Effect of Molybdenum Induced Copper Deficiency on Peripheral Blood Cells and Bone Marrow in Buffalo Calves

Randhawa, C.S.,Randhawa, S.S.,Sood, N.K. Asian Australasian Association of Animal Productio 2002 Animal Bioscience Vol.15 No.4

Copper deficiency was induced in eight male buffalo calves by adding molybdenum (30 ppm wet basis) to their diet. Copper status was monitored from the liver copper concentration and a level below 30 ppm (DM basis) was considered as deficient. Haemoglobin, haematocrit, total and differential leucocyte numbers were determined. The functions of peripheral neutrophils were assessed by in vitro phagocytosis and killing of Staphylococcus aureus. The effect of molybdenum induced copper deficiency on bone marrow was monitored. The mean total leucocyte count was unaffected whereas a significant fall in neutrophil count coincided with the fall in hepatic copper level to $23.9{\pm}2.69$ ppm. Reduced blood neutrophil numbers was not accompanied by any change in the proportion of different neutrophil precursor cells in bone marrow. It was hypothesised that buffalo calves were more tolerant to dietary molybdenum excess than cattle. It was concluded that neutropenia in molybdenum induced copper deficiency occurred without any effect on their synthesis and maturation process. Bone marrow studies in healthy calves revealed higher percentage of neutrophilic myelocytes and metamyelocytes as compared to cattle.

A Review on Chemical-Induced Inflammatory Bowel Disease Models in Rodents

Randhawa, Puneet Kaur,Singh, Kavinder,Singh, Nirmal,Jaggi, Amteshwar Singh The Korean Society of Pharmacology 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.4

Ulcerative colitis and Crohn's disease are a set of chronic, idiopathic, immunological and relapsing inflammatory disorders of the gastrointestinal tract referred to as inflammatory bowel disorder (IBD). Although the etiological factors involved in the perpetuation of IBD remain uncertain, development of various animal models provides new insights to unveil the onset and the progression of IBD. Various chemical-induced colitis models are widely used on laboratory scale. Furthermore, these models closely mimic morphological, histopathological and symptomatical features of human IBD. Among the chemical-induced colitis models, trinitrobenzene sulfonic acid (TNBS)-induced colitis, oxazolone induced-colitis and dextran sulphate sodium (DSS)-induced colitis models are most widely used. TNBS elicits Th-1 driven immune response, whereas oxazolone predominantly exhibits immune response of Th-2 phenotype. DSS-induced colitis model also induces changes in Th-1/Th-2 cytokine profile. The present review discusses the methodology and rationale of using various chemical-induced colitis models for evaluating the pathogenesis of IBD.

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.

A Review on Chemical-Induced Inflammatory Bowel Disease Models in Rodents

Puneet Kaur Randhawa,Kavinder Singh,Amteshwar Singh Jaggi 대한약리학회 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.4

Ulcerative colitis and Crohn’s disease are a set of chronic, idiopathic, immunological and relapsinginflammatory disorders of the gastrointestinal tract referred to as inflammatory bowel disorder (IBD). Although the etiological factors involved in the perpetuation of IBD remain uncertain, developmentof various animal models provides new insights to unveil the onset and the progression of IBD. Variouschemical-induced colitis models are widely used on laboratory scale. Furthermore, these models closelymimic morphological, histopathological and symptomatical features of human IBD. Among thechemical-induced colitis models, trinitrobenzene sulfonic acid (TNBS)-induced colitis, oxazoloneinduced-colitis and dextran sulphate sodium (DSS)-induced colitis models are most widely used. TNBSelicits Th-1 driven immune response, whereas oxazolone predominantly exhibits immune response ofTh-2 phenotype. DSS-induced colitis model also induces changes in Th-1/Th-2 cytokine profile. Thepresent review discusses the methodology and rationale of using various chemical-induced colitismodels for evaluating the pathogenesis of IBD.

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.

Neurological Recovery in Two Patients with Cauda Equina Syndrome Secondary to L5 Lumbar Spine Giant Cell Tumour after Treatment with Denosumab without Surgery

Simret Singh Randhawa,Angel Khor Nee Kwan,Chee Kidd Chiu,Chris Yin Wei Chan,Mun Keong Kwan 대한척추외과학회 2016 Asian Spine Journal Vol.10 No.5

We report two patients with cauda equina syndrome (CES) secondary to L5 giant cell tumour (GCT) who achieved good neurological recovery after treatment with denosumab without surgery. The first patient was a 26-year-old man with L5 GCT causing CES who regained bowel and urinary control, muscle power improvement from grade 2 to grade 4 and Oswestry disability index (ODI) improvement from 48 to 23 after denosumab treatment. The second patient was a 25-year-old woman with L5 GCT causing CES who regained bowel and urinary control, muscle power improvement from grade 0 to grade 4 and ODI improvement from 42 to 20 after denosumab treatment. The usage of denosumab in the treatment of patients with CES due to GCT allows potential neurological recovery without any surgical intervention. If surgery is not contraindicated, more time is obtained to prepare the patient preoperatively to attain safer surgery and to achieve complete tumour clearance.

Neurogenic pathways in remote ischemic preconditioning induced cardioprotection: Evidences and possible mechanisms

Aulakh, Amritpal Singh,Randhawa, Puneet Kaur,Singh, Nirmal,Jaggi, Amteshwar Singh The Korean Society of Pharmacology 2017 The Korean Journal of Physiology & Pharmacology Vol.21 No.2

Remote ischemic preconditioning (RIPC) is an intrinsic phenomenon whereby 3~4 consecutive ischemia-reperfusion cycles to a remote tissue (non-cardiac) increases the tolerance of the myocardium to sustained ischemia-reperfusion induced injury. Remote ischemic preconditioning induces the local release of chemical mediators which activate the sensory nerve endings to convey signals to the brain. The latter consequently stimulates the efferent nerve endings innervating the myocardium to induce cardioprotection. Indeed, RIPC-induced cardioprotective effects are reliant on the presence of intact neuronal pathways, which has been confirmed using nerve resection of nerves including femoral nerve, vagus nerve, and sciatic nerve. The involvement of neurogenic signaling has been further substantiated using various pharmacological modulators including hexamethonium and trimetaphan. The present review focuses on the potential involvement of neurogenic pathways in mediating remote ischemic preconditioning-induced cardioprotection.

Neurogenic pathways in remote ischemic preconditioning induced cardioprotection: Evidences and possible mechanisms

Amritpal Singh Aulakh,Puneet Kaur Randhawa,Nirmal Singh,Amteshwar Singh Jaggi 대한약리학회 2017 The Korean Journal of Physiology & Pharmacology Vol.21 No.2

Remote ischemic preconditioning (RIPC) is an intrinsic phenomenon whereby 3~4 consecutive ischemia-reperfusion cycles to a remote tissue (noncardiac) increases the tolerance of the myocardium to sustained ischemiareperfusion induced injury. Remote ischemic preconditioning induces the local release of chemical mediators which activate the sensory nerve endings to convey signals to the brain. The latter consequently stimulates the efferent nerve endings innervating the myocardium to induce cardioprotection. Indeed, RIPC-induced cardioprotective effects are reliant on the presence of intact neuronal pathways, which has been confirmed using nerve resection of nerves including femoral nerve, vagus nerve, and sciatic nerve. The involvement of neurogenic signaling has been further substantiated using various pharmacological modulators including hexamethonium and trimetaphan. The present review focuses on the potential involvement of neurogenic pathways in mediating remote ischemic preconditioninginduced cardioprotection.

Histopathological changes in gall bladder mucosa in relation to the number, and size of gallstones, and analysis of the findings in the context of age distribution of the patients: A perspective

Sanjeev Sharma,Bhupinder Singh Walia,Mandeep Randhawa,Arjun Sharma,Pankaj Dugg,Jiteshwar Singh Pannu 한국간담췌외과학회 2023 Annals of hepato-biliary-pancreatic surgery Vol.27 No.3

Backgrounds/Aims: To study histopathological changes in gall bladder mucosa in cholelithiasis patients, and analyse their relation to the number and size of gallstones. These findings were evaluated in the context of age distribution of the study population. Methods: One hundred cases of cholecystectomy were part of the study, which was conducted in collaboration with the pathology department. The time period of the study was January 2020 to June 2021. Results: Maximum cases had multiple stones (69.0%), while one third cases (31.0%) had solitary stones. While initial univariate analysis showed age (odds ratio [OR], 6.882; p = 0.043), gallstone number (OR, 9.1; p = 0.050), gallstone size (OR, 17.111; p = 0.013), and duration of symptom (OR, 34.125; p = 0.001) to be significant risk factors associated with gallbladder carcinoma, multivariate analysis found none of these variables to be significant. However, conditional multivariate analysis for the duration of symptom (p = 0.008; OR, 21.118) yielded significant p- value. With histopathological diagnoses, 5% of cases had gallbladder cancer. Conclusions: This study shed light on the rising incidence of cholelithiasis in the young population and the high rate of gallbladder carcinoma in Punjab, India. Although gall stone characteristics (size, number) and patient age appeared to be significant risk factors when their individual relation with gallbladder carcinoma was studied, multivariate analysis, could not prove that. Conditional multivariate analysis showed the duration of symptom to be the only significant risk factor associated with gallbladder carcinoma. Further research with larger sample size is needed to study the rising incidence of gallbladder carcinoma, and the risk factors associated with it.