Floristic inventory and ecological characterization the village Sherpao,District Charsadda,Khyber Pakhtunkhwa- Pakistan

Floristic inventory of village Sherpao, District Charsadda comprised of total 104 plant species belonging to 46 families and 95 genera. The leading families included Fabaceae, Asteraceae, Poaceae and contributed by 8 species one (7.69%).The most pre-dominant life form was therophytes having 35 species (33.65%). Most dominant habit of flora were herbs having 77 species (74%) followed by trees contributed by 18 species (17.30%) and shrubs having 9 species (8.65%). Leaf size spectra of the flora showed that the most dominant leaf size class were microphyll having 38 species (36.53%) followed by nanophyll contributed by 32 species (30.76%), mesophyll represented 22 species (21.15%) and leptophyll contributed by 12 species (11.53%). Based on habitat 77 species (74%) were xerophytic in nature followed by 14 species (13.46%) in wet condition and 13 species (12.5%) were present in both conditions. In 104 plant species 85 were non spiny and 19 were spiny. Plant growth and distribution are having strong correlation with environment. Therefore, it is important to understand the environmental aspects that affect plant growth and distribution.     

Likelihood based population viability analysis in the presence of observation error

Population viability analysis (PVA) entails calculation of extinction risk, as defined by various extinction metrics, for a study population. These calculations strongly depend on the form of the population growth model and inclusion of demographic and/or environmental stochasticity. Form of the model and its parameters are determined based on observed population time series data. A typical population time series, consisting of estimated population sizes, inevitably has some observation error and likely has missing observations. In this paper, we present a likelihood based PVA in the presence of observation error and missing data. We illustrate the importance of incorporation of observation error in PVA by reanalyzing the population time series of song sparrow Melospiza melodia on Mandarte Island, British Columbia, Canada from 1975–1998. Using Akaike information criterion we show that model with observation error fits the data better than the one without observation error. The extinction risks predicted by with and without observation error models are quite different. Further analysis of possible causes for observation error revealed that some component of the observation error might be due to unreported dispersal. A complete analysis of such data, thus, would require explicit spatial models and data on dispersal along with observation error. Our conclusions are, therefore, two‐fold: 1) observation errors in PVA matter and 2) integrating these errors in PVA is not always enough and can still lead to important biases in parameter estimates if other processes such as dispersal are ignored.     

EHD4 and CDH23 Are Interacting Partners in Cochlear Hair Cells

Cadherin 23 (CDH23), a transmembrane protein localized near the tips of hair cell stereocilia in the mammalian inner ear, is important for delivering mechanical signals to the mechano-electric transducer channels. To identify CDH23-interacting proteins, a membrane-based yeast two-hybrid screen of an outer hair cell (OHC) cDNA library was performed. EHD4, a member of the C-terminal EH domain containing a protein family involved in endocytic recycling, was identified as a potential interactor. To confirm the interaction, we first demonstrated the EHD4 mRNA expression in hair cells using in situ hybridization. Next, we showed that EHD4 co-localizes and co-immunoprecipitates with CDH23 in mammalian cells. Interestingly, the co-immunoprecipitation was found to be calcium-sensitive. To investigate the role of EHD4 in hearing, compound action potentials were measured in EHD4 knock-out (KO) mice. Although EHD4 KO mice have normal hearing sensitivity, analysis of mouse cochlear lysates revealed a 2-fold increase in EHD1, but no increase in EHD2 or EHD3, in EHD4 KO cochleae compared with wild type, suggesting that a compensatory increase in EHD1 levels may account for the absence of a hearing defect in EHD4 KO mice. Taken together, these data indicate that EHD4 is a novel CDH23-interacting protein that could regulate CDH23 trafficking/localization in a calcium-sensitive manner.Hair cells located in the mammalian inner ear transform mechanical stimuli into electrical signals that in turn facilitate neurotransmitter release onto auditory neurons. The key element in the transduction process is the mechano-electric transducer (MET)² apparatus located near the top of the stereocilium. CDH23 is a single pass transmembrane protein with 27 extracellular cadherin repeats. It is one of the components of the tip-link (1, 2), which connects the top of a shorter stereocilium to the side of its taller neighbor (3). Vibrations of the basilar membrane of the inner ear ultimately result in deflection of the hair bundles, which modulates tension on the tip-link, thereby controlling the opening probability of cation-selective MET channels (3, 4). Cations, principally K⁺ and Ca²⁺, flow through the MET channels and ultimately change the membrane potential. A mutation in the gene encoding CDH23, the Usher syndrome type 1D factor (USH1D), causes deaf-blindness in humans (5). Several interacting partners of CDH23 have been reported and include another tip-link protein protocadherin 15 (6), a multi-PDZ domain-containing scaffold protein harmonin (7) and a stereociliary scaffolding protein MAGI-1 (8). Protocadherin 15 binds to CDH23 through its extracellular domains (6), whereas the cytoplasmic region of CDH23 interacts with MAGI-1 and harmonin through its PDZ domain-binding interfaces (PBI). Harmonin also associates with other USH1 factors like myosin VIIa, protocadherin 15, and sans (9). These findings indicate that harmonin bridges CDH23 to the cytoskeletal actin core of the stereocilium and is probably essential for the developmental differentiation of stereocilia (10–12). However, it is currently unknown how CDH23 is transported to the tip of stereocilia. To search for additional interacting partners of CDH23, we performed a membrane-based yeast two-hybrid assay, which identified EHD4 as a potential binding partner (13).EHD4 belongs to an evolutionarily conserved EH (Eps 15 homology) domain-containing protein family involved in endocytic trafficking and recycling. Four highly homologous members of this family, EHD1–4, are expressed in mammalian cells. They contain a single C-terminal EH domain, an N-terminal nucleotide-binding loop and a coiled-coil region responsible for oligomerization (14–16). Of the four EHD proteins EHD1 is the best characterized and is involved in regulating the recycling of membrane receptors including the transferrin receptor and the major histocompatibility complex class I (17, 18). EHD1 is also involved in controlling cholesterol recycling and homeostasis (19) and in facilitating endosome to Golgi retrieval (20). EHD3 appears to regulate receptor movements from the early endosome (EE) to the endocytic recycling compartment (ERC) and Golgi (21, 22). EHD2 was isolated from GLUT4-enriched fractions of adipocytes and was shown to regulate insulin-mediated translocation of GLUT4 to the plasma membrane (23, 24). Additionally, EHD2 is involved in the regulation of transferrin receptor internalization (23), recycling (25), and actin cytoskeleton rearrangement (23). EHD4, also called Pincher, was first reported as an extracellular matrix protein (26). Subsequent studies have shown this intracellular protein to be involved in the regulation of neurotrophin receptor TrkA endocytosis in pheochromocytoma (PC12) cells (27). It is also involved in interactions with the cell fate determinant, NUMB, and co-localizes with the small GTP-binding protein, Arf6 (28). Recently, Sharma et al. (29) showed that EHD4 regulates the exit of endocytic cargo from the early endosome toward both the recycling compartment and the late endocytic pathway. They also indicated that EHD4 and EHD1 interact transiently as most of the EHD4 resides on peripheral early endosomes, while EHD1 resides primarily on tubular recycling compartments. This partial overlap/association might be necessary for the transport of proteins through the early endosome to the ERC. Previously, George et al. (25) had also demonstrated that EHD4 interacts with EHD1 and its paralogs, which suggests cooperation and partial overlap of function between EHD4 and EHD1.Unlike other CDH23-binding proteins, EHD4 does not contain a PDZ domain that could bind to the PBI located in the cytoplasmic tail of CDH23. In addition, the cytoplasmic tail of CDH23 lacks an Asn-Pro-Phe (NPF) motif that could mediate an interaction with the EH domain of EHD4. Therefore, we proceeded to characterize the authenticity of interaction between EHD4 and CDH23 identified in yeast and mammalian cells, using both in vitro and in vivo methods. We verified the expression of EHD4 mRNA in mouse cochlea and investigated the physiological role of EHD4 protein in the cochlea using EHD4-KO mice.     

Application of hydrophobic interaction displacement chromatography for an industrial protein purification

Recently it has been established that low molecular weight displacers can be successfully employed for the purification of proteins in hydrophobic interaction chromatography (HIC) systems. This work investigates the utility of this technique for the purification of an industrial protein mixture. The study involved the separation of a mixture of three protein forms, that differed in the C-terminus, from their aggregate impurities while maintaining the same relative ratio of the three protein forms as in the feed. A batch high-throughput screening (HTS) technique was employed in concert with fluorescence spectroscopy for displacer screening in these HIC systems. This methodology was demonstrated to be an effective tool for identifying lead displacer candidates for a particular protein/stationary-phase system. In addition, these results indicate that surfactants can be employed at concentrations above their CMCs as effective displacers. Displacement of the recombinant proteins with PEG-3400 and the surfactant Big Chap was shown to increase the productivity as compared to the existing step-gradient elution process.     

Antiproliferative effect of elevated glucose in human microvascular endothelial cells

Diabetic microangiopathy has been implicated as a fundamental feature of the pathological complications of diabetes including retinopathy, neuropathy, and diabetic foot ulceration. However, previous studies devoted to examining the deleterious effects of elevated glucose on the endothelium have been performed largely in primary cultured cells of macrovessel origin. Difficulty in the harvesting and maintenance of microvascular endothelial cells in culture have hindered the study of this relevant population. Therefore, the objective of this study was to characterize the effect of elevated glucose on the proliferation and involved signaling pathways of an immortalized human dermal microvascular endothelial cell line (HMEC-1) that possess similar characteristics to their in vivo counterparts. Human dermal microvascular endothelial cells (HMEC-1) were grown in the presence of normal (5 mM) or high D-glucose (20 mM) for 14 days. The proliferative response of HMEC-1 was compared under these conditions as well as the cAMP and PKC pathways by in vitro assays. Elevated glucose significantly inhibited (P < 0.05) HMEC-1 proliferation after 7, 10, and 14 days. This effect was not mimicked by 20 mM mannitol. The antiproliferative effect was more pronounced with longer exposure (1–14 days) to elevated glucose and was irreversible 4 days after a 10-day exposure. The antiproliferative effect was partially reversed in the presence of a PKA inhibitor, Rp-cAMP (10–50 μM), and/or a PKC inhibitor, Calphostin C (10 nM). HMEC-1 exposed to elevated glucose (20 mM) for 14 days caused an increase in cyclic AMP accumulation, PKA, and PKC activity but was not associated with the activation of downstream events such as CRE and AP-1 binding activity. These data support the hypothesis that HMEC-1 is a suitable model to study the deleterious effects of elevated glucose on microvascular endothelial cells. Continued studies with HMEC-1 may prove advantageous in delineation of the molecular pathophysiology associated with diabetic microangiopathy. J. Cell. Biochem. 71:491–501, 1998. © 1998 Wiley-Liss, Inc.     

Reproductive tissues-specific meta-QTLs and candidate genes for development of heat-tolerant rice cultivars

Plant Molecular Biology - By integrating genetics and genomics data, reproductive tissues-specific and heat stress responsive 35 meta-QTLs and 45 candidate genes were identified, which could be...     

Security Analysis and Improvement of ‘a More Secure Anonymous User Authentication Scheme for the Integrated EPR Information System’

Over the past few years, secure and privacy-preserving user authentication scheme has become an integral part of the applications of the healthcare systems. Recently, Wen has designed an improved user authentication system over the Lee et al.’s scheme for integrated electronic patient record (EPR) information system, which has been analyzed in this study. We have found that Wen’s scheme still has the following inefficiencies: (1) the correctness of identity and password are not verified during the login and password change phases; (2) it is vulnerable to impersonation attack and privileged-insider attack; (3) it is designed without the revocation of lost/stolen smart card; (4) the explicit key confirmation and the no key control properties are absent, and (5) user cannot update his/her password without the help of server and secure channel. Then we aimed to propose an enhanced two-factor user authentication system based on the intractable assumption of the quadratic residue problem (QRP) in the multiplicative group. Our scheme bears more securities and functionalities than other schemes found in the literature.     

Geographic Wormhole Detection in Wireless Sensor Networks

Wireless sensor networks (WSNs) are ubiquitous and pervasive, and therefore; highly susceptible to a number of security attacks. Denial of Service (DoS) attack is considered the most dominant and a major threat to WSNs. Moreover, the wormhole attack represents one of the potential forms of the Denial of Service (DoS) attack. Besides, crafting the wormhole attack is comparatively simple; though, its detection is nontrivial. On the contrary, the extant wormhole defense methods need both specialized hardware and strong assumptions to defend against static and dynamic wormhole attack. The ensuing paper introduces a novel scheme to detect wormhole attacks in a geographic routing protocol (DWGRP). The main contribution of this paper is to detect malicious nodes and select the best and the most reliable neighbors based on pairwise key pre-distribution technique and the beacon packet. Moreover, this novel technique is not subject to any specific assumption, requirement, or specialized hardware, such as a precise synchronized clock. The proposed detection method is validated by comparisons with several related techniques in the literature, such as Received Signal Strength (RSS), Authentication of Nodes Scheme (ANS), Wormhole Detection uses Hound Packet (WHOP), and Wormhole Detection with Neighborhood Information (WDI) using the NS-2 simulator. The analysis of the simulations shows promising results with low False Detection Rate (FDR) in the geographic routing protocols.