Selective population inversion in NMR

Silver, Michael S.; Joseph, R. I.; Chen, C N; Sank, Victor J.; Hoult, D. I.

doi:10.1038/310681a0

Cited by 193 publications

(113 citation statements)

References 2 publications

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“…Improved fat suppression on SPAIR-SSFSE may be the result of using a nonselective adiabatic IR pulse, compared to a slice-selective adiabatic IR pulse, as used in many commercial IR SSFSE applications. Even though adiabatic pulses are recognized to provide optimal insensitivity to B1 inhomogeneity (11), slight motion and misregistration between IR and imaging slice may become apparent when slice-selective pulses are used.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of optimized inversion‐recovery fat‐suppression techniques for T2‐weighted abdominal MR imaging

Lauenstein

Sharma

Hughes

et al. 2008

Magnetic Resonance Imaging

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Purpose: To test the theoretical benefits of a spectral attenuated inversion-recovery (SPAIR) fat-suppression (FS) technique in clinical abdominal MRI by comparison to conventional inversion-recovery (IR) FS combined with T2-weighted (T2W) partial Fourier single shot fast spin echo (SSFSE).Materials and Methods: 1.5T MRI studies of the abdomen were performed in 28 patients with liver lesions (hemangiomas n ϭ 14; metastases n ϭ 14). T2W sequences were acquired using IR and SPAIR SSFSE. Measurements included retroperitoneal and mesenteric fat signal-to-noise (SNR) to evaluate FS; liver lesion contrast-to-noise (CNR) to evaluate bulk water signal recovery effects; and bowel wall delineation to evaluate susceptibility and physiological motion effects.Results: SPAIR-SSFSE images produce significantly improved FS and liver lesion CNR. The mean SNR of the retroperitoneal and mesenteric fat for SPAIR SSFSE was 20.5 Ϯ 10.2 (Ϯ1 SD) and 12.7 Ϯ 6.2, compared to 43.2 Ϯ 24.1 (P ϭ 0.000006) and 29.3 Ϯ 16.8 (P ϭ 0.0000005) for IR-SSFSE. SPAIR-SSFSE images produced higher CNR for both hemangiomas CNR ϭ 164 Ϯ 88 vs. 126 Ϯ 83 (P ϭ 0.00005) and metastases CNR ϭ 75 Ϯ 27 vs. 53 Ϯ 19 (P ϭ 0.007). Bowel wall visualization was significantly improved using SPAIR-SSFSE (P ϭ 0.002). Conclusion:The theoretical benefits of SPAIR over conventional IR FS translate into significant multiple improvements that can be measured on clinical abdominal MRI scans.

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Section: Discussionmentioning

confidence: 99%

Evaluation of optimized inversion‐recovery fat‐suppression techniques for T2‐weighted abdominal MR imaging

Lauenstein

Sharma

Hughes

et al. 2008

Magnetic Resonance Imaging

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“…Signals from the liver were acquired by image selected in vivo spectroscopy localization technique to remove signals from surface above the liver (22). A 4-ms hyperbolic secant pulse was used to invert the 2.5 cm of the skin surface, and as a result, signals from the surface were eliminated by adding scans with an alternate inverse pulse (23). A 180 Њ pulse at the coil center was used as an excitation pulse.…”

Section: Methodsmentioning

confidence: 99%

Impaired hepatic glycogen synthesis in glucokinase-deficient (MODY-2) subjects.

Velho

Petersen²,

Perseghin³

et al. 1996

J. Clin. Invest.

201

127

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All glucokinase gene mutations identified to date have been localized to exons that are common to the pancreatic and hepatic isoforms of the enzyme. While impaired insulin secretion has been observed in glucokinase-deficient subjects the consequences of this mutation on hepatic glucose metabolism remain unknown. To examine this question hepatic glycogen concentration was measured in seven glucokinasedeficient subjects with normal glycosylated hemoglobin and 12 control subjects using 13 C nuclear magnetic spectroscopy during a day in which three isocaloric mixed meals were ingested. The relative fluxes of the direct and indirect pathways of hepatic glycogen synthesis were also assessed using [1-13 C]glucose in combination with acetaminophen to noninvasively sample the hepatic UDP-glucose pool. Average fasting hepatic glycogen content was similar in glucokinasedeficient and control subjects (279 Ϯ 20 vs 284 Ϯ 14 mM; mean Ϯ SEM), and increased in both groups after the meals with a continuous pattern throughout the day. However, the net increment in hepatic glycogen content after each meal was 30-60% lower in glucokinase-deficient than in the control subjects (breakfast, 46% lower, P Ͻ 0.02; lunch, 62% lower, P ϭ 0.002; dinner; 30% lower, P ϭ 0.04). The net increment over basal values 4 h after dinner was 105 Ϯ 18 mM in glucokinase-deficient and 148 Ϯ 11 mM in control subjects ( P ϭ 0.04). In the 4 h after breakfast, flux through the gluconeogenic pathway relative to the direct pathway of hepatic glycogen synthesis was higher in glucokinase-deficient than in control subjects (50 Ϯ 2% vs 34 Ϯ 5%; P ϭ 0.038). In conclusion glucokinase-deficient subjects have decreased net accumulation of hepatic glycogen and relatively augmented hepatic gluconeogenesis after meals. These results suggest that in addition to the altered ␤ cell function, abnormalities in liver glycogen metabolism play an important role in the pathogenesis of hyperglycemia in patients with glucokinase-deficient maturity onset diabetes of young. ( J. Clin. Invest. 1996. 98:1755-1761.)

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“…Nine healthy control subjects (9 male, mean age±SE was 22±1 yr, mean weight 78±3 kg, mean BMI 23.4±1.0 kg/M2) and six C-peptide negative type I diabetic subjects (4 male, 2 female, mean age 34±2 yr, mean weight 73±3 kg, mean BMI 23.5±2.4 kg/m2, mean duration of diabetes 16±4 yr) were studied. All of the IDDM subjects were on an insulin regimen consisting of a subcutaneous injection of regular insulin (2-14 units, Humulin R; Lilly, Indianapolis, IN) administered 20-30 min before each meal and a subcutaneous injection of intermediate (8)(9)(10)(11)(12) units, Humulin NPH; Lilly) or long acting units, Humulin Ultralente; Lilly) insulin given at bedtime, with the exception of two IDDM subjects who also had a subcutaneous injection of intermediate (8)(9)(10)(11)(12) units, Humulin NPH; Lilly) in the morning in addition to their bedtime dose of NPH insulin. None of the IDDM subjects had any renal complications from diabetes and all were in fair and stable control (mean glycosylated hemoglobin was 10.2±0.3%, normal range 4-8%) for .…”

Section: Methodsmentioning

confidence: 99%

“…Signals from the liver were acquired by image selected in vivo spectroscopy localization technique to remove signals from the surface above the liver (9). A 4-ms hyperbolic secant pulse was used to invert the 2.5 cm of the skin surface, and as a result signals from the surface were eliminated by adding scans with an alternate inversion pulse (10). A 1800 pulse at the coil center was used as an excitation pulse and it was calibrated each time using a 2-cm sphere containing '3C-enriched formic acid that was placed at coil center.…”

Section: Methodsmentioning

confidence: 99%

Impaired net hepatic glycogen synthesis in insulin-dependent diabetic subjects during mixed meal ingestion. A 13C nuclear magnetic resonance spectroscopy study.

Hwang¹,

Perseghin²,

Rothman³

et al. 1995

J. Clin. Invest.

163

130

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Hepatic glycogen concentration was measured in six subjects with insulin-dependent diabetes mellitus (IDDM) and nine weight-matched control subjects using '3C nuclear magnetic resonance spectroscopy during a day in which three isocaloric mixed meals were ingested. The relative fluxes of the direct and indirect (3 carbon units -+ -+ glycogen) pathways of hepatic glycogen synthesis were also assessed using [1-3C]glucose in combination with acetaminophen to noninvasively sample the hepatic UDP-glucose pool. Mean fasting hepatic glycogen content was similar in the two groups. After each meal, hepatic glycogen content increased, peaking 4-5 h after the meal in both groups. By 11:00 p.m. the IDDM subjects had synthesized only 30% of the glycogen that was synthesized by the control group [IDDM subjects, net increment = 44±20 (mean±SE) mM; control subjects, net increment = 144±14 mM; P < 0.05]. After breakfast the flux through the gluconeogenic pathway relative to the direct pathway of hepatic glycogen synthesis was 1.7-fold greater in the IDDM subjects (59±4%) than in the control subjects (35±4%, P < 0.0003). In conclusion, under mixed meal conditions, subjects with poorly controlled IDDM have a major defect in net hepatic glycogen synthesis and augmented hepatic gluconeogenesis. The former abnormality may result in an impaired glycemic response to counterregulatory hormones, whereas both abnormalities may contribute to postprandial hyperglycemia. (J. Clin. Invest. 1995. 95:783-787.)

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Selective population inversion in NMR

Cited by 193 publications

References 2 publications

Evaluation of optimized inversion‐recovery fat‐suppression techniques for T2‐weighted abdominal MR imaging

Evaluation of optimized inversion‐recovery fat‐suppression techniques for T2‐weighted abdominal MR imaging

Impaired hepatic glycogen synthesis in glucokinase-deficient (MODY-2) subjects.

Impaired net hepatic glycogen synthesis in insulin-dependent diabetic subjects during mixed meal ingestion. A 13C nuclear magnetic resonance spectroscopy study.

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