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It is now widely recognized that climate change affects multiple sectors in virtually every part of the world. Impacts on one sector may influence other sectors, including seemingly remote ones, which we call “interconnections of climate risks.” While a substantial number of climate risks are identified in the Intergovernmental Panel on Climate Change Fifth Assessment Report, there have been few attempts to explore the interconnections between them in a comprehensive way. To fill this gap, we developed a methodology for visualizing climate risks and their interconnections based on a literature survey. Our visualizations highlight the need to address climate risk interconnections in impact and vulnerability studies. Our risk maps and flowcharts show how changes in climate impact natural and socioeconomic systems, ultimately affecting human security, health, and well‐being. We tested our visualization approach with potential users and identified likely benefits and issues. Our methodology can be used as a communication tool to inform decision makers, stakeholders, and the general public of the cascading risks that can be triggered by climate change.

Effective clinical therapy to augment intestinal absorption of water and electrolytes does not exist; the gut hormone, peptide YY (PYY), is a potent proabsorptive agent in animal models. The purpose of our study was to evaluate the effects of two novel PYY analogs, BIM-43073D and BIM-43004C, on intestinal absorption. Dogs with ileal Thiry-Vella fistulae (TVF) were treated with either PYY, BIM-43073D, or BIM-43004C. Administration of BIM-43073D significantly increased water and sodium absorption over baseline and maintained this level of increased absorption for a longer duration than an equimolar dose of PYY. Administration of BIM-43004C significantly increased sodium and water absorption over baseline at a level equal to that of PYY. The novel PYY analogs, BIM-43073D and BIM-43004C, are effective proabsorptive agents with BIM-43073D producing more sustained effects than PYY. These compounds may be clinically useful in the treatment of gut malabsorption in conditions such as cholera, Crohn's disease, and the short-bowel syndrome.

Changes in the hemodynamics and urine output were investigated in 19 patients undergoing laparoscopic cholecystectomy, five of whom had heart disease with the New York Heart Association classification I (n = 1) and II (n = 4). Systemic blood pressure, central venous pressure, pulmonary capillary wedge pressure and cardiac output did not significantly change during the procedure including the establishment of pneumoperitoneum. Urine output 30-60 min after starting the pneumoperitoneum was significantly lower in the patients with heart disease compared to the values before and in the initial phase (0-30 min), and also to the values before and during the procedure in the control group. One patient suffered temporary cardiac decompensation following laparoscopic cholecystectomy which prolonged his hospital stay to seven days. The remaining four patients with heart disease could be discharged on the third or fourth day postoperatively. It is concluded that laparoscopic cholecystectomy is feasible in patients with heart disease but attention should be paid to the possibility of oliguria during prolonged pneumoperitoneum.

BACKGROUND & AIMS: Gastrin (G-17) stimulates the growth of certain gastric and colon cancers mostly through gastrin/cholecystokinin (CCK)- B receptors. Glycine-extended gastrin (Gly-G) stimulates growth of a rat pancreatic acinar cell line; however, the effect of Gly-G on human gastric cancers is not known. The purpose of this study was to characterize the trophic effect of G-17 and Gly-G on two human gastric cancer cell lines, AGS and SIIA. METHODS: Binding analyses were performed, and cell growth was assessed by counting cells over a time course. RESULTS: G-17 stimulated growth of both AGS and SIIA cells. In AGS cells, gastrin/CCK-B receptor antagonists inhibited the effect of G- 17 and competitively antagonized 125I-G-17 binding, whereas the CCK- preferring (CCK-A) receptor antagonists had no effect. In contrast, CCK- A receptor antagonists inhibited the stimulatory effect of G-17 in SIIA cells, whereas CCK-B receptor antagonists had no effect. Gly-G stimulated the growth of AGS and SIIA cells; neither the CCK-B nor the CCK-A receptor antagonists blocked this effect. CONCLUSIONS: G-17 stimulates proliferation of AGS cells through the CCK-B receptor; however, G-17-mediated growth of SIIA acts through a CCK-A-like receptor. Furthermore, Gly-G stimulates growth of human gastric cancer cell lines, possibly through a receptor other than the CCK-B or CCK-A receptor. (Gastroenterology 1997 Sep;113(3):782-90)