Refraction and ocular biometric parameters in 3-to 6-year-old preschool children : a large-scale population-based study in Chengdu, China.

PURPOSE: To understand the ocular biometric parameters characteristics and refractive errors in 3-to 6-year-old preschool children in Chengdu, China, and to investigate the prevalence of refractive errors. METHOD: A school-based cross-sectional study was conducted in Chengdu from 2020 to2022 with a total of 666 kindergartens. All children were measured by non-cycloplegic autorefraction and uncorrected visual acuity (UCVA) and ocular biometric parameters. Finally, univariate linear regression models were used to analyze the relationship between ocular biometric parameters and refraction. RESULTS: A total of 108,578 preschool children aged 3-6 underwent examinations, revealing a myopia prevalence of 6.1%. The mean axial length (AL), keratometry (K), corneal radius (CR), axial length/corneal radius (AL/CR) Ratio, central corneal thickness (CCT), anterior chamber depth (ACD), lens thickness (LT), and vitreous chamber depth (VCD) were 22.35 ± 0.69 mm, 43.35 ± 1.58 D, 7.80 ± 0.28 mm, 2.87 ± 0.08, 533.31 ± 32.51 µm, 2.70 ± 0.28 mm, 3.91 ± 0.27 mm, and 15.20 ± 0.68 mm, respectively. With increasing age, AL, CR, AL/CR ratio, CCT, ACD, LT, and VCD also increased. Regardless of age, males consistently exhibited longer AL, flatter corneal curvature, shallower ACD, thicker CCT, thinner LT, and longer VCD compared to females. AL, K, CR, LT, and VCD all showed significant linear relationships with SE (all P < 0.001) in univariate linear regression analysis after adjusting for gender and age. CONCLUSION: The prevalence of myopia among preschool children aged 3-6 in Chengdu is relatively low. Ocular biometric parameters affecting refractive errors include AL, K, CR, LT, and VCD. The preschool period serves as a critical phase for myopia prevention and control.

Correlation between refractive errors and ocular biometric parameters in children and adolescents: a systematic review and meta-analysis.

BACKGROUND: Refractive errors are one of the most common ocular conditions among children and adolescents, with myopia showing an increasing prevalence and early onset in this population. Recent studies have identified a correlation between refractive errors and ocular biometric parameters. METHODS: A systematic search was conducted in electronic databases including PubMed, EMBASE, Cochrane Library, Web of Science, and Medline from January 1, 2012, to May 1, 2023. Various ocular biometric parameters were summarized under different refractive states, including axial length (AL), central corneal thickness (CCT), anterior chamber depth (ACD), lens thickness (LT), corneal curvature (CC), Corneal curvature radius (CR),axial length-to-corneal radius ratio (AL/CR ratio), choroidal thickness (ChT), retinal thickness (RT), retinal nerve fiber layer thickness (RNFL), and retinal blood density (VD). The differences in these parameters among different refractive states were analyzed using Stata software with fixed or random-effects models, taking into account the assessed heterogeneity level. RESULTS: This meta-analysis included a total of 69 studies involving 128,178 eyes, including 48,795 emmetropic eyes, 60,691 myopic eyes, 13,983 hyperopic eyes, 2,040 low myopic eyes, 1,201 moderate myopic eyes, and 1,468 high myopic eyes. The results of our study demonstrated that, compared to the control group (emmetropic group), the myopic group and low, moderate, and high myopic groups showed significant increases in AL, AL/CR ratio, and ACD, while the hyperopic group exhibited significant decreases. Compared to the control group, the myopic group had a significantly increase for CC, while CR, CCT, perifoveal RT, subfoveal ChT, foveal ChT, parafoveal ChT, perifoveal (except nasal) ChT, and pRNFL (except temporal) significantly decreased. Compared to the control group, the hyperopic group had a significantly increase for subfoveal ChT, foveal ChT, parafoveal ChT, perifoveal ChT, and nasal pRNFL. Compared to the control group, the low and moderate myopic groups had a significantly decreases for the CCT, parafoveal RT (except nasal), perifoveal RT (except nasal), and pRNFL (except superior and temporal). Compared to the control group, the high myopic group had a significantly increase for CR, while LT, perifoveal ChT (except nasal), parafoveal RT, perifoveal RT, and pRNFL (except temporal) had significant decreased. CONCLUSION: The changes of ocular biometric parameters in children and adolescents are closely related to refractive errors. Ocular biometric parameters devices, as effective non-invasive techniques, provide objective biological markers for monitoring refractive errors such as myopia.

The Advantages of Levodopa-Carbidopa Intestinal Gel for Patients with Advanced Parkinson's Disease: A Systematic Review.

BACKGROUND: Levodopa-carbidopa intestinal gel (LCIG) is a new type of administration that results in steadier levodopa plasma concentrations in advanced Parkinson's disease (PD) patients and effectively reduces poor mobility and dyskinesia. METHODS: Electronic databases were searched up to January 1, 2018. The inclusion criteria for this review were as follows: LCIG vs oral medication in advanced PD patients. RESULTS: Five trials, with a total of 198 patients, met all the inclusion criteria. The quality score of these studies ranged from 3 to 5. Two clinical trials showed that compared with oral medication, LCIG had a better treatment effect on on-time with troublesome dyskinesia (TSD) (p = 0.02) and on-time without TSD (p < 0.00001) in advanced PD patients. In addition, four of the 5 studies showed that the LCIG may have better efficacy than oral medication for improving the scores of the UPDRS, and two studies found that LCIG demonstrated better efficacy for improving the PDQ-39 scores. The video recording results indicated a potential decline in both dyskinesia and the "off" state in LCIG-treated patients. The incidence of adverse events was not significantly different between the LCIG and oral medication groups. CONCLUSION: Compared with oral treatment, LCIG exerts its effectiveness, mostly by reducing the time of on-time with TSD, increasing the time of on-time without TSD and scores of UPDRS and PDQ-39. It is suggesting that LCIG was likely to be a new type of administration used in clinical applications. However, due to methodological flaws, these findings should be viewed with caution, and more RCTs are needed in the field to complement our findings.

Striatal overexpression of ß-arrestin2 counteracts L-dopa-induced dyskinesia in 6-hydroxydopamine lesioned Parkinson's disease rats.

Prolonged administration of Levodopa (L-dopa) therapy can generate L-dopa-induced dyskinesia (LID). Accumulating evidence indicates that hyper-activation of the dopamine D1 receptor (D1R) and the cAMP signaling cascade in the medium spiny neurons (MSNs) of the striatum are involved in LID. Previous studies have shown that striatal ß-arrestin2 overexpression significantly reduces LID severity and have indicated that ß-arrestin2 may play a causal role in the dyskinesia sensitization process. L-dopa-induced changes in the expression of signaling molecules and other proteins in the striatum were examined immunohistochemically and by western blot. A rAAV (recombinant adeno-associated virus) vector was used to overexpress and ablate ß-arrestin2. We found that striatal overexpression of AAV-mediated ß-arrestin2 produced less severe AIMs (abnormal involuntary movements) in response to L-dopa, whereas selective deletion of ß-arrestin2 in the striatal neurons dramatically enhanced the severity of dyskinesia induced by L-dopa. Furthermore, no significant improvements in motor behavior (FFT: forelimb functional test) were seen with the inhibition or overexpression of ß-arrestin2. Finally, overexpression of ß-arrestin2 diminished L-dopa-induced D1R and phosphor-DARPP32/ERK levels. Viral deletion of ß-arrestin2 markedly enhanced the key biochemical markers in the direct pathway. We found that increased availability of ß-arrestin2 ameliorated dyskinesia severity with no influence on the anti-Parkinsonian action of L-dopa, suggesting a promising approach for controlling LID in Parkinson's disease. In addition, overexpression of ß-Arrestin2 prevented the development of LID by inhibiting G protein-dependent D1R and phosphor-DARPP32/ERK signaling in dyskinetic rats.

Levodopa/Benserazide PLGA Microsphere Prevents L-Dopa-Induced Dyskinesia via Lower ß-Arrestin2 in 6-Hydroxydopamine Parkinson's Rats.

Prolonged pulsatile administration of Levodopa (L-dopa) can generate L-dopa-induced dyskinesia (LID). Numerous research has reported that continuous dopamine delivery (CDD) was useful in reducing the severity of LID. 6-OHDA lesioned rats were divided into two groups to receive intermittent L-dopa stimulation (L-dopa/benserazide) or Levodopa/benserazide PLGA microsphere (LBPM) for 3 weeks. rAAV (recombinant adeno-associated virus) vector was used to overexpress and ablation of ß-arrestin2. We found that LBPM developed less AIM severity compared with standard L-dopa administration, whereas selective deletion of ß-arrestin2 in striatum neurons dramatically enhanced the severity of dyskinesia by LBPM. On the contrary, the effects of LBPM in terms of ALO AIM were further relieved by ß-arrestin2 overexpression. Furthermore, no significant change in motor behavior was seen either in inhibition or overexpression of ß-arrestin2. In short, our experiments provided evidence that LBPM's prevention of LID behavior was likely due to ß-arrestin2, suggesting that a therapy modulating ß-arrestin2 may offer a more efficient anti-dyskinetic method with a low risk of untoward effects.

A comparison of contrast transthoracic echocardiography and contrast transcranial Doppler in cryptogenic stroke patients with patent foramen ovale.

OBJECTIVE: In recent years, increasing attention has been paid to cryptogenic stroke (CS) caused by the patent foramen ovale (PFO). This study aims to compare contrast transthoracic echocardiography (cTTE) and contrast transcranial Doppler (cTCD) to determine whether cTTE is more suitable and reliable than cTCD for clinical use. METHODS: From March 2017 to May 2018, patients who suffered from migraines, stroke, hypomnesis, or asymptomatic stroke found casually were included in our study. Patients with CS were semirandomly divided into two groups (cTTE and cTCD) according to the date of the outpatient visit. Patients with either of the examination above found positive were selected to finish transesophageal echocardiography (TEE). RESULTS: In our study, the sensitivities of group cTTE positive (group cTTE+) and group cTCD positive (group cTCD+) did not have any statistical difference (89% vs. 80%, p = 0.236). Focusing on group cTCD+, we discovered that the semiquantitative shunt grading was not correlated with whether a PFO was present or not (p = 0.194). However, once the PFO has been diagnosed, the shunt grading was shown to be related to the width of the gaps (p = 0.032, pdeviation  = 0.03). CONCLUSION: Both cTTE and the cTCD can be used for preliminary PFO findings. The semiquantitative shunt grading of cTCD and cTTE can suggest the size of the PFO and the next course of treatment. The cTTE may be more significant to a safe PFO (a PFO does not have right-to-left shunts, RLSs). Combining cTTE and TEE could help diagnose PFO and assess CS risk.

Platelet-to-neutrophil ratio is a prognostic marker for 90-days outcome in acute ischemic stroke.

To investigate the prognostic value of platelet-to-neutrophil ratio (PNR) in acute ischemic stroke (AIS) patients. In this study, a total of 400 AIS patients were included. Demographic, clinical, laboratory data were collected on admission, and PNR was calculated according to platelet and neutrophil counts on admission. The prognosis after 3 months was evaluated by the Barthel index (BI), where BI ≤85 was defined as poor prognosis and BI >85 was defined as good prognosis. Regression analyses were performed, adjusting for confounders. (1) Compared with good prognosis group, PNR level on admission in poor prognosis group was significantly lower, the difference between the two groups was statistically significant (P < 0.05). (2) The difference in PNR level between the large infarct volume group and small infarct volume group was no statistically significant, nor between the moderate to severe group and the mild group (all P > 0.05). (3) In multivariate logistic regression analysis, PNR, platelet-to-lymphocyte ratio (PLR), platelet-to-white blood cell ratio (PWR) level were correlated with the 3 month prognosis of AIS. PNR may be an independent protective factor for predicting the prognosis of AIS. PNR level has a higher accuracy in the 3 month prognosis of acute ischemic cerebral infarction than the level of PLR and PWR. The level of PNR is correlated with the 3 month prognosis of acute ischemic cerebral infarction. The level of PNR may be an independent protective factor for predicting the prognosis of AIS.

ß-arrestin2 alleviates L-dopa-induced dyskinesia via lower D1R activity in Parkinson's rats.

The cause of the L-dopa-induced dyskinesia (LID) has been ascribed to G-protein coupled receptor (GPCR) supersensitivity and uncontrolled downstream signaling. It is now supposed that ß-arrestin2 affects GPCR signaling through its ability to scaffold various intracellular molecules. We used the rAAV (recombinant adeno-associated virus) vectors to overexpress and ablation of ß-arrestin2. L-dopa-induced changes in expression of signaling molecules and other proteins in the striatum were examined by western blot and immunohistochemically. Our data demonstrated that via AAV-mediated overexpression of ß-arrestin2 attenuated LID performance in 6-OHDA-lesioned rodent models. ß-arrestin2 suppressed LID behavior without compromising the antiparkinsonian effects of L-dopa. Moreover, we also found that the anti-dyskinetic effect of ß-arrestin2 was reversed by SKF38393, a D1R agonist. On the contrary, the rat knockdown study demonstrated that reduced availability of ß-arrestin2 deteriorated LID performance, which was counteracted by SCH23390, a D1R antagonist. These data not only demonstrate a central role for ß-arrestin2/GPCR signaling in LID, but also show the D1R signal pathway changes occurring in response to dopaminergic denervation and pulsatile administration of L-dopa.

Effects of mGluR5 Antagonists on Parkinson's Patients With L-Dopa-Induced Dyskinesia: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.

Background: Modulation of Metabotropic glutamate receptor 5 (mGluR5) may be a novel therapeutic approach to manage Parkinson's disease (PD) Patients with L-dopa-induced dyskinesia (LID). Objectives: The objective of this meta-analysis was to evaluate the effects of mGluR5 antagonists for the treatment of LID patients. Methods: Several electronic databases were consulted up to July 30, 2017. Randomized clinical trials (RCTs) that compared mGluR5 antagonists vs. placebo in LID patients were included. Pooled weighted mean difference (WMD) with 95% confidence intervals (CIs) were calculated using random-effects models. Results: Nine trials including 776 patients met all inclusion criteria. We pooled the whole data and found apparent difference between mGluR5 antagonists and placebo in terms of mAIMS (p = 0.010). However, there was no significant improvements on antidyskinetic in terms of LFADLDS (p = 0.42) and UPDRS Part IV (p = 0.20). Meanwhile, the effect size of UPDRS part III was similar in mGluR5 antagonist groups with in placebo groups (p = 0.25). Adverse events incidence was higher with mGluR5 antagonists than with placebo, especially at the expense of increased dizziness (16.3 vs. 4.3%), visual hallucination (10.1 vs. 1.1%), or fatigue (10.1 vs. 4.8%). Conclusions: mGluR5 antagonists had a greater treatment effect on the mAIMS in LID patients, however, there was no improvements on antidyskinetic in terms of LFADLDS and UPDRS Part IV compared with placebo. According to these results, we unable to recommend mGluR5 antagonists for the routine treatment of LID patients right now.

Correlation of Changes in Leukocytes Levels 24 Hours after Intravenous Thrombolysis With Prognosis in Patients With Acute Ischemic Stroke.

OBJECTIVE: Leukocytes play a crucial role in inflammation and immune response. This study aims to demonstrate the value of changes in leukocytes levels 24 hours after intravenous thrombolysis to predict prognosis in acute ischemic stroke (AIS). METHODS: From Jan 2016 to Oct 2017, the patients who suffered AIS to our center within 4.5 hours of symptom onset were all treated with recombinant tissue-type plasminogen activator. Data from 213 AIS patients were analyzed. Patients were divided into 4 groups: persistent leukocytosis (PL), transient leukocytosis (TL), leukocytosis 24 hours (L24H) and no leukocytosis (NL). By comparison, the factors with statistically significant were selected in pairwise multiple comparisons. Good clinical outcome was defined as the Modified Rankin Scale score of 2 or lower. Multivariate logistic regression was used to assess the association of the indicators with clinical outcome. RESULTS: By pairwise multiple comparisons, PL and L24H had higher baseline National Institutes of Health Stroke Scale (NIHSS) score than NL and were likely to lead poor clinical outcomes. TL had a better prognosis than L24H. As the results of multivariable analyses shown, PL and L24H were risk factors to poor functional outcomes (odds ratio [OR] = 2.668, 95% confidence interval [CI] = 1.139-6.249, P = .024; OR = 6.648, 95%CI = 2.048-21.584, P = .002). CONCLUSION: Persistent leukocytosis and leukocytosis 24 hours both had higher baseline NIHSS scores, more serious stroke and were more likely to lead to unfavorable outcome. Therefore, changes in leukocytes levels 24 hours after intravenous thrombolysis could be predicted the short-term functional outcome of AIS patients.

Modulation of CaMKIIa-GluN2B interaction in levodopa-induced dyskinesia in 6-OHDA-lesioned Parkinson's rats.

Long-term treatment with L-dopa leads to involuntary aimless movements called L-dopa-induced dyskinesia (LID) has hindered its use in Parkinson's disease (PD) patients. Emerging evidence suggests a possible role of CaMKIIa and its interacting partners in the development of LID. In this study, we found that CaMKIIa was found to form complexes with GluN2B after chronic administration of L-dopa in adult rat striatal neurons. Intrastriatal injection of KN-93 significantly reduced the level of GluN2B in CaMKIIa precipitates with a dose dependent response, as well as reduced the Global ALO AIM score without ablation of the therapeutic response to L-dopa. In parallel, intrastriatal injection of MK-801 significantly alleviated the level of CaMKIIa in GluN2B precipitates compared to LID group (p < 0.01), and this is accompanied by realizing improvement of the Global ALO AIM score also without affect the efficacy of L-dopa. In summary, the present study indicated that CaMKIIa-GluN2B interaction had an important role in the development of LID. Disrupt of this link by intrastriatal infusion of KN-93 or MK-801 ameliorated dyskinesia in 6-OHDA-lesioned PD rats.

Role of sLOX-1 in intracranial artery stenosis and in predicting long-term prognosis of acute ischemic stroke.

Objective: The role of sLOX-1 in acute ischemic stroke still remains unclear. This study aims to demonstrate the value of sLOX-1 in evaluating degrees of intracranial artery stenosis and to predict prognosis in stroke. Methods: Two hundred and seventy-two patients were included in this study and basic data were collected within 72 hr on admission. We assessed the association between sLOX-1 levels and stroke conditions in one-year duration. After adjusting for potential confounders, regression analyses were performed. Results: We found that sLOX-1 levels were increased significantly in severe patients compared to the mild stroke group (p = .011). After adjusting confounders, sLOX-1 was associated with a poor functional outcome in patients with an adjusted OR of 2. 946 (95% CI, 1.788-4.856, p < .001). There was also positive correlation between sLOX-1 levels and the degrees of intracranial artery stenosis in the different groups (p = .029). Conclusions: Our study demonstrated that sLOX-1 levels could be used to evaluate the severity of stroke and the degrees of intracranial artery stenosis. Furthermore, sLOX-1 could be exploited to predict the long-term functional outcome of stroke.

A Meta-Analysis of Folic Acid in Combination with Anti-Hypertension Drugs in Patients with Hypertension and Hyperhomocysteinemia.

Folic acid is generally used to lower homocysteine concentrations and prevent stroke and cardiovascular disease (CVD) at present. However, the efficacy of therapies that lower homocysteine concentrations in reducing the risk of CVD and stroke remains controversial. Our objective was to do a meta-analysis of relevant randomized controlled trials (RCTs) to evaluate the efficacy of folic acid supplementation among patients with hypertension and Hyperhomocysteinemia (HT/HHcy). We included RCTs examining the effects of folic acid plus antihypertensive therapy compared to antihypertensive alone. Weighted Mean Difference (WMD) and Relative risk (RR) were used as a measure of the effect of folic acid on the outcome measures with a random effect model. Sixty-five studies including 7887 patients met all inclusion criteria. Among them, 49 trials reported significant effect of combination therapy for reducing SBP (systolic Blood Pressure) and DBP (Diastolic Blood Pressure) levels compared with antihypertensive alone (WMD = -7.85, WMD = -6.77, respectively). Meanwhile, folic acid supplementation apparently reduced the level of total homocysteine (WMD = 5.5). In addition, folic acid supplementation obviously reduced the risk of cardiovascular and cerebrovascular events (CVCE) by 12.9% compared with control groups. In terms of the stratified analyses, a bigger beneficial effect was seen in those RCTs with treatment duration of more than 12 weeks, a decrease in the concentration of total homocysteine of more than 25%, with folic acid fortification. Our findings indicated that folic acid supplementation was effective in the primary prevention of CVCE among HT/HHcy patients, as well as reducing the blood pressure and total homocysteine levels.

Neuroprotective properties of curcumin in toxin-base animal models of Parkinson's disease: a systematic experiment literatures review.

BACKGROUND: Curcumin (diferuloylmethane), a polyphenol extracted from the plant Curcuma longa, is widely used in Southeast Asia, China and India in food preparation and for medicinal purposes. Meanwhile, the neuroprotective actions of curcumin have been documented for experimental therapy in Parkinson's disease (PD). METHODS: In this study, we used a systematic review to comprehensively assess the efficacy of curcumin in experimental PD. Using electronic and manual search for the literatures, we identified studies describing the efficacy of curcumin in animal models of PD. RESULTS: We identified 13 studies with a total of 298 animals describing the efficacy of curcumin in animal models of PD. The methodological quality of all preclinical trials is ranged from 2 to 5. The majority of the experiment studies demonstrated that curcumin was more significantly neuroprotection effective than control groups for treating PD. Among them, five studies indicated that curcumin had an anti-inflammatory effect in the PD animal models (p < 0.05). Meanwhile, four studies showed the antioxidant capability of curcumin, by which it protected substantia nigra neurons and improved striatal dopamine levels. Furthermore, two studies in this review displayed that curcumin treatment was also effective in reducing neuronal apoptosis and improving functional outcome in animal models of PD. Most of the preclinical studies demonstrated the positive findings while one study reported that curcumin had no beneficial effects against Mn-induced disruption of hippocampal metal and neurotransmitter homeostasis. CONCLUSIONS: The results demonstrated a marked efficacy of curcumin in experimental model of PD, suggesting curcumin probably a candidate neuroprotective drug for human PD patients.

Polymorphisms of heat shock protein 70 genes (HSPA1A, HSPA1B and HSPA1L) and susceptibility of noise-induced hearing loss in a Chinese population: A case-control study.

Noise-induced hearing loss (NIHL) is the second-most frequent form of sensorineural hearing loss. When exposed to the same noise, some workers develop NIHL while others do not, suggesting that NIHL may be associated with genetic factors. To explore the relationship between single nucleotide polymorphisms (SNPs) in heat shock protein 70 (HSP70) genes (HSPA1A, HSPA1B and HSPA1L) and susceptibility to NIHL in Han Chinese workers exposed to noise, a case-control association study was carried out with 286 hearing loss cases and 286 matched with gender, age, type of work, and exposure time, drawn from a population of 3790 noise-exposed workers. Four SNPs were selected and genotyped. Subsequently, the effects of the alleles and genotypes of the three HSP70 genes (HSPA1A, HSPA1B and HSPA1L) on NIHL were analyzed by using a conditional logistic regression. A generalized multiple dimensionality reduction (GMDR) was applied to further detect an interaction between the four SNPs. Compared with the combined genotypes CC/TC, carriers of the TT genotype of rs2763979 appeared to show greater susceptibility to NIHL (P = 0.042, adjusted OR = 1.731, 95% CI 1.021-2.935). A significant interaction between rs2763979 and CNE was found (P = 0.029), and a significant association was found between TT of s2763979 and NIHL (P = 0.024, adjusted OR = 5.694, 95%CI 1.256-25.817) in the 96 dB (A)≤CNE<101 dB (A) group. The results suggest that the rs2763979 locus of the HSP70 genes may be associated with susceptibility to NIHL in Chinese individuals, and other HSP70 genes may also be susceptibility genes for NIHL, but the results must be further replicated in additional independent sample sets.

A Meta-Analysis of Adenosine A2A Receptor Antagonists on Levodopa-Induced Dyskinesia In Vivo.

BACKGROUND: Long-term use of levodopa (l-dopa) is inevitably complicated with highly disabling fluctuations and drug-induced dyskinesias, which pose major challenges to the existing drug therapy of Parkinson's disease. METHODS: In this study, we conducted a systematic review and meta-analysis to assess the efficacy of A2A receptor antagonists on reducing l-dopa-induced dyskinesias (LID). RESULTS: Nine studies with a total of 152 animals were included in this meta-analysis. Total abnormal involuntary movements (AIM) score, locomotor activity, and motor disability were reported as outcome measures in 5, 5, and 3 studies, respectively. Combined standardized mean difference (SMD) estimates were calculated using a random-effects model. We pooled the whole data and found that, when compared to l-dopa alone, A2A receptor antagonists plus l-dopa treatment showed no effect on locomotor activity (SMD -0.00, 95% confidence interval (CI): -2.52 to 2.52, p = 1.0), superiority in improvement of motor disability (SMD -5.06, 95% CI: -9.25 to -0.87, p = 0.02) and more effective in control of AIM (SMD -1.82, 95% CI: -3.38 to -0.25, p = 0.02). CONCLUSION: To sum up, these results demonstrated that A2A receptor antagonists appear to have efficacy in animal models of LID. However, large randomized clinical trials testing the effects of A2A receptor antagonists in LID patients are always warranted.

Genetic variation in EYA4 on the risk of noise-induced hearing loss in Chinese steelworks firm sample.

OBJECTIVES: Noise-induced hearing loss is one of the most serious occupational diseases worldwide. It is caused by interactions between environmental and genetic factors. The purpose of this study was to examine the association between the genetic susceptibility of the eye absent homolog 4 (EYA4) gene and the risk of developing noise-induced hearing loss in China. METHODS: A case-control association study was carried out with 326 hearing loss cases and 326 controls matched with age and duration of noise exposure, drawn from a cohort of steel workers. Five single nucleotide polymorphisms (SNPs) in the EYA4 were selected and genotyped. Logistic regression was performed to analyse the main effect of genotypes and interactions between genotypes and individual/environmental factors adjusted for confounding factors. Moreover, generalised multiple dimensionality reduction was applied to further detect interaction among the 5 selected SNPs. RESULTS: Analysis revealed that locus polymorphism of rs3813346 was associated with the risk of developing noise-induced hearing loss in the dominance model, the codominance model and the addictive model (p=0.004, 0.009 and 0.003, respectively). A significant interaction between rs9321402 and cumulative noise exposure was found (p=0.002). A significant main effect p value (p=0.006) was obtained in the high-level exposure group (cumulative noise exposure ≥98 dB(A)). Generalised multiple dimensionality reduction indicated that the combined interaction of the 2 loci-rs3813346 and rs9493627-significantly affected the incidence of noise-induced hearing loss. CONCLUSIONS: The research suggests that EYA4 genetic variant and its interaction with noise levels may modify the susceptibility to develop noise-induced hearing loss in Chinese population.