Vanadium exposure-induced striatal learning and memory alterations in rats

Occupational and environmental exposure to vanadium has been associated with toxicities in reproductive, respiratory, and cardiovascular systems. The knowledge on whether and how vanadium exposure caused neurobehavioral changes remains incomplete. This study was designed to investigate the changes in learning and memory following drinking water exposure to vanadium, and to conduct the preliminary study on underlying mechanisms. Male Sprague-Dawley rats were exposed to vanadium dissolved in drinking water at the concentration of 0.0, 0.5, 1.0 and 2.0 g/L, as the control, low-, medium-, and high- dose groups, respectively, for 12 weeks. The results by the Morris water maze test showed that the time for the testing animal to find the platform in the high exposed group was increased by 82.9% and 49.7%, as compared to animals in control and low-dose groups (p < 0.05). There were significantly fewer rats in the medium- and high- dose groups than in the control group who were capable of crossing the platform (p < 0.05). Quantitation of vanadium by atomic absorption spectrophotometry revealed a significant dose-dependent accumulation of vanadium in striatum (r = 0.931, p < 0.01). Histopathological examination further demonstrated a degenerative damage in vanadium-exposed striatum. Interestingly, with the increase of the dose of vanadium, the contents of neurotransmitter ACh, 5-HT and GABA in the striatum increased; however, the levels of Syn1 was significantly reduced in the exposed groups compared with controls (p < 0.05). These data suggest that vanadium exposure apparently reduces the animals’ learning ability. This could be due partly to vanadium’s accumulation in striatum and the ensuing toxicity to striatal structure and synaptic plasticity. Further research is warranted for mechanistic understanding of vanadium-induced neurotoxicity.     

Low intensity microwave radiation induced oxidative stress,inflammatory response and DNA damage in rat brain

Over the past decade people have been constantly exposed to microwave radiation mainly from wireless communication devices used in day to day life. Therefore, the concerns over potential adverse effects of microwave radiation on human health are increasing. Until now no study has been proposed to investigate the underlying causes of genotoxic effects induced by low intensity microwave exposure. Thus, the present study was undertaken to determine the influence of low intensity microwave radiation on oxidative stress, inflammatory response and DNA damage in rat brain. The study was carried out on 24 male Fischer 344 rats, randomly divided into four groups (n = 6 in each group): group I consisted of sham exposed (control) rats, group II–IV consisted of rats exposed to microwave radiation at frequencies 900, 1800 and 2450 MHz, specific absorption rates (SARs) 0.59, 0.58 and 0.66 mW/kg, respectively in gigahertz transverse electromagnetic (GTEM) cell for 60 days (2 h/day, 5 days/week). Rats were sacrificed and decapitated to isolate hippocampus at the end of the exposure duration.Low intensity microwave exposure resulted in a frequency dependent significant increase in oxidative stress markers viz. malondialdehyde (MDA), protein carbonyl (PCO) and catalase (CAT) in microwave exposed groups in comparison to sham exposed group (p < 0.05). Whereas, levels of reduced glutathione (GSH) and superoxide dismutase (SOD) were found significantly decreased in microwave exposed groups (p < 0.05). A significant increase in levels of pro-inflammatory cytokines (IL-2, IL-6, TNF-α, and IFN-γ) was observed in microwave exposed animal (p < 0.05). Furthermore, significant DNA damage was also observed in microwave exposed groups as compared to their corresponding values in sham exposed group (p < 0.05). In conclusion, the present study suggests that low intensity microwave radiation induces oxidative stress, inflammatory response and DNA damage in brain by exerting a frequency dependent effect. The study also indicates that increased oxidative stress and inflammatory response might be the factors involved in DNA damage following low intensity microwave exposure.     

Reduced expression of PARK2 in manganese-exposed smelting workers

Manganese (Mn) is widely used in modern industries. Occupational exposure to Mn is known to cause clinical syndromes similar, but not identical to, Parkinson’s disease. This human cohort study was designed to investigate if workers exposed to Mn altered the PARK2 gene expression, leading to Mn-induced neurotoxicity. Workers (n = 26) occupationally exposed to Mn were recruited from a Mn-iron (Fe) alloy smelter, and control workers (n = 20) without Mn-exposure were from an Fe smelter from Zunyi City in China. Subjects were matched with socioeconomic status and background for environmental factors. Metal concentrations were determined by atomic absorption spectrophotometry (AAS). Total RNA from the blood samples was isolated and analyzed by RT-PCR to quantify PARK2. The data showed that Mn concentrations in plasma, red blood cell (RBC) and saliva, and the cumulative Mn-exposure were about 2.2, 2.0, 1.7 and 3.0 fold higher, respectively, in Mn-exposed workers than those in control subjects (p < 0.01). The expression of PARK2 in Mn-exposed workers was significantly decreased by 42% as compared to controls (p < 0.01). Linear regression analysis further established that the expression of PARK2 mRNA was inversely correlated with Mn levels in plasma, RBC and saliva, as well as the cumulative Mn exposure (p < 0.01). Taken together, it seems likely that Mn exposure among smelters may lead to a reduced expression of PARK2, which may partly explain the Mn-induced Parkinsonian disorder.     

Acute exposure to a Mn/Zn ethylene-bis-dithiocarbamate fungicide leads to mitochondrial dysfunction and increased reactive oxygen species production in Caenorhabditis elegans

Mn/Zn ethylene-bis-dithiocarbamate (Mn/Zn-EBDC) fungicides are among some the most widely-used fungicides in the world. Although they have been available for over 50 years, little is known about their mechanism of action in fungi, or their potentially toxic mechanisms in humans. To determine if exposure of Caenorhabditis elegans (C. elegans) to a representative fungicide (Manzate; MZ) from this group inhibits mitochondria or produces reactive oxygen species (ROS), we acutely (30 min) exposed worms to various MZ concentrations. Initial oxygen consumption studies showed an overall statistically significant decrease in oxygen consumption associated with addition of Complex I- and/or II-substrate in treatment groups compared to controls (*p < 0.05). In order to better characterize the individual complex activity, further studies were completed that specifically assessed Complex II or Complex IV. Data indicated that neither of these two complexes were targets of MZ treatment. Results from tetramethylrhodamine ethyl ester (proton gradient) and ATP assays showed statistically significant reductions in both endpoints (*p < 0.05, **p < 0.01, respectively). Additional studies were completed to determine if MZ treatment also resulted in increased ROS production. These assays provided evidence that hydrogen peroxide, but not superoxide or hydroxyl radical levels were statistically significantly increased (*p < 0.05). Taken together, these data indicate exposure of C. elegans to MZ concentrations to which humans are exposed leads to mitochondrial inhibition and concomitant hydrogen peroxide production. Since mitochondrial inhibition and increased ROS are associated with numerous neurodegenerative diseases, we suggest further studies to determine if MZ catalyzes similar toxic processes in mammals.     

Individuals with intellectual disability have lower voluntary muscle activation level

The aim of this study was to explore the voluntary activation level during maximal voluntary contraction (MVC) in individuals with intellectual disability (ID) versus individuals without ID using the twitch interpolation technique. Ten individuals with mild ID (ID group) and 10 sedentary men without ID (control group) participated in this study. The evaluation of neuromuscular function consisted in three brief MVCs (3 s) of the knee extension superimposed with electrical nerve stimulation (NES) to measure voluntary activation. Muscle activity levels were also measured with surface EMG. The root mean square (RMS) was extracted from the EMG signal. The RMS/Mmax ratio and the neuromuscular efficiency (NME) were calculated. Our results reported that individuals with ID present lower muscle strength (p < 0.001), lower voluntary activation level (p < 0.001), lower RMS values of vastus lateralis (p < 0.05), vastus medialis (p < 0.05), and rectus femoris (p < 0.001) muscles. In addition, our results showed lower RMS/Mmax values in the ID group than in the control group for the VM (0.05 ± 0.01 mV vs. 0.04 ± 0.01 mV; p < 0.05) and the RF (0.06 ± 0.02 mV vs. 0.05 ± 0.02 mV; p < 0.05) muscles. However, no significant difference was reported for the VL muscle (0.05 ± 0.02 mV vs. 0.05 ± 0.02 mV; p = 0.463). Moreover, Individuals with ID present smaller potentiated twitch (p < 0.001). However, no significant difference was reported in the NME ratio. These results suggest that the lower muscle strength known in individuals with ID is related to a central nervous system failure to activate motor units and to some abnormal intrinsic muscle properties. It seems that the inactive lifestyle adopted by individuals with ID is one of the most important factors of their lower voluntary activation levels. Therefore, physical activities should be introduced in life style of individuals with ID to improve their neuromuscular function.     

Ectonucleotidase and acetylcholinesterase activities in synaptosomes from the cerebral cortex of streptozotocin-induced diabetic rats and treated with resveratrol

The aim of the present study was to investigate the effects of resveratrol (RV), an important neuroprotective compound on NTPDase, 5′-nucleotidase and acetylcholinesterase (AChE) activities in cerebral cortex synaptosomes of streptozotocin (STZ)-induced diabetic rats. The animals were divided into six groups (n = 8): control/saline; control/RV 10 mg/kg; control/RV 20 mg/kg; diabetic/saline; diabetic/RV 10 mg/kg; diabetic/RV 20 mg/kg. After 30 days of treatment with resveratrol the animals were sacrificed and the cerebral cortex was removed for synaptosomes preparation and enzymatic assays. The results demonstrated that NTPDase and 5′-nucleotidase activities were significantly increased in the diabetic/saline group (p < 0.05) compared to control/saline group. Treatment with resveratrol significantly increased NTPDase, 5′-nucleotidase activities in the diabetic/RV10 and diabetic/RV20 groups (p < 0.05) compared to diabetic/saline group. When resveratrol was administered per se there was also an increase in the activities of these enzymes in the control/RV10 and control/RV20 groups (p < 0.05) compared to control/saline group. AChE activity was significantly increased in the diabetic/saline group (p < 0.05) compared to control/saline group. The treatment with resveratrol prevented this increase in the diabetic/RV10 and diabetic/RV20 groups. In conclusion, this study demonstrated that the resveratrol interfere with the purinergic and cholinergic neurotransmission by altering NTPDase, 5′-nucleotidase and AChE activities in cerebral cortex synaptosomes of diabetic rats. In this context, we can suggest that resveratrol should be considered potential therapeutics and scientific tools to be investigated in brain disorders associated with the diabetes.     

Assessment of physical fitness and exercise tolerance in children with developmental coordination disorder

Children with developmental coordination disorder (DCD) have been shown to be less physically fit when compared to their typically developing peers. The purpose of the present study was to examine the relationships among body composition, physical fitness and exercise tolerance in children with and without DCD. Thirty-seven children between the ages of 7 and 9 years participated in this study. Participants were classified according to results obtained on the Movement Assessment Battery for Children (MABC) and were divided in 2 groups: 19 children with DCD and 18 children without DCD. All children performed the following physical fitness tests: The five-jump test (5JT), the triple-hop distance (THD) and the modified agility test (MAT). Walking distance was assessed using the 6-min walking test (6MWT). Children with DCD showed higher scores than children without DCD in all MABC subscale scores, as well as in the total score (p < 0.001). Participants with DCD were found to perform significantly worse on the MAT (p < 0.001), the THD (p < 0.001) and 5JT (p < 0.05). Moreover, children with DCD had poorer performance on the 6MWT than children without DCD (p < 0.01). Our results found significant correlations among body mass index (BMI), THD (r = 0.553, p < 0.05), 5JT (r = 0.480, p < 0.05) and 6MWT (r = 0.544, p < 0.05) only in DCD group. A significant correlation between MAT and 5JT (r = −0.493, p < 0.05) was found. Similarly, THD and 5JT (r = 0.611, p < 0.01) was found to be correlated in children with DCD. We also found relationships among 6MWT and MAT (r = −0.522, p < 0.05) and the 6MWT and 5JT (r = 0.472, p < 0.05) in DCD group. In addition, we found gender specific patterns in the relationship between exercise tolerance, explosive strength, power, DCD, and BMI. In conclusion, the present study revealed that BMI was indicative of poorer explosive strength, power and exercise tolerance in children with DCD compared to children without DCD probably due to a limited coordination on motor control.     

Attention,locomotor activity and developmental milestones in rats prenatally exposed to ethanol

RationaleDecline of attentional performance as a function of time engaged on a task and hyperactivity are features shared by children and adults with fetal alcohol syndrome or attentional deficit and hyperactivity disorders.ObjectiveTo investigate the effects of prenatal exposure to two doses of ethanol on developmental milestones, locomotor activity and attention.MethodsWistar rats born from dams exposed to one of four maternal treatments during pregnancy were used: A35 – liquid diet with 35% ethanol-derived calories; A10 – liquid diet with 10% ethanol-derived calories; control – ethanol-free liquid diet; chow – laboratory chow and water.ResultsA35 performed worse in grip strength than control and chow (postnatal day – 14, p < 0.05) but not in negative geotaxis (postnatal days 7–10); A35 also showed more locomotor activity than control and A10 (p < 0.05). Regarding attention, acquisition of the five choice reaction time task was similar between groups, but, the percentage of omission errors from A35 group was greater than other groups at baseline parameters, at shorter (2 s) and longer (7 s) inter-trial intervals and at a shorter stimulus duration (0.5 s) (p < 0.05). The percentage of omissions was larger in A35 as the blocks progressed in sessions with either longer or shorter inter-trial intervals (group × block p < 0.05). Animals from A10 group did not show any impairment in the tasks performed.ConclusionsOur study demonstrates that as well as developmental impairments, prenatal ethanol can produce deficits associated with an increase in attentional demand in rodents, analogous to those observed in fetal alcohol syndrome and attentional deficit and hyperactivity disorders.     

Evaluation of neuroprotection by melatonin against adverse effects of prenatal exposure to a nonsteroidal anti-inflammatory drug during peripheral nerve development

The potential ability of melatonin to protect against impairment of the fetal peripheral nerve system due to maternal consumption of diclofenac sodium (DS) was investigated. Eighty-four pregnant rats were divided into seven groups: control (CONT), saline administered (PS), DS administered (DS), DS with low-dose melatonin administered (DS + MLT10), DS with high-dose melatonin administered (DS + MLT50), low-dose melatonin administered (MLT10), and high-dose melatonin administered (MLT50). After the pregnancy, six male newborn rats from each group were sacrificed at 4 and 20 weeks of age. Their right sciatic nerves were harvested, and nerve fibers were evaluated using stereological techniques. Mean numbers of myelinated axons, axon cross-section areas and the mean thickness of the myelin sheet were estimated. Four-week-old prenatally DS-exposed rats had significantly fewer axons, a smaller myelinated axonal area, and a thinner myelin sheath compared to CONT group (p < 0.05). Although melatonin at both doses significantly increased axon numbers, only a high dose of melatonin increased the diameter of those axons (p < 0.05). At 20-weeks of age, myelinated axon number in the DS group was not only significantly lower than all other groups (p < 0.05) but also the cross-sectional area of these axons was smaller than all other groups (p < 0.05). There were no differences between the groups regarding the mean thickness of the myelin sheet. The current study indicates that prenatal exposure to DS decreases the number and the diameter of sciatic nerve axons and that melatonin prophylaxis can prevent these effects.     

Caenorhabditis elegans chronically exposed to a Mn/Zn ethylene-bis-dithiocarbamate fungicide show mitochondrial Complex I inhibition and increased reactive oxygen species

Reports have linked human exposure to Mn/Zn ethylene-bis-dithiocarbamate (Mn/Zn-EBDC) fungicides with multiple pathologies, from dermatitis to central nervous system dysfunction. Although members of this family of agrochemicals have been available for over 50 years, their mechanism of toxicity in humans is still unclear. Since mitochondrial inhibition and oxidative stress are implicated in a wide variety of diseases, we hypothesized that Caenorhabditis elegans (C. elegans) exposed to a commercially-available formulation of an Mn/Zn-EBDC-containing fungicide (Manzate; MZ) would also show these endpoints. Thus, worms were treated chronically (24 h) with various MZ concentrations and assayed for reduced mitochondrial function and increased levels of reactive oxygen species (ROS). Oxygen consumption studies suggested Complex I inhibition in all treatment groups compared to controls (^**p < 0.01). In order to verify these findings, assays specific for Complex II or Complex IV activity were also completed. Data analysis from these studies indicated that neither complex was adversely affected by MZ treatment. Additional data from ATP assays indicated a statistically significant decrease (^***p < 0.001) in ATP levels in all treatment groups when compared to control worms. Further studies were completed to determine if exposure of C. elegans to MZ also resulted in increased ROS concentrations. Studies demonstrated that hydrogen peroxide, but not superoxide or hydroxyl radical, levels were statistically significantly increased (*p < 0.05). Since hydrogen peroxide is known to up-regulate glutathione-S-transferase (GST), we used a GST:green fluorescent protein transgenic worm strain to test this hypothesis. Results from these studies indicated a statistically significant increase (^***p < 0.001) in green pixel number following MZ exposure. Taken together, these data indicate that C. elegans treated with MZ concentrations to which humans are exposed show mitochondrial Complex I inhibition with concomitant hydrogen peroxide production. Since these mechanisms are associated with numerous human diseases, we suggest further studies to determine if MZ exposure induces similar toxic mechanisms in mammals.     

Assessment of COVID-19 trauma responses. Who has been more traumatized during the pandemic?

Background and ObjectiveTo evaluate the effect of cognitive and sociodemographic characteristics of healthcare and non-healthcare workers on their traumatic responses to the COVID-19 pandemic.MethodsData were collected using an online survey between August-September 2020. The survey included the following scales: Beck Anxiety Inventory (BAI), Anxiety Sensitivity Index (ASI), and Impact of Event Scale-Revised (IES-R). Traumatic responses were categorized into three types: avoidance (IES-R_A), intrusion (IES-R_I), and hyperarousal (IES-R_H).ResultsThe study included a total of 672 participants, comprised of 399 (59.4%) men, and 273 (40.6%) women with a mean age of 39.25 ± 933 years. The results indicated that women had higher IES-R_I (r = .5.78, p < 0.001), IES-R_A (r = 4.47, p < 0.001), and IES-R_H (r = .5.20, p < 0.001) scores compared to men. Patients with a history of psychiatric diseases had significantly higher IES-R_I (r = ?3.82, p < 0.001), IES-R_A (r = ?2.00, p < 0.05), and IES-R_H (r = ?4.06, p < 0.001) scores compared to patients with no history of psychiatric diseases. Non-healthcare workers had significantly higher IES-R_A (r = ?2.69, p < 0.01) scores compared to healthcare workers.ConclusionFemale gender and a positive history of psychiatric diseases were found to lead to an increase in the frequency of all three traumatic responses to COVID-19. Contrary to expectation, being a healthcare worker was not found as a factor facilitating trauma response formation in our study.     

An association between neuropeptide Y levels and leukocyte subsets in stress-exacerbated asthmatic mice

Neuropeptide Y (NPY) was recently proposed to be associated with stress and airway inflammation; however, this has rarely been studied in animal models of asthma. Twenty-four C57BL/6 mice were randomly divided into 3 groups of 8 each: naive control group, asthma group (with an established asthma model), and stressed asthma group (with established asthma and stress models). Bronchoalveolar lavage (BAL) fluid was collected for total cell counts using a hemocytometer and for cytological examinations by Wright stain. Differential inflammatory cell counts were performed to identify eosinophils, macrophages, neutrophils, and lymphocytes. NPY and corticosterone serum levels were determined with enzyme immunoassay kits. Stress was associated with increased airway inflammatory response, which was manifested by the accumulation of total leukocytes and eosinophils in the BAL fluid in comparison with the asthma and the control groups. The levels of NPY (p < 0.05) and corticosterone (p < 0.01) were elevated in the stressed asthma group in comparison with the control and asthma groups. The concentration of NPY and corticosterone positively correlated with the total leukocyte count (r = 0.892, p < 0.05 and r = 0.937, p < 0.01 respectively) and eosinophil numbers (r = 0.806, p = 0.053 and r = 0.885, p < 0.01 respectively).Stress may be associated with elevated peripheral NPY level, which was observed to be associated with exacerbated airway inflammation in asthmatic mice.     

Nitrous oxide related behavioral and histopathological changes may be related to oxidative stress

Nitrous oxide (N₂O) toxicity can result in myelin loss and hyperhomocysteinemia similar to cobalamin (Cbl) deficiency. Studies on N₂O exposure can help in understanding the mechanism of demyelination. In view of paucity of studies on N₂O toxicity in rats this study was undertaken. Six male wistar rats were exposed to 1.5 L/min N₂O with 1:1 O₂ for 90 min daily for 1 month. After 1-month exposure blood homocysteine (HCY) and oxidative stress parameters glutathione (GSH) and total antioxidant capacity (TAC) were measured. Brain and spinal cord was subjected to histopathological examination. The neurobehavioral changes, oxidative stress parameters and histopathological changes were correlated with serum B12 and HCY level. After 1-month exposure, the rats appeared sluggish, lethargic and developed predominantly hind limb weakness for 1–1.5 h. In the exposed group, the total distance traveled (2001.66 ± 118.27 cm; p = 0.037), time moving (80.16 ± 5.7 s; p = 0.028), number of rearing (10.33 ± 1.45; p = 0.014) and grip strength (1042.40 ± 51.3 N; p = 0.041) were significantly decreased whereas, resting time significantly increased (219.83 ± 5.7 s; p = 0.030) compared to controls. Serum HCY level was significantly increased (20.56 ± 1.296 μm/ml; p = 0.0007) in the exposed group. However, serum B12 and folic acid levels were not significantly different. GSH significantly decreased (2.21 ± 0.60 mg/dl; p = 0.018) along with TAC (0.76 ± 0.16 Trolox_Eq_mmol/l; p = 0.036). The histopathological studies revealed shrinkage and vacuolation of neurons in cerebral cortex, focal myelin loss, vacuolation in subcortical white matter and spinal cord. N₂O exposure results in behavioral alterations, hyperhomocysteinemia, cortical and spinal cord demyelination which were associated with decrease GSH and TAC highlighting pathophysiological role of oxidative stress.     

The role of PON1 and CYP2D6 genes in susceptibility to organophosphorus chronic intoxication in Egyptian patients

BackgroundParaoxonase-1 (PON1) activity toward organophosphorus(OP) compounds shows inter-individual variations, rendering the identification of individuals’ PON1 allozymes valuable in treating patients suffering from organophosphorus intoxication. One of the most important cytochrome P450 monooxygenases (CYPs) is CYP2D6. The CYP2D6 G1934A polymorphism leads to good, poor or no enzyme activity. Genetic testing helps identification of high risk individuals as well as management of chronic intoxicated patients.Objectiveto investigate a possible association between genetic polymorphisms of PON1 Q192R, and CYP2D6 G1934A as well as PON1 and pseudo-cholinesterase (PChE) enzyme activity levels and chronic organophosphate exposed patients, and hence, susceptibility for organophosphorus chronic poisoning.Design and methodsThirty chronic organophosphate exposed farm workers were compared to 29 healthy controls as regards PON1 Q192R and CYP2D6 G1934A polymorphisms using PCR-RFLP technique. Also serum PON1 and PChE activities were determined spectrophotometrically.ResultsSerum PChE was significantly reduced in chronic intoxicated patients compared to the control group (p = 0.02), while PON1 activity was increased, but just failed to reach significance (p = 0.06). PON1 192 RR genotype and R allele were significantly increased in chronic OP intoxicated patients (p = 0.005 & p = 0.002 respectively). CYP2D6 1934 A allele was significantly increased in chronic OP patients (p = 0.045). combining the two SNPs showed a significant statistical difference between the two groups with PON1QQ and CYP2D6 GG genotypes being more represented in the healthy controls (p = 0.001). Fatigue and motor weakness were the most prevalent neurological symptoms seen in chronic cases (56.7%), followed by headache and lacrimation (30% each), depression (23%), tingling and sensory symptoms (20%), sleep disorders and limb pain (13%).The mean duration of environmental exposure to organophosphates was 7.7 ± 5.2 years and no association was found between chronic symptoms of intoxication and duration of exposure, provided that all workers were exposed for at least 3 years.ConclusionPON1 192RR genotype and CYP2D6 1934 A allele were found to be related to the susceptibility to organophosphate chronic toxicity in Egyptians. Larger scale gene-environmental interaction studies are recommended to confirm results and Genotyping is recommended during selection of agricultural pesticide workers to exclude high risk group.     

Sensorimotor function in preschool-aged children with expressive language disorder

AimThe aim of the study was to evaluate functional motor performance and haptic object recognition in 5-year-old children with mild expressive language disorder (ELD) in comparison with age- and gender-matched healthy children.MethodsThe subjects were classified by speech-language pathologist using The Reynell Developmental Language Scales III and Boehm Test of Basic Concepts: Preschool as children with mild ELD (n = 29, incl. 23 boys and 6 girls) and children with typical language development as controls (n = 29, incl. 23 boys and 6 girls). The children were examined for manual dexterity, ball skills, static and dynamic balance by Movement-ABC, haptic object recognition (HOR), hand-grip strength (HGS) and vertical jumping performance.ResultsChildren with mild ELD demonstrated significantly higher scores (i.e., inferior performance) in all subtests of M-ABC (all p values <0.05), in haptic object recognition (p < 0.01) and vertical jumping height (p < 0.05) compared to controls. However, no statistically significant differences (p > 0.05) emerged from HGS. Boys with mild ELD demonstrated higher results in impairment score (p < 0.001), ball skills (p < 0.01) and balance (p < 0.01) of M-ABC, as well as in HOR (p < 0.05). Girls with mild ELD showed higher impairment score (p < 0.05) with lower percentile (p < 0.05) in M-ABC, indicating inferior motor performance, and lower HGS for the non-dominant hand (p < 0.05). Seven out of 29 (24.1%) children with mild ELD had definite or borderline motor difficulties, while only one child in control group (3.4%) demonstrated borderline motor difficulties.ConclusionsChildren with mild expressive language disorder do not perform as well as controls in tests of functional motor skills, but their results in tests demanding maximal muscle force generation are in level with typically developing children. Boys and girls with mild ELD demonstrated higher impairment scores in M-ABC, indicating the need to follow their overall development more closely.     

Exposure to bright light during evening class hours increases alertness among working college students

ObjectiveTo evaluate the effects of exposure to bright light on sleepiness during evening hours among college students.MethodsTwenty-seven healthy college students, all males, with ages ranging from 21 to 24 years, working during the day and studying in the evening, participated in this study. During the 3 week study, the students wore actigraphs and recorded levels of sleepiness. In a crossover design, on the second and third weeks, the students were exposed to bright light (BL) at either 19:00 or 21:00 h. Salivary melatonin samples were collected before and after BL exposure. ANOVA test for repeated measurements were performed.ResultsAfter BL exposure, sleepiness levels were reduced at 20:30 and 22:00 h (F = 2.2; p < 0.05). ANOVA showed statistical differences between time (F = 4.84; p = 0.04) and between day and time of BL exposure (F = 4.24; p = 0.05). The results showed effects of melatonin onset at 20:00 and 21:30 h and sleepiness levels (F = 7.67; p = 0.02) and perception of sleepiness and intervention time (F = 6.52; p = 0.01).ConclusionControlled exposure to BL during evening hours increased alertness among college students. The effects of BL on sleepiness varied according to the time of melatonin onset.     

Effects of ceftriaxone on ischemia/reperfusion injury in rat brain

The aim of this study was to investigate the effect of ceftriaxone treatment against short-term global brain ischemia/reperfusion (I/R) injury in rats. The study was carried out on 30 Wistar-albino rats that were divided into three groups: control group (n = 10), I/R group (n = 10) and I/R-ceftriaxone group (n = 10). Malondialdehyde (MDA) levels were significantly increased in the I/R group in comparison with the control group (p < 0.001). MDA was significantly lower in the I/R-ceftriaxone group than in the I/R group (p < 0.05). Superoxide dismutase activity was significantly decreased in the I/R group and increased in the I/R-ceftriaxone group as compared with the control group. Glutathione peroxidase activity was significantly decreased in the I/R group and increased in the I/R-ceftriaxone group as compared with the I/R group and the control. Histopathologically, ceftriaxone provided morphological improvement compared with the I/R group. We concluded that ceftriaxone has neuron-protective effects due to its antioxidant properties as shown by a decrease in MDA overproduction and histological improvement in brain tissue.     

Impairment of baroreflex control of heart rate in conscious transgenic mice of type 1 diabetes (OVE26)

Baroreflex control of heart rate (HR) is impaired in human type 1 diabetes mellitus. The goal of this study is to use a transgenic mouse model of type 1 diabetes (OVE26) to assess the diabetes-induced baroreflex impairment in the conscious state. OVE26 transgenic mice (which develop hyperglycemia within the first three weeks after birth due to the specific damage of beta cells) and normal control mice (FVB) 5–6 months of age were anesthetized, and the left femoral artery and both veins were catheterized. On the second day after surgery, baroreflex-mediated HR responses to arterial blood pressure (ABP) changes that were induced by separate microinfusion of phenylephrine (PE) and sodium nitroprusside (SNP) at different doses (0.03–0.4 μg/min) were measured in the conscious state. Compared with FVB control, we found that in OVE26 diabetic mice 1) mean ABP (MABP) and HR were decreased (p < 0.05). 2) PE-induced MABP increases were comparable to those in FVB mice (p > 0.05). 3) Baroreflex-mediated bradycardia was attenuated (p < 0.05). 4) SNP-induced MABP decreases was reduced (p < 0.05). 5) Baroreflex-mediated tachycardia was attenuated (p < 0.05). Since baroreflex control of HR in conscious OVE26 mice is impaired in a similar fashion to human diabetes mellitus, we suggest that OVE26 mice may provide a useful model to study the neural mechanisms of diabetes-induced baroreflex impairment.     

Early postnatal exposure to methylphenidate alters stress reactivity and increases hippocampal ectopic granule cells in adult rats

To mimic clinical treatment with methylphenidate (MPH; Ritalin) for attention deficit/hyperactivity disorder (ADHD), rat pups were injected with MPH (5 mg/kg, I.P.) or placebo twice daily during their nocturnal active phase from postnatal day (PND) 7–35. Thirty-nine days after the last MPH administration (PND 76), four litters of rats experienced stressful conditions during the 2003 New York City blackout. MPH-treated rats that endured the blackout lost more weight and regained it at a slower pace than controls (p < 0.05; N = 7–11 per group). Furthermore, MPH-treated rats had elevated systolic arterial blood pressure (from 115.6 ± 1.2 to 126 ± 1.8 mmHg; p < 0.05), assessed on PND 130 by tail cuff plethysmography. Immunocytochemical studies of transmitter systems in the brain demonstrated rearrangements of catecholamine and neuropeptide Y fibers in select brain regions at PND 135, which did not differ between blackout and control groups. However, MPH-treated rats that endured the blackout had more ectopic granule cells in the hilus of the dorsal hippocampal dentate gyrus compared to controls at PND 135 (p < 0.05; N = 6 per group). These findings indicate that early postnatal exposure to high therapeutic doses of MPH can have long lasting effects on the plasticity of select brain regions and can induce changes in the reactivity to stress that persist into adulthood.     

Belgian Schizophrenia Outcome Survey – Results of a 2-year naturalistic study in patients stabilised on monotherapy with olanzapine,risperidone or haloperidol

ObjectivesThis Schizophrenia Outcome Survey compared medical costs, psychopathology and adverse events in outpatients for 2 years following hospitalisation for an acute schizophrenic episode.MethodsAdults stabilised with haloperidol, olanzapine or risperidone entered this observational study ≤1 month after discharge and were assessed at baseline, 3, 6, 12, 18 and 24 months using Brief Psychiatric Rating Scale (BPRS), Clinical Global Impression (CGI), Global Assessment of Functioning and adverse events reporting.ResultsAmong 323 patients (haloperidol 32, olanzapine 149, risperidone 142), baseline characteristics were similar in the olanzapine and risperidone groups, except for more first episodes in the risperidone group (p = 0.01). Haloperidol patients were more often single and institutionalised, less educated, had more residual schizophrenia, were longer hospitalised in the previous year, took more corrective and psychotropic drugs and had more extrapyramidal symptoms (EPS) and gynaecomastia (all significantly). Sixty-eight percent of patients completed a 2-year follow-up. In all groups, CGI and GAF improved during the first 3 months (both p < 0.0001) while BPRS deteriorated in the first year (all within group changes p < 0.05, between group changes NS) before it stabilised. There were no significant differences in hospitalisations and no change in social profile. At the last visit, 66% of haloperidol (p < 0.01), 35% of olanzapine (NS) and 39% (NS) of risperidone patients had ≥1 EPS; 69% (p < 0.013), 40 and 44%, respectively, had ≥1 sexual problem (NS). Mean weight gain was 0.4 (NS), 2.6 (p < 0.05) and 2.6 kg (p < 0.05), respectively.ConclusionsIn this naturalistic study, treatment allocation might have introduced a bias in the interpretation of efficiency results, but olanzapine and risperidone caused less EPS than haloperidol during 2 years of outpatient follow-up.