Engaging local communities in social learning for inclusive management of native fruit trees in the Central Western Ghats, India

Participatory research and the social learning it supports are increasingly being used to improve forest management. Yet, the participation of women and other marginalized groups is often limited in these processes. This is a serious shortcoming, not only due to concerns for gender and social equity, but also because socially excluded, forest-dependent groups hold specific ecological knowledge, skills and interests that influence prospects for sustainable forest management. Carried out in India’s Central Western Ghats, this study explores the potential participatory research holds for engaging communities in a socially inclusive learning process that can support forest management. Participatory tools – resource mapping, Four Cell Analysis, seasonal fruit calendar, and seasonal activity – were used to elicit information on native fruit tree diversity, phenology, agronomy, uses and marketing. We discuss the benefits of this research set-up which promoted interactions among individuals from different groups, who came to experience a common group identity. The notion of contact zones – where different cultures or groups meet and engage with each other in ways that can reduce conflicts or redress asymmetrical power relations – guides our analysis. We demonstrate that the contact zone created through research process facilitated multi-directional information sharing and supported collective actions for forest management

Women Reproductive Rights in India: Prospective Future.

Reproductive rights were established as a subset of the human rights. Parents have a basic human right to determine freely and responsibly the number and the spacing of their children. Issues regarding the reproductive rights are vigorously contested, regardless of the population’s socioeconomic level, religion or culture. Following review article discusses reproductive rights with respect to Indian context focusing on socio economic and cultural aspects. Also discusses sensitization of government and judicial agencies in protecting the reproductive rights with special focus on the protecting the reproductive rights of people with disability (mental illness and mental retardation)

Formability of Metal-Matrix Composite based on Aluminium Alloy 6061 - Reinforced with Silicon Carbide Particulars

Aluminium alloy reinforced with hard ceramic materials has improved specific strength, specific modulus and wear resistance . Increasing amount of these reinforcing materials decreases ductility and CTE values . Many of these properties are desirable in aerospace , marine and automotive applications . There is no substantial data available as regards to forming characteristics of newly developed composite alloy.The present work has been undertaken with a view to assess quantitatively the forming behavior of 6061-Al/SiCPcomposites developed through conventional casting routes.The cast composites were upset tested and drawn during study of formability. Ring compression tests developed by Male and Cockcroft have been used for determining the friction factor during upsetting of rings . The reduction capacity test was modelled using Avitzur 's equations for forging of thin discs to estimate friction factor during upset forging a solid cylindrical disk under dry conditions . Friction factor has been estimated using a computer based on equation developed by Venugopal et al.Increasing silicon carbide content from 10 vol% to 20 vol% resulted in decreased formability based on upset test. Initially this decrease was of the order of 20% which later decreased by 25%. The rate of decrease of formability was more pronounced beyond 15 vol% of silicon carbide particulate addition . Paper reports the systematic investigation carried out with composite rings of geometry 6:3:2 (OD:ID:Height) under different lubricating conditions to estimate co-efficient of friction.Interfacial frictional value decreased on changing the lubricating conditions from dry to 220 grade lubricant, and this was of the order of 20-25%. Lubricant 220 and furnace oil were foun to have similar characteristics between 25-45% deformation in height. Paper also reports the results of reduction capacity test during upset forging of samples with aspect ratio of 2 and 2.5. It was revealed that the friction factor has strong dependence on deformation percentage. The friction factors determined by means of ring compression test and reduction capacity test with aspect ratio 2 are not in good agreement in cast Al 6061-SIC r composite, however, they are very close when aspect ratio was increased to 2.5. Further work on forming behaviour of the composite is in progress and it is expected that these will fill up the existing gap in the development of metal matrix composites

Role of the ubiquitin proteasome system in Alzheimer's disease

Though Alzheimer's disease (AD) is a syndrome with well-defined clinical and neuropathological manifestations, an array of molecular defects underlies its pathology. A role for the ubiquitin proteasome system (UPS) was suspected in the pathogenesis of AD since the presence of ubiquitin immunoreactivity in AD-related neuronal inclusions, such as neurofibrillary tangles, is seen in all AD cases. Recent studies have indicated that components of the UPS could be linked to the early phase of AD, which is marked by synaptic dysfunction, as well as to the late stages of the disease, characterized by neurodegeneration. Insoluble protein aggregates in the brain of AD patients could result from malfunction or overload of the UPS, or from structural changes in the protein substrates, which prevent their recognition and degradation by the UPS. Defective proteolysis could cause the synaptic dysfunction observed early in AD since the UPS is known to play a role in the normal functioning of synapses. In this review, we discuss recent observations on possible links between the UPS and AD, and the potential for utilizing UPS components as targets for treatment of this disease

Wireless data performance in multi-cell scenarios

The performance of wireless data systems has been extensively studied in the context of a single base station. In the present paper we investigate the flow-level performance in networks with multiple base stations. We specifically examine the complex, dynamic interaction introduced by the strong impact of interference from neighboring base stations. We derive two types of lower and upper bounds for the number of active flows, transfer delays and flow throughputs in the various cells. While the first type of bounds are rather rough and simple to compute, the second type of bounds are sharper, but harder to calculate. In order to obtain closed-form estimates for the latter bounds, we introduce two limit regimes, termed fluid and quasi-stationary regime, where the system dynamics evolve on a very fast and a very slow time scale, respectively. Importantly, the performance in both limit regimes is insensitive, thus yielding simple, explicit estimates that render the detailed statistical characteristics of the system largely irrelevant. Numerical experiments show that the upper bounds evaluated in the quasi-stationary regime provide conservative and extremely tight approximations

On the communication of well-being

The form that any communicatory exchange takes would depend on the extent to which the interests of the signaller and the recipient are at variance. Where such interests coincide, i.e. in cases of mutualism, the signals may be conspicuous when an immediate response is favoured, but rather subtle and variable otherwise. Over 80 % of the events of tactile communication that we have noted in our study of the social behaviour of free ranging groups of tame elephants appear to belong to this latter category. On Smith's standard classification, they can only be classified as 'associative', related to remaining in the company of another individual. However, such signals are commoner by a factor of 20-100 amongst elephant calves and their mothers and allomothers when compared to exchanges between adult cows. We suggest that the function of these signals is mutual monitoring of the state of well being amongst related individuals. The considerable degree of altruistic behaviour displayed in social groups, such as those of elephants is now believed to subserve the function of enhancing the inclusive fitness of the individuals concerned. We explore a mathematical model of exchange of social aid which suggests that animals in social groups may enhance their inclusive fitness further by adjusting the amount of social aid exchanged in relation to the state of well being of the donor as well as the recipient. Our model further suggests that optimal social aid depends on the state of well being in a complex fashion making it difficult for the recipient to deceive the donor so as to extract more aid. We therefore expect that by and large honest communication of the state of well being would be characteristic of the higher social animals. Such communication would be based on normal physiological changes consequent on a change in well being. Thus animals with a superior degree of well being would take postures conducive to greater activity, would be more receptive to sensory inputs and may also shift the balance of production of various metabolites. This monitoring of the well being has greatly advanced in the human species and may be at the base of the elaborate health care amongst human societies

New Perspectives on Oxidized Genome Damage and Repair Inhibition by Pro-Oxidant Metals in Neurological Diseases

The primary cause(s) of neuronal death in most cases of neurodegenerative diseases, including Alzheimer’s and Parkinson’s disease, are still unknown. However, the association of certain etiological factors, e.g., oxidative stress, protein misfolding/aggregation, redox metal accumulation and various types of damage to the genome, to pathological changes in the affected brain region(s) have been consistently observed. While redox metal toxicity received major attention in the last decade, its potential as a therapeutic target is still at a cross-roads, mostly because of the lack of mechanistic understanding of metal dyshomeostasis in affected neurons. Furthermore, previous studies have established the role of metals in causing genome damage, both directly and via the generation of reactive oxygen species (ROS), but little was known about their impact on genome repair. Our recent studies demonstrated that excess levels of iron and copper observed in neurodegenerative disease-affected brain neurons could not only induce genome damage in neurons, but also affect their repair by oxidatively inhibiting NEIL DNA glycosylases, which initiate the repair of oxidized DNA bases. The inhibitory effect was reversed by a combination of metal chelators and reducing agents, which underscore the need for elucidating the molecular basis for the neuronal toxicity of metals in order to develop effective therapeutic approaches. In this review, we have focused on the oxidative genome damage repair pathway as a potential target for reducing pro-oxidant metal toxicity in neurological diseases.The primary cause(s) of neuronal death in most cases of neurodegenerative diseases, including Alzheimer’s and Parkinson’s disease, are still unknown. However, the association of certain etiological factors, e.g., oxidative stress, protein misfolding/aggregation, redox metal accumulation and various types of damage to the genome, to pathological changes in the affected brain region(s) have been consistently observed. While redox metal toxicity received major attention in the last decade, its potential as a therapeutic target is still at a cross-roads, mostly because of the lack of mechanistic understanding of metal dyshomeostasis in affected neurons. Furthermore, previous studies have established the role of metals in causing genome damage, both directly and via the generation of reactive oxygen species (ROS), but little was known about their impact on genome repair. Our recent studies demonstrated that excess levels of iron and copper observed in neurodegenerative disease-affected brain neurons could not only induce genome damage in neurons, but also affect their repair by oxidatively inhibiting NEIL DNA glycosylases, which initiate the repair of oxidized DNA bases. The inhibitory effect was reversed by a combination of metal chelators and reducing agents, which underscore the need for elucidating the molecular basis for the neuronal toxicity of metals in order to develop effective therapeutic approaches. In this review, we have focused on the oxidative genome damage repair pathway as a potential target for reducing pro-oxidant metal toxicity in neurological diseases