Performance Comparison of 8x10Gbps WDM System Using RZ and NRZ Format

Jasleen Kaur,Jyotsana,Jyoteesh Malhotra 보안공학연구지원센터 2015 International Journal of Signal Processing, Image Vol.8 No.11

In this paper, the performance analysis of 8X10 Gbps WDM system for different data formats has been done. The performance is analyzed for Non return-to-zero (NRZ) and Return-to-Zero (RZ) modulation formats to find maximum transmission distance for 80Gbps WDM system. It has been found that for NRZ the system travel transmission distance of 962 km and for RZ the system travel transmission distance of 1203 km. The total of eight channels with data rate of 10Gbps and equal channel spacing of 300 GHZ has been taken.

CHARACTERIZATIONS ON GEODESIC GCR-LIGHTLIKE SUBMANIFOLDS OF AN INDEFINITE KAEHLER STATISTICAL MANIFOLD

Jasleen Kaur,Vandana Rani M 호남수학회 2022 호남수학학술지 Vol.44 No.3

This article introduces the structure of GCR-lightlike submanifolds of an indefinite Kaehler statistical manifold and derives their geometric properties. The characterizations on totally geodesic, mixed geodesic, D-geodesic and D′ -geodesic GCR-lightlike submanifolds have also been obtained.

Animals models of spinal cord contusion injury

Renuka Verma,Jasleen Kaur Virdi,Nirmal Singh,Amteshwar Singh Jaggi 대한통증학회 2019 The Korean Journal of Pain Vol.32 No.1

Spinal cord contusion injury is one of the most serious nervous system disorders, characterized by high morbidity and disability. To mimic spinal cord contusion in humans, various animal models of spinal contusion injury have been developed. These models have been developed in rats, mice, and monkeys. However, most of these models are developed using rats. Two types of animal models, i.e. bilateral contusion injury and unilateral contusion injury models, are developed using either a weight drop method or impactor method. In the weight drop method, a specific weight or a rod, having a specific weight and diameter, is dropped from a specific height on to the exposed spinal cord. Low intensity injury is produced by dropping a 5 g weight from a height of 8 cm, moderate injury by dropping 10 g weight from a height of 12.5–25 mm, and high intensity injury by dropping a 25 g weight from a height of 50 mm. In the impactor method, injury is produced through an impactor by delivering a specific force to the exposed spinal cord area. Mild injury is produced by delivering 100 ± 5 kdyn of force, moderate injury by delivering 200 ± 10 kdyn of force, and severe injury by delivering 300 ± 10 kdyn of force. The contusion injury produces a significant development of locomotor dysfunction, which is generally evident from the 0–14th day of surgery and is at its peak after the 28–56th day. The present review discusses different animal models of spinal contusion injury.

Animals models of spinal cord contusion injury

Verma, Renuka,Virdi, Jasleen Kaur,Singh, Nirmal,Jaggi, Amteshwar Singh The Korean Pain Society 2019 The Korean Journal of Pain Vol.32 No.1

Spinal cord contusion injury is one of the most serious nervous system disorders, characterized by high morbidity and disability. To mimic spinal cord contusion in humans, various animal models of spinal contusion injury have been developed. These models have been developed in rats, mice, and monkeys. However, most of these models are developed using rats. Two types of animal models, i.e. bilateral contusion injury and unilateral contusion injury models, are developed using either a weight drop method or impactor method. In the weight drop method, a specific weight or a rod, having a specific weight and diameter, is dropped from a specific height on to the exposed spinal cord. Low intensity injury is produced by dropping a 5 g weight from a height of 8 cm, moderate injury by dropping 10 g weight from a height of 12.5-25 mm, and high intensity injury by dropping a 25 g weight from a height of 50 mm. In the impactor method, injury is produced through an impactor by delivering a specific force to the exposed spinal cord area. Mild injury is produced by delivering $100{\pm}5kdyn$ of force, moderate injury by delivering $200{\pm}10kdyn$ of force, and severe injury by delivering $300{\pm}10kdyn$ of force. The contusion injury produces a significant development of locomotor dysfunction, which is generally evident from the $0-14^{th}$ day of surgery and is at its peak after the $28-56^{th}$ day. The present review discusses different animal models of spinal contusion injury.

Conditioning-induced cardioprotection

Puneet Kaur Randhawa,Anjana Bali,Jasleen Kaur Virdi,Amteshwar Singh Jaggi 대한생리학회-대한약리학회 2018 The Korean Journal of Physiology & Pharmacology Vol.22 No.5

The aging process induces a plethora of changes in the body including alterations in hormonal regulation and metabolism in various organs including the heart. Aging is associated with marked increase in the vulnerability of the heart to ischemia-reperfusion injury. Furthermore, it significantly hampers the development of adaptive response to various forms of conditioning stimuli (pre/post/remote conditioning). Aging significantly impairs the activation of signaling pathways that mediate preconditioning-induced cardioprotection. It possibly impairs the uptake and release of adenosine, decreases the number of adenosine transporter sites and down-regulates the transcription of adenosine receptors in the myocardium to attenuate adenosine- mediated cardioprotection. Furthermore, aging decreases the expression of peroxisome proliferator-activated receptor gamma co-activator 1-alpha (PGC-1a) and subsequent transcription of catalase enzyme which subsequently increases the oxidative stress and decreases the responsiveness to preconditioning stimuli in the senescent diabetic hearts. In addition, in the aged rat hearts, the conditioning stimulus fails to phosphorylate Akt kinase that is required for mediating cardioprotective signaling in the heart. Moreover, aging increases the concentration of Na+ and K+, connexin expression and caveolin abundance in the myocardium and increases the susceptibility to ischemia-reperfusion injury. In addition, aging also reduces the responsiveness to conditioning stimuli possibly due to reduced kinase signaling and reduced STAT-3 phosphorylation. However, aging is associated with an increase in MKP-1 phosphorylation, which dephosphorylates (deactivates) mitogen activated protein kinase that is involved in cardioprotective signaling. The present review describes aging as one of the major confounding factors in attenuating remote ischemic preconditioninginduced cardioprotection along with the possible mechanisms.

Conditioning-induced cardioprotection: Aging as a confounding factor

Randhawa, Puneet Kaur,Bali, Anjana,Virdi, Jasleen Kaur,Jaggi, Amteshwar Singh The Korean Society of Pharmacology 2018 The Korean Journal of Physiology & Pharmacology Vol.22 No.5

The aging process induces a plethora of changes in the body including alterations in hormonal regulation and metabolism in various organs including the heart. Aging is associated with marked increase in the vulnerability of the heart to ischemia-reperfusion injury. Furthermore, it significantly hampers the development of adaptive response to various forms of conditioning stimuli (pre/post/remote conditioning). Aging significantly impairs the activation of signaling pathways that mediate preconditioning-induced cardioprotection. It possibly impairs the uptake and release of adenosine, decreases the number of adenosine transporter sites and down-regulates the transcription of adenosine receptors in the myocardium to attenuate adenosine-mediated cardioprotection. Furthermore, aging decreases the expression of peroxisome proliferator-activated receptor gamma co-activator 1-alpha ($PGC-1{\alpha}$) and subsequent transcription of catalase enzyme which subsequently increases the oxidative stress and decreases the responsiveness to preconditioning stimuli in the senescent diabetic hearts. In addition, in the aged rat hearts, the conditioning stimulus fails to phosphorylate Akt kinase that is required for mediating cardioprotective signaling in the heart. Moreover, aging increases the concentration of $Na^+$ and $K^+$, connexin expression and caveolin abundance in the myocardium and increases the susceptibility to ischemia-reperfusion injury. In addition, aging also reduces the responsiveness to conditioning stimuli possibly due to reduced kinase signaling and reduced STAT-3 phosphorylation. However, aging is associated with an increase in MKP-1 phosphorylation, which dephosphorylates (deactivates) mitogen activated protein kinase that is involved in cardioprotective signaling. The present review describes aging as one of the major confounding factors in attenuating remote ischemic preconditioning-induced cardioprotection along with the possible mechanisms.

Alveolar Epithelial Cells Express Markers of Senescence in Lungs from Patients With Idiopathic Pulmonary Fibrosis

( Eun Kyung Kim ),( Seung Ick Cha ),( Aaron V Schroeder ),( Jasleen Kukreja ),( Kirk D Jones ),( Jeffrey A Golden ),( Michael A Matthay ),( David J Erle ),( Harold R Collard ),( Paul J Wolters ) 대한결핵 및 호흡기학회 2012 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.114 No.-

Background: The prevalence of idiopathic pulmonary fibrosis (IPF) increases with age. Recent reports have demonstrated that mutations in TERT or TERC and short telomeres are risk factors for the development of IPF. Because short telomeres induce cellular senescence, these findings suggest senescence may occur in IPF lung. Methods: To evaluate for cellular senescence, we compared microRNA (miRNA) expression by miRNA arrays in type II epi-thelial cells. Senescence-associated β-galactosidase staining and immunohistochemical detection of p16, p21 and p53 were examined in sections of lung obtained from IPF patients and normal controls. Results: Expression of miR34-a, -b, and -c, which reportedly induce senescence in human epithelial cells are increased in IPF type II epithelial cells. β-Galactosidase activity is detectable on type II epithelial cells of IPF, but not normal lung. p16, p21 and p53 were detectable by immunostaining in IPF epithelial cells. Conclusions: IPF epithelial cells express several markers of senescence. These results suggest that the senescence of alveolar epithelial cells is accelerated in patients with IPF and may play a role in the pathogenesis of IPF.