Anticipatory anti-colonial writing in R.K. Narayan's Swami and Friends and Mulk Raj Anand's Untouchable

This article uses the term “anticipatory anti-colonial writing” to discuss the workings of time in R.K. Narayan’s Swami and Friends and Mulk Raj Anand’s Untouchable. Both these first novels were published in 1935 with the support of British literary personalities (Graham Greene and E.M. Forster respectively) and both feature young protagonists who, in contrasting ways, are engaged in Indian resistance to colonial rule. This study examines the difference between Narayan’s local, though ironical, resistance to the homogenizing temporal demands of empire and Anand’s awkwardly modernist, socially committed vision. I argue that a form of anticipation that explicitly looks forward to decolonization via new and transnational literary forms is a crucial feature of Untouchable that is not found in Swami and Friends, despite the latter’s anti-colonial elements. Untouchable was intended to be a “bridge between the Ganges and the Thames” and anticipates postcolonial negotiations of time that critique global inequalities and rely upon the multidirectional global connections forged by modernism

PI3K Signaling in Normal B Cells and Chronic Lymphocytic Leukemia (CLL).

B cells provide immunity to extracellular pathogens by secreting a diverse repertoire of antibodies with high affinity and specificity for exposed antigens. The B cell receptor (BCR) is a transmembrane antibody, which facilitates the clonal selection of B cells producing secreted antibodies of the same specificity. The diverse antibody repertoire is generated by V(D)J recombination of heavy and light chain genes, whereas affinity maturation is mediated by activation-induced cytidine deaminase (AID)-mediated mutagenesis. These processes, which are essential for the generation of adaptive humoral immunity, also render B cells susceptible to chromosomal rearrangements and point mutations that in some cases lead to cancer. In this chapter, we will review the central role of PI3K s in mediating signals from the B cell receptor that not only facilitate the development of functional B cell repertoire, but also support the growth and survival of neoplastic B cells, focusing on chronic lymphocytic leukemia (CLL) B cells. Perhaps because of the central role played by PI3K in BCR signaling, B cell leukemia and lymphomas are the first diseases for which a PI3K inhibitor has been approved for clinical use

Cracking the BAFF code.

The tumour necrosis factor (TNF) family members B cell activating factor (BAFF) and APRIL (a proliferation-inducing ligand) are crucial survival factors for peripheral B cells. An excess of BAFF leads to the development of autoimmune disorders in animal models, and high levels of BAFF have been detected in the serum of patients with various autoimmune conditions. In this Review, we consider the possibility that in mice autoimmunity induced by BAFF is linked to T cell-independent B cell activation rather than to a severe breakdown of B cell tolerance. We also outline the mechanisms of BAFF signalling, the impact of ligand oligomerization on receptor activation and the progress of BAFF-depleting agents in the clinical setting

Characterization of hSAA1.1 and MetSAA1.1 by SDS-PAGE, SEC, far UV-CD, tryptophan fluorescence, and thermal denaturation studies.

<p>(A) SDS-PAGE gel (lanes: 1, protein ladder; 2, hSAA1.1; 3, MetSAA1.1 (B) SEC elution profiles of MetSAA1.1 (red solid line) and hSAA1.1 (blue solid line); (C) far UV-CD spectra of MetSAA1.1 (red solid line) and hSAA1.1 (blue solid line); (D) Thermal denaturation profiles of MetSAA1.1 (red solid line) and hSAA1.1 (blue solid line) (E) Tryptophan emission spectra of MetSAA1.1 (red solid line) and hSAA1.1 (blue solid line); (F) Tryptophan fluorescence-based thermal denaturation profiles of MetSAA1.1 (red solid line) and hSAA1.1 (blue solid line). The concentration of protein used in all the experiments was 20 µM. All experiments were performed at 4°C.</p

Characterization of “seeding” properties of MetSAA1.1 and hSAA1.1 by ThT fluorescence assay.

<p>(A) ThT fluorescence intensity profile for freshly refolded MetSAA1.1 only (black bars) and MetSAA1.1+ MetSAA1.1 “seed” (gray bars); (B) ThT fluorescence intensity profile for freshly refolded hSAA1.1 only (black bars) and hSAA1.1+ hSAA1.1 “seed” (gray bars). The concentration of protein was 20 µM. ThT fluorescence intensities were recorded by incubating the samples at 37°C.</p

Characterization of aggregation of MetSAA1.1 and hSAA1.1 by the ThT Fluorescence assay, Congo red binding assay, far UV CD, and solubility assay.

<p>(A) ThT fluorescence intensity profile for MetSAA1.1 (black bars) and hSAA1.1 (red bars); (B) Congo red absorbance spectra for Congo red only (blue solid line); Congo red plus MetSAA1.1 sample (red solid line); MetSAA1.1 difference spectra (red dash line); Congo red plus hSAA1.1 sample (black solid line); hSAA1.1 difference spectra (black dash line); (C) Far UV CD spectra of MetSAA1.1 samples incubated at 37°C for 6 h (red solid line), 24 h (blue solid line), and 72 h (green solid line); (D) Far UV CD spectra of hSAA1.1 samples incubated at 37°C for 6 h (red solid line), 24 h (blue solid line), and 72 h (green solid line); (E) solubility profile for MetSAA1.1 (black solid line) and hSAA1.1 (red solid line). The starting concentration of protein was 20 µM. All assays were performed after the proteins were allowed to aggregate at 37°C.</p