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Articles by S Banerjee
Total Records ( 8 ) for S Banerjee
  S Banerjee , D Williamson , N Habib , M Gordon and J. Chataway
 

Stroke is a leading cause of death and disability. Globally, 15 million people suffer a stroke each year, of whom more than 5 million die, and a further 5 million are left permanently disabled. Current treatment options offer modest benefits, and there is a pressing need for new and effective treatments.

Stem cell therapy is a well-established treatment modality for various haematological diseases, with its use now being explored in different disease processes, including various neurological diseases, as well as vascular conditions such as ischaemic heart disease and peripheral vascular disease. Promising results have been seen in animal models of stroke, with evidence of significant functional benefits. Translation to the bedside, however, is in its early stages. This review will discuss the scientific background to stem cell therapy in ischaemic stroke, including evidence from current clinical trials.

  S Banerjee , M Zvelebil , P Furet , U Mueller Vieira , D. B Evans , M Dowsett and L. A. Martin
 

Endocrine therapy is well established for the treatment of breast cancer, and antiangiogenic agents are showing considerable promise. Targeting the vascular endothelial growth factor (VEGF) and estrogen receptor (ER) signaling pathways concomitantly may provide enhanced therapeutic benefit in ER-positive breast cancer. Therefore, the effects of the VEGF receptor (VEGFR) tyrosine kinase inhibitor PTK787/ZK222584 (PTK/ZK) were investigated using human breast cancer cell lines engineered to express aromatase. As expected in this system, estrogen (E2) or androstenedione induced a proliferative response and increased ER-mediated transcription in ER-positive cell lines expressing aromatase. However, surprisingly, in the presence of androstenedione, PTK/ZK suppressed both the androstenedione-stimulated proliferation and ER-mediated transcription. PTK/ZK alone and in the presence of E2 had no observable effect on proliferation or ER-mediated transcription. These effects result from PTK/ZK having previously unrecognized antiaromatase activity and PTK/ZK being a competitive aromatase inhibitor. Computer-assisted molecular modeling showed that PTK/ZK could potentially bind directly to aromatase. The demonstration that PTK/ZK inhibits aromatase and VEGFR indicates that agents cross-inhibiting two important classes of targets in breast cancer could be developed. [Cancer Res 2009;69(11):4716–23]

  L Lahiry , B Saha , J Chakraborty , A Adhikary , S Mohanty , D. M. S Hossain , S Banerjee , K Das , G Sa and T. Das
 

The most common alterations found in breast cancer are inactivation or mutation of tumor suppressor gene p53. The present study revealed that theaflavins induced p53-mutated human breast cancer cell apoptosis. Pharmacological inhibition of caspase-8 or expression of dominant-negative (Dn)-caspase-8/Fas-associated death domain (FADD) partially inhibited apoptosis, whereas caspase-9 inhibitor completely blocked the killing indicating involvement of parallel pathways that converged to mitochondria. Further studies demonstrated theaflavin-induced Fas upregulation through the activation of c-jun N-terminal kinase, Fas–FADD interaction in a Fas ligand-independent manner, caspase-8 activation and t-Bid formation. A search for the parallel pathway revealed theaflavin-induced inhibition of survival pathway, mediated by Akt deactivation and Bcl-xL/Bcl-2-associated death promoter dephosphorylation. These well-defined routes of growth control converged to a common process of mitochondrial transmembrane potential loss, cytochrome c release and activation of the executioner caspase-9 and -3. Overexpression of either constitutively active myristylated-Akt (Myr-Akt) or Dn-caspase-8 partially blocked theaflavin-induced mitochondrial permeability transition and apoptosis of p53-mutated cells, whereas cotransfection of Myr-Akt and Dn-caspase-8 completely abolished theaflavin effect thereby negating the possibility of existence of third pathways. These results and other biochemical correlates established the concept that two distinct signaling pathways were regulated by theaflavins to induce mitochondrial death cascade, eventually culminating to apoptosis of p53-mutated human breast cancer cells that are strongly resistant to conventional therapies.

  S Banerjee , R Biram , J Chataway and D. Ames
 

Background: South Asians comprise the largest ethnic minority population in the UK. This subgroup is known to have an elevated risk of stroke. However, there is limited data on patterns of cerebrovascular disease and associated risk factors in this population.

Aim: The aim of this study was to analyse differences in stroke subtype and risk factor profile between South Asian and White stroke patients admitted to a central London teaching hospital.

Design: Prospective database of all admissions to the St Mary's Hospital stroke unit.

Methods: We examined ethnicity, stroke subtype and risk factor profile of consecutive patients admitted to the stroke unit between 8 October 2003 and 14 February 2007.

Results: A total of 811 patients were identified of whom 736 had strokes. Four hundred and ninety-six (67%) occurred in the White subgroup, and 72 (10%) in the Asian subgroup. The South Asian subgroup was significantly younger (65 vs. 73 years in the White subgroup; P < 0.001). They had higher rates of hypertension (age adjusted frequency 87% vs. 64%; P < 0.0001), diabetes (54% vs. 15%; P < 0.0001), and hyperlipidaemia (70% vs. 45%; P = 0.001). There were lower rates of smoking (15% vs. 33%; P < 0.0001).There was a trend towards more lacunar infarcts and less total anterior circulation infarcts in South Asians, although after age adjustment this was not significant at the 5% level.

Conclusions: The South Asian subgroup has shown important differences in risk factor profile compared with the White population. The higher frequency of hypertension, diabetes and hyperlipidaemia seen in this subgroup are an important consideration in designing secondary prevention programmes tailored specifically to this community.

  S Banerjee , R Kaniel and I. Kremer
 

Motivated by the insight of Keynes (1936) on the importance of higher-order beliefs in financial markets, we examine the role of such beliefs in generating drift in asset prices. We show that in a dynamic setting, a higher-order difference of opinions is necessary for heterogeneous beliefs to generate price drift. Such drift does not arise in standard difference of opinion models, since investors' beliefs are assumed to be common knowledge. Our results stand in contrast to those of Allen, Morris, and Shin (2006) and others, as we argue that in rational expectation equilibria, heterogeneous beliefs do not lead to price drift.

  J. K Ching , P Rajguru , N Marupudi , S Banerjee and J. S. Fisher
 

Serum starvation is a common cell culture procedure for increasing cellular response to insulin, though the mechanism for the serum starvation effect is not understood. We hypothesized that factors known to potentiate insulin action [e.g., AMP-activated protein kinase (AMPK) and p38] or to be involved in insulin signaling leading to glucose transport [e.g., Akt, PKC, AS160, and ataxia telangiectasia mutated (ATM)] would be phosphorylated during serum starvation and would be responsible for increased insulin action after serum starvation. L6 myotubes were incubated in serum-containing or serum-free medium for 3 h. Levels of phosphorylated AMPK, Akt, and ATM were greater in serum-starved cells than in control cells. Serum starvation did not affect p38, PKC, or AS160 phosphorylation or insulin-stimulated Akt or AS160 phosphorylation. Insulin had no effect on glucose transport in control cells but caused an increase in glucose uptake for serum-starved cells that was preventable by compound C (an AMPK inhibitor), by expression of dominant negative AMPK (AMPK-DN), and by KU55933 (an ATM inhibitor). ATM protein levels increased during serum starvation, and this increase in ATM was prevented by compound C and AMPK-DN. Thus, it appears that AMPK is required for the serum starvation-related increase in insulin-stimulated glucose transport, with ATM as a possible downstream effector.

  A Friggeri , Y Yang , S Banerjee , Y. J Park , G Liu and E. Abraham
 

Phagocytosis of apoptotic cells is critical to resolution of inflammation. High mobility group box 1 protein (HMGB1), a mediator of inflammation, has been shown to diminish phagocytosis through binding to phosphatidylserine (PS) exposed on the surface of apoptotic neutrophils. However, it is currently unknown whether HMGB1 also modulates the activity of receptors involved in PS recognition on the surface of phagocytes. In the present studies, we found that preincubation of macrophages with HMGB1 decreased their ability to engulf apoptotic neutrophils or thymocytes. Preincubation of macrophages with HMGB1 prevented the enhancement of efferocytosis resulting from exposure to milk fat globule EGF factor 8 (MFG-E8), an opsonin that bridges PS and vβ3 as well as vβ5-integrins on the surface of phagocytes. The inhibitory effect of HMGB1 on the phagocytic activity of macrophages was prevented by preincubation of HMGB1 with soluble vβ3, but not with soluble vβ5. HMGB1 colocalized with the β3-integrin on the cell membrane of macrophages and bound to soluble vβ3, but not to soluble vβ5. HMGB1 suppressed the interaction between MFG-E8 and vβ3. HMGB1 also inhibited intracellular signaling events, including ERK phosphorylation and Rac-1 activation, which are activated in macrophages during phagocytosis of apoptotic cells. These results demonstrate that HMGB1 blocks vβ3-dependent recognition and uptake of apoptotic cells.

  Y Zhang , S Banerjee , R Yang , C Lungu and G. Ramachandran
 

Mathematical modeling is being increasingly used as a means for assessing occupational exposures. However, predicting exposure in real settings is constrained by lack of quantitative knowledge of exposure determinants. Validation of models in occupational settings is, therefore, a challenge. Not only do the model parameters need to be known, the models also need to predict the output with some degree of accuracy. In this paper, a Bayesian statistical framework is used for estimating model parameters and exposure concentrations for a two-zone model. The model predicts concentrations in a zone near the source and far away from the source as functions of the toluene generation rate, air ventilation rate through the chamber, and the airflow between near and far fields. The framework combines prior or expert information on the physical model along with the observed data. The framework is applied to simulated data as well as data obtained from the experiments conducted in a chamber. Toluene vapors are generated from a source under different conditions of airflow direction, the presence of a mannequin, and simulated body heat of the mannequin. The Bayesian framework accounts for uncertainty in measurement as well as in the unknown rate of airflow between the near and far fields. The results show that estimates of the interzonal airflow are always close to the estimated equilibrium solutions, which implies that the method works efficiently. The predictions of near-field concentration for both the simulated and real data show nice concordance with the true values, indicating that the two-zone model assumptions agree with the reality to a large extent and the model is suitable for predicting the contaminant concentration. Comparison of the estimated model and its margin of error with the experimental data thus enables validation of the physical model assumptions. The approach illustrates how exposure models and information on model parameters together with the knowledge of uncertainty and variability in these quantities can be used to not only provide better estimates of model outputs but also model parameters.

 
 
 
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