How do psychiatrists in India construct their professional identity? A critical literature review

Psychiatric practice in India is marked by an increasing gulf between largely urban-based mental health professionals and a majority rural population. Based on the premise that any engagement is a mutually constructed humane process, an understanding of the culture of psychiatry including social process of local knowledge acquisition by trainee psychiatrists is critical. This paper reviews existing literature on training of psychiatrists in India, the cultural construction of their professional identities and autobiographical refections. The results reveal a scarcity of research on how identities, knowledge, and values are constructed, contested, resisted, sustained, and operationalized through practice. This paper hypothesizes that psychiatric training and practice in India continues to operate chiefy in an instrumental fashion and bears a circular relationship between cultural, hierarchical training structures and patient–carer concerns. The absence of interpretative social science training generates a professional identity that predominantly focuses on the patient and his/her social world as the site of pathology. Infrequent and often superfuous critical cultural refexivity gained through routine clinical practice further alienates professionals from patients, caregivers, and their own social landscapes. This results in a peculiar brand of theory and practice that is skewed toward a narrow understanding of what constitutes suffering. The authors argue that such omissions could be addressed through nuanced ethnographies on the professional development of psychiatrists during postgraduate training, including the political economies of their social institutions and local cultural landscapes. Further research will also help enhance culturally sensitive epistemology and shape locally responsive mental health training programs. This is critical for majority rural Indians who place their trust in State biomedical care

Hydrogen induced fast-fracture

One of the recurring anomalies in the hydrogen induced fracture of high strength steels is the apparent disconnect between their toughness and uniaxial tensile strength in identical hydrogen environments. Here we propose, supported by detailed atomistic and continuum calculations, that unlike macroscopic toughness, hydrogen-mediated tensile failure is a result of a fast-fracture mechanism. Specifically, we show that failure originates from the fast propagation of cleavage cracks that initiate from cavities that form around inclusions such as carbide particles. The failure process occurs in two stages. In stage-A, hydrides rapidly form around the roots of stressed notches on the cavity surfaces with hydrogen fed from the hydrogen gas within the cavity. These hydrides promote cleavage fracture with the cracks propagating at >100 ms^(-1) until the hydrogen gas in the cavity is exhausted. Predictions of this hydrogen-assisted crack growth mechanism are supported by atomistic calculations of binding energies, mobility barriers and molecular dynamics calculations of the fracture process. Typically, cracks grow by less than 1 μm via this hydrogen-assisted mechanism and thus insufficient to cause macroscopic fracture of the specimen. However, this stage is then followed by a stage-B process where these fast propagating cracks can continue to grow, now in the absence of hydrogen supply, given an appropriate level of remote tensile stress. This is surprising because the fracture energy is now that of Fe in the absence of H and cleavage fracture requires opening tractions on the order of 15 GPa to be generated. Thus, fracture is usually precluded due to plasticity around the crack-tip. Here we show via macroscopic continuum crack growth calculations in a rate dependent elastic-plastic solid with fracture modelled using a cohesive zone that cleavage is possible if the crack propagates fast enough. This is because strain-rates at the tips of fast propagating cracks are sufficiently high for the drag on the motion of dislocations resulting from phonon scattering to limit plasticity. This combined atomistic/continuum model is used to explain a host of well-established experimental observations including (but not limited to): (i) insensitivity of the strength to the concentration of trapped hydrogen; (ii) the extensive microcracking in addition to the final cleavage fracture event and (iii) the higher susceptibility of high strength steels to hydrogen embrittlement. Importantly, we also show that the stage-A hydrogen-assisted fracture process only occurs in certain crystallographic orientations with crack-tip plasticity processes, such as twinning, blunting cracks in other orientations. This inhibits the fast-fracture mechanism in a macroscopic toughness on a polycrystalline material and thus explains the apparent contradiction between the hydrogen-assisted macroscopic toughness and tensile strength of steels.EPSRC EP/L014742/

Growth rate of lithium filaments in ceramic electrolytes

© 2020 Lithium-ion batteries with single ion-conductor ceramic electrolytes short-circuit when subjected to charging currents above a critical current density. Here, we analyse the rate at which a lithium (Li) filament (sometimes referred to as a dendrite) will grow from the cathode towards the anode during charging of such batteries. The filament is modelled as a climbing edge dislocation with its growth occurring by Li+ flux from the electrolyte into the filament tip at constant chemical potential. The growth rate is set by a balance between the reduction of free-energy at the filament tip and energy dissipation associated with the resistance to the flux of Li+ through the filament tip. For charging currents above the critical current density, the filament growth rate increases with decreasing filament tip resistance. Imperfections, such as voids in the Li cathode along the electrolyte/cathode interface, decrease the critical current density but filament growth rates are also lower in these cases as filament growth rates scale with the charging currents. The predictions of the model are in excellent quantitative agreement with measurements and confirm that above the critical current density a filament can traverse the electrolyte in minutes or less. This suggests that initiation of filament growth is the critical step to prevent short-circuiting of the battery

Thermodynamic Modeling of the Statistics of Cell Spreading on Ligand-Coated Elastic Substrates.

Biological spread cells exist in a perpetually fluctuating state and therefore cannot be described in terms of a unique deterministic system. For modeling approaches to provide novel insight and uncover new mechanisms that drive cell behavior, a framework is required that progresses from traditional deterministic methods (whereby simulation of an experiment predicts a single outcome). In this study, we implement a new, to our knowledge, modeling approach for the analysis of cell spreading on ligand-coated substrates, extending the framework for nonequilibrium thermodynamics of cells developed by Shishvan et al. to include active focal adhesion assembly. We demonstrate that the model correctly predicts the coupled influence of surface collagen density and substrate stiffness on cell spreading, as reported experimentally by Engler et al. Low surface collagen densities are shown to result in a high probability that cells will be restricted to low spread areas. Furthermore, elastic free energy induced by substrate deformation lowers the probability of observing a highly spread cell, and, consequentially, lower cell tractions affect the assembly of focal adhesions. Experimentally measurable observables such as cell spread area and aspect ratio can be directly postprocessed from the computed homeostatic ensemble of (several million) spread states. This allows for the prediction of mean and SDs of such experimental observables. This class of cell mechanics modeling presents a significant advance on conventional deterministic approaches.Irish Research Counci

Research Journal of Pharmaceutical, Biological and Chemical Sciences ANTIOXIDANT AND ANTIHYPERGLYCEMIC POTENTIAL OF METHANOLIC EXTRACT OF BARK OF MIMUSOPS ELENGI L. IN MICE

ABSTRACT Ayurveda refers Mimusops elengi L. for the treatment of the diabetes. Considering the traditional claim of M. elengi in management of diabetes and the possible involvement of oxidative stress in pathogenesis of diabetes, the present study was aimed to evaluate the in vitro antioxidant and in vivo antihyperglycemic property of methanolic extract of bark of M. elengi (MEMeOH). In vitro antioxidant activity of MEMeOH was evaluated using reducing power assay, DPPH and hydroxyl radical scavenging assay. MEMeOH offered significant in vitro reducing power capacity and radical scavenging activity. In acute study in alloxan induced diabetes, MEMeOH exhibited significant (p< 0.001) antihyperglycemic effect. The onset of antihyperglycemic effect was observed at 2 nd hr; peak activity was demonstrated at 6 th hr. The antihyperglycemic effect of MEMeOH 400mg/kg, p.o. was persistent up to 24 th hr after drug administration. MEMeOH produced significant (p < 0.01) reduction in elevated glucose levels in glucose loaded non diabetic animals. The onset of action in non diabetic oral glucose tolerance test was found to be at 60 th min and peak activity was observed at 120 th min after oral glucose load. MEMeOH demonstrated significant (p < 0.01) reduction in elevated glucose levels 2hr before glucose administration and 6 hr after glucose load in oral glucose tolerance test in diabetic animals. MEMeOH has demonstrated antihyperglycemic activity in diabetic as well as non diabetic glucose loaded mice. MEMeOH should be further explored against diabetes and related complications

Discrete dislocation plasticity analysis of the high-temperature cyclic response of composites

Discrete dislocation plasticity (DDP) analysis of the high-temperature cyclic deformation of two- phase composites comprising a plastic matrix and elastic precipitates is presented. Deformation of the matrix is by climb-assisted glide of dislocations while the precipitates deform by a combination of bulk elasticity and stress-driven interfacial diffusion. The DDP calculations predict a cyclically softening response due to the formation of dislocation cell structures within the matrix. The dislocation cell sizes decrease with decreasing size of the unit cell (or equivalently matrix channels) and this results in an increased cyclic softening rate in composites with smaller unit cells. Interfacial diffusion also enhances the formation of dislocation cell structures and thereby promotes cyclic softening. These results are consistent with predictions of the creep behaviour that indicate that the increase in the creep rate (i.e. tertiary creep) is also associated with the formation of dislocation cell structures within the matrix

Discrete dislocation plasticity analysis of the effect of interfacial diffusion on the creep response of Ni single-crystal superalloys

© 2017 Acta Materialia Inc. Discrete dislocation plasticity (DDP) analysis of the high temperature creep deformation of a single crystal Ni superalloy comprising Ni3Al precipitates (γ′) in a Ni matrix (γ) is presented. The γ′ precipitates remain elastic but can also deform due to the stress-driven inter-diffusion of the Al within the Ni on the γ/γ′ interface while plastic deformation of the γ phase occurs by a combination of dislocation glide and dislocation climb coupled to the diffusion of vacancies. At relatively low applied uniaxial tensile stresses, the creep strain rates are very low in the absence of interfacial diffusion. This is due to the stress-induced pile up of dislocations at γ/γ′ interfaces that serves to inhibit further nucleation and suppresses continued plastic flow in the γ phase. When interfacial diffusion is permitted, the creep rates not only increase but the superalloy also exhibits distinct secondary and tertiary creep regimes. While this change in behaviour is a result of interfacial diffusion, the contribution of the average γ′ strain to the deformation of the superalloy is small. Rather, the diffusional deformation at the interface results in the development of a wavy interface which relaxes the back-stresses of dislocations piled-up at the γ/γ′ interfaces. This permits continued dislocation activity within the γ phase with dislocations arranging themselves into low energy cell-structures in the γ phase via dislocation climb. The formation of these structures results in an increase in the creep strain rate and the onset of the tertiary creep regime. At high applied stresses, the high initial dislocation density within the γ phase results in the continued climb motion of dislocations and an evolving spatial distribution of vacancies within the superalloy. Thus, creep deformation occurs even in the absence of interfacial diffusion although the creep rates are significantly increased when interfacial diffusion is present. The DDP analysis presented here demonstrates the critical role of interfacial diffusion in controlling the creep rates of Ni superalloys and suggests that interface engineering to reduce interfacial diffusion rates will aid in improving the creep performance of these alloys

Response of cells on a dense array of micro-posts

AbstractWe have analysed the response of cells on a bed of micro-posts idealized as a Winkler foundation using a homeostatic mechanics framework. The framework enables quantitative estimates of the stochastic response of cells along with the coupled analysis of cell spreading, contractility and mechano-sensitivity. In particular the model is shown to accurately predict that: (i) the extent of cell spreading, actin polymerisation as well as the traction forces that cells exert increase with increasing stiffness of the foundation; (ii) the traction forces that cells exert are primarily concentrated along the cell periphery; and (iii) while the total tractions increase with increasing cell area the average tractions are reasonably independent of cell area, i.e. for a given substrate stiffness, the average tractions that are normalized by cell area do not vary strongly with cell size. These results thus suggest that the increased foundation stiffness causes both the cell area and the average tractions that the cells exert to increase through higher levels of stress-fibre polymerization rather than the enhanced total tractions being directly linked through causation to the larger cell areas. A defining feature of the model is that its predictions are statistical in the form of probability distributions of observables such as the traction forces and cell area. In contrast, most existing models present solutions to specific boundary value problems where the cell morphology is imposed a priori. In particular, in line with observations we predict that the diversity of cell shapes, sizes and measured traction forces increase with increasing foundation stiffness. The homeostatic mechanics framework thus suggests that the diversity of observations in in vitro experiments is inherent to the homeostatic equilibrium of cells rather than being a result of experimental errors.</jats:p

Mental illness, poverty and stigma in India: a case-control study

OBJECTIVE: To assess the effect of experienced stigma on depth of multidimensional poverty of persons with severe mental illness (PSMI) in Delhi, India, controlling for gender, age and caste. DESIGN: Matching case (hospital)–control (population) study. SETTING: University Hospital (cases) and National Capital Region (controls), India. PARTICIPANTS: A case–control study was conducted from November 2011 to June 2012. 647 cases diagnosed with schizophrenia or affective disorders were recruited and 647 individuals of same age, sex and location of residence were matched as controls at a ratio of 1:2:1. Individuals who refused consent or provided incomplete interview were excluded. MAIN OUTCOME MEASURES: Higher risk of poverty due to stigma among PSMI. RESULTS: 38.5% of PSMI compared with 22.2% of controls were found poor on six dimensions or more. The difference in multidimensional poverty index was 69% between groups with employment and income of the main contributors. Multidimensional poverty was strongly associated with stigma (OR 2.60, 95% CI 1.27 to 5.31), scheduled castes/scheduled tribes/other backward castes (2.39, 1.39 to 4.08), mental illness (2.07, 1.25 to 3.41) and female gender (1.87, 1.36 to 2.58). A significant interaction between stigma, mental illness and gender or caste indicates female PSMI or PSMI from ‘lower castes’ were more likely to be poor due to stigma than male controls (p<0.001) or controls from other castes (p<0.001). CONCLUSIONS: Public stigma and multidimensional poverty linked to SMI are pervasive and intertwined. In particular for low caste and women, it is a strong predictor of poverty. Exclusion from employment linked to negative attitudes and lack of income are the highest contributors to multidimensional poverty, increasing the burden for the family. Mental health professionals need to be aware of and address these issues