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Oct 2025 DOI 10.14302/issn.3070-2313.jeh-25-5757
P. Austin DavidCorresponding author
The Ames dwarf mice have a recessive mutation of the PROP-1 gene that produces hereditary dwarfism. The abnormality is responsible for an anterior-pituitary deficiency that results in a substantial reduction of growth hormone, thyroid-stimulating hormone, and prolactin. These mice are smaller in size than their normal siblings but live approximately twice as long. The normal siblings do not have the mutation, and therefore still have the typical levels of the three hormones. The purpose of the present research was to determine if the reduced hormones in the Ames dwarf mice affected their ability to learn and delayed the age-related loss of memory. In general, the hypotheses proposed indicate that there will be no significant differences on the tasks in regards to the genotype or the age of the mice. These hypotheses would support previous research and suggest a delay in the age-related loss of memory and the ability to learn in the Ames dwarf mice. Learning was assessed using a matching-to-sample procedure, while memory was evaluated using a modified radial-arm procedure. Generally, the age of the animals had little to do with their performance on any of the tasks. Taken together, the overall results showed no significant differences in accuracy between any of the groups of mice or a behavioral decline as the mice age. The present results are consistent with the theory of a delayed age-related behavioral decline in the Ames dwarf mice.
Nov 2022 DOI 10.14302/issn.2641-4538.jphi-22-4235
E. Obeten KebeCorresponding author
Department of Human Anatomy, Faculty of Biomedical sciences, Kampala International university, Uganda
This study investigates the effect of Aqueous extract of abelmoschus esculentus on the microanatomy of the small, large intestine and stomach and the body weight of Wister rats. Twenty-one adults male wistar rats weighing between 100-120 grams were assigned into three groups consisting of seven rats each; Group A (control), Group B (low dose), and Group C (high dose). The rats in the control group were fed with fed with feed and water only while the rats in groups B and C were treated with 0.1mg/kg body weight and 3.0mg/kg body weight of abelmoschus esculentus respectively for 14 days. At the end of administration, the final weights of all rats were recorded before sacrifice using cervical dislocation and the small, large intestine and the stomach were harvested, processed and stained using H&E stain. The results were revealed as significant (p<0.05) increased in the mean body weight compared with the weight in the control groups and experimental groups. The treated animal groups revealed increased cellularity, focal metaplasia of the mucosal cells with villous disruption in the small intestine and dysplasia of the mucosal with loss of epithelial shape in large intestine. The stomach histology showed gastric pits with goblet cells smooth muscles layer and surface epithelium in the control group. Sections from the low dose treated group showed deep epithelical gastric pit areas with marked depletion of pits and goblet cells while the high dose treated group revealed dysplasia of gastric pits, goblet cells and smooth muscles appear mildly eroded.
Jan 2020 DOI 10.14302/issn.2474-9273.jbtm-19-3157
Jana SnehasisCorresponding author
Trivedi Science Research Laboratory Pvt. Ltd., Thane (W), Maharashtra, India.
Sleep biomarkers in brain such as melatonin, BDNF (Brain-derived neurotrophic factor), PGD2 (Prostaglandin D2), leptin, orexin-A, and acetylcholine were evaluated in the unpredictable chronic stress (UCS) rodent model in the presence of Consciousness Energy Healing Treated (the Trivedi Effect®) novel test formulation in male Sprague Dawley (SD) rats using ELISA assay. The test formulation was consisted of minerals (Zn, Fe, Cu, Se, Ca, Mg), vitamins (C, E, B6, B12, D3), β-carotene, ginseng, and cannabidiol isolate. The test formulation constituents were divided into two parts, one part of each ingredient was distinct as the untreated test formulation, while the other portion of the test formulation and a group of animals received Biofield Energy Healing Treatment by a renowned Biofield Energy Healer, Mr. Mahendra Kumar Trivedi. The level of melatonin in groups viz. G5 (Biofield Energy Treated Test formulation) and G7 (15-days pre-treatment of Biofield Energy Treated Test formulation) was significantly increased by 17.6% (p≤0.01) and 16%, respectively as compared with the disease control group (G2). Brain-derived neurotrophic factor (BDNF) level in brain was increased by 5.2% in G7 group as compared with the G4. Prostaglandins D2 (PGD2) level was significantly (p≤0.001) increased by 12.7%, 18.1%, 23.7%, and 30.7% in the G6, G7, G8 (15 days pre-treatment of Biofield Energy Treated Test formulation to the Biofield Energy Treatment per se rats), and G9 (untreated test formulation to the Biofield Energy Treatment per se to the rats) groups, respectively as compared with the G2. The level of leptin after Biofield Energy Treatment and with the test formulation was altered. However, orexin-A level was significantly decreased by 37.1% (p≤0.05), 32.6%, 40.5% (p≤0.05), 44.4% (p≤0.05), and 28.2% in the G5, G6, G7, G8, and G9 groups respectively, as compared with the G2. Similarly, acetylcholine (Ach) level was significantly (p≤0.001) decreased by 42.5%, 49.2%, 40.1%, 47.9%, and 45% in the G5, G6, G7, G8, and G9 groups, respectively as compared with the G2. Overall, the results showed the significant slowdown the stress-related disease progression and its complications/symptoms in the preventive in the Biofield Energy Treatment group per se and/or Biofield Energy Treated Test formulation groups (viz. G6, G7, G8, and G9) comparatively with the disease group. The Trivedi Effect® showed increased level of melatonin and decreased levels of insomnia related brain biomarkers which might be helpful to induce better sleep in human.
May 2017 DOI 10.14302/issn.2470-0436.jos-17-1453
Zhang JieCorresponding author
Department of Ophthalmology, Faculty of Medical and Health Sciences, University of Auckland, Private bag 92019, Auckland 1142, New Zealand.
Purpose: High intraocular pressure (IOP) is known to result in retinal ganglion cell (RGC) loss, both with chronically raised intraocular pressure (such as with glaucoma) and with acute raises in pressure (due to injury or acute angle closure). Because IOP is often raised during ocular surgery, the purpose of this study was to evaluate the effect of transient moderate IOP on retinal function, RGC survival and the expression of Connexin 43 (Cx43) and glial fibrillary acidic protein (GFAP), ubiquitously expressed central nervous system (CNS) proteins that are known to be elevated during the retinal inflammatory response to injury. Materials and Methods: Wistar rats were exposed to transient IOP at 40 mmHg for 5 or 30 minutes, and 60 mmHg for 5 minutes (via cannulation of the anterior chamber with a saline reservoir raised to a height corresponding to the desired IOP), mimicking potential IOP rises during surgery such as DSAEK and some laser procedures (LASIK and femtosecond laser cataract surgery). Separate groups of animals had IOP maintained at 10 mmHg for 5 or 30 minutes as cannulation controls, or 120 mmHg for 60 minutes as positive controls. Changes in the optic nerve and retina were assessed immunohistochemically for GFAP and Cx43 expression. Retinal function was assessed using electroretinography (ERG) recorded at baseline and 14 days after the IOP rise and compared with RGC counts. Results: Results showed that there was a differential GFAP labelling pattern observed in the anterior optic nerve in the 40 mmHg 30 minute and 60 mmHg 5 minute groups 4 hours after manipulation. Gap junction protein Cx43 was minimally up-regulated in the retina in the short-term. There was, however, minimal long-term effect on retinal function and no RGC loss. Conclusions: n conclusion, elevations of IOP that are short in duration such as those occurring during surgical procedures, do not cause significant changes long-term in retinal function or RGC survival. Key Messages: Cx43 and GFAP are known to be elevated during the retinal inflammatory response to injury. No previous study has explored the effect of moderate and relatively short increases in IOP on the initial inflammatory response. We observed a mild glial inflammatory response in the anterior optic nerve, but only a minimal up-regulation of Cx43. However, transient and moderate IOP rises did not induce long term disruption to RGC function or number as measured by electrophysiology and RGC counts, respectively. This is applicable to clinical practice, as it means the IOP elevations that occur during some surgical procedures are unlikely to be causing long term damage in retinal function or RGC survival.
Apr 2024 DOI 10.14302/issn.2997-2086.jfs-23-4651
Osama Siddiqui MuhammadCorresponding author
This article has been retracted on April 10, 2025. VIEW THE RETRACTION NOTICE (https://doi.org/10.14302/issn.2997-2086.jfs-25-5857) Myelomeningocele (MMC), a class of spina bifida is a type of neural tube defect. According to the U.S. Centers for Disease Control and Prevention, each year approximately 1,400 babies born in the United States have spina bifida. The disease manifests with the lack of skin and bone covering the caudal part of the spinal cord. The patient developing such a condition often develops lifelong impaired lower limb mobility accompanied by hydrocephalus, and urinary and bowel incontinence. The available interventions include prenatal and postnatal surgery to fuse the dura. Prenatal surgery performed before 26 weeks of gestation reduces the risk of death or the need for ventriculoperitoneal shunting. It also enhanced results on a comprehensive index for mental and motor function. When compared to postnatal surgery, prenatal surgery reduces the manifestation of several secondary outcomes, including the degree of hindbrain herniation seen in the Chiari II malformation. Stem cell therapy for MMC on animal models of chick, ovine, and rodents with reported cases 15/63, 15, and 136, respectively, using human Embryonic Stem Cells (hESCs), Neural Stem Cells (NSCs), Mesenchymal Stem Cells (MSCs) showed significant coverage of MMC defect and slight neurogenesis was also observed. With an understanding of medical literature about in-utero regenerative capacity, it is to be appreciated that placental stem cells surgically seeded within a biocompatible scaffold of the cell patches can play a part in alleviating the spinal cord manifestation associated with MMC. Documented animal studies show that incorporating Placental Mesenchymal Stem Cells in prenatal surgery has reported improved neurogenesis and lower limb mobility. In an ovine myelomeningocele model, the development of in-utero myelomeningocele repair with human Placental Mesenchymal Stem Cells seeded onto an extracellular matrix (PMSC-ECM) enhances motor findings. The clinical trial for the first stem cell therapy on human subjects known as the “CuRe Trial: Cellular Therapy for In Utero Repair of Myelomeningocele.” is expected to be finished by 2030. So far, the cases undergoing treatment have shown significant leg movement and a greater degree of bowel and urinary control. This FDA-approved clinical trial is envisioned to be the future of treating MMC.
Feb 2021 DOI 10.14302/issn.2471-2140.jaa-21-3704
Jana SnehasisCorresponding author
Trivedi Science Research Laboratory Pvt. Ltd., Thane (W), Maharashtra, India.
The aim of the study was to evaluate the antioxidant potential of Biofield Energy Healing (the Trivedi Effect®) based test formulation using TNBS-induced colitis animal model. Each ingredient of the test formulation was divided into two parts. One part was denoted as the control without any Biofield Energy Treatment, while the other part was treated with Biofield Energy Treatment by Mr. Mahendra Kumar Trivedi and defined as the Biofield Energy Treated test formulation. The colon tissue was used for the estimation of anti-oxidation activity for catalase (CAT), glutathione (GSH), lipid peroxidation (LPO) product, myeloperoxidase (MPO), superoxide dismutase (SOD), and glutathione peroxidase (GPx) using standard procedure. The antioxidant results showed that the CAT level was significantly increased by 95.4% (p≤0.001), 72.3%, 47.6%, and 13.9% in the Biofield Energy Treated test formulation (G5), Biofield treatment per se to animals (-15 days)(G6), Biofield Energy Treatment per se to animals plus Biofield Energy Treated test formulation (-15 day) (G8), and Biofield Energy Treatment per se to animals plus untreated test formulation (G9) groups, respectively as compared to the untreated test formulation group (G4). Further, colon GSH activity was found to be significantly increased by 23.2% (p≤0.05) 15.4%, and 15.5%, in G5, G6, and G9 groups, respectively with respect to G2 group. In addition, colon LPO activity data suggested that it was decreased by 12%, 17%, 18%, and 19.1% in G5, G6, Biofield Energy Treated test formulation (-15 day) (G7), and G8 groups, respectively, as compared with the G2 group. The level of MPO showed a significant (p≤0.001) reduced level by 27.9%, 22%, 14.5%, 16.6%, and 25.3% in G5, G6, G7, G8, and G9 groups, respectively as compared with the G2 group. The level of colon SOD was increased by 16.7% and 14.2% in the G5 and G9 groups, respectively as compared with the untreated test formulation, G4 group. Colon GPx level was increased by 177.6%, 71.4%, 71.4%, 161.2%, and 114.3% in G5, G6, G7, G8, and G9 groups, respectively as compared with the G2 group. Thus, it can be concluded that the Trivedi Effect®-Consciousness Energy Healing based test formulation and Biofield Energy per se has significant colon anti-oxidation profile, which can be used to improve many autoimmune and inflammatory diseases, stress management and prevention, and anti-aging by improving overall health.
May 2019 DOI 10.14302/issn.2644-1101.jhp-19-2766
Crespi FrancescoCorresponding author
Biology, CSK, Verona, Italy
Cholecystokinin (CCK) is found in high concentrations in cortical and limbic structures including the amygdala of rodents, and evidence has been gathered supporting a role for CCK in the neurobiology of anxiety. A variety of animal models have been used to study a central state of fear or anxiety, state that appears to produce a complex pattern of behaviors highly correlated with each other. It is now well established that the amygdala in particular is a critical link in the pathway through which sensory stimuli come to acquire fear evoking properties. The purpose of the proposed experiments is to study the role of the putative neurotransmitter CCK in fear and anxiety in vivo by means of a methodology coupling electrochemical and electrophysiological measurements in various brain areas. Indeed, the association of in vivo differential pulse voltammetry (DPV) with in vivo extracellular single unit recording could be able to provide concomitant physiological and neurochemical indications and to relate them to behavioral events. To further study and support the initial observations pharmacological experiments will also be performed by means of CCK receptor agonists and antagonists. This may eventually lead to development of more effective pharmacological strategies for treating clinical anxiety disorders.
Mar 2019 DOI 10.14302/issn.2379-7835.ijn-19-2578
E. Ahmed FaridCorresponding author
GEM Tox Labs, Institute for Research in Biotechnology, 2905 South Memorial Drive, Greenville, NC 27834, USA.
We present below a mechanistic cellular and molecular approaches for the development of Anti-Inflammatory biomarkersof Probiotic Bacteria in Fermented Foods. Probiotics are live microorganisms that promote human health by counteracting the noxious toxic gut microflora in human intestine, by modulating of the tight junctions, and by increasing mucin production, enforcing intestinal epithelial cell barrier function, modifying microbial community within the gut intestinal disorders, and improving immune responses associated with chronic inflammation in experimental animal models, collectively enhancing human health. Cytokine secretion by intestinal epithelial cells and macrophages are regulated by probiotics through key signaling pathways such as nuclear factor-κB and mitogen-activated kinases, resulting in alleviation of several disorders such as allergies, diabetes, obesity, heart diseases and cancer. MicroRNAs are small non-coding RNA molecules involved in transcriptional and post-translational regulation of gene expression by inhibiting gene translation. Using in vitro and in vivo approaches in cell lines and mice models to study effects of probiotic conditional media and heat-killed bacterial strains with anti-inflammatory effect to elucidate the mechanisms by which probiotics affect signaling pathways, and by using global cytokine and microRNA gene expression analyses approaches to develop biomarkers for studying different pro- and anti-inflammatory activities, and using statistical approaches to analyse the data, we show that cytokines and miRNAs have an essential role in regulation of cancerous and inflammatory pathways. This mechanistic approach will result in developing specific disease biomarkers for the early diagnosis of certain pathogenic states, as well as evaluating the effect of different dietary components on developed biomarkers in health states that will promote and enhance human health. Comparing the concordance of the in vitro to the in vivo research findings will confirm the correspondence of both approaches to each other. Moreover, this study will have a major public health relevance in elucidating the role of miRNAs and their targets in inflammation, paving the way to diagnosing and treating of pathogenic human disease stages.
Aug 2018
Bai QifengCorresponding author
Key Lab of Preclinical Study for New Drugs of Gansu Province, School of Basic Medical Sciences, Lanzhou University, Lanzhou, Gansu 730000, P. R. China
Drug design, referred to the fields of pharmacology, biotechnology and medicine, is in silico, in vitro and in vivo assay processes of finding new candidate medications based on the biological targets. The in silicoexperiments of drug discovery are involved in the macromolecular structure databases, small molecule databases, molecular docking, de novo drug design and molecular dynamics simulations. The in vitro experiments of drug discovery need evaluate the direct interaction information between ligands and targets as well as the function of ligands on signaling pathway in the cell. The in vivo experiments of drug discovery give the convincing evidence for preclinical trial at the physiological level. In this review, we outline the drug design components of databases, virtual screening tools, biochemical assays, cell-based system and animal models.
Mar 2017 DOI 10.14302/issn.2572-5424.jgm-16-1352
Qaiser Shah SyedCorresponding author
Biochemistry Section, Institute of Chemical Sciences, University of Peshawar, Peshawar, KPK, Pakistan.
In this investigation, Rifabutin dithiocarbamate (RFND) was labeled with Technetium-99m (99mTc) using tricarbonyl technique. The labeled RFND was further characterized in terms of radiochemical purity, stability in saline & serum, in vitro bacterial binding, biodistribution in animal model rats and for scintigraphic accuracy in animal model rabbit. Finally different radiobiological characteristics of the 99mTc(CO)3-RFND was compared with the recently reported 99mTc-RFN. It was observed that the dithiocarbamate form of RFN showed better radiochemical purity, stability in saline, bacterial binding, biodistribution and targeted imaging than the recently reported 99mTc-RFN. These better radiobiological parameters posed 99mTc(CO)3-RFND as a more reliable agent for tuberculosis imaging.
Aug 2016 DOI 10.14302/issn.2474-9273.jbtm-16-1151
Xing GuoqiangCorresponding author
Departments of Anesthesiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814
Oxidative stress mediated neural cell death is thought to be involved in the progression of secondary cell injury following brain trauma. Agents that can block oxidative stress-related injury could be potential therapies for TBI. Resveratrol, a polyphenol found in plants and red wine, is cytoprotective due to its potent antioxidant activities. To further understand how resveratrol could affect oxidative stress-induced injury, we hypothesized that the cytoprotective activities of resveratrol could be dose-dependent. In this study, resveratrol-induced cytoprotection was evaluated in cultured astrocytes. Primary rat astrocytes were cultured in T-75 flasks to a confluence of 80% before being plated onto 96-well plates. After 24 hours of acclimation, astrocytes were treated with various doses of hydrogen peroxide (H2O2) (0.1, 0.25, 0.5 and 1 µM) and resveratrol (25, 50, 75, 100 µM), respectively. Cell viability was determined 24 hours later using Alamar Blue Assay. Treatment of astrocytes with 0.5 mM H2O2, left 65% of astrocytes non-viable whereas treatment of astrocytes with 0.1 mM H2O2 had no effect on astrocytes viability; whereas 1 mM, H2O2 caused total loss of astrocyte viability. Resveratrol treatment at 75 µM and 100 µM has reduced 0.5 mM H2O2-induced cytotoxicity in astrocytes by 50%. Immunostaining with GFAP also confirmed these findings about the cytoprotective effects of resveratrol in astrocytes exposed to H2O2. These results suggest that resveratrol could be a potential neuroprotective agent in TBI due to its antioxidant properties. Further studies are needed to evaluate the long- term effects of resveratrol in animal models of TBI.
Jul 2016 DOI 10.14302/issn.2644-0105.jbfb-16-1121
Anderson GeorgeCorresponding author
CRC Scotland & London, Eccleston Square, London, UK.
The biological underpinnings that drive the plethora of breastfeeding benefits over formula-feeding is an area of intense research, given the cognitive and emotional benefits as well as the offsetting of many childhood- and adult-onset medical conditions that breast-feeding provides. In this article, we review the research on the role of melatonin in driving some of these breastfeeding benefits. Melatonin is a powerful antioxidant, anti-inflammatory and antinociceptive as well as optimizing mitochondrial function. Melatonin is produced by the placenta and, upon parturition, maternal melatonin is passed to the infant upon breastfeeding with higher levels in night-time breast milk. As such, some of the benefits of breastfeeding may be mediated by the higher levels of maternal circulating night-time melatonin, allowing for circadian and antioxidant effects, as well as promoting the immune and mitochondrial regulatory aspects of melatonin; these actions may positively modulate infant development. Herein, it is proposed that some of the benefits of breastfeeding may be mediated by melatonin's regulation of the infant's gut microbiota and immune responses. As such, melatonin is likely to contribute to the early developmental processes that affect the susceptibility to a range of adult onset conditions. Early research on animal models has shown promising results for the regulatory role of melatonin.
Mar 2016 DOI 10.14302/issn.2470-5020.jnrt-15-800
Huang LiliCorresponding author
Dept. Biological Psychology, Donders Center for Cognition, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen.
Although clinical trials in refractory epilepsy are currently carried out, the field of deep brain stimulation (DBS) in epilepsy is still at its initial stage. Little is known about where, when and how to stimulate and what would be the short and long consequences. Animal studies might provide clinicians with new ideas regarding targets for DBS. Here an overview is given regarding old and new targets in rodent models of temporal lobe epilepsy. The evidence from animal models showed that stimulation of the subiculum – either in responsive or scheduled manner - is anticonvulsant in different seizure and epilepsy models, indicating that the subiculum might be a promising candidate for DBS targets. For the rest, the antiepileptic effects of low frequency stimulation were established mostly in kindling models. The presence of a critical time window in which stimulation was effective following after discharges on kindling acquisition, demonstrates that timing of DBS is an important factor for the anticonvulsant effects of DBS.
Mar 2016 DOI 10.14302/issn.2470-0436.jos-15-739
P. Sarthy VijayCorresponding author
Department of Ophthalmology, Northwestern University Feinberg School of Medicine, Chicago, IL 606111.
Ciliary neurotrophic factor (CNTF) is a well-tested, neuroprotective agent that has been shown to retard photoreceptor degeneration in several animal models of retinitis pigmentosa. The molecular mechanisms underlying CNTF-mediated neuroprotection are currently not understood. CNTF could act directly on photoreceptors or it could act indirectly by stimulating Müller glial cells to produce photoreceptor neuroprotective agents. To better characterize CNTF action on Müller cells, we have studied signaling pathways activated by CNTF using an established retinal Müller cell line, rMC-1. RNA was isolated from CNTF-treated cultures, and suppressor of signal transducer and activator of transcription (SOCS3) and Glial fibrillary acidic protein (GFAP) transcript levels were assessed by quantitative real-time PCR. Immunoblotting was used to examine activation ofmitogen activated protein kinase (ERK1/2/MAPK) and phosphoinositide 3-kinase (PI3-K)/Aktpathways in response to CNTF. Additionally, the level of5' AMP-activated protein kinase (AMPK), an enzyme that plays a key role in cellular energy homeostasis levels, was determined by immunoblotting. CNTF treatment resulted strong upregulation of SOCS3 and GFAP transcripts that were blocked by expression of a dominant-negative STAT3 mutant. CNTF treatment also resulted in transient activation of ERK1/2/MAPK but not PI3K/Akt signaling pathway. There was no change in activation of AMPK. We conclude that CNTF treatment leads to stimulation of JAK-STAT and MAPK signaling pathways but not the PI3K/AKT pathway, associated with cell death, in Müller cells.
Sep 2013 DOI 10.14302/issn.2374-9431.jbd-13-226
Jayne McKnight AmyCorresponding author
Nephrology Research, Centre for Public Health, Queen’s University of Belfast
The number of individuals with diabetes is increasing worldwide and a large subset of those affected will develop diabetic nephropathy. Diabetic nephropathy is the leading cause of end-stage renal disease, has serious health consequences for affected individuals, and represents a major monetary cost to healthcare providers. Technological and analytical developments have enabled large-scale, collaborative studies that are revealing risk factors associated with diabetic nephropathy. However, much of the inherited predisposition and biological mechanisms underpinning risk of this disease remain to be identified. Meta-analyses and integrated pathway studies are becoming an increasingly important part of research for diabetic nephropathy including, genetic, epigenetic, transcriptomic, proteomic research, clinical observations and the development of animal models. This report highlights current bioinformatic resources and standards of reporting to maximise interdisciplinary research for diabetic nephropathy. The identification of an -Omics profile that can lead to earlier diagnosis and / or offer improved clinical evaluation of individuals with diabetes would not only provide significant health benefits to affected individuals, but may also have major utility for the efficient use of healthcare resources.