Biology subjects

Homolak, J.

Publications and source records attributed to Homolak, J..

At least 19 recordsLinked to original sources

bioRxiv2026

Ethical Considerations of Mitigating Data Loss: VLADISLAV, a Manifesto for Reliable Home Cage Systems

Home cage monitoring (HCM) captures longitudinal animal behavioural data without human intervention. However, the systems complexity is rarely addressed in their design, increasing the risk of data loss, which wastes workhours, resources, and animal lives. To assess the feasibility of implementing modern, robust architectures in complex operant HCM paradigms, the VersatiLe Autonomous DevIce for Scheduled Learning Assessment Via Wi-Fi (VLADISLAV) was developed and employed to test cognitive deficits in the intracerebroventricular streptozotocin-induced rat model of sporadic Alzheimers disease (sAD). Reliability was modelled against a system architecture common in commercial HCM systems by modelling the failure rate of the devices critical components across typical durations of animal experiments. VLADISLAV assessed multiple cognitive dimensions of a rat model of sAD with automated, scheduled testing. Its design enabled simultaneous, redundant recording to multiple devices in real time, as well as batch remote control and supervision of tens of VLADISLAVs. VLADISLAV is estimated to reduce component failure rate [~]200-fold at {euro}40/device. Data loss due to system failure shouldnt be accepted as a normal occurrence and robust system design is an ethical imperative. VLADISLAVs robustness and utility demonstrate the potential of embedded networked systems, used in other industries and consumer electronics for over a decade. Today, the open source ecosystem enables cost-effective implementation of such architectures in HCM by biomedical researchers with no electronic engineering education, preventing data loss and facilitating researchers and technicians day-to-day work. Considering these findings, it is apparent that the implementation of modern architectures in HCM is long overdue.

animal behavior and cognition↗

bioRxiv2024

MIROSLAV: A complete open-source hardware and software toolkit for high-throughput circadian activity measurement and analysis in rodents

While conventional behavioural tests offer valuable insight into rodent behaviour in specific paradigms, rodents spend most of their time in a safe, undisturbed environment - their home cage. However, home cage monitoring (HCM) is often impractical at scale over prolonged periods of time without significant loss of data. To achieve this, we developed MIROSLAV, the Multicage InfraRed Open Source Locomotor Activity eValuator, a home cage activity and environmental monitoring device designed to be open, adaptable, and robust. Its transparent and modular design allows the device to be tailored to varying experimental requirements and environmental conditions, while its wireless operation and multiple redundancies minimise loss of data and animal disturbance. Data quality is maintained by a modular software workflow for data preparation (Prepare-a-SLAV) and cleaning (TidySLAV), followed by exploratory (MIROSine - MIRO The Explorer) and statistical (MIROSine - StatistiSLAV) analysis of circadian periodicity. Here, using MIROSLAV, we demonstrate circadian dysrhythmia and a disrupted response to regular stimuli (e.g. behavioural testing, bedding change) in a rat model of sporadic Alzheimers disease, showcasing MIROSLAVs utility in a typical animal study of disease. In accordance with the 3Rs, every rodent study and laboratory performing them can benefit from HCM, provided the existence of transparent and customisable tools which allow robust deployment to tens or hundreds of cages in various conditions. MIROSLAV provides this opportunity to researchers in a cost-effective manner.

animal behavior and cognition↗

bioRxiv2023

Insights into Gastrointestinal Redox Dysregulation in a Rat Model of Alzheimer's Disease and the Assessment of the Protective Potential of D-galactose

IntroductionRecent evidence suggests that the gut plays a vital role in the development and progression of Alzheimers disease (AD) by triggering systemic inflammation and oxidative stress. The well-established rat model of AD, induced by intracerebroventricular administration of streptozotocin (STZ-icv), provides valuable insights into the GI implications of neurodegeneration. Notably, this model leads to pathophysiological changes in the gut, including redox dyshomeostasis, resulting from central neuropathology. Our study aimed to investigate the mechanisms underlying gut redox dyshomeostasis and assess the effects of D-galactose, which is known to benefit gut redox homeostasis and alleviate cognitive deficits in this model. Materials and MethodsDuodenal rings isolated from STZ-icv animals and control groups were subjected to a prooxidative environment using AAPH or H2O2 with or without D-galactose in oxygenated Krebs buffer ex vivo. Redox homeostasis was analyzed through protein microarrays and functional biochemical assays, alongside cell survival assessment. Structural equation modeling, univariate, and multivariate models were employed to evaluate the differential response of STZ-icv and control samples to the controlled prooxidative challenge. ResultsSTZ-icv samples showed suppressed expression of catalase and glutathione peroxidase 4 (GPX4) and increased baseline activity of enzymes involved in H2O2 and superoxide homeostasis. The altered redox homeostasis status was associated with an inability to respond to oxidative challenges and D-galactose. Conversely, the presence of D-galactose increased antioxidant capacity, enhanced catalase and peroxidase activity, and upregulated superoxide dismutases in the control samples. ConclusionSTZ-icv-induced gut dysfunction is characterized by a diminished ability of the redox regulatory system to maintain long-term protection through the transcription of antioxidant response genes, as well as compromised activation of enzymes responsible for immediate antioxidant defense. D-galactose can exert beneficial effects on gut redox homeostasis under physiological conditions.

neuroscience↗

bioRxiv2023

An exploratory study of gastrointestinal redox biomarkers in the presymptomatic and symptomatic Tg2576 mouse model of familial Alzheimer's disease - phenotypic correlates and the effects of chronic oral D-galactose

The gut might play an important role in the etiopathogenesis of Alzheimers disease (AD) as gastrointestinal alterations often precede the development of neuropathological changes in the brain and correlate with disease progression in animal models. The gut has an immense capacity to generate free radicals whose role in the etiopathogenesis of AD is well known; however, it remains to be clarified whether gastrointestinal redox homeostasis is associated with the development of AD. The aim was to i) examine gastrointestinal redox homeostasis in the presymptomatic and symptomatic Tg2576 mouse model of AD; ii) investigate the effects of chronic oral D-galactose previously shown to alleviate cognitive deficits and metabolic changes in animal models of AD; iii) investigate the association between gastrointestinal redox biomarkers and behavioral alterations in Tg2576 mice. Presymptomatic Tg2576 have a heightened gastrointestinal electrophilic tone reflected in increased lipid peroxidation and activity of Mn/Fe-SOD. Chronic oral D-galactose treatment was associated with detrimental effects on redox homeostasis only in the wild-type controls. In the symptomatic stage, Tg2576 mice demonstrate compensated redox disbalance characterized by normalized lipid peroxidation and increased hydrogen peroxide dissociation capacity but diminished total antioxidant reserve alleviated with chronic oral D-galactose treatment. Conversely, D-galactose reduced antioxidant capacity and increased lipid peroxidation in the controls. Total antioxidant capacity was associated with greater spatial memory, while other biomarkers had a complex relationship with exploration, nesting, and grooming. Gut redox homeostasis might be involved in the development and progression of AD pathophysiology and should be further explored in this context.

neuroscience↗

bioRxiv2022

Altered secretion, constitution, and functional properties of the gastrointestinal mucus in a rat model of sporadic Alzheimer's disease

Accumulating evidence supports the involvement of the gastrointestinal (GI) system in Alzheimers disease (AD), however, it is currently unknown whether GI alterations arise as a consequence of central nervous system (CNS) pathology or play a causal role in the pathogenesis of the disease. The GI mucus system is a possible mediator of GI dyshomeostasis in neurological disorders as CNS controls mucus production and secretion via the efferent arm of the brain-gut axis. The aim was to use a brain-first model of sporadic AD induced by intracerebroventricular streptozotocin (STZ-icv) to dissect the efferent (i.e. brain-to-gut) effects of isolated central neuropathology on the GI mucus system. Quantification and morphometric analysis of goblet cell mucigen granules revealed altered GI mucus secretion in the AD model possibly mediated by the insensitivity of AD goblet cells to neurally-evoked mucosal secretion confirmed by ex vivo cholinergic stimulation of isolated duodenal rings. The dysfunctional efferent control of the GI mucus secretion results in altered biochemical composition of the mucus associated with reduced glycoprotein aggregation and binding capacity in vitro. Finally, functional consequences of the reduced barrier-forming capacity of the AD mucus are demonstrated using the in vitro two-compartment caffeine diffusion interference model. Isolated central AD-like neuropathology results in the loss of efferent control of GI homeostasis via the brain-gut axis characterized by the insensitivity to neurally-evoked mucosal secretion, altered mucus constitution, and reduced barrier-forming capacity potentially increasing the susceptibility of STZ-icv rat model of AD to GI and systemic inflammation induced by intraluminal toxins, microorganisms, and drugs.

neuroscience↗

bioRxiv2022

The absence of gastrointestinal redox dyshomeostasis in the brain-first rat model of Parkinson's disease induced by bilateral intrastriatal 6-hydroxydopamine

The gut-brain axis plays an important role in Parkinsons disease (PD) by acting as a route for vagal propagation of aggregated -synuclein in the gut-first endophenotype and as a mediator of gastrointestinal dyshomeostasis via the nigro-vagal pathway in the brain-first endophenotype of the disease. One important mechanism by which the gut-brain axis may promote PD is by regulating gastrointestinal redox homeostasis as overwhelming evidence suggests that oxidative stress plays a key role in the etiopathogenesis and progression of PD and the gastrointestinal tract maintains redox homeostasis of the organism by acting as a critical barrier to environmental and microbiological electrophilic challenges. The present aim was to utilize the bilateral intrastriatal 6-hydroxydopamine (6-OHDA) brain-first PD model to study the effects of isolated central pathology on redox homeostasis of the gastrointestinal tract. Three-month-old male Wistar rats were either not treated (intact controls; CTR) or treated bilaterally intrastriatally with vehicle (CIS) or 6-OHDA (6-OHDA). Motor deficits were assessed with the rotarod performance test and the duodenum, ileum, and colon were dissected for biochemical analyses 12 weeks after the treatment. Lipid peroxidation, total antioxidant capacity, low-molecular thiols, and protein sulfhydryls, the activity of total and Mn/Fe superoxide dismutases, and total and azide-insensitive catalase/peroxidase were measured. Univariate and multivariate models of redox biomarkers provide solid evidence against the existence of pronounced gastrointestinal redox dyshomeostasis. The results indicate that the dysfunction of the nigro-vagal system and not motor deficit may be a key mediator of gastrointestinal dyshomeostasis in brain-first 6-OHDA-induced rodent models of PD.

neuroscience↗

bioRxiv2022

Proposal of a simple open-source quantitative tribometric assay and its implementation for the assessment of the effects of redox-related alterations on the lubrication capacity of a commercial water-based lubricant gel

BackgroundUnderstanding molecular and biochemical mechanisms affecting biotribological properties of tissues, biological fluids, and drugs may accelerate the invention of novel drug formulations and targets and facilitate the discovery of etiopathogenetic mechanisms. Unfortunately, biotribometric equipment is expensive and unaffordable. The first aim was to assess whether PASTA, an open-source platform based on a hacked kitchen scale, can be adapted for the analysis of biotribometric properties. The second aim was to demonstrate the use of PASTA by studying the effects of oxidation on the lubricating properties of the commercial water-based lubricant. MethodsThe PASTA platform was adapted using a custom-made tribometric adapter attached to the bottom of the hacked kitchen scale connected to a computer via the NodeMCU ESP-32S. A commercial water-based lubricant was oxidized with 2,2-azobis(2-amidinopropane) dihydrochloride and/or protected against oxidation with glutathione. The samples were analyzed using a simple tribometric assay with the PASTA platform and the ORP-146S redox microsensor. ResultsA mastPASTA custom-made adapter enables the use of PASTA for reliable quantitative tribometric studies. Oxidation of the commercial water-based lubricant does not reduce its lubrication capacity, however, the addition of the antioxidant glutathione protects against the loss of its lubrication capacity upon exposure to air by a redox-unrelated mechanism. ConclusionPASTA can easily be adapted for studying tribological properties. The effects of the addition of antioxidants to water-based vaginal lubricants should be explored as a possible way to enhance durability and efficacy and increase their health benefits.

pharmacology and toxicology↗

bioRxiv2022

Sudan black lipid blot - a rapid and simple method for quantification of lipids in biological samples

Bioanalytical techniques for the isolation and quantification of total lipids in biological samples are an integral part of lipidomic workflows and widely used tools for metabolic assessment at the cellular and organismic levels. The most widely used protocol for the isolation, extraction, and quantification of total lipids in biological tissues was originally introduced by Folch et al.. It requires a relatively large amount of tissue and large volumes of lipid extracts for reliable assessment of lipid content using the gravimetric technique. Here, we propose a new method to overcome the aforementioned challenges based on the hypothesis that the partitioning coefficient of the widely used lysochrome diazo dye Sudan Black B between the lipid extract and ethylene glycol can be used to indirectly estimate the absolute concentration of lipids. The proposed method demonstrates great precision and linearity, requires minimal equipment, and enables the analysis of total lipid content in biological specimens available only in limited amounts by reducing the requirements for the input quantity by >300-fold for some tissues (e.g. fecal samples).

biochemistry↗

bioRxiv2022

In vitro analysis of catalase and superoxide dismutase mimetic properties of blue tattoo ink

Tattoo inks are comprised of different combinations of bioactive chemicals with combined biological effects that are insufficiently explored. Tattoos have been associated with oxidative stress; however, a recent N-of-1 study suggested that blue tattoos may be associated with suppressed local skin oxidative stress. The present study aimed to explore the attributes of the blue tattoo ink (BTI) that may explain its possible effects on redox homeostasis, namely the catalase (CAT) and superoxide dismutase (SOD)-mimetic properties that have been reported for copper(II) phthalocyanine (CuPC) - the main BTI constituent. Intenze Persian blue (PB) BTI has been used in the experiment. CAT and SOD-mimetic properties of PB and its pigment-enriched fractions were analyzed using the carbonato-cobaltate (III) formation-derived H2O2 dissociation and 1,2,3-trihydroxybenzene autoxidation rate assays utilizing simple buffers and biochemical matrix of normal skin tissue as chemical reaction environments. CuPC-based tattoo ink PB and both its blue and white pigment-enriched fractions demonstrate CAT and SOD-mimetic properties in vitro with effect sizes demonstrating a substantial dependence on the biochemical environment. PB constituents act as inhibitors of CAT but potentiate its activity in the biochemical matrix of the skin. CuPC-based BTI can mimic antioxidant enzymes, however chemical constituents other than CuPC (e.g. the photoreactive TiO2) seem to be at least partially responsible for the BTI redox-modulating properties.

pharmacology and toxicology↗

bioRxiv2022

Non-alcoholic components of Pelinkovac, a Croatian wormwood-based strong liquor, counteract the inhibitory effect of high ethanol concentration on catalase in vitro

Antioxidant enzyme catalase protects the cells against alcohol-induced oxidative stress by scavenging free radicals and metabolizing alcohol. Concentrations of ethanol present in alcoholic beverages can inhibit catalase and foster oxidative stress and alcohol-induced injury. Non-alcoholic components of pelinkovac counteract the inhibitory effects of high ethanol concentration and acidic pH on catalase in vitro.

pharmacology and toxicology↗

bioRxiv2021

The effect of acute oral galactose administration on the redox system of the rat small intestine

Galactose is a ubiquitous monosaccharide with important yet incompletely understood nutritive and physiological roles. Chronic parenteral D-galactose administration is used for modeling aging-related pathophysiological processes in rodents due to its ability to induce oxidative stress (OS). Conversely, chronic oral D-galactose administration prevents and alleviates cognitive decline in a rat model of sporadic Alzheimers disease indicating galactose may exert beneficial health effects by acting in the gut. The present aim was to explore acute time-response of intestinal redox homeostasis following oral administration of D-galactose. Male Wistar rats were euthanized at baseline (n=6), 30 (n=6), 60 (n=6), and 120 (n=6) minutes following orogastric administration of D-galactose (200 mg/kg). The overall reductive capacity, lipid peroxidation, the concentration of low molecular weight thiols (LMWT) and protein sulfhydryls (SH), the activity of Mn and Cu/Zn superoxide dismutases (SOD), reduced and oxidized fractions of nicotinamide adenine dinucleotide phosphates (NADPH/NADP), and hydrogen peroxide dissociation rate were analyzed in duodenum and ileum. Acute oral administration of D-galactose increased the activity of SODs and decreased intestinal lipid peroxidation and nucleophilic substrates (LMWT, SH, NADPH) indicating activation of peroxidative damage defense pathways. The redox system of the small intestine can acutely tolerate even high luminal concentrations of galactose (0.55 M) and oral galactose treatment is associated with a reduction rather than the increment of the intestinal OS. The ability of oral D-galactose to modulate intestinal OS should be further explored in the context of intestinal barrier maintenance, and beneficial cognitive effects associated with long-term administration of low doses of D-galactose.

biochemistry↗

bioRxiv2021

DIVERGENT EFFECT OF CENTRAL INCRETIN RECEPTORS INHIBITION IN A RAT MODEL OF SPORADIC ALZHEIMER'S DISEASE

The incretin system is an emerging new field that might provide valuable contributions to the research of both pathophysiology and therapeutic strategies in the treatment of diabetes, obesity, and neurodegenerative disorders. This study aimed to explore the role of central glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP) on cell metabolism and energy in the brain as well as on the levels of these incretins, insulin and glucose, by inhibiting the central incretins receptors following intracerebroventricular administration of the respective antagonists in healthy rats and a streptozotocin-induced rat model of sporadic Alzheimers disease (sAD). Chemical ablation of the central GIP receptor (GIPR) or GLP-1 receptor (GLP-1R) in healthy and diseased animals indicated a region-dependent role of incretins in the brain cell energy and metabolism and central incretin-dependent modulation of peripheral hormone secretion, markedly after GIPR inhibition, as well as a dysregulation of the GLP-1 system in experimental sAD.

neuroscience↗

bioRxiv2021

Disbalance of the intestinal epithelial cell turnover and apoptosis in a rat model of sporadic Alzheimer's disease

BackgroundDyshomeostasis of the gastrointestinal (GI) system is investigated as a potential contributor to metabolic dysfunction, systemic and neuro-inflammation recognized as important pathophysiological drivers of neurodegeneration. Gastrointestinal redox dyshomeostasis and dysfunctional brain-gut incretin axis have been reported in the rat model of insulin-resistant brain state (IRBS)-driven neurodegeneration induced by intracerebroventricular administration of streptozotocin (STZ-icv). The aim was to assess i) whether GI oxidative stress is accompanied by structural and functional changes of the epithelial barrier; ii) whether the brain glucose-dependent insulinotropic polypeptide receptor (GIP-R) is also involved in redox regulation of the gut; and iii) whether the STZ-icv brain-gut axis is resistant to pharmacological inhibition of the brain GIP-R. MethodsForty three-month-old male Wistar rats were treated with 3mg/kg STZ-icv or vehicle. One month later the animals were randomized to receive either saline or 85 g/kg GIP-R inhibitor [Pro3]-GIP intracerebroventricularly and sacrificed 30 minutes later. Thiobarbituric acid reactive substances (TBARS) were measured in plasma and duodenum. Duodenal sections were subjected to morphometric analysis. Caspase-3 expression and activation were analyzed by western blot and spatial signal analysis was done by multiplex fluorescent signal amplification (MFSA). Data were analyzed by linear and linear mixed modeling, and exploration was done by principal component analysis. ResultsInhibition of the brain GIP-R decreased plasma TBARS in the controls and the STZ-icv animals and increased duodenal TBARS only in the controls. Acute inhibition of brain GIP-R affects duodenal epithelial cell, but not villus structure, while all morphometric parameters were altered in the STZ-icv-treated animals. Morphometric changes in the STZ-icv animals were accompanied by reduced levels of activated and total regulator of apoptosis - caspase-3. Acute inhibition of brain GIP-R inactivated duodenal apoptosis at the level of caspase-3 activation. ConclusionsBrain GIP-R is involved in the regulation of the systemic and duodenal redox homeostasis and epithelial function. Duodenal oxidative stress in the STZ-icv rats is accompanied by the resistance of the brain-gut GIP axis and morphological changes indicative of abnormal epithelial cell turnover and dysfunctional GI barrier. Dysfunction of the brain-gut incretin axis might be an important etiopathogenetic factor in neurodegeneration and a potential pharmacological target.

neuroscience↗

bioRxiv2021

Failure of the brain glucagon-like peptide-1-mediated control of intestinal redox homeostasis in a rat model of sporadic Alzheimer's disease

The gastrointestinal system may be involved in the etiopathogenesis of the insulin-resistant brain state (IRBS) and Alzheimers disease (AD). Gastrointestinal hormone glucagon-like peptide-1 (GLP-1) is being explored as a potential therapy as activation of brain GLP-1 receptors (GLP-1R) exerts neuroprotection and controls peripheral metabolism. Intracerebroventricular administration of streptozotocin (STZ-icv) is used to model IRBS and GLP-1 dyshomeostasis seems to be involved in the development of neuropathological changes. The aim was to explore i) gastrointestinal homeostasis in the STZ-icv model ii) assess whether the brain GLP-1 is involved in the regulation of gastrointestinal redox homeostasis and iii) analyze whether brain-gut GLP-1 axis is functional in the STZ-icv animals. Acute intracerebroventricular treatment with exendin-3(9-39)amide was used for pharmacological inhibition of brain GLP-1R in the control and STZ-icv rats, and oxidative stress was assessed in plasma, duodenum and ileum. Acute inhibition of brain GLP-1R increased plasma oxidative stress. TBARS were increased, and LMWT, SH, and superoxide dismutase (SOD) were decreased in the duodenum, but not in the ileum of the controls. In the STZ-icv, TBARS and CAT were increased, LMWT and SH were decreased at baseline, and no further increment of oxidative stress was observed upon central GLP-1R inhibition. The presented results indicate that i) oxidative stress is increased in the duodenum of the STZ-icv rat model of AD, ii) brain GLP-1R signaling is involved in systemic redox regulation, iii) brain-gut GLP-1 axis regulates duodenal, but not ileal redox homeostasis, and iv) brain-gut GLP-1 axis is dysfunctional in the STZ-icv model.

neuroscience↗

bioRxiv2021

Is galactose a hormetic sugar? Evidence from rat hippocampal redox regulatory network

Galactose is a ubiquitous simple monosaccharide with yet incompletely understood biochemical and physiological role. Most of what we currently know about galactose is based on induction from the research on inherited disorders of galactose metabolism and animal models that exploit galactose-induced oxidative stress to model aging in rodents, however, recent evidence also demonstrates unique properties of galactose to conserve cellular function during the periods of starvation, and prevent and alleviate cognitive deficits in a rat model of sporadic Alzheimers disease. Here, we try to understand the molecular background of both detrimental and beneficial effects of galactose by exploring the acute systemic and hippocampal biochemical changes upon oral administration of galactose solution focusing primarily on the components of the redox regulatory network (RRN). Although orogastric gavage of galactose solution (200 mg/kg) was insufficient to induce systemic RRN disbalance in the first two hours upon administration, analysis of hippocampal RRN revealed a mild pro-oxidative shift accompanied by a paradoxical increase in tissue reductive capacity, suggesting overcompensation of endogenous antioxidant systems in the response to the pro-oxidative stimulus. The more thorough analysis revealed that galactose-induced increment of reductive capacity was accompanied by inflation of the hippocampal pool of nicotinamide adenine dinucleotide phosphates indicating ROS detoxification through disinhibition of the oxidative pentose phosphate pathway flux, reduced neuronal activity, and upregulation of Leloir pathway gatekeeper enzyme galactokinase-1. Based on the observed findings, and in the context of previous work on galactose, we propose a hormetic hypothesis of galactose action suggesting that the protective effects of galactose might be inseparable from its pro-oxidative effects at the biochemical level.

neuroscience↗

bioRxiv2020

Publishing of COVID-19 Preprints in Peer-reviewed Journals, Preprinting Trends, Public Discussion and Quality Issues

IntroductionCOVID-19-related (vs. non-related) articles appear to be more expeditiously processed and published in peer-reviewed journals. We aimed to evaluate: (i) whether COVID-19-related preprints were favored for publication, (ii) preprinting trends and public discussion of the preprints, and (iii) the relationship between the publication topic (COVID-19-related or not) and quality issues. MethodsManuscripts deposited at bioRxiv and medRxiv between January 1 and September 27 were assessed for the probability of publishing in peer-reviewed journals, and those published were evaluated for submission-to-acceptance time. The extent of public discussion was assessed based on Altmetric and Disqus data. The Retraction Watch Database and PubMed were used to explore the retraction of COVID-19 and non-COVID-19 articles and preprints. ResultsWith adjustment for the preprinting server and number of deposited versions, COVID-19-related preprints were more likely to be published within 120 days since the deposition of the first version (OR=2.04, 95%CI 1.87-2.23) as well as over the entire observed period (OR=1.42, 95%CI 1.33-1.52). Submission-to-acceptance was by 38.67 days (95%CI 34.96-42.39) shorter for COVID-19 articles. Public discussion of preprints was modest and COVID-19 articles were overrepresented in the pool of retracted articles in 2020. ConclusionCurrent data suggest a preference for publication of COVID-19-related preprints over the observed period.

scientific communication and education↗

bioRxiv2020

griPASTA: A hacked kitchen scale for quantification of grip strength in rodents

Assessment of neuromuscular function is critical for understanding pathophysiological changes related to motor system dysfunction in many rodent disease models. Among methods used for quantification of grip performance in rodents, gauge-based grip strength meters provide the most reliable results, however, such instruments are unaffordable by many laboratories. Here we demonstrate how to build a rodent grip strength apparatus from scratch using a digital kitchen scale, an empty cage, and a microcontroller, with both hardware and software being completely open-source to enable maximal modularity and flexibility of the instrument in concordance with the principles of open-source bioinstrumentation. Furthermore, we test the griPASTA system for assessment of increased muscular rigidity in the proof-of-concept experiment in the rat model of Parkinsons disease induced by intrastriatal administration of 6-hydroxydopamine (6-OHDA). Finally, the importance of bioinstrumental customization is demonstrated by utilizing griPASTA for assessment of trial speed from initial-to-maximal deflection time segments and controlling for its potential confounding effects on the grip strength. Significance StatementNeuromuscular function analyzed by grip strength performance tests is an integral part of motor system neuroscience and neurotoxicology. Strain gauge-based grip strength meters provide the most reliable results, however, commercial solutions are unaffordable by many. Consequently, cheap semi-quantitative tests are often used at the expense of precision and reliability. We propose griPASTA - a simple and robust open-source grip strength platform made from an ordinary kitchen scale. griPASTA could improve the quality and reproducibility of grip strength experiments by enabling researchers to obtain quantitative grip strength data in high resolution using a highly customizable platform.

neuroscience↗

bioRxiv2020

Nitrocellulose redox permanganometry: a simple method for reductive capacity assessment

We propose a rapid, simple and robust method for measurement of reductive capacity of liquid and solid biological samples based on potassium permanganate reduction followed by trapping of manganese dioxide precipitate on a nitrocellulose membrane. Moreover, we discuss how nitrocellulose redox permanganometry (NRP) can be used for high-throughput analysis of biological samples and present HistoNRP, its modification used for detailed analysis of reductive capacity spatial distribution in tissue with preserved anatomical relations.

biochemistry↗