Human Resource Management in India: Performance and Complementarity

This is a study of the relationship between HR practices and organisational performance of large-scale enterprises in India. The main survey yielded 252 usable replies from the HR directors. Results show that mutually supportive sets of HR practices do not yield disproportionately superior outcomes than limited and focused individual practices. This highlights the limitations of strategic HRM in an Indian context. It seems there is little immediate benefit in developing sophisticated mutually supporting HR systems if particular firm or regionally relevant interventions yield clear benefits on their own right. These results highlight the limitations in national level institutions made for a general lack of complementarities, and/or that firms do not want to take the risk of over-relying on a specific institutional feature that may be subject to change. We also find that innovative firms are not in any way more likely to adopt best HR practices to a greater degree than their less innovative counterparts. India’s weak and uneven institutional coverage may open up more opportunities for HR innovation, but the lack of systemic support means that there are fewer opportunities for the latter to realise its fullest potential

D-serine improves learning and memory in epileptic animals

The N-methyl-D-aspartate receptor (NMDAR) is critical for the induction of synaptic plasticity and is essential for many forms of learning and memory. Activation of NMDAR by glutamate requires the presence of D-Serine, which is an endogenous physiological coagonist of the receptor and plays an important role in glutamate mediated NMDAR-dependent synaptic plasticity in the brain. However, the role of D-serine in synaptic plasticity and learning in chronic epilepsy is not known

D-serine improves learning and memory in epileptic animals

The N-methyl-D-aspartate receptor (NMDAR) is critical for the induction of synaptic plasticity and is essential for many forms of learning and memory. Activation of NMDAR by glutamate requires the presence of D-Serine, which is an endogenous physiological coagonist of the receptor and plays an important role in glutamate mediated NMDAR-dependent synaptic plasticity in the brain. However, the role of D-serine in synaptic plasticity and learning in chronic epilepsy is not known

Entsorgungsbergwerk. Machbarkeitsstudie zur Ablagerung von Abfaellen und Rueckstaenden in Steinkohlenbergwerken

SIGLETIB Hannover: FR 2602 / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekDEGerman

GABAA receptors-dependent synchronization leads to ictogenesis in the human dysplastic cortex

Patients with Taylor's type focal cortical dysplasia (FCD) present with seizures that are often medically intractable. Here, we attempted to identify the cellular and pharmacological mechanisms responsible for this epileptogenic state by using ®eld potential and K+- selective recordings in neocortical slices obtained from epileptic patients with FCD and, for purposes of comparison, with mesial temporal lobe epilepsy (MTLE), an epileptic disorder that, at least in the neocortex, is not characterized by any obvious structural aberration of neuronal networks. Spontaneous epileptiform activity was induced in vitro by applying 4-aminopyridine (4AP)-containing medium. Under these conditions, we could identify in FCD slices a close temporal relationship between ictal activity onset and the occurrence of slow interictal-like events that were mainly contributed by GABAA receptor activation. We also found that in FCD slices, pharmacological procedures capable of decreasing or increasing GABAA receptor function abolished or potentiated ictal discharges, respectively. In addition, the initiation of ictal events in FCD tissue coincided with the occurrence of GABAA receptordependent interictal events leading to [K+]o elevations that were larger than those seen during the interictal period. Finally, by testing the effects induced by baclofen on epileptiform events generated by FCD and MTLE slices, we discovered that the function of GABAB receptors (presumably located at presynaptic inhibitory terminals) was markedly decreased in FCD tissue. Thus, epileptiform synchronization leading to in vitro ictal activity in the human FCD tissue is initiated by a synchronizing mechanism that paradoxically relies on GABAA receptor activation causing sizeable increases in [K+]o. This mechanism may be facilitated by the decreased ability of GABAB receptors to control GABA release from interneuron terminals