weeks. The proliferation, migration, and survival of DCX-positive cells in the subventricular zone (SVZ), and the dendritic complexity of DCX-positive cells in the dentate gyrus (DG), as well as the inflammatory response in the infarcted striatum were analyzed by immunohistochemistry. Functional recovery was assessed in beam-walking and water maze tests. RESULTS: Forced limb-use enhanced the proliferation, migration, dendritic complexity and the survival of newborn neurons. Furthermore, forced limb-use suppressed the inflammatory response and improved both motor and cognitive functions after stroke. AMD3100 significantly abrogated the enhanced neurogenesis and behavioral recovery induced by forced limb-use without influencing the inflammatory response. CONCLUSIONS: SDF-1/CXCR4 pathway seems to be involved in the enhancement of neurogenesis and behavioral recovery induced by post-stroke forced limb-use.

Training the motor cortex by observing the actions of others during immobilization.

Limb immobilization and nonuse are well-known causes of corticomotor depression. While physical training can drive the recovery from nonuse-dependent corticomotor effects, it remains unclear if it is possible to gain access to motor cortex in alternative ways, such as through motor imagery (MI) or action observation (AO). Transcranial magnetic stimulation was used to study the excitability of the hand left motor cortex in normal subjects immediately before and after 10 h of right arm immobilization. During immobilization, subjects were requested either to imagine to act with their constrained limb or to observe hand actions performed by other individuals. A third group of control subjects watched a nature documentary presented on a computer screen. Hand corticomotor maps and recruitment curves reliably showed that AO, but not MI, prevented the corticomotor depression induced by immobilization. Our results demonstrate the existence of a visuomotor mechanism in humans that links AO and execution which is able to effect cortical plasticity in a beneficial way. This facilitation was not related to the action simulation, because it was not induced by explicit MI.

The embodied nature of motor imagery processes highlighted by short-term limb immobilization.

We investigated the embodied nature of motor imagery processes through a recent use-dependent plasticity approach, a short-term limb immobilization paradigm. A splint placed on the participants' left-hand during a brief period of 24 h was used for immobilization. The immobilized participants performed two mental rotation tasks (a hand mental rotation task and a number mental rotation task) before (pre-test) and immediately after (post-test) the splint removal. The control group did not undergo the immobilization procedure. The main results showed an immobilization-induced effect on left-hand stimuli, resulting in a lack of task-repetition benefit. By contrast, accuracy was higher and response times were shorter for right-hand stimuli. No immobilization-induced effects appeared for number stimuli. These results revealed that the cognitive representation of hand movements can be modified by a brief period of sensorimotor deprivation, supporting the hypothesis of the embodied nature of motor simulation processes.

Increased resistance of immobilized-stressed mice to infection: correlation with behavioral alterations.

Immobilization is an easy and convenient method to induce both psychological and physical stress resulting in restricted motility and aggression and is believed to be the most severe type of stress in rodent models. Although it has been generally accepted that chronic stress often results in immunosuppression while acute stress has been shown to enhance immune responses, the effects of IS on the host resistance to Escherichia coli (E. coli) infection and associated behavioral changes are still not clear. In a series of experiments aimed at determining the level of hypothalamic COX-2, HSP-90, HSP-70, SOD-1 and plasma level of corticosterone, cytokine, antibody titer and their association with behavioral activities, mice were infected with viable E. coli during acute and chronic IS by taping their paws. In this study we show that acute and chronic IS enhances the resistance of mice to E. coli infection via inhibiting the production of pro-inflammatory cytokines, free radicals, and by improving the exploratory behavior. Altogether, our findings support the notion that cytokines released during immune activation and under the influence of corticosterone can modulate the open field behavior both in terms of locomotor activity as well as exploration. One of the features observed with chronic stressor was a lower ability to resist bacterial infection, although in case of acute stress, a better clearance of bacterial infection was observed in vivo with improvement of exploratory behavior and cognitive functions.

Impaired physical function, loss of muscle mass and assessment of biomechanical properties in critical ill patients.

Intensive care unit (ICU) admission is associated with muscle weakness and ICU survivors report sustained limitation of physical capacity for years after discharge. Limited information is available on the underlying biomechanical properties responsible for this muscle function impairment. A plausible contributor to the accentuated catabolic drive in ICU patients is a synergistic response to inflammation and inactivity leading to loss of muscle mass. As these entities are predominantly present in the early phase of ICU stay, interventions employed during this time frame may exhibit the greatest potential to counteract loss of muscle mass. Despite the obvious clinical significance of muscle atrophy for the functional impairment observed in ICU survivors, no preventive therapies have been identified as yet. The overall aim of the present dissertation is to characterize aspects of physical function and biomechanical properties in ICU patients and to provide new insights into ICU-induced muscle wasting and the underlying biomechanical mechanisms responsible for the residual impairment of physical function in ICU survivors.

Influencia del vendaje neuromuscular sobre la presión plantar durante la marcha / Influence of the neuromuscular bandage on plantar pressure during walking

Durante los últimos años, la aplicación del vendaje neuromuscular (VN) ha sido empleada en el ámbito deportivo y la rehabilitación. Varios son los beneficios asociados al VN, aunque su influencia y efectos en el patrón de presión plantar es desconocida. En este sentido, mediante el sistema de pedobarografía Biofoot IBV® 6.0 se ha analizado la presión plantar en 5 zonas del pie, así como la cadencia y el tiempo de apoyo. Veintinueve sujetos participaron en el estudio, caminando sobre una cinta rodante a 1 m/s, con/sin VN en peroneos y tríceps sural. Los resultados no mostraron diferencias significativas (p<0,05) en las presiones plantares por el uso del VN en ambos grupos musculares. Tan sólo el efecto de este vendaje aplicado en el tríceps sural durante la marcha mostró un ligero incremento en el tiempo de apoyo (p=0,045) (AU)

Application of the neuromuscular bandage has frequently been used in sports and rehabilitation. There are several benefits associated with this bandage, although its influence and effects on the plantar pressure pattern have not been analyzed. In this sense, our study has analyzed plantar pressure in 5 foot zones with the pedobarographic system Biofoot IBV® 6.0 as well as cadence and contact time. A total of 29 subjects participated in the study, walking on a treadmill at 1 m/s with and without the neuromuscular bandage on the peroneus and triceps surae. The results did not show any significant differences (p<0.05) in plantar pressure using the neuromuscular bandage in both muscle groups. Only the effect of this bandage applied on the triceps surae during walking showed a slight increase in contact time (p=0.045) (AU)

[Secondary restless legs syndrome].

Restless legs syndrome (RLS) is known to occur secondary to various medical conditions such as iron deficiency, pregnancy, end-stage renal disease, and neuropathy. Secondary RLS usually occurs later in the life and in the absence of a family history of RLS. Diagnosis of secondary RLS may be difficult, particularly in patients with neurological comorbidities. Sensory disturbance due to neurological disorder may mimic the symptoms of RLS symptom. In distinguishing between RLS and RLS mimics, neurophysiological findings, in addition to a detailed neurological examination, are helpful. Treatment of secondary RLS often requires management of the background medical condition. Iron supplementation is useful in patients with iron deficiency. Dopamine agonists are usually effective for both primary and secondary RLS; however, an increased dose of dopamine agonist may be necessary in some secondary RLS cases, particularly in uremic RLS. In patients with end-stage renal disease on hemodialysis, management of daytime symptoms, particularly during the hemodialysis sessions, may be necessary. Secondary RLS is still an unrecognized and underdiagnosed disorder. Medical practitioners should be aware of comorbid RLS in patients with neurological conditions that could be the cause of RLS.

Effect of creatine supplementation during cast-induced immobilization on the preservation of muscle mass, strength, and endurance.

Muscle and strength loss will occur during periods of physical inactivity and immobilization. Creatine supplementation may have a favorable effect on muscle mass and strength independently of exercise. The purpose of this study was to determine the effects of creatine supplementation on upper limb muscle mass and muscle performance after immobilization. Before the study, creatine-naïve men (n = 7; 18-25 years) were assessed for lean tissue mass (dual-energy X-ray absorptiometry), strength (1-repetition maximum [1RM] isometric single arm elbow flexion/extension), and muscle endurance (maximum number of single-arm isokinetic elbow flexion/extension repetitions at 60% 1RM). After baseline measures, subjects had their dominant or nondominant (random assignment) upper limb immobilized (long arm plaster cast) at 90 degrees elbow flexion. Using a single-blind crossover design, subjects received placebo (maltodextrin; 4 x 5 gxd-1) during days 1-7 and creatine (4 x 5 gxd-1) during days 15-21. The cast was removed during days 8-14 and 22-29. The dependent measures of lean tissue mass, strength, and endurance were assessed at baseline, postcast, and after the study. During immobilization, compared with isocaloric placebo, creatine supplementation better maintained lean tissue mass (Cr +0.9% vs. PLA -3.7%, p < 0.05), elbow flexor strength (Cr -4.1% vs. PLA -21.5%, p < 0.05), and endurance (Cr -9.6% vs. PLA -43%, p < 0.05), and elbow extensor strength (Cr -3.8% vs. PLA -18%, p < 0.05) and endurance (Cr -6.5% vs. PLA -35%, p < 0.05). These results indicate that short-term creatine supplementation attenuates the loss in muscle mass and strength during upper-arm immobilization in young men.

Force-displacement relationship during anteroposterior mobilization of the ankle joint.

OBJECTIVE: The purpose of this study was to determinate the correlation between force and displacement during passive anteroposterior mobilization of the talus and the effect of this treatment technique on ankle dorsiflexion range of motion (ROM). METHODS: This is an exploratory, methodological study. Maitland grades III and IV mobilization were applied on the right ankle of 25 healthy subjects (mean age +/- standard deviation, 25.08 +/- 3.01 years) by 2 randomized raters (A and B). Applied forces were measured using a small force plate and displayed for the rater on a computer monitor. Linear displacement of the ankle joint was quantified by a motion analysis system. Synchronization of these 2 systems was obtained by software. Dorsiflexion active ROM, before and after mobilization, was assessed using a biplane goniometer. Statistical analysis was performed using the Pearson correlation coefficient for force and displacement variables and the paired t test to compare dorsiflexion ROM mean values. RESULTS: A fair positive correlation was found between force range and displacement (r = 0.370; P = .049, 1-tailed), and a fair negative correlation was found between minimum forces and displacement (r = 0.404; P = .035, 1-tailed), only for rater A data. Significant increase in dorsiflexion was found in the right ankle (P = .035), comparing ROM before and after mobilization, which did not occur in the left ankle. CONCLUSIONS: These data do not support a linear force-displacement relationship during Maitland grades III and IV passive joint mobilization, although they confirmed an increase in ankle dorsiflexion ROM immediately after joint mobilization. The use of visual feedback may increase interrater reliability of forces applied during ankle joint mobilization.

Flexores. Avances en fisioterapia / Flexor muscles. Advances in physical therapy

Introducción. A pesar de contradecir técnicasde rehabilitación tradicionales en las que se inicianlos ejercicios pasivos para posteriormente pasara los activos, con este protocolo se pretende inmovilizarselectivamente las articulaciones más proximalespermitiendo una movilización activa de la articulacióndistal.Material y método. Hemos documentado las lesionestendinosas traumáticas tratadas en nuestro centromediante movilización activa inmediata, comparandolos resultados con un grupo control en el que se haefectuado un protocolo de movilización pasivainmediata.Conclusiones. La utilización de esta técnica permitesolucionar tres problemas simultáneamente: a) resolverla debilidad articular y de tejidos blandos; b) cambiar el patrón de movilidad activa haciéndolo más productivo,y c) movilizar el edema crónico. Cuando se intenta disminuir el estrés de una articulación mediante la utilización de ortesis fijas, estamos dando origen a una debilidad que no puede ser tratada mediante movilizaciones pasivas. Sólo se han documentado efectos negativos de la movilización pasiva; además, una mejora del movimiento pasivo no se corresponde con una mejora de la movilidad activa. Los patrones anormales de movimiento originan cambios en la corteza somatosensorial. La recuperación de la movilidad abarca una rehabilitación mecánica y una reeducación de lospatrones normales de movimiento en la corteza.El empleo de esta metodología nos permite crearpatrones de movimiento deseados sin que aparezcanmovimientos compensatorios

Introduction. In spite of contradict techniques oftraditional rehabilitation where passive exercises arebegun in order to go to the active ones later, this protocol is expected to inmobilize selectively the most proximal articulations permiting an active mobilization of the distal articulation.Material and method. we have documented thetendinous injuries treated in our centre by inmediateactive mobilization and we have checked the results witha controlled group followed by immediate passivemobilization.Conclusions. the use of this technique,allows us to solvethree problems simultaneously. a) To solve the articularweakness and soft tissues; b) to change the active mobility pattern becoming more productive, and c) tTo mobilize the chronic oedema. When it is tried to reduce the stress of an articulation through the use of fixed orthosis, we are provoking a weakness of the passive mobilization which cannot be treated with passive mobilizations.Only negative effects have been researched, also a better passive movementwhich does not correspond with a better active mobility.The abnormal patterns of movement provoke changes atthe somesthetic cortex level. The recovery of the mobility cover a mechanic rehabilitation and normal patterns of movement rehabilitation at the cortex level.Using this methodology allows us to create movementpatterns wanted without the appearance of compensatorymovements

Study of the force applied during anteroposterior articular mobilization of the talus and its effect on the dorsiflexion range of motion.

OBJECTIVE: The aim of this study was to investigate the behavior of the force applied during the Maitland grade III anteroposterior joint mobilization of the talus and its effect on dorsiflexion range of motion (ROM). METHODS: Two examiners performed measurements of dorsiflexion ROM on both ankles of healthy volunteers using a universal goniometer. The anteroposterior talus mobilization was first applied by examiner A for 30 seconds. Examiner B then repeated the same procedure. A platform was placed under the volunteer's leg to register the forces obtained during mobilization. After the procedure, examiner A assessed the ankle dorsiflexion. RESULTS: The results showed consistency regarding maximal forces applied throughout the 30 seconds of mobilization as well as low consistency upon the minimal forces. A significant increase in dorsiflexion ROM of the ankle was found immediately after joint mobilization. CONCLUSIONS: The results of the present study have shown consistent maximal forces applied by one examiner and inconsistent minimal forces during an ankle mobilization in healthy volunteers when the same examiner was compared. Moreover, the applied force was able to increase dorsiflexion ROM after the Maitland grade III anteroposterior mobilization of the talus.

Cytokine secretion and latent herpes virus reactivation with 28 days of horizontal hypokinesia.

INTRODUCTION: Hypokinesia is associated with spaceflight and prolonged illnesses and may lead to secondary immune deficiency. METHODS: The distribution of immunocytes in whole blood, mitogen-induced cytokine secretion in vitro, Epstein-Barr virus (EBV) reactivation, and plasma cortisol levels were studied in 13 healthy volunteers subjected to a horizontal bed rest (BR) regime for 28 d. Samples were collected before the study, weekly during BR, and then 3-5 d after the regime ended. Additionally, subjects were treated with hydrocortisone on the 1st and 27th d of BR to simulate the hypercortisolemia that occurs during stress. RESULTS: The factors of 28-d BR regime accompanied by acute hypercortisolemia significantly decreased the relative and absolute number of total lymphocytes, CD3+ T-cells, T-helper subset, and monocytes, but increased the percentage of the CD8+ T-cells, and NK cells at the 4th wk compared with the baseline. A significant decrease in mitogen-activated secretion of IL-2, IFN-gamma, TNF-beta, IL-6, and IL-10 was registered at the same interval. Also, secretion of IL-2 and IFN-gamma declined at the 2nd week of the BR regime. Secretion of IL-4 was significantly higher at the 2nd and 3rd weeks compared with the baseline. A significant increase in the shedding of EBV DNA in saliva was observed as early as the 3rd wk of BR. CONCLUSIONS: Stress factors associated with BR significantly alter immune responsiveness in vitro and in vivo. Changes in the cytokine secretion and cytokine imbalance precede latent EBV reactivation. PHA/LPS-activated cytokine secretion in whole blood can be used as a test system for predicting latent virus activation.

High-dose risedronate treatment partially preserves cancellous bone mass and microarchitecture during long-term disuse.

Disuse induces rapid and severe bone loss in larger mammals as a result of greatly elevated osteoclastic resorption. In this study, we tested whether risedronate (RIS), a potent inhibitor of osteoclastic activity, would effectively prevent cancellous bone loss in female beagles (5-7 years old, N = 28) subjected to single forelimb immobilization (IM) for 12 months. Age-matched, non-IM dogs served as controls (Con). Half the animals from each group received RIS 1 mg/kg p.o. daily (Con + RIS, IM + RIS). Remaining dogs received sterile water (Con, IM). Histomorphometry showed that IM caused a dramatic reduction in cancellous bone mass (-71%) of distal 2nd metacarpals, characterized by marked decreases in trabecular width (-51%) and number (-41%), and 4-fold increases in the indices of bone resorption (eroded surface, osteoclast number, and surface). Bone formation indices (calcein-labeled surface, osteoid surface, and bone formation rate) were also significantly higher in IM than in controls. Activation frequency in IM increased about 4-fold beyond control level. RIS treatment reduced, but did not abolish cancellous bone loss due to immobilization. IM animals treated with RIS lost nearly 50% of cancellous bone mass, while trabecular width and number were reduced by 31% and 25%, respectively. In both RIS-treated control and IM animals, overall bone formation parameters (mineralized bone surface fraction and bone formation rate) remained roughly at intact control levels; however, mineral apposition rate relative to intact control was reduced 40% in RIS-treated control and 86% in RIS-treated IM animals. These results indicate that high-dose RIS treatment might suppress osteoblastic function, especially under long-term disuse. Interestingly, bone resorption parameters in RIS-treated IM animals reached levels even higher than in vehicle-treated IM animals; values for eroded surface, osteoclast number, and surface were 84%, 53%, and 83% above vehicle-treated IM values, respectively. Our data indicate that risedronate treatment is partially effective in preventing cancellous bone loss during long-term disuse. Moreover, our results suggest that bisphosphonates can impair the ability of mature osteoclasts to resorb bone, but cannot overcome the strong stimulus for osteoclast recruitment caused by long-term disuse.