Transforming water scarcity conflict: community responses in Yemen and Australia

When water is scarce, disputes over how to share it fairly and effectively are frequent. Understanding how people view and respond to water scarcity conflict is essential if it is to be addressed constructively. Through an interdisciplinary lens of hydropolitics and peace and conflict studies, this research used semi-structured interviews and interpretive phenomenological analysis (IPA) to investigate lived experience of sharing scarce water resources in Australia’s Murray-Darling/Barka Basin and Yemen’s Jibal as-Sarawat. Across divergent hydrological, cultural and political contexts, the study gained rich insight into how top decision-makers, mid-level community leaders and grassroots water sharers make sense of their relationships to water and emergent conflict in the face of water scarcity, as well as barriers to and opportunities for fair and peaceful water sharing. The study demonstrated that water scarcity conflict can wear down community resilience long before physiological needs arise, with devastating effects on mental health and social cohesion. Unpredictability, lack of information, social division and perceived injustice among basin stakeholders represent barriers to constructive water sharing outcomes. Opportunities to transform this conflict lie in expanding understandings of hydro-hegemony to incorporate the satisfaction of basic human water needs best understood as social in nature. However, this represents an ongoing process which is costly and replete with paradox. Despite water scarcity theory, policy and practice being dominated by positivist approaches, community resilience to the immense stresses of water scarcity can be found in acknowledging and holding emergent tensions between predictability and adaptability; simplicity and complexity; and personal and social responsibility

An investigation of the inflammatory response in patients with prostate cancer

Prostate cancer remains a major global health problem. Each year, in the UK, more than 27,000 patients are diagnosed with prostate cancer and approximately 9,500 die of their disease. The therapeutic options range from treatments primarily aimed at cure, such as radical surgery or radical radiotherapy, in patients with organ-confined disease to palliative treatments such as homrone therapy or chemotherapy used in patients with advanced disease. In chapter 1, the epidemiology, pathology, clinical features and treatment of prostate cancer are discussed. In chapter 2, the specific cellular and non-specific systemic inflammatory responses are discussed. In chapter three, the influence of tumour-bed lymphocyte infiltration on survival in patients with prostate cancer was evaluated. In chapter four, the effect of the systemic inflammatory response on outcome in patients with metastatic prostate cancer was investigated. In chapter five, the relationship between IL-6 and C-reactive protein in patients with untreated prostate cancer and benign prostatic disease was evaluated. Given that the inflammatory response appears to be important in predicting outcome in patients with prostate cancer, the question of whether C-reactive protein, could be used in the diagnostic setting to detect prostate cancer was explored in chapter 6. In conclusion, these studies suggest that in patients with prostate cancer, both the presence of a systemic inflammatory response and a profuse CD4+ lymphocyte infiltration of the tumour bed, predict poor survival. The negative impact of the systemic inflammatory response has been well documented in a variety of other common solid tumours. In contrast, the effect on survival of tumour bed lymphocyte infiltration appears to differ between tumour types. Whereas the presence of tumour-bed lymphocyte infiltration appears to be protective in patients with colorectal cancer, it appears to be detrimental in patients with prostate cancer. The reasons for these differences are as yet not clear. However, given that tumour lymphocyte infiltration parallels that of other inflammatory cells and that an elevated C-reactive protein is associated with poor survival in both tumour types, it may be that the source of interleukin-6 differs in different tumours. In colorectal cancer patients it has been reported that interleukin-6 concentrations increase with tumour stage and correlate with CEA concentrations. This would suggest that in colorectal cancer patients, interleukin-6 is produced by the tumour cells. In contrast, in patients with prostate cancer there is no significant correlation between serum interleukin-6 and PSA concentrations. It may therefore be that in patients with prostate cancer, interleukin-6 is produced by the host inflammatory cells rather than the tumour. If this were so, it might have implications for the treatment of the systemic inflammatory response in patients with different tumour types. (Abstract shortened by ProQuest.)

Asn 102 of the Gonadotropin-releasing Hormone Receptor Is a Critical Determinant of Potency for Agonists Containing C-terminal Glycinamide

We demonstrate a critical role for Asn102 of the human gonadotropin-releasing hormone (GnRH) receptor in the binding of GnRH. Mutation of Asn102, located at the top of the second transmembrane helix, to Ala resulted in a 225-fold loss of potency for GnRH. Eight GnRH analogs, all containing glycinamide C termini like GnRH, showed similar losses of potency between 95- and 750-fold for the [Ala102]GnRHR, compared with wild-type receptor. In contrast, four GnRH analogs that had ethylamide in place of the C-terminal glycinamide residue, showed much smaller decreases in potency between 2.4- and 11-fold. In comparisons of three agonist pairs, differing only at the C terminus, glycinamide derivatives showed an 11-20-fold greater loss of potency for the mutant receptor than their respective ethylamide derivatives. Thus Asn102 is a critical determinant of potency specifically for ligands with C-terminal glycinamide, while ligands with C-terminal ethylamide are less dependent on Asn102. These findings indicate a role for Asn102 in the docking of the glycinamide C terminus and are consistent with hydrogen bonding of the Asn102 side chain with the C-terminal amide moiety. Taken with previous data, they suggest a region of the GnRH receptor formed by the top of helices 2 and 7 as a binding pocket for the C-terminal part of the ligand

Reclassification of the Fuhrman grading system in renal cell carcinoma-does it make a difference?

PURPOSE: The aim of this study was to determine whether reclassifying the Fuhrman grading system provides further prognostic information. MATERIALS AND METHODS: We studied the pathological features and cancer specific survival of 237 patients with clear cell cancer undergoing surgery between 1997–2007 in a single centre. The original Fuhrman grading system was investigated as well as various simplified models utilising the original Fuhrman grade. RESULTS: The median follow up was 69 months. On univariate analysis, the conventional Fuhrman grading system as well various simplified models were predicative of cancer specific survival. On multivariate analysis, only the three tiered modified model in which grades 1 and 2 were combined whilst grades 3 and 4 were kept separate was an independent predictor of cancer specific survival (p=0.001, HR 2.17, 95% CI 1.37-3.43). Furthermore this simplified model demonstrated a stronger relationship to recurrence than the conventional 4 tiered Fuhrman grading system. CONCLUSIONS: A modified, three-tiered Fuhrman grading system has been demonstrated to be an independent predictor of cancer specific survival

(η5-Cyclo­penta­dien­yl){[3-(2,2-dicyano­ethen­yl)bicyclo­[2.2.1]hepta-2,5-dien-2-yl]ethyn­yl}(triphenyl­phosphine)nickel(II)

The title compound, [Ni(C5H5)(C13H7N2)(C18H15P)] or (η5-C5H5)(PPh3)Ni—C C—C7H6—C(H)=C(CN)2, contains an unusual disubstituted norbornadienyl (NBD) ligand containing ethynyl (–C C–) and dicyano­vinyl [–C(H)=C(CN)2] groups. Disorder is present in the NBD group with site occupancies of 0.636 (10) and 0.364 (10) for two distinct orientations. There are no strong hydrogen bonds and the primary inter­actions are weak C—H⋯π(arene) inter­actions

Environmental, dietary and case-control study of Nodding Syndrome in Uganda: A post-measles brain disorder triggered by malnutrition?

AbstractNodding Syndrome (NS) is an epileptic encephalopathy characterized by involuntary vertical head nodding, other types of seizures, and progressive neurological deficits. The etiology of the east African NS epidemic is unknown. In March 2014, we conducted a case-control study of medical, nutritional and other risk factors associated with NS among children (aged 5–18years) of Kitgum District, northern Uganda (Acholiland). Data on food availability, rainfall, and prevalent disease temporally related to the NS epidemic were also analyzed. In NS Cases, the mean age of reported head nodding onset was 7.6years (range 1–17years). The epidemiologic curve of NS incidence spanned 2000–2013, with peaks in 2003 and 2008. Month of onset of head nodding was non-uniform, with all-year-aggregated peaks in April and June when food availability was low. Families with one or more NS Cases had been significantly more dependent on emergency food and, immediately prior to head nodding onset in the child, subsistence on moldy plant materials, specifically moldy maize. Medical history revealed a single significant association with NS, namely prior measles infection. NS is compared with the post-measles disorder subacute sclerosing panencephalitis, with clinical expression triggered by factors associated with poor nutrition

Anti-tumour therapeutic efficacy of OX40L in murine tumour model

OX40 ligand (OX40L), a member of TNF superfamily, is a co-stimulatory molecule involved in T cell activation. Systemic administration of mOX40L fusion protein significantly inhibited the growth of experimental lung metastasis and subcutaneous (s.c.) established colon (CT26) and breast (4T1) carcinomas. Vaccination with OX40L was significantly enhanced by combination treatment with intra-tumour injection of a disabled infectious single cycle-herpes simplex virus (DISC-HSV) vector encoding murine granulocyte macrophage-colony stimulating factor (mGM-CSF). Tumour rejection in response to OX40L therapy required functional CD4+ and CD8+ T cells and correlated with splenocyte cytotoxic T lymphocytes (CTLs) activity against the AH-1 gp70 peptide of the tumour associated antigen expressed by CT26 cells. These results demonstrate the potential role of the OX40L in cancer immunotherapy