Suppression of bacterial cell wall-induced polyarthritis by recombinant gamma interferon

Group A streptococcal cell wall fragments (SCW) induce erosive polyarthritis, characterized by synovial cell hyperplasia and intense mononuclear cell infiltration, in susceptible rats. Because of the known antiproliferative and immunomodulatory effects of interferon (IFN), we evaluated the effect of systemically administered alpha, beta and gamma IFN on the evolution of these destructive lesions. Treatment with gamma IFN not only reduced the acute response, but had an even greater suppressive effect on the chronic mononuclear cell-mediated destructive phase of the disease (articular index 10.2 +/- 1.2 for SCW only versus 3.8 +/- 0.7 for SCW + gamma IFN; p less than 0.01). Treatment with gamma IFN was more effective in the suppression of the arthritis than alpha, beta IFN. Histopathologic evaluation of the joints demonstrated that gamma IFN-treated animals had significantly fewer inflammatory cells, and less synovial hyperplasia and erosions than the SCW controls. gamma IFN suppression of mononuclear cell prostaglandin synthesis and synovial fibroblast proliferation was consistent with its anti-arthritic effects. These data indicate that the pathophysiology of SCW-induced erosive polyarthritis is subject to regulatory control by gamma IFN and that the mechanisms of suppression may be relevant in the treatment of rheumatoid arthritis.     

Apoptosis: mode of cell death induced in T cell leukemia lines by dexamethasone and other agents

Glucocorticoids can mediate the destruction of thymocytes and T cell-derived leukemia cells through a mechanism known as apoptosis. The characteristic feature of apoptosis is fragmentation of DNA at internucleosomal linkers through the activity of a specific endonuclease. In this study, an attempt was made to compare dexamethasone-induced apoptosis in two T cell-derived human leukemia lines (CEM-C1 and CEM-C7) to the cell killing brought about by selected cytotoxic agents. In the CEM-C7 cell line (dexamethasone-sensitive), apoptosis was induced not only by dexamethasone but by actinomycin D, cycloheximide, and 25-OH cholesterol. In the CEM-C1 cell line (dexamethasone-resistant) cycloheximide, 25-OH cholesterol, or cell starvation could induce apoptosis. It appears that in leukemic cells apoptosis may be induced by a variety of unrelated toxic agents and is not limited to glucocorticoids.     

A novel Z-structure for poly d(GC).poly d(GC)

A novel zig-zag (Z) structure is proposed for poly d(GC).poly d(GC). The proposed model closely resembles the crystal structure of d(CG)₃.     

Isolation and characterisation of cathepsin-B from bovine pancreas

A simple procedure for the isolation of cathepsin-B from bovine pancreas employing ammonium sulphate fractionation, DEAE cellulose chromatography and Sephadex G-200 gel filtration is described. The purified enzyme gave a single band on polyacrylamide gel electrophoresis. The molecular weight as determined by gel filtration of the enzyme was 26,850. ItsK _m andV _max values were 12.8 mM and 0.303 Μmol/min/mg, respectively. TheK _i for iodoacetamide was 0.16 mM.     

Studies on a strain of Fusarium solani (Mart.) Sacc. Isolated from a case of mycotic keratitis

A strain of Fusarium solani (Mart.) Sacc. (IMI-216517), isolated from a patient of mycotic keratitis, produced experimental keratomycosis in albino rabbit cornea and survived in internal tissues of albino mice for varying periods. Alantolactone, isolated from the plant — Inula racemosa Hook. f. exhibited marked in vitro fungistatic activity against this strain of F. solani at 100–200 g/ml concentrations. The strain was less sensitive to amphotericin B and showed more acid than alkaline proteinase and phosphatase activities.Communication No. 2526.     

Range edges in heterogeneous landscapes: Integrating geographic scale and climate complexity into range dynamics

The impacts of climate change have re‐energized interest in understanding the role of climate in setting species geographic range edges. Despite the strong focus on species' distributions in ecology and evolution, defining a species range edge is theoretically and empirically difficult. The challenge of determining a range edge and its relationship to climate is in part driven by the nested nature of geography and the multidimensionality of climate, which together generate complex patterns of both climate and biotic distributions across landscapes. Because range‐limiting processes occur in both geographic and climate space, the relationship between these two spaces plays a critical role in setting range limits. With both conceptual and empirical support, we argue that three factors—climate heterogeneity, collinearity among climate variables, and spatial scale—interact to shape the spatial structure of range edges along climate gradients, and we discuss several ways that these factors influence the stability of species range edges with a changing climate. We demonstrate that geographic and climate edges are often not concordant across species ranges. Furthermore, high climate heterogeneity and low climate collinearity across landscapes increase the spectrum of possible relationships between geographic and climatic space, suggesting that geographic range edges and climatic niche limits correspond less frequently than we may expect. More empirical explorations of how the complexity of real landscapes shapes the ecological and evolutionary processes that determine species range edges will advance the development of range limit theory and its applications to biodiversity conservation in the context of changing climate.     

A robust KASP marker for selection of four pairs of linked leaf rust and stripe rust resistance genes introgressed on chromosome arm 5DS from different wheat genomes

Molecular Biology Reports - Stripe rust and leaf rust are among the most devastating diseases of wheat, limiting its production globally. Wheat wild relatives harbour genetic diversity for new...     

Seeing the Quiet Politics in Unquiet Woods: A Different Vantage Point for a Future Forest Agenda

Human Ecology - We address two aspects of forest lives—violence and care—that are central to forest outcomes but often invisible in mainstream discussions on forests. We argue that...     

Xanthomonas sontii sp. nov., a non-pathogenic bacterium isolated from healthy basmati rice (Oryza sativa) seeds from India

Antonie van Leeuwenhoek - We report three yellow-pigmented, Gram-negative, aerobic, rod-shaped, motile bacterial isolates designated as PPL1T, PPL2, and PPL3 from healthy basmati rice seeds....     

Role of HRTPT in kidney proximal epithelial cell regeneration: Integrative differential expression and pathway analyses using microarray and scRNA-seq

Damage to proximal tubules due to exposure to toxicants can lead to conditions such as acute kidney injury (AKI), chronic kidney disease (CKD) and ultimately end-stage renal failure (ESRF). Studies have shown that kidney proximal epithelial cells can regenerate particularly after acute injury. In the previous study, we utilized an immortalized in vitro model of human renal proximal tubule epithelial cells, RPTEC/TERT1, to isolate HRTPT cell line that co-expresses stem cell markers CD133 and CD24, and HREC24T cell line that expresses only CD24. HRTPT cells showed most of the key characteristics of stem/progenitor cells; however, HREC24T cells did not show any of these characteristics. The goal of this study was to further characterize and understand the global gene expression differences, upregulated pathways and gene interaction using scRNA-seq in HRTPT cells. Affymetrix microarray analysis identified common gene sets and pathways specific to HRTPT and HREC24T cells analysed using DAVID, Reactome and Ingenuity software. Gene sets of HRTPT cells, in comparison with publicly available data set for CD133+ infant kidney, urine-derived renal progenitor cells and human kidney-derived epithelial proximal tubule cells showed substantial similarity in organization and interactions of the apical membrane. Single-cell analysis of HRTPT cells identified unique gene clusters associated with CD133 and the 92 common gene sets from three data sets. In conclusion, the gene expression analysis identified a unique gene set for HRTPT cells and narrowed the co-expressed gene set compared with other human renal–derived cell lines expressing CD133, which may provide deeper understanding in their role as progenitor/stem cells that participate in renal repair.