Probing magnetism in 2D van der Waals crystalline insulators via electron tunneling.

Magnetic insulators are a key resource for next-generation spintronic and topological devices. The family of layered metal halides promises varied magnetic states, including ultrathin insulating multiferroics, spin liquids, and ferromagnets, but device-oriented characterization methods are needed to unlock their potential. Here, we report tunneling through the layered magnetic insulator CrI3 as a function of temperature and applied magnetic field. We electrically detect the magnetic ground state and interlayer coupling and observe a field-induced metamagnetic transition. The metamagnetic transition results in magnetoresistances of 95, 300, and 550% for bilayer, trilayer, and tetralayer CrI3 barriers, respectively. We further measure inelastic tunneling spectra for our junctions, unveiling a rich spectrum consistent with collective magnetic excitations (magnons) in CrI3.

High-K diets reduce brain haemorrhage and infarcts, death rate and mesenteric arteriolar hypertrophy in stroke-prone spontaneously hypertensive rats.

Male stroke-prone spontaneously hypertensive rats (SHRSP) were fed 4% NaCl diets containing either 0.75% normal K or 2.11% high K, starting at 6 weeks of age. After 8 months on these diets 69% of 58 SHRSP rats on 0.75% K had died, whereas 2% of 95 rats of 2.11% K died, a 98% reduction in mortality, P less than 0.000 001. After 20 weeks the daytime and night-time blood pressure (BP) of each rat were measured intra-arterially. We selected two groups precisely matched for BP. One matched SHRSP group (BP 182 mmHg) ate the 0.75% K diet and 30 of 47 rats died (64% mortality). The other matched SHRSP group (BP 182 mmHg) ate the 2.11% K diet, and two of 35 died (6% mortality, a 91% reduction of mortality, P less than 0.0001). Seemingly, the striking reduction in mortality rate with the 2.11% hig-K diet does not depend on a lowering of BP. High-K diets do not change body Na or K. The dry weight of mesenteric arterioles was reduced by 22% on 2.11% K diet versus 75% K (7.5 versus 9.7 mg) (P less than 0.001), indicating a greatly reduced hypertensive hypertrophy. In nine surviving SHRSP on 0.75% K, 13 of 36 brain hemisphere slides (four slides per rat) showed infarcts (36%). In 11 surviving SHRSP on 2.11% K, one of 44 brain slides showed infarcts (2%, a 94.5% reduction, P less than 0.0001). Brain haemorrhage was reduced by 92% on the 2.11% K diet. High-K diets allow cerebral arteries to carry very high BPs without sustaining damage to the artery wall, thereby drastically reducing brain infarcts and lowering the death rate.

Potassium protection against lesions of the renal tubules, arteries, and glomeruli and nephron loss in salt-loaded hypertensive Dahl S rats.

Dahl S rats (20/group) were given three Purina diets for 24 weeks: 4% NaCl-no added potassium (BP 171 mm Hg); 4% NaCl-3.8% K citrate (BP 174 mm Hg); 4% NaCl-2.6% KCl (BP 173 mm Hg). The added potassium did not lower blood pressure (BP) but strikingly reduced microscopic renal lesions. Focal tubular dilation was scored blindly (100, severest lesions; 0, normal). Scores were: renal cortex: no potassium (41); K citrate (20); KCl (22), 50% improvement p less than 0.001; outer medulla: no potassium (79); K citrate (54); KCl (58), 30% improvement p less than 0.001; renal papilla: no potassium (49); K citrate (28); KCl (28), 43% improvement, p less than 0.001. Both K citrate and KCl also eliminated the thickened walls and relatively narrowed lumens of the hypertensive renal arterioles, without lowering BP. In these same rats, the wall thickness of arterioles from 20 normotensive salt-resistant (R) rats on 4% NaCl averaged 18.9 mu vs 26.1 mu in arterioles from 18 hypertensive salt-sensitive (S) rats on 4% NaCl with no added potassium. Adding either KCl or K citrate to the 4% NaCl diet strikingly reduced the wall thickness to that found in the R rat, even though the BP was not reduced at all. Potassium did not lower the high BP but apparently reduced the severity of the arteriolar lesions resulting from that high BP.(ABSTRACT TRUNCATED AT 250 WORDS)