Abnormalities In Animals Research Articles

High NaCl Concentrations in Water Are Associated with Developmental Abnormalities and Altered Gene Expression in Zebrafish.

Salt is frequently introduced in ecosystems, where it acts as a pollutant. This study examined how changes in salinity affect the survival and development of zebrafish from the two-cell to the blastocyst stage and from the blastocyst to the larval stage. Control zebrafish embryos were cultured in E3 medium containing 5 mM Sodium Chloride (NaCl), 0.17 mM Potassium Chloride (KCL), 0.33 mM Calcium Chloride (CaCl2), and 0.33 mM Magnesium Sulfade (MgSO4). Experiments were conducted using increasing concentrations of each individual salt at 5×, 10×, 50×, and 100× the concentration found in E3 medium. KCL, CaCl2, and MgSO4 did not result in lethal abnormalities and did not affect early embryo growth at any of the concentrations tested. Concentrations of 50× and 100× NaCl caused embryonic death in both stages of development. Concentrations of 5× and 10× NaCl resulted in uninflated swim bladders in 12% and 65% of larvae, compared to 4.2% of controls, and caused 1654 and 2628 genes to be differentially expressed in blastocysts, respectively. The ATM signaling pathway was affected, and the Sonic Hedgehog pathway genes Shh and Ptc1 implicated in swim bladder development were downregulated. Our findings suggest that increased NaCl concentrations may alter gene expression and cause developmental abnormalities in animals found in affected ecosystems.

Knockdown of the Non-canonical Wnt Gene Prickle2 Leads to Cerebellar Purkinje Cell Abnormalities While Cerebellar-Mediated Behaviors Remain Intact.

Autism spectrum disorders (ASD) involve brain wide abnormalities that contribute to a constellation of symptoms including behavioral inflexibility, cognitive dysfunction, learning impairments, altered social interactions, and perceptive time difficulties. Although a single genetic variation does not cause ASD, genetic variations such as one involving a non-canonical Wnt signaling gene, Prickle2, has been found in individuals with ASD. Previous work looking into phenotypes of Prickle2 knock-out (Prickle2-/-) and heterozygous mice (Prickle2-/+) suggest patterns of behavior similar to individuals with ASD including altered social interaction and behavioral inflexibility. Growing evidence implicates the cerebellum in ASD. As Prickle2 is expressed in the cerebellum, this animal model presents a unique opportunity to investigate the cerebellar contribution to autism-like phenotypes. Here, we explore cerebellar structural and physiological abnormalities in animals with Prickle2 knockdown using immunohistochemistry, whole-cell patch clamp electrophysiology, and several cerebellar-associated motor and timing tasks, including interval timing and eyeblink conditioning. Histologically, Prickle2-/- mice have significantly more empty spaces or gaps between Purkinje cells in the posterior lobules and a decreased propensity for Purkinje cells to fire action potentials. These structural cerebellar abnormalities did not impair cerebellar-associated behaviors as eyeblink conditioning and interval timing remained intact. Therefore, although Prickle-/- mice show classic phenotypes of ASD, they do not recapitulate the involvement of the adult cerebellum and may not represent the pathophysiological heterogeneity of the disorder.

Virus as Teratogenic Agents.

Viral infectious diseases are important causes of reproductive disorders, as abortion, fetal mummification, embryonic mortality, stillbirth, and congenital abnormalities in animals and in humans. In this chapter, we provide an overview of some virus, as important agents in teratology.We begin by describing the Zika virus, whose infection in humans had a very significant impact in recent years and has been associated with major health problems worldwide. This virus is a teratogenic agent in humans and has been classified as a public health emergency of international concern (PHEIC).Then, some viruses associated with reproductive abnormalities on animals, which have a significant economic impact on livestock, are described, as bovine herpesvirus, bovine viral diarrhea virus, Schmallenberg virus, Akabane virus, and Aino virus.For all viruses mentioned in this chapter, the teratogenic effects and the congenital malformations associated with fetus and newborn are described, according to the most recent scientific publications.

Herbal therapies for weight gain and metabolic abnormalities induced by atypical antipsychotics: a review article.

Psychosis is a state of mind that makes it difficult to determine what is real and what is not. Psychosis can have serious negative effects. Like many psychiatric phenomena, psychosis has a variety of causes, such as schizophrenia, bipolar disorder, and psychotic depression. Antipsychotic medications, psychotherapy, and social support are the most common treatments. Antipsychotic drugs reduce the symptoms of psychosis by changing brain chemistry. Based on the mechanism of action, antipsychotics have two groups, typical and atypical. Most people who take antipsychotics experience side effects. People taking typical antipsychotics tend to have higher rates of extrapyramidal side effects, but some atypical drugs, especially olanzapine, are associated with the risk of significant weight gain, diabetes, and metabolic syndrome, which, in turn, increases the risk of atherosclerotic cardiovascular disease and premature death. Physical exercise, diet regimen, psychoeducation, monotherapy, or switching to an alternative antipsychotic are strategies to correct metabolic aberrates in atypical antipsychotic users. In light of several successful studies on the use of medicinal plants to control metabolic syndrome, this article briefly reviews the studies on some herbal medications for the management of metabolic disorders associated with atypical antipsychotics and discusses probable mechanisms. Therefore, we searched the Cochrane, Scopus, PubMed, and Google Scholar databases for works published before July, 2022, on the effect of herbal medications on antipsychotic-related metabolic abnormalities in animals or humans. We recommend that some herbal medicines may be efficient for regulating the metabolic changes related to atypical antipsychotics due to their multipotential action, and more efforts should be made to make herbal drug treatments more effective. We hope this review will be a reference for research on developing herbal therapeutics for metabolic alterations in antipsychotic customers.

Simultaneous Occurrence of Hypospadias and Bilateral Cleft Lip and Jaw in a Crossbred Calf: Clinical, Computer Tomographic, and Genomic Characterization.

Congenital abnormalities in animals, including abnormalities of the cleft lip and jaw and hypospadias have been reported in all domesticated species. They are a major concern for breeders due to the increased economic loss they entail. In this article, we described a congenital bilateral cheilognathoschisis (cleft lip and jaw) with campylognathia in association with penile hypospadias and preputial hypoplasia with failure of preputial fusion in a Bos taurus crossbred Piedmontese × Wagyu calf. Clinical examination, computed tomography, and whole genome sequencing were performed to describe and identify a possible cause of the abnormalities. Clinical examination revealed a bilateral cheilognathoschisis of approximately 4 cm in length and 3 cm in width in the widest part, with computer tomography analyses confirming the bilateral absence of the processus nasalis of the incisive bone and the lateral deviation of the processus palatinus towards the left side. Genomic data analyses identified 13 mutations with a high impact on the products of the following overlapped genes: ACVR1, ADGRA2, BHMT2, BMPR1B, CCDC8, CDH1, EGF, F13A1, GSTP1, IRF6, MMP14, MYBPHL, and PHC2 with ADGRA2, EGF, F13A1, GSTP1, and IRF6 having mutations in a homozygous state. The whole genome investigation indicates the involvement of multiple genes in the birth defects observed in this case.

Multi-tensor diffusion abnormalities of gray matter in an animal model of cortical dysplasia.

Focal cortical dysplasias are a type of malformations of cortical development that are a common cause of drug-resistant focal epilepsy. Surgical treatment is a viable option for some of these patients, with their outcome being highly related to complete surgical resection of lesions visible in magnetic resonance imaging (MRI). However, subtle lesions often go undetected on conventional imaging. Several methods to analyze MRI have been proposed, with the common goal of rendering subtle cortical lesions visible. However, most image-processing methods are targeted to detect the macroscopic characteristics of cortical dysplasias, which do not always correspond to the microstructural disarrangement of these cortical malformations. Quantitative analysis of diffusion-weighted MRI (dMRI) enables the inference of tissue characteristics, and novel methods provide valuable microstructural features of complex tissue, including gray matter. We investigated the ability of advanced dMRI descriptors to detect diffusion abnormalities in an animal model of cortical dysplasia. For this purpose, we induced cortical dysplasia in 18 animals that were scanned at 30 postnatal days (along with 19 control animals). We obtained multi-shell dMRI, to which we fitted single and multi-tensor representations. Quantitative dMRI parameters derived from these methods were queried using a curvilinear coordinate system to sample the cortical mantle, providing inter-subject anatomical correspondence. We found region- and layer-specific diffusion abnormalities in experimental animals. Moreover, we were able to distinguish diffusion abnormalities related to altered intra-cortical tangential fibers from those associated with radial cortical fibers. Histological examinations revealed myelo-architectural abnormalities that explain the alterations observed through dMRI. The methods for dMRI acquisition and analysis used here are available in clinical settings and our work shows their clinical relevance to detect subtle cortical dysplasias through analysis of their microstructural properties.

Dysfunctional microRNA-144-3p/ZBTB20/ERK/CREB1 signalling pathway is associated with MK-801-induced schizophrenia-like abnormalities

Schizophrenia is a group of severe mental disorders. ZBTB20 is critical in brain development and corticogenesis and its dysfunction induces various neural disorders. ERK/CREB signalling is a potential downstream pathway of ZBTB20. Up-regulated microRNA-144-3p (miR-144-3p) were found in schizophrenic model rats in our previous study. This study investigated whether suppressed ZBTB20/ERK/CREB1 signalling caused by up-regulated miR-144-3p is associated with schizophrenia-like abnormalities in animals. A MK-801 rat model was established by 2-week MK-801 administration. An RNA-Seq test was performed to reveal differentially expressed genes in model rat hippocampus (HIP). MiR-144-3p-overexpressed SK-N-SH and 293T cell models were constructed by lentivirus, respectively. The in vitro and in vivo levels of miR-144-3p and ZBTB20, and the activation of the ERK/CREB1 signalling were examined by qRT-PCR, Western blots, or immunohistochemistry. The interaction between miR-144-3p and ZBTB20 was predicted and assessed by using bioinformatic methods and a luciferase reporter gene assay on 293T cells, respectively. The RNA-Seq test revealed that ZBTB20 was altered in the model rat HIP. Further experiments confirmed the reduced ZBTB20 mRNA and protein levels in the model rat HIP and caudate putamen (CPu), accompanied by increased miR-144-3p levels. Moreover, the ZBTB20 expression and ERK/CREB1 phosphorylation was decreased in the miR-144-3p-overexpressed 293T cells. These abnormal changes in the ZBTB20 expression and ERK/CREB1 phosphorylation levels were also observed in the model rat brain, but could be reversed by risperidone. In conclusion, this study revealed that dysfunctional miR-144-3p/ZBTB20/ERK/CREB1 signalling might be associated with schizophrenia-like abnormalities, suggesting potential therapeutic targets for future schizophrenia treatment.

Granulocyte-macrophage colony-stimulating factor-triggered innate immune tolerance against chronic stress-induced behavioral abnormalities in mice

Pre-stimulation of the innate immune is considered a potential strategy to prevent chronic stress-induced behavioral abnormalities in animals. In this study, we investigated whether granulocyte–macrophage colony-stimulating factor (GM-CSF), an immunostimulant used in the clinic to treat diseases of the hematopoietic system, can prevent chronic stress-induced behavioral abnormalities in mice. Our results showed that a single intraperitoneal injection of GM-CSF (100 μg/kg) one day before stress exposure prevented the depression- and anxiety-like behaviors induced by chronic social defeat stress (CSDS) in mice, including preventing the CSDS-induced increase in the immobility time in the tail suspension test and forced swimming test and decrease in the time spent in the interaction zone in the social interaction test, as well as preventing the CSDS-induced decrease in the time spent (i) in open arms in the elevated plus maze test, (ii) on the illuminated side in the light–dark test, and (iii) in the central region of the open field test. The single GM-CSF preinjection (100 μg/kg) also prevented the CSDS-induced increase in the expression levels of interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-α (TNF-α) mRNA in the hippocampus and medial prefrontal cortex of the mice. Further analysis showed that the preventive effect of GM-CSF on CSDS-induced depression- and anxiety-like behaviors and neuroinflammatory responses was abolished by pretreatment with minocycline (an innate immune inhibitor). These results indicate that a single low dose of GM-CSF before injection could be a potential way to prevent behavioral abnormalities induced by chronic stress in mice.

Degradation and transformation of all-

Environmental context Excessive amounts of retinoic acids (RAs), the main derivatives of vitamin A, cause developmental abnormalities in animals, yet information on their fate in the marine environment is limited. This study investigated the degradation of all-trans-RA in seawater and found that over 90% was degraded and transformed in unfiltered natural seawater within 24 h. The results provide essential insights on the fate and risks of RAs in marine environments. Rationale Retinoic acids (RAs) are crucial to the development of various animals. However, exposure to excessive concentrations of RAs can lead to teratogenic effects in aquatic species during their developmental stages. Some urbanised coastal marine environments receive a large amount of partially treated wastewater effluent and occasionally suffer from algal bloom incidents, both of which are considered important sources of RAs in the marine environment. Yet information on degradation and transformation of RAs in seawater is currently unavailable for assessment of their environmental risk. This study, therefore, aimed to investigate the degradation and transformation of all-trans-RA (at-RA), which is the most abundant and widely distributed RA in the marine environment. Methodology A laboratory experiment was conducted to examine the degradation and transformation of at-RA in six different types of seawater (i.e. artificial seawater, unfiltered and filtered natural seawater, each with or without autoclave treatment). Degradation and transformation products of at-RA were analysed using high-performance liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS). Results The experiment showed that at-RA could be instantly degraded and transformed into other isomers such as 9-cis-RA and 13-cis-RA when entering seawater. Over 80% of at-RA was degraded in the first 48 h regardless of the type of seawater. Discussion The presence of microorganisms and suspended organic matters could jointly facilitate the degradation and removal of at-RA from the water column. Further investigation is encouraged to reveal the influence of other factors (e.g. temperature, solar radiation, aeration) on the transformation and degradation of at-RA in seawater.

Brachygnathia Inferior in Cloned Dogs Is Possibly Correlated with Variants of Wnt Signaling Pathway Initiators.

Abnormalities in animals cloned via somatic cell nuclear transfer (SCNT) have been reported. In this study, to produce bomb-sniffing dogs, we successfully cloned four healthy dogs through SCNT using the same donor genome from the skin of a male German shepherd old dog. Veterinary diagnosis (X-ray/3D-CT imaging) revealed that two cloned dogs showed normal phenotypes, whereas the others showed abnormal shortening of the mandible (brachygnathia inferior) at 1 month after birth, even though they were cloned under the same conditions except for the oocyte source. Therefore, we aimed to determine the genetic cause of brachygnathia inferior in these cloned dogs. To determine the genetic defects related to brachygnathia inferior, we performed karyotyping and whole-genome sequencing (WGS) for identifying small genetic alterations in the genome, such as single-nucleotide variations or frameshifts. There were no chromosomal numerical abnormalities in all cloned dogs. However, WGS analysis revealed variants of Wnt signaling pathway initiators (WNT5B, DVL2, DACT1, ARRB2, FZD 4/8) and cadherin (CDH11, CDH1like) in cloned dogs with brachygnathia inferior. In conclusion, this study proposes that brachygnathia inferior in cloned dogs may be associated with variants in initiators and/or regulators of the Wnt/cadherin signaling pathway.

The Development of Phyto- and Tissue Origin Medicines for Veterinary Reproductive Issues

Modern conditions of practical veterinary medicine require the use of effective and safe drugs. Along with the already known and common medicines, the search for new drugs which are harmless for the body and have the physiological direction of action is still required. In recent years, the attention to the use of phyto- and tissue-derived drugs increased. However, the problem of their use is insufficiently studied – many aspects of their clinical use require further development, expansion of the spectrum of used medicinal plants, study, and implementation into veterinary practice. Therefore, the purpose of this work was to develop a comprehensive vitamin-hormone drugs based on phyto- and tissue medicines for the treatment and prevention of reproductive abnormalities in animals. Based on the information on the etiopathogenesis of disorders of reproductive function indicators: homeostasis, reducing of the concentration of hormones (estrogen or progesterone), changes in the morphofunctional state of endocrine (pituitary, thyroid, and adrenal gland) and reproductive (ovaries) organs, the application of vitamin-hormone drugs in veterinary medicine is scientifically sound. Drugs in terms of pathogenetic therapy can optimise homeostasis, hormone concentrations, stimulate rehabilitation processes in the regulatory organs of reproductive function (pituitary, adrenal, and thyroid) and reproductive organs (ovaries), which, in turn, contributes to the normalisation of follicles which are a prerequisite for the full reproductive capacity of females. Vitamin-hormonal medicines of herbal and tissue origin were developed, with high efficiency for the treatment and prevention of reproductive pathologies of various species of animals, providing the stimulation of reproductive function (estrus signs) for therapy of females with gonadopathies (“Carafest”, “Caplaestrol” and “Caplagonìn”) and males (display of sexual reflexes and sperm quality) for reproductive activity dysfunction (“Carafand”), increase in the viability of the newborn (increasing the number of lambs and goatlings with satisfactory clinical condition with a high-growth potential, reduce in their morbidity and lethality), preventing the incidence of ìntra- and postnatal (labor hypofunction, diseases of post-labor period) pathology (“Carafest”, and “Caplaestrol”)

Gut dysbiosis and systemic inflammation promote cardiomyocyte abnormalities in an experimental model of steatohepatitis.

BACKGROUNDCardiovascular disease is the main cause of death in metabolic-associated fatty liver disease, and gut microbiota dysbiosis is associated with both of them.AIMTo assess the relationship between gut dysbiosis and cardiovascular risk (CVR) in an experimental model of steatohepatitis.METHODSAdult male Sprague-Dawley rats were randomized to a control group (n = 10) fed a standard diet and an intervention group (n = 10) fed a high-fat choline-deficient diet for 16 wk. Biochemical, molecular, hepatic, and cardiac histopathology. Gut microbiota variables were evaluated.RESULTSThe intervention group had a significantly higher atherogenic coefficient, Castelli’s risk index (CRI)-I and CRI-II, interleukin-1β, tissue inhibitor of metalloproteinase-1 (all P < 0.001), monocyte chemoattractant protein-1 (P = 0.005), and plasminogen activator inhibitor-1 (P = 0.037) than the control group. Gene expression of miR-33a increased (P = 0.001) and miR-126 (P < 0.001) decreased in the intervention group. Steatohepatitis with fibrosis was seen in the intervention group, and heart computerized histological imaging analysis showed a significant decrease in the percentage of cardiomyocytes with a normal morphometric appearance (P = 0.007), reduction in the mean area of cardiomyocytes (P = 0.037), and an increase of atrophic cardiomyocytes (P = 0.007). There were significant correlations between the cardiomyocyte morphometry markers and those of progression and severity of liver disease and CVR. The intervention group had a lower Shannon diversity index and fewer changes in the structural pattern of gut microbiota (both P < 0.001) than controls. Nine microbial families that are involved in lipid metabolism were differentially abundant in intervention group and were significantly correlated with markers of liver injury and CVR.CONCLUSIONThe study found a link between gut dysbiosis and significant cardiomyocyte abnormalities in animals with steatohepatitis.

The influence of low-carbohydrate diets on the metabolic response to androgen-deprivation therapy in prostate cancer.

Prostate cancer (PC) is the second most lethal cancer for men. For metastatic PC, standard first-line treatment is androgen deprivation therapy (ADT). While effective, ADT has many metabolic side effects. Previously, we found in serum metabolome analysis that ADT reduced androsterone sulfate, 3-hydroxybutyric acid, acyl-carnitines but increased serum glucose. Since ADT reduced ketogenesis, we speculate that low-carbohydrate diets (LCD) may reverse many ADT-induced metabolic abnormalities in animals and humans. In a multicenter trial of patients with PC initiating ADT randomized to no diet change (control) or LCD, we previously showed that LCD intervention led to significant weight loss, reduced fat mass, improved insulin resistance, and lipid profiles. To determine whether and how LCD affects ADT-induced metabolic changes, we analyzed serum metabolites after 3-, and 6-months of ADT on LCD versus control. We found androsterone sulfate was most consistently reduced by ADT and was slightly further reduced in the LCD arm. Contrastingly, LCD intervention increased 3-hydroxybutyric acid and various acyl-carnitines, counteracting their reduction during ADT. LCD also reversed the ADT-reduced lactic acid, alanine, and S-adenosyl methionine (SAM), elevating glycolysis metabolites and alanine. While the degree of androsterone reduction by ADT was strongly correlated with glucose and indole-3-carboxaldehyde, LCD disrupted such correlations. Together, LCD intervention significantly reversed many ADT-induced metabolic changes while slightly enhancing androgen reduction. Future research is needed to confirm these findings and determine whether LCD can mitigate ADT-linked comorbidities and possibly delaying disease progression by further lowering androgens.

Neuroprotective Effect of p38 MAPKs Inhibitor (SB239063) and Vitamin B12 against Lipopolysaccharide Induced Neuroinflammation

Objectives: To evaluate the effect of MAP kinase inhibitor (SB239063) on neuroinflammation along with Vitamin B12. Materials and Methods: Male wistar albino rats divided in to eight groups each group having six animals. Neuroinflammation was induced in animals by the lipopolysaccharides/ LPS (100μg/ml) fallowed by treatment with MAPK inhibitor (SB239063) alone (5mg/kg) and along with Vit B12 (0.5mg/kg) for 30 days. Subsequently, animals were screened in the behavioral tests by using radial arm apparatus and actophotometer apparatus followed by biochemical and histopathological estimations. Results: Chronic LPS, 100 μg/kg i.p., caused physical and mental abnormalities in animals, including memory impairment, reduced locometer activity abnormal posture and cognitive deficit. Biochemical analysis of brain homogenate in LPS treated rats showed altered biochemical marker. Neurohistological alterations of various parts of brain of LPS treated rats exhibit severe neuronal space, irregular damaged cells. MAP Kinase inhibitor (SB239063) alone and along with Vit B12 administered for 15 days significantly improved motor performance and cognitive behavior task and restored the histopathological changes. Conclusion: MAP Kinase inhibitor (SB239063) alone show significant effect at dose 5 mg/kg, I.V and whenever it was used in combination at reduced concentration with Vitamin B12 provided slow neuroprotective effect.

Review of Mucuna pruriens L. therapeutic potential for Parkinson’s disease

Parkinson’s disease is a multifactorial disorder of the nervous system, the main features of which are progressive degeneration of dopaminergic neurons in the nigra pars compacta nigrostriatal tract and subsequent deficiency of the neurotransmitter dopamine in the areas of the brain, leading to the loss of motor function, the emergence of non-motor symptoms, rigidity, akinesia or bradykinesia, motor block, and decline in cognitive functions. Parkinson’s disease has high prevalence throughout the world, and has no curative treatment in modern medicine. The available drugs such as anticholinergics, levodopa and a DOPA-decarboxylase inhibitor provide symptomatic relief only. Although dopaminergic therapy is the standard treatment of motor disabilities associated with Parkinson’s disease, it does not managed all the aspects of the disease. For this reason, the increasing numbers of patients are looking for more holistic approach to the treatment of this disease. Mucuna pruriens L. – an annual self-pollinating legume plant, can be considered as a potential complementary therapy for patients with Parkinson’s disease, as it is an extremely rich source of levodopa. Numerous studies have shown that Mucuna pruriens extracts restore biochemical and behavioral abnormalities in animals with the experimental model of Parkinson’s disease. The plant also demonstrates some antioxidant activity. The clinical effects of high-dose Mucuna pruriens are similar to levodopa, but have a more favorable tolerance profile. If long-term use of Mucuna pruriens proves safe and effective in controlled clinical trials, it could become a sustainable complementary therapy for the treatment of Parkinson’s disease, especially in low-income countries.

(−)-Hydroxycitric acid regulates energy metabolism by activation of AMPK - PGC1α - NRF1 signal pathway in primary chicken hepatocytes

As the most important bioactive substance in Garcinia cambogia, (−)-hydroxycitric acid (HCA) is widely used in food additives to regulate obesity and diabetes in animals or humans, while the mechanism is poorly understood. The purpose of this study was to elucidate the regulatory effect and mechanism of (−)-HCA in regulating glucose and lipid metabolism in chicken primary hepatocytes. The results showed that (−)-HCA obviously decreased triglyceride content through inhibiting the fatty acid synthase protein level, and enhancing the protein level of phosphorylated acetyl CoA carboxylase, enoyl coenzyme A hydratase short chain 1 and carnitine palmitoyltransferase 1A in hepatocytes. Moreover, (−)-HCA markedly enhanced the protein level of phosphofructokinase-1, pyruvate dehydrogenase, succinate dehydrogenase A and complex IV, and which led to the enhancing of glucose uptake and catabolism in hepatocytes. Importantly, the regulation of (−)-HCA on these key factors associated with lipid and glucose metabolism in hepatocytes was mainly achieved through activation of AMP-activated protein kinase/peroxisome proliferator-activated receptor gamma coactivator 1α-nuclear respiratory factor 1 signaling pathway. These results convincingly demonstrated the mechanism of (−)-HCA's regulating on glucose and lipid metabolism, and provided a strategy in prevention of diseases associated with glycolipid metabolic abnormalities in animals, even in humans.

Endocrine disruptors in breeding ponds and reproductive health of toads in agricultural, urban and natural landscapes

Many chemical pollutants have endocrine disrupting effects which can cause lifelong reproductive abnormalities in animals. Amphibians are the most threatened group of vertebrates, but there is little information on the nature and quantity of pollutants occurring in typical amphibian breeding habitats and on the reproductive capacities of amphibian populations inhabiting polluted areas. In this study we investigated the occurrence and concentrations of endocrine disrupting chemicals in the water and sediment of under-studied amphibian breeding habitats in natural, agricultural and urbanized landscapes. Also, we captured reproductively active common toads (Bufo bufo) from these habitats and let them spawn in a ‘common garden’ to assess among-population differences in reproductive capacity. Across 12 ponds, we detected 41 out of the 133 contaminants we screened for, with unusually high concentrations of glyphosate and carbamazepine. Levels of polycyclic aromatic hydrocarbons, nonylphenol and bisphenol-A increased with urban land use, whereas levels of organochlorine and triazine pesticides and sex hormones increased with agricultural land use. Toads from all habitats had high fecundity, fertilization rate and offspring viability, but the F1 generation originating from agricultural and urban ponds had reduced development rates and lower body mass both as larvae and as juveniles. Females with small clutch mass produced thicker jelly coat around their eggs if they originated from agricultural and urban ponds compared with natural ponds. These results suggest that the observed pollution levels did not compromise reproductive potential in toads, but individual fitness and population viability may be reduced in anthropogenically influenced habitats, perhaps due to transgenerational effects and/or costs of tolerance to chemical contaminants.

Molecular Markers and its applications in livestock

Molecular markers are the positions on genome where certain alterations in DNA sequences present among members of the same species which reveals polymorphism at the DNA level. A molecular marker shows an alteration in expression of mRNA leads to abnormal protein function that correlates with the certain phenotypic or genetic abnormality in animals or cause progression of a disease, with the susceptibility of the disease. The most broadly used of molecular markers in livestock genomic research include Restriction Fragment Length Polymorphism (RFLP) that recognize and cut DNA at specific alteration sites, Random Amplified Polymorphic DNA (RAPD) may used in analysis of mixed genome samples and for development of target specific probes, microsatellite markers that help in scoring of alleles and single Nucleotide Polymorphism (SNP) markers that recognizes single base modification in DNA sequences. Genetic improvement or genetic selection of livestock has been mainly dependent on the selective breeding with superior phenotypes. The uses of molecular genetics techniques in with association of usual animal breeding tools are important to equilibrate the process of selection to optimize the animal breeding program. In this regard, the use of molecular markers is significantly crucial and it certainly has added advantages over conventional breeding techniques. The present review deals with molecular markers and their application in livestock research leads to the association of molecular markers with certain livestock trait viz. milk production, growth, reproduction, and genetic diseases assist researcher and breeders for production of elite livestock.

Neuroprotective effect of solanesol against 3-nitropropionic acid-induced Huntington's disease-like behavioral, biochemical, and cellular alterations: Restoration of coenzyme-Q10-mediated mitochondrial dysfunction.

OBJECTIVE:The aim of the present study was to evaluate the solanesol (SNL)-mediated coenzyme-Q10 restoration to ameliorate 3-nitropropionic (3-NP)-induced behavioral, biochemical, and histological changes which resemble Huntington's disease (HD)-like symptoms in men.MATERIALS AND METHODS:Various behavioral and biochemical parameters were carried out to evaluate the activity of SNL on 3-NP-treated rats. To determine the therapeutic significance of SNL on HD, different behavioral tests such as memory task, locomotor activity, grip strength, and beam cross and some biochemical test along with histopathological findings were done.RESULTS:Chronic 3-NP, 10 mg/kg i.p., caused physical and mental abnormalities in animals, including memory impairment, weak grip strength, abnormal posture, and cognitive deficit. Biochemical analysis of brain homogenate in 3-NP-treated rats showed altered mitochondrial complexes, oxidative stress, and elevated lipid biomarkers. Neurohistological alterations of hippocampus, basal ganglia, and cerebral cortex of 3-NP-treated rats exhibit severe neuronal space, irregular damaged cells, and dense pyknotic nuclei-associated marked focal diffused gliosis. SNL administered for 15 days significantly improved motor performance and cognitive behavior task and restored the histopathological changes. Further, SNL treatment significantly improved mitochondrial complexes such as coenzyme-Q10 enzyme activity and attenuated inflammatory and oxidative damage of rat brain.CONCLUSION:In the present research work, SNL (5, 10, and 15 mg/kg p.o.) provided notable neuroprotective effect, which was confirmed by behavioral paradigms and biochemical test. It restored the behavioral and biochemical alteration caused by 3-NP and confirmed the strong neuroprotective mechanism of SNL in 3-NP-intoxicated memory and cognitive abnormalities.

Lanthanum chloride reduces lactate production in primary culture rat cortical astrocytes and suppresses primary co-culture rat cortical astrocyte-neuron lactate transport.

Lanthanum (La) can impair learning memory and induce behavioral abnormalities in animals. However, the mechanism underlying these adverse effects of La is still elusive. It has been demonstrated that lactate derived from astrocytes is the major energy source for neurons during long-term memory (LTM) formation and the deficiency of lactate supply can result in LTM damage. However, little work has been done with respect to the impact of La on the lactate production in astrocytes and astrocyte-neuron lactate transport (ANLT). Herein, experiments were undertaken to explore if there was such an adverse effect of La. Primary culture rat cortical astrocytes and primary co-culture rat cortical astrocyte-neuron were treated with (0.125, 0.25 and 0.5mM) lanthanum chloride (LaCl3) for 24h. The results showed that LaCl3 treatment significantly downregulated the mRNA and protein expression of glucose transporter 1 (GLUT1), glycogen synthase (GS), glycogen phosphorylase (GP), lactate dehydrogenase A (LDHA), and monocarboxylate transporter 1, 2 and 4 (MCT 1 2 and 4); upregulated the mRNA and protein expression of lactate dehydrogenase B (LDHB); and decreased the glycogen level, total LDH and GP activity, GS/p-GS ratio and lactate contents. Moreover, rolipram (20, 40μM) or forskolin (20, 40μM) could increase the lactate content by upregulating GP expression and the GS/p-GS ratio, as well as antagonize the effects of La. These results suggested that La-induced learning-memory damage was probably related to its suppression of lactate production in astrocytes and ANLT. This study provides some novel clues for clarifying the mechanism underlying the neurotoxicity of La.