206 research outputs found
Green recovery featuring Dr Jagannadha Pawan Tamvada
No full textGreen Recovery has been adopted as a term proposing a package of environmental, regulatory and fiscal reforms to recover the prosperity after the COVID-19 pandemic. In the fourth episode of 'Policy Pod', Giles talks to Dr Jagannadha Pawan Tamvada, Associate Professor at the Southampton Business School. Pawan explains the role of microentreprenurship and why gong green links with a better company performance. He is a co-founder of iPowerz, the global entrepreneurship platform that serves to unleash the entrepreneurial spirit worldwide and author. His book 'Microentreprenurship in a Developing Country' examines the nexus between the entrepreneur, the firm, and the region for drawing a comprehensive picture of entrepreneurship in a developing country context
New Economic Science by Pawan Upadhyay
No full text[Copyright © 2025–2026 Pawan Upadhyay]
Economic Science by Pawan Upadhyay — The Best Economy Model :-
This repository presents “Economic Science by Pawan Upadhyay,” a comprehensive and balanced economic framework built on the combined strength of Domestic Consumption and Export-Driven Growth. This model defines the foundation of a stable, resilient, and growth-oriented national economy capable of withstanding both internal and external shocks.
At the core of this framework is the principle that a nation must cultivate a solid domestic economy while simultaneously boosting exports. When domestic demand weakens, export demand fills the gap; when global markets slow down, strong internal consumption sustains growth. This dual-engine approach ensures long-term economic stability.
The model emphasizes that economic strength is not dependent on a single variable, but on the coordinated functioning of multiple factors:
Key Components of the Model :-
Domestic Consumption + Export: The two main drivers of national growth.
Deficit Management: Strong savings, efficient taxation, investment inflows, and tourism revenue help reduce both fiscal and current account deficits.
Demand, Supply & Production: Stable demand, timely supply, and expansion of production capacity drive continuous growth.
Consumer Purchasing Power: Strong income, job creation, and affordable pricing strengthen domestic demand.
Strong but Comfortable Currency: A balanced strong currency reduces import costs without harming export competitiveness.
Cash Inflow vs. Outflow: Increasing foreign exchange inflow and reducing unnecessary outflow fortify national reserves.
Savings & Reserves: National savings act as a shield during inflation spikes, droughts, or global recessions.
Insights on Export Dynamics :-
The model explains how companies profit even with a strong currency by increasing export quantity or reducing production costs through cheaper imports. Profit = Earning − Expenditure A strong currency lowers import costs, increasing profit margins and making the economy more efficient.
Purpose of This Repository :-
This repository documents the complete economic model, provides theoretical foundations, and offers policymakers, students, and researchers a structured approach to understanding sustainable economic development.
Explanation
Economic Science by Pawan Upadhyay
A Balanced and Resilient Economic Growth Model :-
This repository presents “Economic Science by Pawan Upadhyay,” a comprehensive economic framework built on the dual strength of Domestic Consumption and Export-Driven Growth. The model outlines how nations can achieve long-term stability, strong financial health, and sustainable growth by balancing internal demand with external trade performance.
Key Principles of the Model :-
Domestic Consumption + Export = Best Economy
A nation becomes resilient when it has:
Strong domestic demand
Strong export performance
If one weakens, the other fills the gap — stabilizing the economy.
Managing Fiscal & Current Account Deficits
The model highlights four essential strategies:
Strong national saving
Efficient tax revenue collection
Increased domestic + foreign investment
Growth in tourism and foreign currency inflow
These pillars help control deficits and strengthen national finances.
Inflation, Income & Demand
Stable growth requires:
Low to moderate inflation
Rising income levels
Affordable product pricing
Strong consumer purchasing power
Demand and supply must remain balanced to avoid shocks.
Production Capacity & Supply Chain
Timely production and efficient supply chains meet both:
Domestic demand
Export demand
Higher production capacity drives economic expansion.
Strong but Comfortable Currency
A strong currency:
Makes imports cheaper
Reduces production cost
Increases profitability
A “comfortable level” of strength ensures exports remain competitive.
Cash Inflow vs Cash Outflow
A strong economy ensures:
More money flows into the country
Less money flows out unnecessarily
This boosts foreign reserves and economic security.
Savings & Economic Stability
National savings and reserves help during:
Drought
Inflation spikes
Global recessions
Domestic economic shocks
Export Profitability Formula
Profit = Earning − Expenditure
A strong currency lowers import-related expenditure, increasing profits even if export prices remain competitive.
Purpose of This Repository
This repository documents the complete economic model, offering:
Theoretical insights
Policy frameworks
Practical explanations
Real-world economic logic
It is suitable for students, researchers, economists, and policymakers.
✍️ Author and Independent Researcher
Pawan Upadhyay
[email protected]
Discoveries by Pawan Upadhyay
Official research page:
https://sites.google.com/view/discoveriesbypawanupadhyay/research-project
S): As a Potent Modulator and Therapeutic Prodrug in Cancer
No full textHydrogen sulfide (H2S) is an endogenous gaseous molecule present in all living organisms that has been traditionally studied for its toxicity. Interestingly, increased understanding of H2S effects in organ physiology has recently shown its relevance as a signalling molecule, with potentially important implications in variety of clinical disorders, including cancer. H2S is primarily produced in mammalian cells under various enzymatic pathways are target of intense research biological mechanisms, and therapeutic effects of H2S. Herein, we describe the physiological and biochemical properties of H2S, the enzymatic pathways leading to its endogenous production and its catabolic routes. In addition, we discuss the role of currently known H2S-releasing agents, or H2S donors, including their potential as therapeutic tools. Then we illustrate the mechanisms known to support the pleiotropic effects of H2S, with a particular focus on persulfhydration, which plays a key role in H2S-mediating signalling pathways. We then address the paradoxical role played by H2S in tumour biology and discuss the potential of exploiting H2S levels as novel cancer biomarkers and diagnostic tools. Finally, we describe the most recent preclinical applications focused on assessing the anti-cancer impact of most common H2S-releasing compounds. While the evidence in favour of H2S as an alternative cancer therapy in the field of translational medicine is yet to be clearly provided, application of H2S is emerging as a potent anticancer therapy in preclinical trails
Endolysosomal Ca2+ Signalling and Cancer Hallmarks: Two-Pore Channels on the Move, TRPML1 Lags Behind!
No full textThe acidic vesicles of the endolysosomal (EL) system are emerging as an intracellular Ca2+ store implicated in the regulation of multiple cellular functions. The EL Ca2+ store releases Ca2+ through a variety of Ca2+-permeable channels, including Transient Receptor Potential (TRP) Mucolipin 1-3 (TRPML1-3) and two-pore channels 1-2 (TPC1-2), whereas EL Ca2+ refilling is sustained by the proton gradient across the EL membrane and/or by the endoplasmic reticulum (ER). EL Ca2+ signals may be either spatially restricted to control vesicle trafficking, autophagy and membrane repair or may be amplified into a global Ca2+ signal through the Ca2+-dependent recruitment of ER-embedded channels. Emerging evidence suggested that nicotinic acid adenine dinucleotide phosphate (NAADP)-gated TPCs sustain multiple cancer hallmarks, such as migration, invasiveness and angiogenesis. Herein, we first survey the EL Ca2+ refilling and release mechanisms and then focus on the oncogenic role of EL Ca2+ signaling. While the evidence in favor of TRPML1 involvement in neoplastic transformation is yet to be clearly provided, TPCs are emerging as an alternative target for anticancer therapies
Targeting the endothelial Ca 2+ tool kit to rescue endothelial dysfunction in obesity associated-hypertension
No full textObesity is a major cardiovascular risk factor which dramatically impairs endothelium-dependent vasodilation and leads to hypertension and vascular damage. The impairment of the vasomotor response to extracellular autacoids, e.g. acetylcholine, mainly depends on the reduced nitric oxide (NO) bioavailability, which hampers vasorelaxation in large conduit arteries. In addition, obesity may affect endothelium-dependent hyperpolarization (EDH), which drives vasorelaxation in small resistance arteries and arterioles. Of note, endothelial Ca 2+ signals drive NO release and trigger EDH
Optical excitation of organic semiconductors as a highly selective strategy to induce vascular regeneration and tissue repair
No full textTherapeutic neovascularization represents a promising strategy to rescue the vascular network and restore organ function in cardiovascular disorders (CVDs), including acute myocardial infarction, heart failure, peripheral artery disease, and brain stroke. Endothelial colony forming cells (ECFCs), which are mobilized in circulation upon an ischemic insult, are commonly regarded as the most suitable cellular tool to achieve therapeutic neovascularization. ECFCs can be genetically or pharmacologically manipulated to enhance their vasoreparative potential by boosting specific pro-angiogenic signalling pathways. However, optical stimulation represents the most reliable approach to control cellular activity because of its high selectivity and unprecedented spatio-temporal resolution. Herein, we discuss a novel strategy to drive ECFC angiogenic activity in ischemic tissues by combining geneless optical excitation with photosensitive organic semiconductors. We describe how photoexcitation of the conducting polymer poly(3-hexylthiophene-2,5-diyl), also known as P3HT, stimulates extracellular Ca2+ entry through Transient Receptor Potential Vanilloid 1 (TRPV1) channels upon the production of hydrogen peroxide (H2O2) in the cleft between the nanomaterial and the cell membrane. H2O2-induced TRPV1-dependent Ca2+ entry stimulates ECFC proliferation and tube formation, thereby providing the proof-of-concept that photoexcitation of organic semiconductors may offer a reliable strategy to stimulate ECFCs-dependent neovascularization in CVDs
New clues for the role of cerebellum in schizophrenia and the associated cognitive impairment
No full text: Schizophrenia (SZ) is a complex neuropsychiatric disorder associated with severe cognitive dysfunction. Although research has mainly focused on forebrain abnormalities, emerging results support the involvement of the cerebellum in SZ physiopathology, particularly in Cognitive Impairment Associated with SZ (CIAS). Besides its role in motor learning and control, the cerebellum is implicated in cognition and emotion. Recent research suggests that structural and functional changes in the cerebellum are linked to deficits in various cognitive domains including attention, working memory, and decision-making. Moreover, cerebellar dysfunction is related to altered cerebellar circuit activities and connectivity with brain regions associated with cognitive processing. This review delves into the role of the cerebellum in CIAS. We initially consider the major forebrain alterations in CIAS, addressing impairments in neurotransmitter systems, synaptic plasticity, and connectivity. We then focus on recent findings showing that several mechanisms are also altered in the cerebellum and that cerebellar communication with the forebrain is impaired. This evidence implicates the cerebellum as a key component of circuits underpinning CIAS physiopathology. Further studies addressing cerebellar involvement in SZ and CIAS are warranted and might open new perspectives toward understanding the physiopathology and effective treatment of these disorders
Targeting endothelial ion signalling to rescue cerebral blood flow in cerebral disorders
No full textThe mechanism whereby an increase in neuronal activity (NA) leads to a local elevation in cerebral blood flow to supply the active neurons with oxygen and nutrients and remove the catabolic waste has been termed neurovascular coupling (NVC). Although it has long been thought that the vasoactive mediators involved in NVC are generated by neurons and astrocytes, recent evidence unveiled the crucial role of cerebrovascular endothelial cells in NVC. Brain capillary endothelial cells express a complement of ion channels, including inward-rectifier K+ (Kir2.1) channels, Transient Receptor Potential Ankyrin 1 channels and N-methyl-d-aspartate receptors that enable them to sense NA and thereby initiate the retrograde transmission of both electrical (via endothelium-dependent hyperpolarization) and chemical (via intercellular Ca2+ waves also sustained by TRP Vanilloid 4 channels and inositol-1,4,5-trisphosphate receptors) signals that induce vasodilation in upstream pial arteries and parenchymal arteries. Notably, a defect in the endothelial ion channel machinery (particularly, Kir2.1 channels) contributes to vascular cognitive impairment and dementia that features many cerebral disorders, including Alzheimer's disease, cerebral small vessel diseases, and traumatic brain injury. Targeting endothelial ion channels through appropriate pharmacological approaches might represent a hitherto unappreciated strategy to rescue CBF and prevent cognitive impairment and dementia in patients affected by cerebral disorders
Store-Operated Ca2+ Entry as a Putative Target of Flecainide for the Treatment of Arrhythmogenic Cardiomyopathy
No full textArrhythmogenic cardiomyopathy (ACM) is a genetic disorder that may lead patients to sudden cell death through the occurrence of ventricular arrhythmias. ACM is characterised by the progressive substitution of cardiomyocytes with fibrofatty scar tissue that predisposes the heart to life-threatening arrhythmic events. Cardiac mesenchymal stromal cells (C-MSCs) contribute to the ACM by differentiating into fibroblasts and adipocytes, thereby supporting aberrant remodelling of the cardiac structure. Flecainide is an Ic antiarrhythmic drug that can be administered in combination with fi-adrenergic blockers to treat ACM due to its ability to target both Nav1.5 and type 2 ryanodine receptors (RyR(2)). However, a recent study showed that flecainide may also prevent fibro-adipogenic differentiation by inhibiting store-operated Ca2+ entry (SOCE) and thereby suppressing spontaneous Ca2+ oscillations in C-MSCs isolated from human ACM patients (ACM C-hMSCs). Herein, we briefly survey ACM pathogenesis and therapies and then recapitulate the main molecular mechanisms targeted by flecainide to mitigate arrhythmic events, including Nav1.5 and RyR(2). Subsequently, we describe the role of spontaneous Ca2+ oscillations in determining MSC fate. Next, we discuss recent work showing that spontaneous Ca2+ oscillations in ACM C-hMSCs are accelerated to stimulate their fibro-adipogenic differentiation. Finally, we describe the evidence that flecainide suppresses spontaneous Ca2+ oscillations and fibro-adipogenic differentiation in ACM C-hMSCs by inhibiting constitutive SOCE
Arachidonic Acid Evokes an Increase in Intracellular Ca2+ Concentration and Nitric Oxide Production in Endothelial Cells from Human Brain Microcirculation
No full textIt has long been known that the conditionally essential polyunsaturated arachidonic acid (AA) regulates cerebral blood flow (CBF) through its metabolites prostaglandin E2 and epoxyeicosatrienoic acid, which act on vascular smooth muscle cells and pericytes to vasorelax cerebral microvessels. However, AA may also elicit endothelial nitric oxide (NO) release through an increase in intracellular Ca2+ concentration ([Ca2+]i). Herein, we adopted Ca2+ and NO imaging, combined with immunoblotting, to assess whether AA induces intracellular Ca2+ signals and NO release in the human brain microvascular endothelial cell line hCMEC/D3. AA caused a dose-dependent increase in [Ca2+]i that was mimicked by the not-metabolizable analogue, eicosatetraynoic acid. The Ca2+ response to AA was patterned by endoplasmic reticulum Ca2+ release through type 3 inositol-1,4,5-trisphosphate receptors, lysosomal Ca2+ mobilization through two-pore channels 1 and 2 (TPC1-2), and extracellular Ca2+ influx through transient receptor potential vanilloid 4 (TRPV4). In addition, AA-evoked Ca2+ signals resulted in robust NO release, but this signal was considerably delayed as compared to the accompanying Ca2+ wave and was essentially mediated by TPC1-2 and TRPV4. Overall, these data provide the first evidence that AA elicits Ca2+-dependent NO release from a human cerebrovascular endothelial cell line, but they seemingly rule out the possibility that this NO signal could acutely modulate neurovascular coupling
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