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Introduction: The leading cause of childhood blindness globally is paediatric cataract. Bilateral cataract surgery can help to improve visual performance and to diminish the burden of childhood blindness., Objective: To report in a retrospective observational cohort study the long-term outcomes of 298 children who had bilateral cataract surgery with IOL implantation from 2001-2016 in Kinshasa., Methods: A standardized surgical treatment of paediatric cataract was practiced on 298 children. Patient's follow-up, complications, and visual outcomes were recorded and analysed., Results: The mean age was 5.7 ± 4.3 years and males were predominant (64.9%). Most of children were living mainly in urban poorest areas (96.3%). Strabismus, nystagmus and microcornea were encountered in 20.1%, 25.1% and 8.7% of children, respectively. Using WHO criteria most of patients were classified as blind preoperatively and 81.9% of them had improved visual outcomes after surgery. Main reasons for reduced vision during follow-up were secondary cataract (5.7%), IOL decentration (1.2%), retinal detachment (1.2%), and secondary glaucoma (1.5%)., Conclusion: In spite of the post conflict challenges, elimination of cataract blindness in children remains a priority. Children present at a late age for surgery and long term follow-up is poor. There is need for program strengthening in these areas., (© 2020 Ngoy JK et al.)

Background: Glaucoma is one of the most common causes of blindness worldwide. The only evidence-based treatment to slow down the progression of glaucoma is the reduction of intraocular pressure (IOP) using local medication or through surgery. During the last years, a large number of microinvasive glaucoma surgery techniques (MIGS) has been developed, in order to reduce the IOP in glaucoma patients safely and effectively. Until now, efficacy of MIGS has been assessed mainly according to the postoperative IOP and the number of medications used. Results from long-term studies are rare or not available in the majority of the cases. In order to better evaluate the functionality of MIGS, a new examination method has been developed with the help of a new oculopressor device. In this study the efficacy of different MIGS techniques will be examined using the new oculopressor., Material/methods: At first, glaucoma patients that had previously received a MIGS surgery (iStent inject, XEN Stent, ELT) were examined with the new oculopression test. Their results were compared with those of non-operated patients and healthy individuals. Overall, 38 healthy subjects (group 1), 10 non-operated patients (group 2), 19 patients after iStent inject implantation (group 3), 14 patients after XEN Stent implantation (group 4) and 5 patients after ELT (group 5) were examined. The new examination measures the IOP-reduction that occurs after oculopression and can be seen as an indirect measurement of the outflow facility of the eye., Results: The IOP-reduction after oculopression differed among the study groups. Non-operated patients showed a significantly lower IOP-reduction compared to healthy individuals. Patients after iStent inject and XEN stent implantation showed a larger reduction of IOP after oculopression in relation to non-operated patients and their results approximated those of healthy individuals. These patients needed fewer medications postoperatively in relation to non-operated patients. Patients after ELT showed postoperatively a smaller reduction of IOP after oculopression compared to iStent inject and XEN stent patients., Conclusion: MIGS can increase the outflow facility of the eye in patients with glaucoma. Though ELT had the lowest impact on the aqueous outflow among the studied procedures in this study. The new test can help in the evaluation of current and further development of new MIGS in the future., Competing Interests: The authors declare that they have no conflict of interest./Die Autorinnen/Autoren geben an, dass kein Interessenkonflikt besteht., (Thieme. All rights reserved.)

Parkinson's disease (PD) is an age-related neurodegenerative disease that produces changes in movement, cognition, sleep, and autonomic function. Motor learning involves acquisition of new motor skills through practice, and is affected by PD. The purpose of the present study was to evaluate regional differences in resting cerebral blood flow (rCBF), measured using arterial spin labeling (ASL) MRI, during a finger-typing task of motor skill acquisition in PD patients compared to age- and gender-matched controls. Voxel-wise multiple linear regression models were used to examine the relationship between rCBF and several task variables, including initial speed, proficiency gain, and accuracy. In these models, a task-by-disease group interaction term was included to investigate where the relationship between rCBF and task performance was influenced by PD. At baseline, perfusion was lower in PD subjects than controls in the right occipital cortex. The task-by-disease group interaction for initial speed was significantly related to rCBF (p < 0.05, corrected) in several brain regions involved in motor learning, including the occipital, parietal, and temporal cortices, cerebellum, anterior cingulate, and the superior and middle frontal gyri. In these regions, PD patients showed higher rCBF, and controls lower rCBF, with improved performance. Within the control group, proficiency gain over 12 typing trials was related to greater rCBF in cerebellar, occipital, and temporal cortices. These results suggest that higher rCBF within networks involved in motor learning enable PD patients to compensate for disease-related deficits.

Mycophenolate mofetil (MMF) is a prodrug active only after its hydrolysis to mycophenolic acid (MPA). The UGT1A9 enzyme is of special interest since it is the main enzyme involved in the glucuronidation of MPA. Single nucleotide polymorphisms (SNPs) in the UGT1A9 gene may be responsible for individual differences in the pharmacokinetics of MMF. Expression levels and the activity of UGT1A9 may depend on the presence of some SNPs located in the gene promoter region (-2152C>T and -275T>A), as well as changes in the coding region (c.98T>C). The objective of this study was to evaluate the effect of allelic variants of the UGT1A9 c.98T>C polymorphism (rs72551330; g. 87289T>C) on MMF metabolism in renal transplant patients. MPA and MPA 7-O glucuronide (MPAG) levels were determined on plasma samples of kidney transplant patients (N = 39) by high-performance liquid chromatography using ultraviolet detection. DNA was isolated from leukocytes and stored at -20°C. The presence of SNPs was investigated using polymerase chain reaction, followed by amplicon sequencing. The analysis of the UGT1A9 c.98T>C polymorphism revealed that all study patients presented the TT genotype. Diverse MPA and MPAG plasma concentrations were detected, including therapeutic, subtherapeutic, and toxic levels. A standardized molecular method permitted identification of UGT1A9 c.98T>C polymorphism genotypes in the examined renal transplant patients. All individuals of the study group presented the same genotype (c.98TT) for that polymorphism. Thereby, no association between the c.98T>C polymorphism and MPA and MPAG plasma levels could be evaluated, despite different levels of these compounds being observed.

Several studies have associated exposure to environmental pollutants, especially polycyclic aromatic hydrocarbons (PAHs), with the development of cardiovascular diseases. Considering that 1-hydroxypyrene (1-OHP) is the major biomarker of exposure to pyrenes, the purpose of this study was to evaluate the potential association between 1-OHP and oxidative stress/inflammatory biomarkers in patients who had suffered an acute myocardial infarction (AMI). After adopting the exclusion criteria, 58 post-infarction patients and 41 controls were sub-divided into smokers and non-smokers. Urinary 1-OHP, hematological and biochemical parameters, oxidative stress biomarkers (MDA, SOD, CAT, GPx and exogenous antioxidants) and the inflammatory biomarker (hs-CRP) were analyzed. 1-OHP levels were increased in post-infarct patients compared to controls (p < 0.05) and were correlated to MDA (r = 0.426, p < 0.01), CAT (r = 0.474, p < 0.001) and β-carotene (r = -0.309; p < 0.05) in non-smokers. Furthermore, post-infarction patients had elevated hs-CRP, MDA, CAT and GPx levels compared to controls for both smokers and non-smokers. Besides, β-carotene levels and SOD activity were decreased in post-infarction patients. In summary, our findings indicate that the exposure to pyrenes was associated to lipid damage and alterations of endogenous and exogenous antioxidants, demonstrating that PAHs contribute to oxidative stress and are associated to acute myocardial infarction.

Toluene is an organic solvent used in numerous processes and products, including industrial paints. Toluene neurotoxicity and reproductive toxicity are well recognized; however, its genotoxicity is still under discussion, and toluene is not classified as a carcinogenic solvent. Using the comet assay and the micronucleus test for detection of possible genotoxic effects of toluene, we monitored industrial painters from Rio Grande do Sul, Brazil. The putative involvement of oxidative stress in genetic damage and the influences of age, smoking, alcohol consumption, and exposure time were also assessed. Although all biomarkers of toluene exposure were below the biological exposure limits, painters presented significantly higher DNA damage (comet assay) than the control group; however, in the micronucleus assay, no significant difference was observed. Painters also showed alterations in hepatic enzymes and albumin levels, as well as oxidative damage, suggesting the involvement of oxidative stress. According to multiple linear regression analysis, blood toluene levels may account for the increased DNA damage in painters. In summary, this study showed that low levels of toluene exposure can cause genetic damage, and this is related to oxidative stress, age, and time of exposure., (Copyright © 2012 Elsevier B.V. All rights reserved.)

This work has investigated the effects of prolonged exposure of young rats to nicotine on some physiological and biochemical parameters. Wistar male rats (30 days old) were treated (s.c.) with saline or nicotine 5mg/kg/day for 28 or 56 days. They received five injections (1mg/kg) per day (8, 10, 12:00 a.m., 2 and 4:00 p.m.) on the dark period of the cycle. Nicotine exposure for 56 days reduced body and liver weights. Moreover, nicotine exposure for 28 or 56 days decreased the hepatic glycogen but not blood glucose levels. The activities of blood and hepatic PBG-synthase, and blood and cerebral acetylcholinesterase were not affected by in vivo exposure. However, these activities were inhibited by nicotine in vitro. Results show that although high levels of plasma cotinine were found in both intervals of exposures, the parameters here analyzed were not affected by prolonged nicotine exposure except the storage of glucose, and body and liver weights.

Early assessment of neurological and behavioral effects is extremely valuable for early identification of intoxications because preventive measures can be taken against more severe or chronic toxic consequences. The time course of the effects of an oral dose of the anticholinesterase agent propoxur (8.3 mg/kg) was determined on behaviors displayed in the open-field and during an active avoidance task by rats and on blood and brain cholinesterase activity. Maximum inhibition of blood cholinesterase was observed within 30 min after administration of propoxur. The half-life of enzyme-activity recovery was estimated to be 208.6 min. Peak brain cholinesterase inhibition was also detected between 5 and 30 min of the pesticide administration, but the half-life for enzyme activity recovery was much shorter, in the range of 85 min. Within this same time interval of the enzyme effects, diminished motor and exploratory activities and decreased performance of animals in the active avoidance task were observed. Likewise, behavioral normalization after propoxur followed a time frame similar to that of brain cholinesterase. These data indicate that behavioral changes that occur during intoxication with low oral doses of propoxur may be dissociated from signs characteristic of cholinergic over-stimulation but accompany brain cholinesterase activity inhibition.