Peter Pushparaj

Peter Pushparaj

orcid

Research Focus & Metrics

Academic Career Length

27Years (2000-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 April 2016 in Methods
Verified
Journal Article
Open access
SRStephen M Richardson
Stephen M Richardson
GKGauthaman Kalamegam
Gauthaman Kalamegam
PPPeter Pushparaj
Peter Pushparaj
CMCsaba Matta
Csaba Matta
Adnan MemicAdnan Memic
Adnan Memic
Ali MobasheriAli Mobasheri
Ali Mobasheri
Musculoskeletal disorders represent a major cause of disability and morbidity globally and result in enormous costs for health and social care systems. Development of cell-based therapies is rapidly proliferating in a number of disease areas, including musculoskeletal disorders. Novel biological therapies that can effectively treat joint and spine degeneration are high priorities in regenerative medicine. Mesenchymal stem cells (MSCs) isolated from bone marrow (BM-MSCs), adipose tissue (AD-MSCs) and umbilical cord (UC-MSCs) show considerable promise for use in cartilage and intervertebral disc (IVD) repair. This review article focuses on stem cell-based therapeutics for cartilage and IVD repair in the context of the rising global burden of musculoskeletal disorders. We discuss the biology MSCs and chondroprogenitor cells and specifically focus on umbilical cord/Wharton's jelly derived MSCs and examine their potential for regenerative applications. We also summarize key components of the molecular machinery and signaling pathways responsible for the control of chondrogenesis and explore biomimetic scaffolds and biomaterials for articular cartilage and IVD regeneration. This review explores the exciting opportunities afforded by MSCs and discusses the challenges associated with cartilage and IVD repair and regeneration. There are still many technical challenges associated with isolating, expanding, differentiating, and pre-conditioning MSCs for subsequent implantation into degenerate joints and the spine. However, the prospect of combining biomaterials and cell-based therapies that incorporate chondrocytes, chondroprogenitors and MSCs leads to the optimistic view that interdisciplinary approaches will lead to significant breakthroughs in regenerating musculoskeletal tissues, such as the joint and the spine in the near future.

1 May 2007 in Journal of Ethnopharmacology
Verified
Journal Article
Closed access
PPPeter Pushparaj
Peter Pushparaj
HLH.K. Low
H.K. Low
JMJ. Manikandan
J. Manikandan
BTB.K.H. Tan
B.K.H. Tan
CTC.H. Tan
C.H. Tan

15 January 2015 in BMC Medical Genomics
Verified
Journal Article
Open access
PDF file
MFMuhammad Faheem
Muhammad Faheem
MNMuhammad Imran Naseer
Muhammad Imran Naseer
MRMahmood Rasool
Mahmood Rasool
ACAdeel Chaudhary
Adeel Chaudhary
TKTaha A Kumosani
Taha A Kumosani
HJHasan Saleh Jamal
Hasan Saleh Jamal
Autosomal recessive primary microcephaly (MCPH) is a neurodevelopmental disorder that is characterised by microcephaly present at birth and non-progressive mental retardation. Microcephaly is the outcome of a smaller but architecturally normal brain; the cerebral cortex exhibits a significant decrease in size. MCPH is a neurogenic mitotic disorder, though affected patients demonstrate normal neuronal migration, neuronal apoptosis and neural function. Twelve MCPH loci (MCPH1-MCPH12) have been mapped to date from various populations around the world and contain the following genes: Microcephalin, WDR62, CDK5RAP2, CASC5, ASPM, CENPJ, STIL, CEP135, CEP152, ZNF335, PHC1 and CDK6. It is predicted that MCPH gene mutations may lead to the disease phenotype due to a disturbed mitotic spindle orientation, premature chromosomal condensation, signalling response as a result of damaged DNA, microtubule dynamics, transcriptional control or a few other hidden centrosomal mechanisms that can regulate the number of neurons produced by neuronal precursor cells. Additional findings have further elucidated the microcephaly aetiology and pathophysiology, which has informed the clinical management of families suffering from MCPH. The provision of molecular diagnosis and genetic counselling may help to decrease the frequency of this disorder.

1 September 2000 in Journal of Ethnopharmacology
Verified
Journal Article
Closed access
PPPeter Pushparaj
Peter Pushparaj
CTC.H Tan
C.H Tan
BTB.K.H Tan
B.K.H Tan

21 October 2007 in Nature Medicine
Verified
Journal Article
Closed access
AMAlirio J Melendez
Alirio J Melendez
MHMargaret M Harnett
Margaret M Harnett
PPPeter Pushparaj
Peter Pushparaj
WWWs Fred Wong
Ws Fred Wong
HTHwee Kee Tay
Hwee Kee Tay
WHWilliam Harnett
William Harnett

15 June 2016 in Bioinformation
Verified
Journal Article
Open access
SAShazia Ali
Shazia Ali
MRMahmood Rasool
Mahmood Rasool
HCHani Chaoudhry
Hani Chaoudhry
PPPeter Pushparaj
Peter Pushparaj
PJParkash Jha
Parkash Jha
MJMohammad Sarwar Jamal
Mohammad Sarwar Jamal
Breast cancer is one of the most common cancers in women around the globe Tamoxifen is used for the last 40 years as an endocrine therapy for breast cancer. This resulted in the reduction of mortality rate by 30% and it still remains one of the most effective therapies against breast cancer. However, resistance against tamoxifen is still one of the major hurdles in the effective management of breast cancer. Intense research has been conducted in the past decade to further explore its resistance mechanism, but still a lot of research will be needed to effectively alleviate this problem. Several biochemical factors and molecular pathways, such as the modulation of ER signaling, upregulation of growth factors had been observed as key factors for tamoxifen resistance (TR). After, initial therapy of five to ten years, breast cancer patients develops resistance towards this drug. The resistance leads to the development of other cancers like uterine cancer. Here, we briefly explore all the molecular events related to tamoxifen resistance and focus on its mechanism of action as well as other pharmacological approaches to better its beneficial effects in the treatment of breast carcinoma.