Karthik Krishnamurthy

Bio: Karthik Krishnamurthy is an academic researcher from Thomas Jefferson University. The author has contributed to research in topics: Air traffic control & Friction stir welding. The author has an hindex of 29, co-authored 101 publications receiving 2720 citations. Previous affiliations of Karthik Krishnamurthy include Missouri University of Science and Technology & National Institute of Mental Health and Neurosciences.

A neural network thrust force controller to minimize delamination during drilling of graphite-epoxy laminates

Abstract: Delamination is a well-recognized problem associated with drilling fiber-reinforced composite materials (FRCMs). The most noted problems occur as the drill enters and exits the FRCM. Since drilling is often a final operation during assembly, any defects introduced in parts through the drilling process that result in the part being rejected represent an expensive loss. Studies based on linear-elastic fracture mechanics theory have proposed critical cutting and thrust forces in the various drilling regions that can be used as a guide in preventing crack growth or delamination. Using these critical force curves as a guide, a thrust force controller was developed to minimize the delamination while drilling a graphite-epoxy laminate. A neural network control scheme was implemented which required a neural network identifier to model the drilling dynamics and a neural network controller to learn the relationship between feed rate and the desired thrust force. Experimental results verifying the validity of this control approach as well as the robustness of the design are presented. Visual measurements of the delamination zones were used to quantify the benefits of the thrust force controlled drilling process versus the conventional constant feed rate drilling process.

Agrobacterium mediated transformation of chickpea (Cicer arietinum L.) embryo axes.

Abstract: Embryo axes of four accessions of chickpea (Cicer arietinum L.) were treated with Agrobacterium tumefaciens strains C58C1/GV2260 carrying the plasmid p35SGUSINT and EHA101 harbouring the plasmid pIBGUS. In both vectors the GUS gene is interrupted by an intron. After inoculation shoot formation was promoted on MS medium containing 0.5 mg/l BAP under a selection pressure of 100 mg/l kanamycin or 10 mg/l phosphinothricin, depending on the construct used for transformation. Expression of the chimeric GUS gene was confirmed by histochemical localization of GUS activity in regenerated shoots. Resistant shoots were grafted onto 5-day-old dark-grown seedlings, and mature plants could be recovered. T-DNA integration was confirmed by Southern analysis by random selection of putative transformants. The analysis of 4 plantlets of the T1 progeny revealed that none of them was GUS-positive, whereas the presence of the nptII gene could be detected by polymerase chain reaction.

Direct shoot regeneration from node, internode, hypocotyl and embryo explants of Withania somnifera

Abstract: In vitro studies were initiated with Withania somnifera (L.) Dun. for rapid micropropagation of selected chemotypes using nodes, internodes, hypocotyls and embryo explants. Direct regeneration of shoot buds was observed in MS basal medium supplemented with various concentrations of either benzyladenine (BA) or thidiazouron (TDZ) depending on the explant. Nodal explants formed multiple shoots both from pre-existing and de novo buds on Murashige and Skoog's medium (MS) containing 0.1–5.0 mg l−1 BA and a ring of de novo shoot buds on MS medium containing 0.2 and 0.3 mg l−1 TDZ. Internodal explants formed shoot buds on MS with 1.0 and 5.0 mg l−1 BA while the hypocotyl explants gave rise to multiple shoots only on MS with 0.5 mg l−1 BA. Isolated embryos gave rise to many shoot buds on MS with 0.2 and 0.3 mg l−1 TDZ. The shoot buds elongated and rooted either on MS medium with 0.01 mg l−1 BA or on half strength MS medium lacking growth regulators, which depended upon the growth regulator used in the shoot bud induction medium. Except for the embryo-derived plantlets, all other plantlets could be acclimatized with 100% success.

Decoding ALS: from genes to mechanism

Abstract: Amyotrophic lateral sclerosis (ALS) is a progressive and uniformly fatal neurodegenerative disease. A plethora of genetic factors have been identified that drive the degeneration of motor neurons in ALS, increase susceptibility to the disease or influence the rate of its progression. Emerging themes include dysfunction in RNA metabolism and protein homeostasis, with specific defects in nucleocytoplasmic trafficking, the induction of stress at the endoplasmic reticulum and impaired dynamics of ribonucleoprotein bodies such as RNA granules that assemble through liquid-liquid phase separation. Extraordinary progress in understanding the biology of ALS provides new reasons for optimism that meaningful therapies will be identified.

GGGGCC repeat expansion in C9orf72 compromises nucleocytoplasmic transport

Abstract: The GGGGCC (G4C2) repeat expansion in a noncoding region of C9orf72 is the most common cause of sporadic and familial forms of amyotrophic lateral sclerosis and frontotemporal dementia. The basis for pathogenesis is unknown. To elucidate the consequences of G4C2 repeat expansion in a tractable genetic system, we generated transgenic fly lines expressing 8, 28 or 58 G4C2-repeat-containing transcripts that do not have a translation start site (AUG) but contain an open-reading frame for green fluorescent protein to detect repeat-associated non-AUG (RAN) translation. We show that these transgenic animals display dosage-dependent, repeat-length-dependent degeneration in neuronal tissues and RAN translation of dipeptide repeat (DPR) proteins, as observed in patients with C9orf72-related disease. This model was used in a large-scale, unbiased genetic screen, ultimately leading to the identification of 18 genetic modifiers that encode components of the nuclear pore complex (NPC), as well as the machinery that coordinates the export of nuclear RNA and the import of nuclear proteins. Consistent with these results, we found morphological abnormalities in the architecture of the nuclear envelope in cells expressing expanded G4C2 repeats in vitro and in vivo. Moreover, we identified a substantial defect in RNA export resulting in retention of RNA in the nuclei of Drosophila cells expressing expanded G4C2 repeats and also in mammalian cells, including aged induced pluripotent stem-cell-derived neurons from patients with C9orf72-related disease. These studies show that a primary consequence of G4C2 repeat expansion is the compromise of nucleocytoplasmic transport through the nuclear pore, revealing a novel mechanism of neurodegeneration.