TASK DEFINITION: Given a question and a context passage, generate the answer having the word or phrase from the context passage. Here, the answer should be a shortest continous span from the passage.
PROBLEM: Context: Can you name some fossils? How about dinosaur bones or dinosaur footprints? Animal skeletons, teeth, shells, coprolites (otherwise known as feces), or any other remains or traces from a living creature that becomes rock is a fossil. The same processes that formed these fossils also created some of our most important energy resources, fossil fuels. Coal, oil, and natural gas are fossil fuels. Fossil fuels come from living matter starting about 500 million years ago. Millions of years ago, plants used energy from the Sun to form sugars, carbohydrates, and other energy-rich carbon compounds. As plants and animals died, their remains settled on the ground on land and in swamps, lakes, and seas (Figure 1.1). Over time, layer upon layer of these remains accumulated. Eventually, the layers were buried so deeply that they were crushed by an enormous mass of earth. The weight of this earth pressing down on these plant and animal remains created intense heat and pressure. After millions of years of heat and pressure, the material in these layers turned into chemicals called hydrocarbons (Figure 1.2). Hydrocarbons are made of carbon and hydrogen atoms. This molecule with one carbon and four hydrogen atoms is methane. Hydrocarbons can be solid, liquid, or gaseous. The solid form is what we know as coal. The liquid form is petroleum, or crude oil. Natural gas is the gaseous form. The solar energy stored in fossil fuels is a rich source of energy. Although fossil fuels provide very high quality energy, they are non-renewable. Click image to the left or use the URL below. URL: 
 Question: hydrocarbons in solid form are called _________________.

SOLUTION: coal

PROBLEM: Context: 1836 Komarov, provisional designation 1971 OT, is a main-belt asteroid discovered on 26 July 1971 by Nikolai Chernykh at the Crimean Astrophysical Observatory in Nauchnyj. 
 Question: Who discovered 1836 Komarov?

SOLUTION: nikolai chernykh

PROBLEM: Context: Sodium-glucose cotransporter 2 (SGLT2) inhibitors lower glycemia by enhancing urinary glucose excretion. The physiologic response to pharmacologically induced acute or chronic glycosuria has not been investigated in human diabetes. We evaluated 66 patients with type 2 diabetes (62 7 years, BMI = 31.6 4.6 kg/m(2), HbA1c = 55 8 mmol/mol, mean SD) at baseline, after a single dose, and following 4-week treatment with empagliflozin (25 mg). At each time point, patients received a mixed meal coupled with dual-tracer glucose administration and indirect calorimetry. Both single-dose and chronic empagliflozin treatment caused glycosuria during fasting (median, 7.8 [interquartile range {IQR}, 4.4] g/3 hours and 9.2 [IQR, 5.2] g/3 hours) and after meal ingestion (median, 29.0 [IQR, 12.5] g/5 hours and 28.2 [IQR, 15.4] g/5 hours). After 3 hours of fasting, endogenous glucose production (EGP) was increased 25%, while glycemia was 0.9 0.7 mmol/l lower (P < 0.0001 vs. baseline). After meal ingestion, glucose and insulin AUC decreased, whereas the glucagon response increased (all P < 0.001). While oral glucose appearance was unchanged, EGP was increased (median, 40 [IQR, 14] g and 37 [IQR, 11] g vs. 34 [IQR, 11] g, both P < 0.01). Tissue glucose disposal was reduced (median, 75 [IQR, 16] g and 70 [IQR, 21] g vs. 93 [IQR, 18] g, P < 0.0001), due to a decrease in both glucose oxidation and nonoxidative glucose disposal, with a concomitant rise in lipid oxidation after chronic administration (all P < 0.01). Cell glucose sensitivity increased (median, 55 [IQR, 35] pmol min(-1) m(-2) mM(-1) and 55 [IQR, 39] pmol min(-1) m(-2) mM(-1) vs. 44 [IQR, 32] pmol min(-1) m(-2) mM(-1), P < 0.0001), and insulin sensitivity was improved. Resting energy expenditure rates and those after meal ingestion were unchanged. In patients with type 2 diabetes, empagliflozin-induced glycosuria improved cell function and insulin sensitivity, despite the fall in insulin secretion and tissue glucose disposal and the rise in EGP after one dose, thereby lowering fasting and postprandial glycemia. Chronic dosing shifted substrate utilization from carbohydrate to lipid. Trial registration. ClinicalTrials.Gov NCT01248364 (EudraCT no. 2010-018708-99). Funding. This study was funded by Boehringer Ingelheim. 
 Question: Which protein does empagliflozin inhibit?

SOLUTION:
sglt2