جستجوی مقالات مرتبط با کلیدواژه « motor activity » در نشریات گروه « پزشکی »

The sensory and mobility failure associated with spinal cord injury (SCI) is desperately complicated due to the pathological events that occur sequentially in consequent to the injury.

Herein, we applied neural stem cells, derived from human iPSCs (hiPSC-NSCs), to ameliorate the behavioral complications of contusive SCI in Rhesus monkeys, in sub-acute phase.

hiPSC-NSCs were maintained and characterized in vitro for general NSCs as well as hind-limb specific gene and protein expression prior to transplantation. Moreover, Masson's trichrome staining (MTS) in addition to luxol fast blue (LFB) were performed to determine the fibrotic scar reduction and myelination respectively. Tarlov’s scale were utilized to score the motor improvement, plus, sensory perception evaluation throughout six months following the injury.

hiPSC-NSCs were identified to own NSCs’ exclusive properties in vitro by SOX2, DCX and NESTIN in addition to NESTIN , PAX6 , SOX1 , HOXA2 and HOXB2 protein and gene expression. Additionally, hiPSC-NSCs caused remarkable depletion in fibrotic scar and enhance myelination; spinal shock, sensory responses, reflexes and motor function were improved over six months.

Our findings suggest that hiPSC-NSCs lead to promising recovery after SCI, therefore, this source of NSCs provide a therapeutic potential in clinical studies.

Viral encephalitis (VE) refers to an acute intracranial inflammation mainly caused by various viral infections.

Viral encephalitis (VE) refers to an acute inflammation of the brain primarily caused by various viral infections.

Data from 60 children with acute viral encephalitis (VE) who received 4 weeks of rehabilitation nursing from July 2019 to July 2020 were collected for retrospective analysis. These children were divided into two groups: An early intervention group (n = 30), where rehabilitation nursing started in the second week after admission, and a late intervention group (n = 30), where rehabilitation nursing began in the fourth week after admission. Motor function, daily living abilities, and limb spasticity were compared before and four weeks after nursing. Additionally, the outcomes of rehabilitation nursing—including recovery times from convulsions, cranial nerve disorders, and consciousness disorders—were also compared.

The scores for motor function and daily living ability were significantly higher, while the score for limb spasticity was lower in the early intervention group compared to the late intervention group (P < 0.05). Additionally, the early intervention group experienced a significantly shorter recovery time from convulsions, cranial nerve disorders, and consciousness disorders than the late intervention group (P < 0.05).

Early rehabilitation nursing is effective in enhancing motor function, relieving limb spasticity, and improving the nursing outcomes for children with acute viral encephalitis (VE).

This study aimed to investigate the effect of four weeks of selected endurance training on neurotrophin-3 (NT-3) and tropomyosin receptor kinase C (TrkC) gene expression in hippocampal areas of rats with spinal cord injury (SCI).

In this experimental study, the rats were separated into six equal groups. First, the animals were put under general anesthesia and had their SCI. Then, for four weeks, they were subjected to two kinds of endurance training programs. However, the control injury group received no intervention or training. Following the completion of the training regimes, molecular tests were done using the qRT-PCR technique to evaluate changes in the gene expression of NT-3 and TrkC from the animals' hippocampus.

The expression of NT-3 and TrkC genes were significantly reduced in the SCI model compared to the healthy control group, but it was increased in the SCI + exercise 1 and SCI + exercise 2 groups compared to the SCI group. NT-3 levels did not vary significantly between the SCI + exercise 1 and SCI + exercise 2 groups, although alterations in TrkC levels altered.

In addition to enhancing locomotion in animals with SCI, the endurance training regimens in this research were effective on the expression of NT-3 and TrkC genes and may play a role in axonal development and neuronal survival in SCI recovery.

The current study aims to investigate the protective effect of iron oxide nanoparticles capped with curcumin (FeONPs-Cur) against motor impairment and neurochemical changes in a rat model of Parkinson’s disease (PD) induced by reserpine.

Rats were grouped into control, PD model induced by reserpine, and PD model treated with FeONPs-Cur (8 rats/group). The open field test was used to assess motor activity. The concentration of dopamine (DA), norepinephrine (NE), serotonin (5-HT), lipid peroxidation (MDA), reduced glutathione (GSH), and nitric oxide (NO), and the activities of Na+,K+,ATPase, acetylcholinesterase (AchE), and monoamine oxidase (MAO) were determined in the midbrain and striatum. Data were analyzed by ANOVA at P-value<0.05. 

The PD model exhibited a decrease in motor activity. In the midbrain and striatum of the PD model, DA, NE, and 5-HT levels decreased significantly (P-value<0.05). However, an increase in MAO, NO, and MDA was observed. GSH, AchE and Na+,K+,ATPase decreased significantly in the two brain areas. FeONPs-Cur prevented the decline of dopamine and norepinephrine and reduced oxidative stress in both areas.  It also prevented the increased MAO activity in the two areas and the inhibited activity of AchE and Na+,K+,ATPase in the midbrain. These changes were associated with improvements in motor activity.

The present data indicate that FeONPs-Cur could prevent the motor deficits induced in the PD rat model by restoring dopamine and norepinephrine in the midbrain and striatum. The antioxidant activity of FeONPs-Cur contributed to its protective effect. These effects nominate FeONPs-Cur as an antiparkinsonian candidate.

An ankle sprain is one of the most common musculoskeletal injuries and has various complications. Various factors can predict post-injury complications, including ankle muscle strength, pain, and activity level. So far, no study has exclusively investigated the predictive role of these factors. Therefore, this study aims to investigate the role of these factors in ankle instability, functional mobility, and gait speed in individuals with ankle sprain.

This study was conducted on 140 individuals with ankle sprains who were referred to medical centers in Shiraz City, Iran. The demographic information of the patients (including the time elapsed since the sprain, etc.) was recorded by a demographic questionnaire. Related tests were also used to evaluate ankle muscle strength, pain, activity level, ankle functional instability, functional mobility, and gait speed, respectively. 

In the regression models, the predictive value for each outcome of ankle functional instability, functional mobility, and walking speed was 45.5%, 58.8%, and 65.3% of the variance, respectively. In all stepwise models, ankle muscle strength was the strongest predictor for the outcomes of functional ankle instability, functional mobility, and gait speed.

Ankle muscle strength, level of education, history of sprain in the last year, and age were the vital predictors of ankle functional instability. Muscle strength, age, and sprain status were the critical predictors of functional mobility respectively. Muscle strength, pain, age, duration of sprain, and activity level were the crucial predictors of gait speed.

Stress can alter behavioral parameters, oxidative stress markers, and electrocardiographic (ECG) records. Also, metal oxide nanoparticles can affect behavioral and oxidative stress parameters in animal models, but their effects on the physiological functions of the body in stress situations and ECG changes are not yet clear.

In this study, motor activity, ECG records, and oxidant/antioxidant balance changes were investigated following administration of nanoparticles of magnesium oxide (nano-MgO) and zinc oxide (nano-ZnO) in normal and acute restraint stressed rats.

Adult male Wistar rats were divided into 16 groups, including control (saline), restraint stress (90, 180, and 360 minutes + saline), nano-MgO, and nano-ZnO (1, 5, and 10mg/kg, intraperitoneally) groups, with or without restraint stress of 90minutes. Motor activities were evaluated by the elevated plus maze (EPM) and open field tests. Electrocardiographic parameters were evaluated in the 6 groups. Catalase (CAT) activity and malondialdehyde (MDA) level were measured in the cerebellum + brain stem and brain hemispheres of animals.

Motor activity was decreased by the stress of 90 minutes, nano-MgO 10 mg/kg, and nano-ZnO 10 mg/kg. The PR interval and ST height were decreased by the stress of 90 minutes. The QRS interval was increased by nano-MgO 5 mg/kg, and QRS amplitude, T amplitude, and ST height were decreased by nano-MgO 5mg/kg. The QT interval and QTc were increased by nano-ZnO 5mg/kg, and ST height was decreased by nano-ZnO 5 mg/kg. The PR interval, QRS interval, QTc, and QT interval were increased by nano-MgO 5 mg/kg in the stress of 90 minutes, and the heart rate (HR) and ST height were decreased by nano-MgO 5 mg/kg in the stress of 90 minutes. HR, QRS interval, and QTc were increased by nano-ZnO 5 mg/kg in the stress of 90 minutes, and T amplitude and ST height were decreased by nano-ZnO 5 mg/kg in the stress of 90 minutes. The MDA level was increased by nano-MgO and nano-ZnO in the brain hemisphere and cerebellum + brain stem, and CAT activity was decreased by nano-MgO and nano-ZnO in the brain hemisphere and cerebellum + brain stem. The MDA level was increased by the restraint stress of 360 minutes in the cerebellum + brain stem while it was not changed in the brain hemispheres.

It seems that the side effects of these nanoparticles on motor activity could be related to the imbalance of oxidant/antioxidant systems in the cerebellum + brain stem. Also, it is possible that nanoparticles increase the effects of acute stress on changes in ECG parameters.

Neuroinflammation and oxidative stress play critical roles in the pathophysiology of Parkinson’s disease (PD), and neuroprotective agents could be helpful to slow down the dopaminergic neurodegeneration. Neuroprotective and antioxidant properties of exercise and sesamol have been previously reported. The current research evaluated the influences of sesamol and exercise on memory and motor impairments, oxidative stress and inflammatory markers in an experimental model of PD.

6-hydroxydopamine (6-OHDA) was microinjected into the medial forebrain bundle of male rats. Treatment with sesamol (50mg/kg) or treadmill exercise was performed for 7 weeks. Behavioral and biochemical assessments were performed at the end of 6th week after 6-OHDA injection.

Net number of rotations and tumor necrosis factor (TNF)-α level was significantly enhanced in 6-OHDA group in comparison with sham group. Also, step-through latency was decreased in this group along with increased lipid peroxidation and decreased total thiol levels in the hippocampus. Moreover, sesamol and exercise, alone or in combination, improved rotational behavior, which was accompanied by decreased striatal TNF-α level. However, sesamol and/or treadmill exercise had no effect on aversive memory, although exercise enhanced hippocampal total thiol level.

Beneficial properties of sesamol and treadmill exercise for amelioration of motor impairments might be due to their anti-inflammatory activities.

The main aim of the study was to identify selected factors that determine patients with multiple sclerosis (MS’) failure to take home therapeutic exercises (HTE) and other physical activity (OPA).

The study was conducted using a self‑completed online survey that was aimed at adult people diagnosed with MS, registered on the portal TacyJakJa.pl. In total, 335 persons were involved.

Almost half of all people who completed the survey (49.9%), reported that no one encouraged them to use HTE, and only 16.1% were encouraged by their doctor. As many as 51% of the respondents reported also that no one encouraged them to undertake OPA, and only 18.5% were encouraged by their doctor. As the most important reason for not using HTE, the respondents chose fear that exercises may worsen their condition (47.3%). However, the most important reason for not using the OPA was high fatigue (61.9%). The number of people exercising at home increased with age (P = 0.013). Those surveyed with relapsing–remitting MS significantly more often (P = 0.002) took up OPA (60.7%) than the respondents with a secondary progressive MS (10.0%) and a primary progressive (4.4%).

Physicians relatively rarely encourage patients with MS to undertake HTE and OPA. The patients do not perform HTE primarily because of fears of health deterioration or fatigue. Undertaking HTE is influenced by age but undertaking other forms of physical activity by the type of MS. Actions should be taken to popularize HTE and OPA, especially HTE among young patients.

Astrocyte dysfunction is the common pathology failing astrocyte-neuron interaction in neurological diseases, including Parkinson’s Disease (PD). The present study aimed to evaluate the impacts of astrocytic dysfunction caused by striatal injections of selective glial toxin L-Aminoadipic Acid (L-AA) on the rats’ locomotor activity in normal conditions and under alpha-methyl-p-tyrosine depletion of catecholamines synthesis.

Thirty-three male Wistar rats were used in the experiments. Intrastriatal L-AA injections (100 µg) were performed into the right striatum. Alpha-methyl-p-tyrosine (a-MT, 100 mg/kg, inhibitor of tyrosine hydroxylase) was intraperitoneally injected for catecholamine depletion. The animals were divided into 5 groups, as follows: 1. L-AA treated (n=7), 2. L-AA+a-MT treated (n=5), 3. Sham-operated (n=7), 4. Sham+a-MT treated (n=5), 5. Intact control (n=9). For assessing motor function, open field and beam walking tests were used on the third day after the operation. Neuronal and astrocyte markers (glial fibrillary acidic protein, glutamine synthetase, tyrosine hydroxylase, & neuronal nuclear antigen) were examined in the striatum by immunohistochemistry.

Administrating L-AA led to astrocytic degeneration in the striatum. No neuronal death and disruption of dopaminergic terminals were detected. L-AA and a-MT-treated animals’ distance traveled was significantly (P=0.047) shorter than the Sham-operated group injected with a-MT. In the walking beam test, the number of unilateral paw slippings was significantly (P<0.01) higher in the L-AA-treated group than Sham-operated animals. Administrating a-MT alone and L-AA did not change rats’ performance in walking beam tests.

Astrocyte ablation in dopamine depleted striatum resulted in reduced motor activity and asymmetrical gait disturbances. These findings demonstrated the role of astroglia in motor function regulation in the nigrostriatal system and suggest the possible association of glial dysfunction with motor dysfunction in PD.

Methylphenidate (MPH), as a central nervous system stimulant, is often used to manage hyperactive disorders. The literature is scarce regarding the behavioral consequences of chronic MPH treatment and the role of involved receptors. Thus, in the current study involved receptors in MPH induced-anxiety, depression and motor activity disorders were evaluated.

Seventy rats were randomly distributed to seven groups (n = 10, per group); they were treated with normal saline, Domoic acid (DOM) (as AMPA/kainite receptor agonist), Bicuculline (BIC) (as GABAA receptor antagonist), Ketamine (KET) (as NMDA receptor antagonist ), Yohimbine (YOH) (as Alpha-2 adrenergic receptor antagonist), or Haloperidole (HAL) (as D2 dopamine receptor antagonist), simultaneously with MPH (10 mg/kg). On days 11, 17 and 24, some standard behavior tests including Elevated Plus Maze (EPM), Forced Swim Test (FST) and Open Field Test (OFT) were used to investigate anxiety, depression and motor activity disturbances, respectively.

Our study indicated that pretreatment of rats with KET, HAL and YOH abolished MPH induced - mood and motor activity disturbances. 

 MPH by interacting with Dopaminergic, NMDA and ɑ2-adrenergic receptors induces anxiety, depression and motor activity disorders.

The major secondary complications of spinal cord injury (SCI) are neuropathic pain and motor dysfunction, which remained medical challenges for clinicians. Due to the major role of glutamate in excitotoxicity and central sensitization, the present experiment was to evaluate the effects of ketamine (KET), an n-methyl-D-aspartate (NMDA) receptor blocker, on sensory-motor functions in a rat model of clip compression SCI.

Wistar rats were divided into sham, SCI and KET-treated groups. The sham group received laminectomy without any compression lesion. KET and SCI groups were subjected to severe compression injury for 1min with an aneurysm clip and then treated with KET (10mg/kg) or 5% dimethyl sulfoxide (as vehicle), respectively. The rats were assessed by pain-related and motor behavioral tests inclusive of von Frey, acetone drop, hot plate, inclined plane and Basso-Beattie-Bresnahan on day 0 prior to the injury and the 7th, 14th, 21st and 28th days following SCI.

KET group compared with the SCI group showed a significant decline in the mechanical allodynia on the 21st and 28th days, and in cold allodynia from the 1st week to the 4th week post-injury. KET treatment improved the motor function but not weight loss and auricle temperature rise during the 4 weeks of follow up from the 1st week until the 4th week.

It was ultimately attained that the advantageous effects of intrathecal KET on sensory-motor dysfunction of SCI rats could provide new approaches for KET as a neuroprotective agent toward clinical applications.

The neuroprotective effects of duloxetine and neurodegenerative effects of methamphetamine have been shown in previous studies, but their exact mechanism remain unclear. In the current study it involved molecular mechanisms of neuroprotective effects of duloxetine against methamphetamine induced neurodegeneration were clarified.

About 40 adult male rats randomly were divided to 5 groups. Group 1 and 2, as control and methamphetamine treated, received normal saline and methamphetamine (10 mg/kg) respectively. Groups 3, 4 and 5 concurrently treated with methamphetamine and duloxetine at doses of 10, 20 and 30 mg/kg respectively. All treatments were undertaken for 21 days. On day 22 Open Field Test (OFT) were used to examine the level of motor activity disturbance and anxiety in animals. After that hippocampus was isolated from each rat and oxidative, antioxidant, inflammatory factors and also level or expression of total and phosphorylated forms of CREB and P‑CREB and BDNF proteins were measured.

Duloxetine in all mentioned doses could inhibit the effects of methamphetamine induced motor activity disturbance in MWM. Chronic abuse of methamphetamine could increase malondialdehyde (MDA), tumor necrosis factor‑Alpha (TNF‑α) and interleukine‑1beta (IL‑1β) while caused decreases in superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GR) activities and decreased CREB (both forms) and BDNF proteins, while duloxetine could prevent these malicious effects of methamphetamine.

We conclude that P‑CREB/ BDNF signaling pathways might have critical role in duloxetine neuroprotective effects against methamphetamine induced neurodegeneration.

Regarding the many applications of nanomaterials in various industries and the existence of many hypotheses on the harmful effects of nanoparticles on living things, the research in this field is of great significance. Thus, the present study aimed to investigate the effect of zinc and vitamin C nanoparticles as antioxidants and administration both on locomotor activity and anxiety.

In this experimental study, rats were divided into seven groups including one saline group and six treatment groups. Zinc oxide nanoparticles (ZnO) were injected intraperitoneally in six groups at three concentrations of 1.25, 2.5, 5 mg/kg and vitamin C at three concentrations of 30, 60 and 120 mg/kg. At the end of the prescription period, the number of lines crossed in the open field test for motor activity and the number of stools for anxiety in each group were evaluated over a 5-min period.

Prescription of different doses of ZnO and vitamin C did not indicate any significant change in motor activity compared to the saline group. The injection of 30 and 120 mg/kg of vitamin C decreased the number of defecation (anxiety) compared to the saline group (P < 0.001and P < 0.01, respectively) and also significant decrease was observed at 5 and 1.25 mg/kg doses of ZnO compared to the saline group (P < 0.001).

Based on these observations, vitamin C and ZnO reduced anxiety but had no effect on the motor activity of animals.

Frequent and regular exercises in the first six months of stroke may cause return of a significant portion of sensory and motor function of patients. This study aimed to examine the effects of passive range of motion exercise in the acute phase after stroke on motor function of the patients. A randomized controlled trial study was conducted. The patients with first ischemic stroke were randomly allocated to either experimental (n=33) or control (n=19) group. Passive range of motion exercises was performed in the experimental group during the first 48 hours of admission as 6 to 8 times of 30 minute exercise. Before intervention, and one and three months after intervention, motor function were measured by muscle strength grading scale (Oxford scale) and compared. SPSS version 13.0 for Windows was used for statistical analysis. Frequency distribution was used to describe the data. For comparisons, paired t-test, independent t-test was used, and repeated measures test was used. In acute phase, the intervention in the experimental group led to significant improvement of motor function between the first and third month in both the upper and lower extremities. In control group, improvement was observed only in the muscle strength of upper extremity in the first and third month compared to pre-intervention measurement. The greatest improvement was observed in the interval from base to one month in the upper extremity, and base to the first month and the first to the third month in the lower extremity. It is recommended to use early passive range of motion exercise as part of care for people with stroke during the acute phase of the disease.