One of the quantum theory concepts on which quantum information processing stands is superposition. Here we provide experimental evidence for the existence of classical analogues to the coherent ...superposition of energy states, which is made possible by the Hertz-type nonlinearity of the granules together with the external driving field. The granules' nonlinear vibrations are projected into the linear modes of vibration, which depend on one another through the phase and form a coherent superposition. We show that the amplitudes of the coherent states form the components of a state vector that spans a two-dimensional Hilbert space, and time enables the system to span its Hilbert space parametrically. Thus, the superposition of states can be exploited in two-state quantum-like computations without decoherence and wave function collapse. Finally, we demonstrate the experimental realization of applying a reversible Hadamard gate to a pure base state that brings the state into a superposition.
Bangladesh, one of the most densely populated countries in the world has been ranked 9th on the Climate Risk Index for 2017: the 10 most affected countries & 7th on the Long-Term Climate Risk Index: ...the 10 countries most affected from 1998 to 2017. Every year it is afflicted with various climatic disasters including floods, hurricanes and cyclones. Apart from the obvious devastation of lives and property, there is a huge increase in clinical diseases when these disasters occur. Mental health of affected persons after these disasters is a topic that is often neglected by local and national level.
A qualitative case study was conducted on perceived need on mental health support & availability of such services in a cyclone affected area in rural Bangladesh. Ten (10) key informant interviews (KIIs) with different stakeholders and ten (10) in-depth interviews (IDIs) with affected people were taken.
We found that cyclones had numerous psychosocial impacts on the population including acute stress disorder, sleep disorder, post-traumatic stress disorders (PTSDs), generalized anxiety disorders, suicidal ideation and depression. The survivors had specific needs for receiving support. Children, elderly and women were perceived to be more vulnerable. The government and NGOs had no specific action plans and initiatives to address these issues and support the mental health of affected population. There was a visible gap in finding effective ways to provide affected people with the required mental health & psycho-social services (MHPSS).
Resilient, responsive and self-sustaining health systems for this vulnerable population are required. Implementation of effective mental health programs and strong mental health policies remain a challenge in Bangladesh where there is a cultural fatalistic acceptance of mental health issues.
•Norepinephrine acts on the ventromedial hypothalamic nucleus (VMN) to control counter-regulation.•Estrogen receptor-alpha (ERα)- and -beta (ERβ) control VMN gluco-inhibitory signaling.•ERα- or -β ...antagonist was delivered to rats of each sex before insulin-induced hypoglycemia (IIH).•VMN γ-aminobutyric acid (GABA) and nitric oxide (NO) neurons were analyzed by Western blot.•GABA and NO neurons exhibit ER-dependent sex-specific reactivity to NE and estradiol during IIH.
The ventromedial hypothalamic nucleus (VMN) is a vital component of the neural circuitry that regulates glucostasis. Norepinephrine (NE) controls VMN gluco-inhibitory γ-aminobutyric acid (GABA) and gluco-stimulatory nitric oxide (NO) transmission. Sex-specific insulin-induced hypoglycemic (IIH) patterns of VMN GABA signaling are estrogen receptor-alpha (ERα)- and -beta (ERβ)-dependent. Current research utilized combinatory immunocytochemistry, laser-microdissection, and Western blot techniques in a pharmacological approach to address the hypothesis that ERα and/or -β mediate sex-dimorphic VMN GABAergic and/or nitrergic nerve cell receptivity to NE and estradiol during IIH. The impact of these ER on expression of the pyruvate recycling pathway marker proteins glutaminase (GLS) and malic enzyme-1 (ME-1) was also examined. Both VMN neuron populations express ERα, ERβ, and G protein-coupled estrogen receptor-1 (GPER), along with alpha1, alpha2, and beta1 adrenergic receptor (AR) proteins. NO neurons exhibited ERα/β-dependent (beta1 AR, GPER) and -independent (alpha1 AR) sex differences in receptor protein responses to hypoglycemia. Similarly, sex-dimorphic effects of IIH on alpha1 AR, alpha2 AR, and ERα profiles in GABA neurons involve ERα/β. These ERs also underlie divergent adjustments in gluco-regulatory nerve cell GLS and ME-1 protein expression in hypoglycemic males and females. Sex-specific nitrergic and GABAergic nerve cell sensitivity to NE and E, respectively, during IIH may contribute to sex-contingent patterns of neurotransmitter signaling.
The mediobasal hypothalamus (MBH) shapes the neural regulation of glucostasis by 5'-AMP-activated protein kinase (AMPK)-dependent mechanisms. Yet, the neurochemical identity and neuroanatomical ...distribution of MBH neurons that express glucoprivic-sensitive AMPK remain unclear. The neurotransmitters γ-aminobutyric acid (GABA) and nitric oxide (NO) act within the MBH to correspondingly inhibit or stimulate glucose counter-regulation. The current review highlights recent findings that GABA and NO, neurons located in the ventromedial hypothalamic nucleus (VMN), a distinct important element of the MBH, are direct targets of noradrenergic regulatory signaling, and thereby, likely operate under the control of hindbrain metabolic-sensory neurons. The ovarian hormone estradiol acts within the VMN to govern energy homeostasis. Discussed here is current evidence that estradiol regulates GABA and NO nerve cell receptivity to norepinephrine and moreover, controls the noradrenergic regulation of AMPK activity in each cell type. Future gains in insight on mechanisms underpinning estradiol's impact on neurotransmitter communication between the hindbrain and hypothalamic AMPKergic neurons are expected to disclose viable new molecular targets for the therapeutic simulation of hormonal enhancement of neuro-metabolic stability during circumstances of diminished endogenous estrogen secretion or glucose dysregulation.
The catecholamine norepinephrine (NE) links hindbrain metabolic-sensory neurons with key glucostatic control structures in the brain, including the ventromedial hypothalamic nucleus (VMN). In the ...brain, the glycogen reserve is maintained within the astrocyte cell compartment as an alternative energy source to blood-derived glucose. VMN astrocytes are direct targets for metabolic stimulus-driven noradrenergic signaling due to their adrenergic receptor expression (AR). The current review discusses recent affirmative evidence that neuro-metabolic stability in the VMN may be shaped by NE influence on astrocyte glycogen metabolism and glycogen-derived substrate fuel supply. Noradrenergic modulation of estrogen receptor (ER) control of VMN glycogen phosphorylase (GP) isoform expression supports the interaction of catecholamine and estradiol signals in shaping the physiological stimulus-specific control of astrocyte glycogen mobilization. Sex-dimorphic NE control of glycogen synthase and GP brain versus muscle type proteins may be due, in part, to the dissimilar noradrenergic governance of astrocyte AR and ER variant profiles in males versus females. Forthcoming advances in the understanding of the molecular mechanistic framework for catecholamine stimulus integration with other regulatory inputs to VMN astrocytes will undoubtedly reveal useful new molecular targets in each sex for glycogen mediated defense of neuronal metabolic equilibrium during neuro-glucopenia.
The enzyme aromatase is expressed at high levels in the ventromedial hypothalamic nucleus (VMN), a principal component of the brain gluco-regulatory network. Current research utilized selective gene ...knockdown tools to investigate the premise that VMN neuroestradiol controls glucostasis. Intra-VMN aromatase siRNA administration decreased baseline aromatase protein expression and tissue estradiol concentrations and either reversed or attenuated the hypoglycemic regulation of these profiles in a VMN segment-specific manner. Aromatase gene repression down-regulated protein biomarkers for gluco-stimulatory (nitric oxide; NO) and -inhibitory (gamma-aminobutyric acid; GABA) neurochemical transmitters. Insulin-induced hypoglycemia (IIH) up- or down-regulated neuronal nitric oxide synthase (nNOS) and glutamate decarboxylase
(GAD), respectively, throughout the VMN. Interestingly, IIH caused divergent changes in tissue aromatase and estradiol levels in rostral (diminished) versus middle and caudal (elevated) VMN. Aromatase knockdown prevented hypoglycemic nNOS augmentation in VMN middle and caudal segments, but abolished the GAD inhibitory response to IIH throughout this nucleus. VMN nitrergic and GABAergic neurons monitor stimulus-specific glycogen breakdown. Here, glycogen synthase (GS) and phosphorylase brain- (GPbb; AMP-sensitive) and muscle- (GPmm; noradrenergic -responsive) type isoform responses to aromatase siRNA were evaluated. Aromatase repression reduced GPbb and GPmm content in euglycemic controls and prevented hypoglycemic regulation of GPmm but not GPbb expression while reversing glycogen accumulation. Aromatase siRNA elevated baseline glucagon and corticosterone secretion and abolished hypoglycemic hyperglucagonemia and hypercorticosteronemia. Outcomes document the involvement of VMN neuroestradiol signaling in brain control of glucose homeostasis. Aromatase regulation of VMN gluco-regulatory signaling of hypoglycemia-associated energy imbalance may entail, in part, control of GP variant-mediated glycogen disassembly.
Neural substrates for estrogen regulation of glucose homeostasis remain unclear. Female rat dorsal vagal complex (DVC) A2 noradrenergic neurons are estrogen- and metabolic-sensitive. The ventromedial ...hypothalamic nucleus (VMN) is a key component of the brain network that governs counter-regulatory responses to insulin-induced hypoglycemia (IIH). Here, the selective estrogen receptor-alpha (ERα) or -beta (ERβ) antagonists MPP and PHTPP were administered separately to the caudal fourth ventricle to address the premise that these hindbrain ER variants exert distinctive control of VMN reactivity to IIH in the female sex. Data show that ERα governs hypoglycemic patterns of VMN astrocyte glycogen metabolic enzyme, e.g. glycogen synthase and phosphorylase protein expression, whereas ERβ mediates local glycogen breakdown. DVC ERs also regulate VMN neurotransmitter signaling of energy sufficiency γ-aminobutyric acid or deficiency nitric oxide, steroidogenic factor-1 during IIH. Neither hindbrain ER mediates IIH-associated diminution of VMN norepinephrine (NE) content. Both ERs oppose hypoglycemic hyperglucagonemia, while ERβ contributes to reduced corticosterone output. Outcomes reveal that input from the female hindbrain to the VMN is critical for energy reserve mobilization, metabolic transmitter signaling, and counter-regulatory hormone secretion during hypoglycemia, and that ERs control those cues. Evidence that VMN NE content is not controlled by hindbrain ERα or -β implies that these receptors may regulate VMN function via NE-independent mechanisms, or alternatively, that other neurotransmitter signals to the VMN may control local substrate receptivity to NE.
•Estrogen receptor-alpha (ERα) or -beta (ERβ) antagonist was injected icv to hypoglycemic female rat hindbrain (HB).•HB ERα governs ventromedial hypothalamic nucleus (VMN) glycogen enzyme protein levels; ERβ controls VMN glycogen mass.•HB ERs regulate VMN transmitters that signal metabolic stability, e.g. γ-aminobutyric acid and nitric oxide.•Hypoglycemic diminution of VMN norepinephrine content is HB ER-independent.•HB ERα and -β oppose hypoglycemic hyperglucagonemia, while ERβ suppresses corticosterone output.
ObjectiveWe aimed to rapidly assess the health system impact of COVID-19 in the urban slums of Bangladesh.DesignSetting and participantsA cross-sectional survey among 476 households was conducted ...during October–December 2020 in five selected urban slums of Dhaka North, Dhaka South and Gazipur City Corporation. In-depth interviews with purposively selected 22 slum dwellers and key informant interviews with 16 local healthcare providers and four policymakers and technical experts were also conducted.Outcome measuresPercentage of people suffering from general illness, percentage of people suffering from chronic illness, percentage of people seeking healthcare, percentage of people seeking maternal care, health system challenges resulting from COVID-19.ResultsAbout 12% of members suffered from general illness and 25% reported chronic illness. Over 80% sought healthcare and the majority sought care from informal healthcare providers. 39% of the recently delivered women sought healthcare in 3 months preceding the survey. An overall reduction in healthcare use was reported during the lockdown period compared with prepandemic time. Mismanagement and inefficient use of resources were reported as challenges of health financing during the pandemic. Health information sharing was inadequate at the urban slums, resulting from the lack of community and stakeholder engagement (51% received COVID-19-related information, 49% of respondents knew about the national hotline number for COVID-19 treatment). Shortage of human resources for health was reported to be acute during the pandemic, resulting from the shortage of specialist doctors and uneven distribution of health workforce. COVID-19 test was inadequate due to the lack of adequate test facilities and stigma associated with COVID-19. Lack of strong leadership and stakeholder engagement was seen as the barriers to effective pandemic management.ConclusionThe findings of the current study are expected to support the government in tailoring interventions and allocating resources more efficiently and timely during a pandemic.
•Catecholamine neurons likely convey caudal hindbrain input to hypothalamic AMPK.•Insulin-induced hypoglycemia (IIH) elevated lateral hypothalamic phospho-AMPK (pAMPK).•6-Hydroxydopamine (6-OHDA) ...reversed IIH inhibition of ventromedial nucleus pAMPK.•6-OHDA elevated VMH steroidogenic factor-1 protein expression in IIH rats.•6-OHDA normalized or elevated arcuate neuropeptide Y and proopiomelanocortin profiles.
The hypothalamic energy sensor adenosine 5′-monophosphate-activated protein kinase (AMPK), an important regulator of counter-regulatory responses to hypoglycemia, responds to pharmacological manipulation of hindbrain AMPK activity. Dorsomedial hindbrain A2 noradrenergic neurons express hypoglycemia-sensitive metabolo-sensory biomarkers, including AMPK. Here, adult male rats were pretreated by intra-caudal fourth ventricular administration of the selective neurotoxin 6-hydroxydopamine (6-OHDA) to determine if catecholamine signaling from the aforesaid site governs hypothalamic AMPK activation during insulin-induced hypoglycemia (IIH). Micropunched arcuate (ARH), ventromedial (VMH), paraventricular (PVH), dorsomedial (DMH) nuclei and lateral hypothalamic area (LHA) tissues were obtained at the neutral protamine Hagedorn insulin-induced hypoglycemic nadir, coincident with A2 AMPK activation, for Western blot analysis of AMPK, phospho-AMPK (pAMPK), and relevant metabolic neuropeptides. ARH, VMH, LHA, and DMH norepinephrine levels were altered according to insulin dose; 6-OHDA-mediated reversal of these responses was site-specific. IIH elevated LHA and reduced VMH pAMPK protein, profiles that were respectively unchanged or increased by 6-OHDA. PVH and ARH pAMPK was resistant to IIH, but augmented in ARH of neurotoxin- plus insulin-treated rats. ARH neuropeptide Y (NPY) and pro-opiomelanocortin (POMC) proteins were correspondingly increased or refractory to IIH; 6-OHDA pretreatment normalized NPY and elevated POMC expression after insulin injection. Results demonstrate site-specific bi-directional adjustments in hypothalamic AMPK reactivity to hypoglycemia. Intensification of ARH/VMH pAMPK by 6-OHDA implies dorsomedial hindbrain improvement of energy balance in those sites during IIH. Neurotoxin-mediated augmentation versus suppression of basal catabolic (ARH POMC/VMH steroidogenic factor-1) or IIH-associated anabolic (ARH NPY) neuropeptide profiles, respectively, may involve local AMPK-dependent against independent mechanisms.
Central endozepinergic signaling is implicated in glucose homeostasis. Ventromedial hypothalamic nucleus (VMN) metabolic monitoring governs glucose counter-regulation. VMN glucose-stimulatory nitric ...oxide (NO) and glucose-inhibitory γ-aminobutyric acid (GABA) neurons express the energy gauge 5’-AMP-activated protein kinase (AMPK). Current research addresses the premise that the astrocyte glio-peptide octadecaneuropeptide (ODN) imposes sex-dimorphic control of metabolic sensor activity and neurotransmitter signaling in these neurons. The ODN G-protein coupled-receptor antagonist cyclo(1−8)DLeu5OP (LV-1075) was administered intracerebroventricularly (icv) to euglycemic rats of each sex; additional groups were pretreated icv with the ODN isoactive surrogate ODN11−18 (OP) before insulin-induced hypoglycemia. Western blotting of laser-catapult-microdissected VMN NO and GABA neurons showed that hypoglycemia caused OP-reversible augmentation of phospho-, e.g., activated AMPK and nitric oxide synthase (nNOS) expression in rostral (female) or middle (male) VMN segments or ODN-dependent suppression of nNOS in male caudal VMN. OP prevented hypoglycemic down-regulation of glutamate decarboxylase profiles in female rat rostral VMN, without affecting AMPK activity. LV-1075 treatment of male, not female rats elevated plasma glucagon and corticosterone concentrations. Moreover, OP attenuated hypoglycemia-associated augmentation of these hormones in males only. Results identify, for each sex, regional VMN metabolic transmitter signals that are subject to endozepinergic regulation. Directional shifts and gain-or-loss of ODN control during eu- versus hypoglycemia infer that VMN neuron receptivity to or post-receptor processing of this stimulus may be modulated by energy state. In male, counter-regulatory hormone secretion may be governed principally by ODN-sensitive neural pathways, whereas this endocrine outflow may be controlled by parallel, redundant ODN-dependent and -independent mechanisms in female.
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