Clinical and histopathological correlation of breast lesions

Background: To study the histopathological features of neoplastic and non neoplastic lesions of breast.  To correlate the pathological findings with clinical parameters.Methods: We have studied total 170 cases of breast lesions over a period of two years in our institute. The specimens were received in histopathology section of our department. Detailed gross examination of specimens was done followed by fixation, thorough sampling, and tissue processing. The different lesions were studied by histopathological examination and analysed. Neoplastic lesions were classified according to the WHO classification.Results: Out of the 170 cases, 128 cases had neoplastic lesions and 41 cases had non-neoplastic lesions, and one case had coexistent neoplastic and nonneoplastic lesions. Out of the total 129 cases with neoplastic lesions, 76 cases had benign breast tumors, 51 cases had malignant breast tumors, and 2 cases had precursor lesions. Fibroadenoma was the most common benign tumour with 62 cases. Invasive carcinoma no special type was the most common malignant tumour with 43 cases. Special subtypes of invasive carcinoma found in our study were mucinous carcinoma (2 case). The most common nonneoplastic lesion was mastitis with 12 cases, followed by duct ectasia and fibrocystic change. There were 6 cases of gynaecomastia. All the tumors involved upper outer quadrant most frequently. The benign tumors were most frequent in second, third and fourth decades, malignant tumours were seen beyond 4th decade. The nonneoplastic lesions were common in 4th decade.Conclusions: Histopathological study is important in the management of breast lesions

Differential effects of interleukin-13 and interleukin-6 on Jak/STAT signaling and cell viability in pancreatic β-cells

This is an Accepted Manuscript of an article published by Taylor & Francis in islets on 1 March 2013, available online: http://www.tandfonline.com/10.4161/isl.24249Open Access articlePro-inflammatory cytokines are important mediators of β-cell demise in type 1 diabetes, and similar mechanisms are increasingly implicated in type 2 diabetes, where a state of chronic inflammation may persist. It is likely that the actions of anti-inflammatory cytokines are also altered in diabetes. Cytokines are released from immune cells, which may be recruited to the islets in diabetes, but they can also be produced by islet endocrine cells in response to environmental factors, including enteroviral infection. Since enteroviral infection of islet cells may influence the development of diabetes in humans, we examined the actions of two cytokines, IL-13 and IL-6, whose expression are reported to be altered in β-cells during enteroviral infection. Human and rodent islet cells were shown to express receptors for both IL-13 and IL-6, and treatment with either cytokine resulted in the rapid phosphorylation of STAT3 and STAT6. However, while β-cells were protected against a range of cytotoxic insults during exposure to IL-13, treatment with IL-6 enhanced cytotoxicity and western blotting revealed that IL-13 induced one specific isoform of phospho-STAT6 preferentially. Upon incubation with both cytokines together, the isoform of STAT6 that was upregulated by IL-13 alone was again induced, and the effects of IL-6 on β-cell viability were attenuated. Overall, the results suggest that induction of specific isoforms of STAT family transcription factors may underlie the cytoprotective actions of IL-13, and they imply that selective targeting of specific STAT-mediated signaling components could provide a means to ameliorate the loss of β-cell viability in diabetes.Nuffield Foundation - Bursary schemeEuropean Union’s Seventh Framework Programme PEVNET (FP7/2007-2013

Effect of foliar application of zinc and salicylic acid on growth, flowering and chemical constitute of African marigold cv. pusa narangi gainda (Targets erecta L.)

A field experiment on African marigold (Targets erecta L.) was conducted during winter season of 2014-15to study the foliar effect of Zn and SA of 20 treatment combinations having five concentrations of zinc (0.0, 0.25, 0.50, 0.75, and 1.0 %) and salicylic acid (0.0, 0.25, 0.50 and 1.0 mM/L).The treatmentZn4SA3 (Zinc 1% + Salicylic acid 1.0 mM/L) recorded the maximum plant height (77.41 cm), number of leaves per plant (314.10),earliest first flower bud appearance (39.78 days), maximum number of flowers per plant (62.33), maximum chlorophyll content (3.83mg/g) and maximum carotene content (3.07 mg/g)as compared to control where it was recorded minimum. These results are conclusive that foliar spraying with zinc 1.0% + salicylic acid 1.0 mM/L may positively increasedthe growth and flowering parametersof marigold

Studies on variability in cumin (Cuminum cyminum L.) on normal and saline soil

Studies on variability in nine genotypes of cumin (Cuminum cyminum) (VC-217, VC-198, VC-216, VC-209, Local, VC-218, VC-89, RS-1 & VC-208) conducted at Jobner, India, indicated higher estimates of genotypic coefficient of variance, phenotypic coefficient of variance, heritability and genetic advance for plant height, number of umbels per plant, number of grains per umbel, test weight;grain yield per 10 plants, on normal soil and number of grains per umbel and test weight on saline soil, suggesting the probable role of additive gene effects on character expression. &nbsp

Studies on variability in cumin (Cuminum cyminum L.) on normal and saline soil

Studies on variability in nine genotypes of cumin (Cuminum cyminum) (VC-217, VC-198, VC-216, VC-209, Local, VC-218, VC-89, RS-1 & VC-208) conducted at Jobner, India, indicated higher estimates of genotypic coefficient of variance, phenotypic coefficient of variance, heritability and genetic advance for plant height, number of umbels per plant, number of grains per umbel, test weight;grain yield per 10 plants, on normal soil and number of grains per umbel and test weight on saline soil, suggesting the probable role of additive gene effects on character expression. &nbsp

Salinity tolerance of cumin (Cuminum cyminum L.) genotypes during germination

A laboratory experiment was conducted to identify cumin (Cuminum cyminum L.) genotypes tolerant to salt at germination stage. Four salinity levels having electrical conductivity of 2.61 (control), 5.17 (low), S.10 (medium) and 12.15 (high) dSm-1 were tested. There is an increase in the suppression of seed germination with increase in salinity in all the genotypes tested. The genotype UC-20S showed maximum salt tolerance, followed by UC-209 and UC-2IS. &nbsp

Salinity tolerance of cumin (Cuminum cyminum L.) genotypes during germination

A laboratory experiment was conducted to identify cumin (Cuminum cyminum L.) genotypes tolerant to salt at germination stage. Four salinity levels having electrical conductivity of 2.61 (control), 5.17 (low), S.10 (medium) and 12.15 (high) dSm-1 were tested. There is an increase in the suppression of seed germination with increase in salinity in all the genotypes tested. The genotype UC-20S showed maximum salt tolerance, followed by UC-209 and UC-2IS. &nbsp

Differential effects of saturated and unsaturated fatty acids on autophagy in pancreatic β-cells

Long-chain saturated fatty acids are lipotoxic to pancreatic β-cells, whereas most unsaturates are better tolerated and some may even be cytoprotective. Fatty acids alter autophagy in β-cells and there is increasing evidence that such alterations can impact directly on the regulation of viability. Accordingly, we have compared the effects of palmitate (C16:0) and palmitoleate (C16:1) on autophagy in cultured β-cells and human islets. Treatment of BRIN-BD11 β-cells with palmitate led to enhanced autophagic activity, as judged by cleavage of microtubule-associated protein 1 light chain 3-I (LC3-I) and this correlated with a marked loss of cell viability in the cells. In addition, transfection of these cells with an mCherry-YFP-LC3 reporter construct revealed the accumulation of autophagosomes in palmitate-treated cells, indicating an impairment of autophagosome-lysosome fusion. This was also seen upon addition of the vacuolar ATPase inhibitor, bafilomycin A1. Exposure of BRIN-BD11 cells to palmitoleate (C16:1) did not lead directly to changes in autophagic activity or flux, but it antagonised the actions of palmitate. In parallel, palmitoleate also improved the viability of palmitate-treated BRIN-BD11 cells. Equivalent responses were observed in INS-1E cells and in isolated human islets. Taken together, these data suggest that palmitate may cause an impairment of autophagosome-lysosome fusion. These effects were not reproduced by palmitoleate which, instead, antagonised the responses mediated by palmitate suggesting that attenuation of β-cell stress may contribute to the improvement in cell viability caused by the mono-unsaturated fatty acid.This article is freely available via Open Access. Click on the Publisher URL to access it via the publisher's site.The authors are grateful to Diabetes UK for financial support via project grants 14/0005093 and 15/0005156 (to N G M) and a PhD studentship (14/0005093) to Patricia Thomas. They also thank Dr Jon Lane (University of Bristol) for the kind gift of a dual-fluorescence LC3 reporter construct.accepted version (12 month embargo), submitted versio

GPR120 (FFAR4) is preferentially expressed in pancreatic delta cells and regulates somatostatin secretion from murine islets of Langerhans

Open Access articleThe final publication is available at Springer via http://dx.doi.org/10.1007/s00125-014-3213-0AIMS/HYPOTHESIS: The NEFA-responsive G-protein coupled receptor 120 (GPR120) has been implicated in the regulation of inflammation, in the control of incretin secretion and as a predisposing factor influencing the development of type 2 diabetes by regulation of islet cell apoptosis. However, there is still considerable controversy about the tissue distribution of GPR120 and, in particular, it remains unclear which islet cell types express this molecule. In the present study, we have addressed this issue by constructing a Gpr120-knockout/β-galactosidase (LacZ) knock-in (KO/KI) mouse to examine the distribution and functional role of GPR120 in the endocrine pancreas. METHODS: A KO/KI mouse was generated in which exon 1 of the Gpr120 gene (also known as Ffar4) was replaced in frame by LacZ, thereby allowing for regulated expression of β-galactosidase under the control of the endogenous GPR120 promoter. The distribution of GPR120 was inferred from expression studies detecting β-galactosidase activity and protein production. Islet hormone secretion was measured from isolated mouse islets treated with selective GPR120 agonists. RESULTS: β-galactosidase activity was detected as a surrogate for GPR120 expression exclusively in a small population of islet endocrine cells located peripherally within the islet mantle. Immunofluorescence analysis revealed co-localisation with somatostatin suggesting that GPR120 is preferentially produced in islet delta cells. In confirmation of this, glucose-induced somatostatin secretion was inhibited by a range of selective GPR120 agonists. This response was lost in GPR120-knockout mice. CONCLUSIONS/INTERPRETATION: The results imply that GPR120 is selectively present within the delta cells of murine islets and that it regulates somatostatin secretion.BBSRC-CASE studentshipDiabetes U

Investigation of the utility of the 1.1B4 cell as a model human beta cell line for study of persistent enteroviral infection.

This is the final version. Available on open access from Nature Research via the DOI in this record. Data availability: The research data supporting this publication are provided within this paper.The generation of a human pancreatic beta cell line which reproduces the responses seen in primary beta cells, but is amenable to propagation in culture, has long been an important goal in diabetes research. This is particularly true for studies focussing on the role of enteroviral infection as a potential cause of beta-cell autoimmunity in type 1 diabetes. In the present work we made use of a clonal beta cell line (1.1B4) available from the European Collection of Authenticated Cell Cultures, which had been generated by the fusion of primary human beta-cells with a pancreatic ductal carcinoma cell, PANC-1. Our goal was to study the factors allowing the development and persistence of a chronic enteroviral infection in human beta-cells. Since PANC-1 cells have been reported to support persistent enteroviral infection, the hybrid 1.1B4 cells appeared to offer an ideal vehicle for our studies. In support of this, infection of the cells with a Coxsackie virus isolated originally from the pancreas of a child with type 1 diabetes, CVB4.E2, at a low multiplicity of infection, resulted in the development of a state of persistent infection. Investigation of the molecular mechanisms suggested that this response was facilitated by a number of unexpected outcomes including an apparent failure of the cells to up-regulate certain anti-viral response gene products in response to interferons. However, more detailed exploration revealed that this lack of response was restricted to molecular targets that were either activated by, or detected with, human-selective reagents. By contrast, and to our surprise, the cells were much more responsive to rodent-selective reagents. Using multiple approaches, we then established that populations of 1.1B4 cells are not homogeneous but that they contain a mixture of rodent and human cells. This was true both of our own cell stocks and those held by the European Collection of Authenticated Cell Cultures. In view of this unexpected finding, we developed a strategy to harvest, isolate and expand single cell clones from the heterogeneous population, which allowed us to establish colonies of 1.1B4 cells that were uniquely human (h1.1.B4). However, extensive analysis of the gene expression profiles, immunoreactive insulin content, regulated secretory pathways and the electrophysiological properties of these cells demonstrated that they did not retain the principal characteristics expected of human beta cells. Our data suggest that stocks of 1.1B4 cells should be evaluated carefully prior to their use as a model human beta-cell since they may not retain the phenotype expected of human beta-cells.JDRFJDRFMedical Research Council (MRC)Diabetes UKNorman Family TrustEuropean Foundation for the Study of Diabete