Turismo de vida silvestre: una síntesis de la agenda de investigación pasada, presente y futuro

Wildlife tourism (WT) is an emerging sector of tourism, majorly meant to view and/or encounter wildlife in the wild, captive, and semi-captive settings. Because of the new emerging economies, there is an increased demand for wildlife destinations in both, developing and developed nations. However, a comprehensive study is lacking in WT. In this context, the present study seeks to bring together and discuss the key findings on WT from the present literature and propose new approaches to research using co-citation, co-authorship, and co-occurrence analyses. Further, the study also considers research on WT conducted so far like attitudes, bird-watching, conservation, economics, hunting, mammals, management, marine monitoring, negative impacts, positive impacts, captive wildlife, and guidelines. A data set is created that includes authors, article titles, citations, countries, co-authorship, institutions, publication years and sources, keywords, and abstracts by collecting the bibliographies from Scopus and Web of Science (WoS) indexed journals with keywords search “Wild Life, Jungle and Tourism.” The study collected 1,519 and used 1,259 published articles from 1990 to 2020, and analyzed employing VOS viewer software, which has enabled us to understand the relationship and structure of the literatureEl turismo de vida silvestre (WT) es un sector emergente del turismo, destinado principalmente a ver y / o encontrar vida silvestre en entornos silvestres, cautivos y semi-cautivos. Debido a las nuevas economías emergentes, existe una mayor demanda de destinos de vida silvestre tanto en países desarrollados como en desarrollo. Sin embargo, falta un estudio completo en WT. En este contexto, el presente estudio busca reunir y discutir los hallazgos clave sobre WT de la literatura actual y proponer nuevos enfoques de investigación utilizando análisis de co-cita, coautoría y co-ocurrencia. Además, el estudio también considera la investigación sobre WT realizada hasta ahora como actitudes, observación de aves, conservación, economía, caza, mamíferos, manejo, monitoreo marino, impactos negativos, impactos positivos, vida silvestre cautiva y pautas. Se crea un conjunto de datos que incluye a los autores, títulos de artículos, citas, países, coautoría, instituciones, años de publicación y fuentes, palabras clave y resúmenes mediante la recopilación de bibliografías de revistas indexadas de Scopus y Web of Science (WoS) con la búsqueda de palabras clave "Wild Life, Jungle and Tourism". El estudio recopiló 1.519 y utilizó 1.259 artículos publicados entre 1990 y 2020, y analizó utilizando el software de visualización VOS, lo que nos ha permitido comprender la relación y la estructura de la literatur

Delayed cystectomy for T 1 G 3 TCC of urinary bladder managed initially by TURBT & intravesical immunotherapy (BCG + interferon) rationale & our result

Objectives: Management of pT 1 G 3 TCC of urinary bladder is always a dilemma for urologists due to its high recurrence & disease progression rate. We evaluated the role of conservative management for this subgroup with TURBT and intravesical immunotherapy; and delayed cystectomy for progressive disease with an aim to salvage bladder. Patients & Methods: Between Jan.1996 to Dec.2002, 66 patients (15%) of pT 1 G 3 , out of a total 440 patients of superficial bladder cancer treated in this department were subjected to low dose BCG (40mg) and Interferon 3 million IU intravesically with maintenance therapy after complete TURBT and followed up for average 60 months. The mean tumor free interval was 26 months & 18 months in superficial recurrences & muscle progression disease respectively. Delayed cystectomy being preserved only for disease progression patients and the mean period of delayed cystectomy was 24 months (18-30 months). Results: 19 patients (29%) had no tumor recurrence, 35 patients (53%) showed superficial recurrence and 12 patients (18%) progressed to higher stage at end of five year follow up thereby giving a disease progression free interval of 60 months in 82% of our patients. Five patients of disease progression group died due to metastatic disease process and 7 patients are alive after delayed cystectomy at the end of follow up. Side effects from intravesical therapy were confined to local irritative symptoms only. Conclusion: Our data only confirms the benefit of adjuvant intravesical low dose immunotherapy in management of pT 1 G 3 tumor after TURBT with bladder salvage in 82% of patients, simultaneously not compromising the survival rate

Development and Characterization of Inducible Astrocyte-Specific Aromatase Knockout Mice

17β-estradiol (E2) is produced in the brain as a neurosteroid, in addition to being an endocrine signal in the periphery. The current animal models for studying brain-derived E2 include global and conditional non-inducible knockout mouse models. The aim of this study was to develop a tamoxifen (TMX)-inducible astrocyte-specific aromatase knockout mouse line (GFAP-ARO-iKO mice) to specifically deplete the E2 synthesis enzymes and aromatase in astrocytes after their development in adult mice. The characterization of the GFAP-ARO-iKO mice revealed a specific and robust depletion in the aromatase expressions of their astrocytes and a significant decrease in their hippocampal E2 levels after a GCI. The GFAP-ARO-iKO animals were alive and fertile and had a normal general brain anatomy, with a normal astrocyte shape, intensity, and distribution. In the hippocampus, after a GCI, the GFAP-ARO-iKO animals showed a major deficiency in their reactive astrogliosis, a dramatically increased neuronal loss, and increased microglial activation. These findings indicate that astrocyte-derived E2 (ADE2) regulates the ischemic induction of reactive astrogliosis and microglial activation and is neuroprotective in the ischemic brain. The GFAP-ARO-iKO mouse models thus provide an important new model to help elucidate the roles and functions of ADE2 in the brain

Neuron-Derived Estrogen—A Key Neuromodulator in Synaptic Function and Memory

In addition to being a steroid hormone, 17β-estradiol (E2) is also a neurosteroid produced in neurons in various regions of the brain of many species, including humans. Neuron-derived E2 (NDE2) is synthesized from androgen precursors via the action of the biosynthetic enzyme aromatase, which is located at synapses and in presynaptic terminals in neurons in both the male and female brain. In this review, we discuss evidence supporting a key role for NDE2 as a neuromodulator that regulates synaptic plasticity and memory. Evidence supporting an important neuromodulatory role of NDE2 in the brain has come from studies using aromatase inhibitors, aromatase overexpression in neurons, global aromatase knockout mice, and the recent development of conditional forebrain neuron-specific knockout mice. Collectively, these studies demonstrate a key role of NDE2 in the regulation of synapse and spine density, efficacy of excitatory synaptic transmission and long-term potentiation, and regulation of hippocampal-dependent recognition memory, spatial reference memory, and contextual fear memory. NDE2 is suggested to achieve these effects through estrogen receptor-mediated regulation of rapid kinase signaling and CREB-BDNF signaling pathways, which regulate actin remodeling, as well as transcription, translation, and transport of synaptic proteins critical for synaptic plasticity and function

Brain-Derived Estrogen and Neurological Disorders

Astrocytes and neurons in the male and female brains produce the neurosteroid brain-derived 17β-estradiol (BDE2) from androgen precursors. In this review, we discuss evidence that suggest BDE2 has a role in a number of neurological conditions, such as focal and global cerebral ischemia, traumatic brain injury, excitotoxicity, epilepsy, Alzheimer’s disease, and Parkinson’s disease. Much of what we have learned about BDE2 in neurological disorders has come from use of aromatase inhibitors and global aromatase knockout mice. Recently, our group developed astrocyte- and neuron-specific aromatase knockout mice, which have helped to clarify the precise functions of astrocyte-derived 17β-estradiol (ADE2) and neuron-derived 17β-estradiol (NDE2) in the brain. The available evidence to date suggests a primarily beneficial role of BDE2 in facilitating neuroprotection, synaptic and cognitive preservation, regulation of reactive astrocyte and microglia activation, and anti-inflammatory effects. Most of these beneficial effects appear to be due to ADE2, which is induced in most neurological disorders, but there is also recent evidence that NDE2 exerts similar beneficial effects. Furthermore, in certain situations, BDE2 may also have deleterious effects, as recent evidence suggests its overproduction in epilepsy contributes to seizure induction. In this review, we examine the current state of this quickly developing topic, as well as possible future studies that may be required to provide continuing growth in the field

Brain-derived estrogen and neural function

Brain-derived estrogen (BDE2) produced by the enzyme aromatase has several important functions in the brain. Work using aromatase inhibitors, aromatase knockdown models, and conditional forebrain neuron-specific and astrocyte-specific aromatase knockout mouse models have provided evidence that BDE2 has a critical role in regulating synaptic function and plasticity, cognitive function, sexual differentiation and reproduction, socio-sexual behavior, and neuroprotection. [Display omitted] •Aromatase is localized at synaptic and non-synaptic locations in the brain.•Neuron-derived E2 functions as a neuromodulator to regulate plasticity, memory and behavior.•Neuron-derived E2 is also neuroprotective and anti-inflammatory.•Following brain injury or ischemia, astrocytes also produce E2.•Astrocyte-derived E2 regulates gliosis, neuroinflammation, and is neuroprotective. Although classically known as an endocrine signal produced by the ovary, 17β-estradiol (E2) is also a neurosteroid produced in neurons and astrocytes in the brain of many different species. In this review, we provide a comprehensive overview of the localization, regulation, sex differences, and physiological/pathological roles of brain-derived E2 (BDE2). Much of what we know regarding the functional roles of BDE2 has come from studies using specific inhibitors of the E2 synthesis enzyme, aromatase, as well as the recent development of conditional forebrain neuron-specific and astrocyte-specific aromatase knockout mouse models. The evidence from these studies support a critical role for neuron-derived E2 (NDE2) in the regulation of synaptic plasticity, memory, socio-sexual behavior, sexual differentiation, reproduction, injury-induced reactive gliosis, and neuroprotection. Furthermore, we review evidence that astrocyte-derived E2 (ADE2) is induced following brain injury/ischemia, and plays a key role in reactive gliosis, neuroprotection, and cognitive preservation. Finally, we conclude by discussing the key controversies and challenges in this area, as well as potential future directions for the field

Regulation and Role of Neuron-Derived Hemoglobin in the Mouse Hippocampus

Hemoglobin (Hb) is the oxygen transport protein in erythrocytes. In blood, Hb is a tetramer consisting of two Hb-alpha (Hb-α) chains and two Hb-beta (Hb-β) chains. A number of studies have also shown that Hb-α is also expressed in neurons in both the rodent and human brain. In the current study, we examined for age-related regulation of neuronal Hb-α and hypoxia in the hippocampus and cerebral cortex of intact male and female mice. In addition, to confirm the role and functions of neuronal Hb-α, we also utilized lentivirus CRISPR interference-based Hb-α knockdown (Hb-α CRISPRi KD) in the non-ischemic and ischemic mouse hippocampus and examined the effect on neuronal oxygenation, as well as induction of hypoxia-inducible factor-1α (HIF-1α) and its downstream pro-apoptotic factors, PUMA and NOXA, and on neuronal survival and neurodegeneration. The results of the study revealed an age-related decrease in neuronal Hb-α levels and correlated increase in hypoxia in the hippocampus and cortex of intact male and female mice. Sex differences were observed with males having higher neuronal Hb-α levels than females in all brain regions at all ages. In vivo Hb-α CRISPRi KD in the mouse hippocampus resulted in increased hypoxia and elevated levels of HIF-1α, PUMA and NOXA in the non-ischemic and ischemic mouse hippocampus, effects that were correlated with a significant decrease in neuronal survival and increased neurodegeneration. As a whole, these findings indicate that neuronal Hb-α decreases with age in mice and has an important role in regulating neuronal oxygenation and neuroprotection

Therapeutic Targeting of Ovarian Cancer Stem Cells Using Estrogen Receptor Beta Agonist

Ovarian cancer (OCa) is the deadliest gynecologic cancer. Emerging studies suggest ovarian cancer stem cells (OCSCs) contribute to chemotherapy resistance and tumor relapse. Recent studies demonstrated estrogen receptor beta (ERβ) exerts tumor suppressor functions in OCa. However, the status of ERβ expression in OCSCs and the therapeutic utility of the ERβ agonist LY500307 for targeting OCSCs remain unknown. OCSCs were enriched from ES2, OV90, SKOV3, OVSAHO, and A2780 cells using ALDEFLUOR kit. RT-qPCR results showed ERβ, particularly ERβ isoform 1, is highly expressed in OCSCs and that ERβ agonist LY500307 significantly reduced the viability of OCSCs. Treatment of OCSCs with LY500307 significantly reduced sphere formation, self-renewal, and invasion, while also promoting apoptosis and G2/M cell cycle arrest. Mechanistic studies using RNA-seq analysis demonstrated that LY500307 treatment resulted in modulation of pathways related to cell cycle and apoptosis. Western blot and RT-qPCR assays demonstrated the upregulation of apoptosis and cell cycle arrest genes such as FDXR, p21/CDKN1A, cleaved PARP, and caspase 3, and the downregulation of stemness markers SOX2, Oct4, and Nanog. Importantly, treatment of LY500307 significantly attenuated the tumor-initiating capacity of OCSCs in orthotopic OCa murine xenograft models. Our results demonstrate that ERβ agonist LY500307 is highly efficacious in reducing the stemness and promoting apoptosis of OCSCs and shows significant promise as a novel therapeutic agent in treating OCa

Harnessing Genetic Variation in Physiological and Molecular Traits to Improve Heat Tolerance in Food Legumes

Plant genetic variations provide opportunity to develop new and improved cultivars with desired characteristics, hence gaining major attention from the scientists and breeders all over the world. Harnessing genetic variability is the key factor in the adaptation of plants to ever-rising temperature. Nowadays, such characteristic traits among the population can be used to develop various heat-resilient crop varieties and have a profound effect on restoring the balance between climate change and agriculture. Genetic variations in physiological and molecular traits proved to be the major components for breeding programs to augment the gene pool. With genetic variations, it is possible to identify the phenotypic variations governed either by a single gene or by many genes that will be helpful for mapping associated quantitative trait loci. Genetic variations can also be traced by examining various physiological traits of a crop plant like growth traits (biomass, plant height, and root growth), leaf traits (stomatal conductance, chlorophyll content, chlorophyll fluorescence, photosynthetic rate, membrane stability, sucrose content, and canopy temperature depression), and floral traits (mainly associated with male gametophyte). Yield traits can also display enormous variation, making it highly useful/reliable for screening purposes. Further, genetic variation at the biochemical level can be assessed by measuring the expression of enzymes (related to oxidative stress and antioxidants) and metabolites (both primary and secondary). Evaluating how genetic variation influences phenotype is the ultimate objective of genetics, and using omics approaches can improve the understanding of heat tolerance-governing mechanisms. Further, collecting molecular data at different levels of plant growth and development will help to accelerate our understanding of the mechanisms linking genotype to phenotype

Inhibition of LIFR Blocks Adiposity-Driven Endometrioid Endometrial Cancer Growth

Endometrial cancer (EC) is the fourth most common cancer in women, and half of the endometrioid EC (EEC) cases are attributable to obesity. However, the underlying mechanism(s) of obesity-driven EEC remain(s) unclear. In this study, we examined whether LIF signaling plays a role in the obesity-driven progression of EEC. RNA-seq analysis of EEC cells stimulated by adipose conditioned medium (ADP-CM) showed upregulation of LIF/LIFR-mediated signaling pathways including JAK/STAT and interleukin pathways. Immunohistochemistry analysis of normal and EEC tissues collected from obese patients revealed that LIF expression is upregulated in EEC tissues compared to the normal endometrium. Treatment of both primary and established EEC cells with ADP-CM increased the expression of LIF and its receptor LIFR and enhanced proliferation of EEC cells. Treatment of EEC cells with the LIFR inhibitor EC359 abolished ADP-CM induced colony formation andcell viability and decreased growth of EEC organoids. Mechanistic studies using Western blotting, RT-qPCR and reporter assays confirmed that ADP-CM activated LIF/LIFR downstream signaling, which can be effectively attenuated by the addition of EC359. In xenograft assays, co-implantation of adipocytes significantly enhanced EEC xenograft tumor growth. Further, treatment with EC359 significantly attenuated adipocyte-induced EEC progression in vivo. Collectively, our data support the premise that LIF/LIFR signaling plays an important role in obesity-driven EEC progression and the LIFR inhibitor EC359 has the potential to suppress adipocyte-driven tumor progression