Notes

A Novel Aldo-Keto Reductase (AKR17A1) associated with Anabaena sp. PCC 7120 Degrades the Hemp Industry Herbicide Butachlor and also Confers Ability to tolerate Abiotic Tensions in Electronic. coli.
Aging is characterized by a progressive loss of physiological function leading to increase in the vulnerability to death. This deterioration process occurs in all living organisms and is the primary risk factor for pathological conditions including obesity, type 2 diabetes mellitus, Alzheimer's disease and cardiovascular diseases. Most of the age-related diseases have been associated with impairment of action of an important hormone, namely insulin. It is well-known that this hormone is a critical mediator of metabolism, growth, proliferation and differentiation. Insulin action depends on two processes that determine its circulating levels, insulin secretion and clearance, and insulin sensitivity in its target tissues. Aging has deleterious effects on these three mechanisms, impairing insulin action, thereby increasing the risk for diseases and death. Thus, improving insulin action may be an important strategy to have a healthier and longer life.Falls result in multiple adverse health outcomes including mortality in older persons. Impaired balance is known to increase the risk of falls. Numerous factors play a role in the etiology of balance disturbance. Among the calciotropic hormones, the role of vitamin D in falls risk has been extensively studied. There is evolving interest in the role of parathyroid hormone (PTH) in this area. Elevated PTH hormone levels have been associated with age-related syndromes such as frailty, osteoporosis, and sarcopenia. Among the existing studies, most have focused on muscle strength with few studies evaluating its role in balance disturbances. In this chapter, we will summarize the aspects of PTH and aging, its biological effects on muscle, and the known associations between PTH and balance.It is the heterogeneous changes of hypothalamic functions that determine the chronological sequence of aging in mammals. Recently, it was hypothesized by Cai the decrease in slow-wave sleep (SWS) resulting from skin aging as responsible for the degeneration of hypothalamic suprachiasmatic nucleus (SCN). It was soon hypothesized by the European people in television that the increase in body fat as responsible for the degeneration of male preoptic sexually dimorphic nucleus (SDN-POA), via the aromatase converting testosterone to estradiol as proposed by Cohen. It is the hypothalamic paraventricular nucleus (PVN) that remains unchanged in neuron number during aging for psychological stress. In this chapter, it is briefly reviewed more manifestations of hypothalamic related mammalian aging processes, including (1) the aging of ovary by lipid, estradiol and hypothalamus; (2) the aging of muscle, stomach, intestine, thymus, and the later aging of brain, regulated by growth hormone/insulin-like growth factor 1(GH/IGF1); (3) the cardiovascular hypertension from PVN activation, the bone and other peripheral aging by psychological stress, and that of kidney by vasopressin. It is classified these aging processes by the primary regulation from one of the three hypothalamic nuclei, although still necessary to investigate and supplement their secondary regulation by the hypothalamic nuclei in future. It is the hypothalamic structural changes that shift the functional balance among these three hypothalamic systems toward aging.Aging is associated with changes in hormones, slowing of metabolism, diminished physiological processes, chronic inflammation and high exposure to oxidative stress factors, generally described as the biological cost of living. Lifestyle interventions of diet and exercise can improve the quality of life during aging and lower diet-related chronic disease. The endocannabinoid system (ECS) has important effects on systemic metabolism and physiological systems, including the central and peripheral nervous systems. Exercise can reduce the loss of muscle mass and improve strength, and increase the levels of endocannabinoids (eCB) in brain and blood. Although the ECS exerts controls on multiple systems throughout life it affords benefits to natural aging. The eCB are synthesized from polyunsaturated fatty acids (PUFA) and the primary ones are produced from arachidonic acid (n-6 PUFA) and others from the n-3 PUFA, namely eicosapentaenoic and docosahexaenoic acids. The eCB ligands bind to their receptors, CB1 and CB2, with effects on appetite stimulation, metabolism, immune functions, and brain physiology and neuroplasticity. Dietary families of PUFA are a primary factor that can influence the types and levels of eCB and as a consequence, the downstream actions when the ligands bind to their receptors. Furthermore, the association of eCB with the synthesis of oxylipins (OxL) is a connection between the physiological actions of eCB and the lipid derived immunological OxL mediators of inflammation. OxL are ubiquitous and influence neuroinflammation and inflammatory processes. The emerging actions of eCB on neuroplasticity, well-being and pain are important to aging. Herein, we present information about the ECS and its components, how exercise and diet affects specific eCB, their role in neuroplasticity, neuroinflammation, pain, mood, and relationship to OxL. Poor nutrition status and low nutrient intakes observed with many elderly are reasons to examine the role of dietary PUFA actions on the ECS to improve health.It is widely accepted that the metabolic hormone leptin regulates food intake and body weight via activation of hypothalamic leptin receptors. Selleckchem Atamparib However, as leptin receptors are also highly expressed in other brain regions, such as the hippocampus, alterations in leptin responsiveness also impacts on key functions of the hippocampus, like learning and memory. Within the hippocampus, high levels of leptin receptors are expressed at excitatory synapses, and in accordance with a synaptic localization, leptin potently regulates synaptic transmission at both Schaffer collateral (SC) and temporoammonic (TA) inputs to CA1 pyramidal neurons. Increasing evidence from cellular and behavioral studies examining leptin action at CA1 synapses support the notion that leptin is a potential cognitive enhancer. link2 However, the capacity of leptin to regulate synaptic efficacy at SC-CA1 and TA-CA1 synapses declines in an age-dependent manner. Moreover, clinical evidence that supports a link between circulating leptin levels and the risk of the age-related neurodegenerative disorder, Alzheimer's disease (AD) is accumulating. link3 Consequently, it has been proposed that the leptin system is a potential therapeutic target in AD, and that boosting the hippocampal actions of leptin may be beneficial in the treatment of AD. Here we review recent progress in our understanding of the neuronal and hippocampal synaptic functions that are regulated by leptin and how alterations in the leptin system influence age-related CNS-related disorders like AD.The world's population is increasingly aging, this noted particularly in the Western world where there are ever greater numbers of centenarians and those over 85 years. Given the immense importance of the thyroid gland for optimal health and the fact that morphological and functional changes in the hypothalamic-pituitary-thyroid (HPT) axis take place as a natural adaptation to the aging process, a clear distinction must be made in older individuals between these and the onset of disease. However, this is problematic since, frequently, subtle differences exist between them, making diagnosis a challenging task, especially as concerns subclinical disease. The newly emerging interdisciplinary field of geroscience offers the prospect of being used as a platform to investigate the effect of disrupted HPT function on functional capacity and cognitive ability among the aged, as well as the risk or onset of age-associated diseases, thus enhancing healthspan and lifespan. Because optimal functioning of the thyroid gland is a prerequisite for longevity as well as for mental and physical wellbeing, this review summarizes the recent scientific data regarding HPT and aging while discussing alternative and personalized treatment approaches to maintaining a healthy thyroid as a means to ensuring a long, active, and healthy life.This is a commentary on the manuscript by Sullivan G, Skertich N, Gulack B, et al., titled "Shifting Paradigms The Top Most Disruptive Papers in Core Pediatric Surgery Journals".
Information is needed regarding the complex relationships between long-term functional outcomes and health-related quality of life (HRQoL) in Hirschsprung's Disease (HSCR). We describe long-term outcomes across multiple domains, completing a core outcome set through to adulthood.

HSCR patients operated at a single center over a 35-year period (1978-2013) were studied. Patients completed detailed questionnaires on bowel and urologic function, and HRQOL. Patients with learning disability (LD) were excluded. Outcomes were compared to normative data. Data are reported as median [IQR] or mean (SD).

186 patients (median age 28 [18-32] years; 135 males) completed surveys. Bowel function was reduced (BFS 17 [14-19] vs. 19 [19-20], p<0•0001;η
=0•22). Prevalence and severity of fecal soiling and fecal awareness improved with age (p<0•05 for both). Urinary incontinence was more frequent than controls, most of all in 13-26y females (65% vs. 31%,p=0•003). In adults, this correlated independently with constipats.Paul Greengard brought to neuroscience the idea of, and evidence for, the role of second messenger systems in neuronal signaling. The fundamental nature of his contributions is evident in the far reach of his work, relevant to various subfields and topics in neuroscience. In this review, we discuss some of Greengard's work from the perspective of nicotinic acetylcholine receptors and their relevance to nicotine addiction. Specifically, we review the roles of dopamine- and cAMP-regulated phospho-protein of 32kDa (DARPP-32) and Ca2+/calmodulin-dependent kinase II (CaMKII) in nicotine-dependent behaviors. For each protein, we discuss the historical context of their discovery and initial characterization, focusing on the extensive biochemical and immunohistochemical work conducted by Greengard and colleagues. We then briefly summarize contemporary understanding of each protein in key intracellular signaling cascades and evidence for the role of each protein with respect to systems and behaviors relevant to nicotine addiction.DARPP-32 (dopamine- and cAMP-regulated phosphoprotein with an apparent Mr of 32,000), now also known as phosphoprotein phosphatase 1 regulatory subunit 1B (PPP1R1B), is a potent inhibitor of protein phosphatase 1 (PP1, also known as PPP1) when phosphorylated at Thr34 by cAMP-dependent protein kinase (PKA). DARPP-32 exhibits a remarkable regional distribution in brain, roughly similar to that of dopamine innervation. Its discovery was a culmination of the long-standing effort of Paul Greengard to understand the mechanisms through which neurotransmitters such as dopamine exert their effects on target neurons. DARPP-32 is particularly enriched in striatal projection neurons where it is regulated by numerous signals through which it integrates and amplifies responses to many stimuli. Molecular studies of DARPP-32 have revealed that its regulation and function are more complex than anticipated. It is phosphorylated on multiple sites by several protein kinases that modulate DARPP-32 properties. Primarily, when phosphorylated at Thr34 DARPP-32 is a potent inhibitor of PP1, whereas when phosphorylated at Thr75 by Cdk5 it inhibits PKA.
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