Morphoelectric and transcriptomic divergence of the layer 1 interneuron repertoire in human versus mouse neocortex.

Neocortical layer 1 (L1) is a site of convergence between pyramidal-neuron dendrites and feedback axons where local inhibitory signaling can profoundly shape cortical processing. Evolutionary expansion of human neocortex is marked by distinctive pyramidal neurons with extensive L1 branching, but whether L1 interneurons are similarly diverse is underexplored. Using Patch-seq recordings from human neurosurgical tissue, we identified four transcriptomic subclasses with mouse L1 homologs, along with distinct subtypes and types unmatched in mouse L1. Subclass and subtype comparisons showed stronger transcriptomic differences in human L1 and were correlated with strong morphoelectric variability along dimensions distinct from mouse L1 variability. Accompanied by greater layer thickness and other cytoarchitecture changes, these findings suggest that L1 has diverged in evolution, reflecting the demands of regulating the expanded human neocortical circuit.

Signature morphoelectric properties of diverse GABAergic interneurons in the human neocortex.

Human cortex transcriptomic studies have revealed a hierarchical organization of γ-aminobutyric acid-producing (GABAergic) neurons from subclasses to a high diversity of more granular types. Rapid GABAergic neuron viral genetic labeling plus Patch-seq (patch-clamp electrophysiology plus single-cell RNA sequencing) sampling in human brain slices was used to reliably target and analyze GABAergic neuron subclasses and individual transcriptomic types. This characterization elucidated transitions between PVALB and SST subclasses, revealed morphological heterogeneity within an abundant transcriptomic type, identified multiple spatially distinct types of the primate-specialized double bouquet cells (DBCs), and shed light on cellular differences between homologous mouse and human neocortical GABAergic neuron types. These results highlight the importance of multimodal phenotypic characterization for refinement of emerging transcriptomic cell type taxonomies and for understanding conserved and specialized cellular properties of human brain cell types.

Peripheral and Autonomic Neuropathy Status of Young Patients With Type 1 Diabetes Mellitus at the Time of Transition From Pediatric Care to Adult-Oriented Diabetes Care.

Introduction: The prevalence of neuropathic lesions in young patients with type 1 diabetes mellitus (T1DM) at the time of transition from pediatric care to adult-oriented diabetes care is poorly studied. A comparative study with healthy volunteers to assess the possible neuropathic condition of this special population and to identify the potential early screening needs has not been performed yet. The results may provide important feedback to pediatric diabetes care and a remarkable baseline reference point for further follow up in adult diabetes care. Patients and Methods: Twenty-nine young patients with T1DM [age: 22.4 ± 2.9 years; HbA1c: 8.5 ± 2.1%, diabetes duration: 12.2 ± 5.8 years; (mean ± SD)] and 30 healthy volunteers (age: 21.5 ± 1.6 years; HbA1c: 5.3 ± 0.3%) were involved in the study. Autonomic function was assessed by standard cardiovascular reflex tests. Complex peripheral neuropathic testing was performed by Neurometer®, Neuropad®-test, Tiptherm®, Monofilament®, and Rydel-Seiffer tuning fork tests. Results: T1DM patients had significantly higher diastolic blood pressure than controls (80 ± 9 vs. 74 ± 8 mmHg, p < 0.01), but there was no significant difference in systolic blood pressure (127 ± 26 vs. 121 ± 13 mmHg). Cardiovascular reflex tests had not revealed any significant differences between the T1DM patients and controls. No significant differences with Neurometer®, Neuropad®-test, and Monofilament® were detected between the two groups. The vibrational sensing on the radius on both sides was significantly impaired in the T1DM group compared to the controls with Rydel-Seiffer tuning fork test (right: 7.5 ± 1.0 vs. 7.9 ± 0.3; left: 7.5 ± 0.9 vs. 7.9 ± 0.3, p < 0.05). The Tiptherm®-test also identified a significant impairment in T1DM patients (11 sensing failures vs. 1, p < 0.001). In addition, the neuropathic complaints were significantly more frequently present in the T1DM patient group than in the controls (9 vs. 0, p < 0.01). Conclusion: In this young T1DM population, cardiovascular autonomic neuropathy and cardiac morphological alterations could not be found. However, Rydel-Seiffer tuning fork and Tiptherm®-tests revealed peripheral sensory neurological impairments in young T1DM patients at the time of their transition to adult diabetes care.

Expression of GLP-1 receptors in insulin-containing interneurons of rat cerebral cortex.

AIMS/HYPOTHESIS: Glucagon-like peptide 1 (GLP-1) receptors are expressed by pancreatic beta cells and GLP-1 receptor signalling promotes insulin secretion. GLP-1 receptor agonists have neural effects and are therapeutically promising for mild cognitive impairment and Alzheimer's disease. Our previous results showed that insulin is released by neurogliaform neurons in the cerebral cortex, but the expression of GLP-1 receptors on insulin-producing neocortical neurons has not been tested. In this study, we aimed to determine whether GLP-1 receptors are present in insulin-containing neurons. METHODS: We harvested the cytoplasm of electrophysiologically and anatomically identified neurogliaform interneurons during patch-clamp recordings performed in slices of rat neocortex. Using single-cell digital PCR, we determined copy numbers of Glp1r mRNA and other key genes in neurogliaform cells harvested in conditions corresponding to hypoglycaemia (0.5 mmol/l glucose) and hyperglycaemia (10 mmol/l glucose). In addition, we performed whole-cell patch-clamp recordings on neurogliaform cells to test the effects of GLP-1 receptor agonists for functional validation of single-cell digital PCR results. RESULTS: Single-cell digital PCR revealed GLP-1 receptor expression in neurogliaform cells and showed that copy numbers of mRNA of the Glp1r gene in hyperglycaemia exceeded those in hypoglycaemia by 9.6 times (p < 0.008). Moreover, single-cell digital PCR confirmed co-expression of Glp1r and Ins2 mRNA in neurogliaform cells. Functional expression of GLP-1 receptors was confirmed with whole-cell patch-clamp electrophysiology, showing a reversible effect of GLP-1 on neurogliaform cells. This effect was prevented by pre-treatment with the GLP-1 receptor-specific antagonist exendin-3(9-39) and was absent in hypoglycaemia. In addition, single-cell digital PCR of neurogliaform cells revealed that the expression of transcription factors (Pdx1, Isl1, Mafb) are important in beta cell development. CONCLUSIONS/INTERPRETATION: Our results provide evidence for the functional expression of GLP-1 receptors in neurons known to release insulin in the cerebral cortex. Hyperglycaemia increases the expression of GLP-1 receptors in neurogliaform cells, suggesting that endogenous incretins and therapeutic GLP-1 receptor agonists might have effects on these neurons, similar to those in pancreatic beta cells.

MEN1 mutations and potentially MEN1-targeting miRNAs are responsible for menin deficiency in sporadic and MEN1 syndrome-associated primary hyperparathyroidism.

Inherited, germline mutations of menin-coding MEN1 gene cause multiple endocrine neoplasia type 1 (MEN1), while somatic MEN1 mutations are the sole main driver mutations in sporadic primary hyperparathyroidism (PHPT), suggesting that menin deficiency has a central role in the pathogenesis of PHPT. MiRNAs are small, noncoding RNAs posttranscriptionally regulating gene expression. Our aim was to investigate both the role of MEN1 mutations and potentially MEN1-targeting miRNAs as the underlying cause of menin deficiency in MEN1-associated and sporadic PHPT tissues. Fifty six PHPT tissues, including 16 MEN1-associated tissues, were evaluated. Diagnosis of MEN1 syndrome was based on identification of germline MEN1 mutations. In silico target prediction was used to identify miRNAs potentially targeting MEN1. Menin expression was determined by immunohistochemistry while expression of miRNAs was analyzed by quantitative real-time PCR. Sporadic PHPT tissues were subjected to somatic MEN1 mutation analysis as well. Lack of nuclear menin was identified in all MEN1-associated and in 28% of sporadic PHPT tissues. Somatic MEN1 mutations were found in 25% of sporadic PHPTs. The sensitivity and specificity of menin immunohistochemistry to detect a MEN1 mutation were 86 and 87%, respectively. Expression levels of hsa-miR-24 and hsa-miR-28 were higher in sporadic compared to MEN1-associated PHPT tissues; however, no difference in miRNA levels occurred between menin-positive and menin-negative PHPT tissues. Menin deficiency is the consequence of a MEN1 mutation in most menin-negative PHPT tissues. Elevated expression of hsa-miR-24 and hsa-miR-28 mark the first epigenetic changes observed between sporadic and MEN1-associated PHPT.

Cerebral cortex: a target and source of insulin?

Recent results suggest that insulin is synthesised by a subpopulation of neurons in the cerebral cortex and neural progenitor cells of the hippocampus. Supplementing the slow supply of insulin to the brain by pancreatic beta cells, the insulin locally released by neurons provides a rapid means of regulating local microcircuits, effectively modulating synaptic transmission and on-demand energy homeostasis of neural networks. Modulation of insulin production by brain neurons via glucagon-like peptide 1 (GLP-1) agonists might be useful in counteracting diabetes, obesity and neurodegenerative diseases. Replacement of lost pancreatic beta cells by autologous transplantation of insulin-producing neural progenitor cells could be a viable therapy for diabetes.

Increased Short-Term Beat-To-Beat Variability of QT Interval in Patients with Acromegaly.

Cardiovascular diseases, including ventricular arrhythmias are responsible for increased mortality in patients with acromegaly. Acromegaly may cause repolarization abnormalities such as QT prolongation and impairment of repolarization reserve enhancing liability to arrhythmia. The aim of this study was to determine the short-term beat-to-beat QT variability in patients with acromegaly. Thirty acromegalic patients (23 women and 7 men, mean age±SD: 55.7±10.4 years) were compared with age- and sex-matched volunteers (mean age 51.3±7.6 years). Cardiac repolarization parameters including frequency corrected QT interval, PQ and QRS intervals, duration of terminal part of T waves (Tpeak-Tend) and short-term variability of QT interval were evaluated. All acromegalic patients and controls underwent transthoracic echocardiographic examination. Autonomic function was assessed by means of five standard cardiovascular reflex tests. Comparison of the two groups revealed no significant differences in the conventional ECG parameters of repolarization (QT: 401.1±30.6 ms vs 389.3±16.5 ms, corrected QT interval: 430.1±18.6 ms vs 425.6±17.3 ms, QT dispersion: 38.2±13.2 ms vs 36.6±10.2 ms; acromegaly vs control, respectively). However, short-term beat-to-beat QT variability was significantly increased in acromegalic patients (4.23±1.03 ms vs 3.02±0.80, P<0.0001). There were significant differences between the two groups in the echocardiographic dimensions (left ventricular end diastolic diameter: 52.6±5.4 mm vs 48.0±3.9 mm, left ventricular end systolic diameter: 32.3±5.2 mm vs 29.1±4.4 mm, interventricular septum: 11.1±2.2 mm vs 8.8±0.7 mm, posterior wall of left ventricle: 10.8±1.4 mm vs 8.9±0.7 mm, P<0.05, respectively). Short-term beat-to-beat QT variability was elevated in patients with acromegaly in spite of unchanged conventional parameters of ventricular repolarization. This enhanced temporal QT variability may be an early indicator of increased liability to arrhythmia.

GABAergic neurogliaform cells represent local sources of insulin in the cerebral cortex.

Concentrations of insulin in the brain are severalfold higher than blood plasma levels. Insulin in the brain regulates the metabolism, molecular composition, and cognitive performance of microcircuits and reduces food intake; cerebral insulin levels are altered in diabetes, aging, obesity, and Alzheimer's disease. Released by pancreatic ß cells, insulin passes the blood-brain barrier, but sources of locally released insulin still remain unclear. We find that insulin is strongly expressed in GABAergic neurogliaform cells in the cerebral cortex of the rat detected by single-cell digital PCR. Focal application of glucose or glibenclamide to neurogliaform cells mimics the excitation suppressing effect of external insulin on local microcircuits via insulin receptors. Thus, neurogliaform cells might link GABAergic and insulinergic action in cortical microcircuits.

[In the labyrinth of calcium metabolism]. / A kalcium-anyagcsere útvesztoi.

The authors present the case of a 27-year-old male patient. In 2010, he suffered from a bone fracture of the pelvis. As imaging techniques showed multiple osseal lytic lesions, diagnostic investigations were performed for multiple myeloma. Later, a mass lesion measuring 37 mm in size was removed from the left side of his mandible. Histology revealed a giant-cell tumour of the bone and oncologic therapy was considered. However, before this planned treatment a PET-CT was performed, which showed numerous distinct lesions with enhanced glucose metabolism in the skeleton as well as in soft tissue behind the right lobe of the thyroid. Hence, the patient was referred to endocrinologists. On the basis of severe hypercalcemia (serum calcium 3.66 mmol/l) and high serum parathyroid hormone level (162.5 pmol/l) the diagnosis of a right sided parathyroid tumour was established. After surgical excision of the parathyroid tumour, high levels of serum calcium and parathyroid hormone returned to normal. Histology failed to show malignancy and the patient recovered soon. This case report may shed some light on the importance of serum calcium measurements and the differential diagnostic significance of primary hyperparathyroidism.

[Endoscopic, posterior transseptal pituitary surgery--learning curve of the surgical technique and equipment in 61 operations]. / Endoszkópos posterior transseptalis hypophysismutét. A sebészi technika fejlodése a teljes endoszkópos tumoreltávolításig 61 eset elemzése alapján.

INTRODUCTION: The removal of hypophyseal tumor by transsphenoidal pituitary surgery using microsurgical instruments was first performed over 100 years ago. Operating techniques for this surgery are constantly being renewed, first by using a microscope and later on with the use of an endoscop. The authors provide an overview of the minimal invasive posterior transseptal-transsphenoidal aproach with the combined utilization of classical techniques with the assistance of the endoscop. METHOD: Sixty-one patients (33 female, 28 male, 21-84 yrs) were treated for sellar region tumor resection using an endonasal transsphenoidal aproach with the help of an endoscope. Follow ups were performed within 2-21 months. RESULTS: Total tumor resection was successful in 91.8%, and partial resection in 8.2% of the patients. The rate of complications using the endoscopic method was not higher compared to that of the classical microscopic method. There was no major bleeding in any of the cases. Adverse events such as minor epistaxis occurred in 4.9%, transitional diabetes insipidus in 6.5%, inraoperative CSF leak in 16.67%, postoperative CSF leak in 11.5% and meningitis in 8.2% of the patients. After the operation the pathological hormonal production stoped in all patients except in two patients who were acromegalic. However their GH level normalized and they did not require further treatment, the IGF-1 still remained high. CONCLUSION: The success of the surgical treatment is based on both, the proficient pre- and postoperative endocrinological care, and the minimal invasive surgical technique. The endoscope was used partially or continuously during the operation for better visualization of the operation field in multiple angles (30 degrees, 45 degrees). It was useful in differentiating between normal and tumorous glandular tissue, and also offered an enhanced view of the intrasellar (via hydroscopy) and parasellar region. Moreover the endoscopic method is able to decrease the operating time, reduce blood loss. In different stages of the surgery, depending on the anatomical and pathological situation, switching back and forth from microscope to endoscope technique, gives us the benefit of a clearer view in each situation.

Over-representation of the G12S polymorphism of the SDHD gene in patients with MEN2A syndrome.

OBJECTIVE: To evaluate whether germline variants of the succinate dehydrogenase genes might be phenotypic modifiers in patients with multiple endocrine neoplasia type 2. Mutations of genes encoding subunits of the succinate dehydrogenase are associated with hereditary paraganglioma/pheochromocytoma syndrome. Pheochromocytoma is one of the main manifestations of multiple endocrine neoplasia type 2 caused by germline mutation of the rearranged during transfection proto-oncogene. METHODS: Polymorphisms of the succinate dehydrogenase genes were analyzed in 77 rearranged during transfection mutation carriers, 47 patients with sporadic medullary thyroid cancer, 48 patients with sporadic Pheo, and 100 healthy individuals. Exons 10-16 of the rearranged during transfection proto-oncogene were analyzed by direct DNA sequencing, and all exons of the von Hippel-Lindau, succinate dehydrogenase B, and succinate dehydrogenase subunit D genes were tested by direct DNA sequencing and multiple ligation probe analysis. The G12S polymorphism of the succinate dehydrogenase subunit D gene was determined by restriction fragment length polymorphism. RESULTS: Of the 77 rearranged during transfection mutation carriers, 55 from 16 families had multiple endocrine neoplasia type 2A, three from three families had multiple endocrine neoplasia type 2B, and 19 from two families had familial medullary thyroid carcinoma. Eight of 55 (14.5%) patients with multiple endocrine neoplasia type 2A had this variant whereas it was absent in multiple endocrine neoplasia type 2B, familial medullary thyroid carcinoma, sporadic medullary thyroid carcinoma, and sporadic pheochromocytoma groups, and its prevalence in controls was 1% (p<0.002 multiple endocrine neoplasia type 2A versus controls). No associations between G12S and age of manifestation, incidence of pheochromocytoma or hyperparathyroidism, or level of serum calcitonin were observed. CONCLUSION: The high prevalence of the G12S variant in patients with multiple endocrine neoplasia type 2A raises questions about its role as a genetic modifier, but this proposal remains to be established.

Over-representation of the G12S polymorphism of the SDHD gene in patients with MEN2A syndrome

OBJECTIVE: To evaluate whether germline variants of the succinate dehydrogenase genes might be phenotypic modifiers in patients with multiple endocrine neoplasia type 2. Mutations of genes encoding subunits of the succinate dehydrogenase are associated with hereditary paraganglioma/pheochromocytoma syndrome. Pheochromocytoma is one of the main manifestations of multiple endocrine neoplasia type 2 caused by germline mutation of the rearranged during transfection proto-oncogene. METHODS: Polymorphisms of the succinate dehydrogenase genes were analyzed in 77 rearranged during transfection mutation carriers, 47 patients with sporadic medullary thyroid cancer, 48 patients with sporadic Pheo, and 100 healthy individuals. Exons 10-16 of the rearranged during transfection proto-oncogene were analyzed by direct DNA sequencing, and all exons of the von Hippel-Lindau, succinate dehydrogenase B, and succinate dehydrogenase subunit D genes were tested by direct DNA sequencing and multiple ligation probe analysis. The G12S polymorphism of the succinate dehydrogenase subunit D gene was determined by restriction fragment length polymorphism. RESULTS: Of the 77 rearranged during transfection mutation carriers, 55 from 16 families had multiple endocrine neoplasia type 2A, three from three families had multiple endocrine neoplasia type 2B, and 19 from two families had familial medullary thyroid carcinoma. Eight of 55 (14.5%) patients with multiple endocrine neoplasia type 2A had this variant whereas it was absent in multiple endocrine neoplasia type 2B, familial medullary thyroid carcinoma, sporadic medullary thyroid carcinoma, and sporadic pheochromocytoma groups, and its prevalence in controls was 1% (p<0.002 multiple endocrine neoplasia type 2A versus controls). No associations between G12S and age of manifestation, incidence of pheochromocytoma or hyperparathyroidism, or level of serum calcitonin were observed. CONCLUSION: The high prevalence of the G12S variant in patients with multiple endocrine neoplasia type 2A raises questions about its role as a genetic modifier, but this proposal remains to be established.

Obesity is associated with aortic enlargement and increased stiffness: an echocardiographic study.

BACKGROUND: Obesity may be associated with early vascular changes. The current study was designed to assess the relationship between obesity and aortic stiffness in two populations, one aged 18-40 years and one aged 41-64 years. METHODS: The study complied 121 subjects, all of them underwent a physical examination, transthoracic echocardiography and blood pressure measurement. Aortic stiffness index (beta) was evaluated from aortic diameter and blood pressure data. RESULTS: beta was higher in obese subjects both in the young (4.26 +/- 1.57 vs. 6.88 +/- 5.96, P < 0.05) and old patient populations (7.13 +/- 4.99 vs. 14.89 +/- 14.64, P < 0.05). Systolic (SD) aortic diameters (in mm) were enlarged in obese young patients (25.7 +/- 2.8 vs. 27.1 +/- 2.5, P < 0.05) and obese old subjects (28.0 +/- 3.0 vs. 30.3 +/- 3.3, P < 0.05). Diastolic (DD) aortic diameter (in mm) showed similar tendency in youngs (22.8 +/- 2.9 vs. 24.9 +/- 2.5, P < 0.05) and old subjects (25.9 +/- 2.7 vs. 28.0 +/- 3.1, P < 0.05). CONCLUSIONS: Aortic stiffness is higher in young obese patients and similar to older subjects without obesity. Both SD and DD are increasing with age, but subjects within similar age group have larger SD and DD suggesting early vascular remodelling in obesity.

Aortic stiffness is increased in acromegaly--a transthoracic echocardiographic study.

BACKGROUND: Acromegaly is associated with increased cardiovascular risk. Recent studies suggested a direct effect of growth hormone and insuline-like growth factor 1 excess on the vasculature over the conventional risk factors. The aim of the present study was to evaluate the stiffness of ascending aorta by means of transthoracic echocardiography (TTE) in patients with acromegaly. PATIENTS AND METHODS: The following patient populations were compared: 20 subjects with negative coronary angiograms, 16 acromegalics and 21 patients with significant coronary artery disease (CAD). Aortic stiffness index (beta) was evaluated by means of TTE by use of the formula: beta=ln (SBP/DBP)/(DeltaD/DD), where SBP and DBP are the systolic and diastolic blood pressures, DD is the diastolic aortic diameter, DeltaD is the pulsatile change in aortic diameter (systolic diameter minus diastolic diameter) and 'ln' is the natural logarithm. RESULTS: The average time from diagnosis was 162+/-127 days in acromegalic patients. Transsphenoidal hypophysectomy was performed in 12 patients, while the mean growth hormone level was 10.8+/-11.7 mIU/ml. beta was similarly increased in acromegalics and in CAD patients as compared to controls (6.23+/-3.29 vs 16.47+/-14.53 and 16.66+/-15.49, p<0.05, respectively). CONCLUSIONS: Stiffness of ascending aorta evaluated by a routine TTE examination is increased in acromegalics without overt cardiovascular disease as compared to controls and similar to CAD patients.

Increased aortic stiffness in glycogenosis type 2 (Pompe's disease).

BACKGROUND: Pompe's disease, also known as acid maltase deficiency or glycogen storage disease type II, is an autosomal recessive disorder in which deficient activity of the enzyme acid alpha-glucosidase causes intra-lysosomal accumulation of glycogen in muscle and other tissues. The current study was designed to assess aortic stiffness index (beta), as a characteristic of aortic elasticity during transthoracic echocardiography in patients with Pompe's disease. METHODS: A total of 17 patients (age 44+/-8 years, 5 males) with Pompe's disease were studied. Their results were compared to 17 age- and gender-matched controls. In all patients, the ascending aorta was recorded with M-mode echocardiography. Beta was calculated as ln(SBP/DBP)/[(SD-DD)/DD], where SBP and DBP are the systolic and diastolic blood pressures, SD and DD are the systolic and diastolic aortic diameters, and 'ln' is the natural logarithm. RESULTS: Diastolic aortic diameter was 27.4+/-2.4 mm in Pompe patients and 25.6+/-2.7 mm in controls (P<0.05). Systolic aortic diameters did not differ between the groups (29.4+/-2.5 mm vs 28.3+/-2.4 mm, P=ns). Aortic stiffness index (beta) was increased in Pompe patients compared to controls (14.6+/-10.1 vs 5.1+/-2.6, P<0.001). CONCLUSIONS: The results of this study indicate that aortic stiffness is increased in patients with Pompe's disease. This may be due to glycogen storage in the vessel wall causing reduced vascular elasticity.

Gadolinium(III)-loaded nanoparticulate zeolites as potential high-field MRI contrast agents: relationship between structure and relaxivity.

The effects of dealumination, pore size, and calcination on the efficiency (as expressed in the relaxivity) of Gd3+-loaded zeolites for potential application as magnetic resonance imaging (MRI) contrast agents were studied. Partial dealumination of zeolites NaY or NaA by treatment with (NH4)2SiF6 or diluted HCl resulted in materials that, upon loading with Gd3+, had a much higher relaxivity than the corresponding non-dealuminated materials. Analysis of the 1H NMR dispersion profiles of the various zeolites showed that this can be mainly ascribed to an increase of the amount of water inside the zeolite cavities as a result of the destruction of walls between cavities. However, the average residence time of water inside the Gd3+-loaded cavities did not change significantly, which suggests that the windows of the Gd3+-loaded cavities are not affected by the dealumination. Upon calcination, the Gd3+ ions moved to the small sodalite cavities and became less accessible for water, resulting in a decrease in relaxivity. The important role of diffusion for the relaxivity was demonstrated by a comparison of the relaxivity of Gd3+-loaded zeolite NaY and NaA samples. NaA had much lower relaxivities due to the smaller pore sizes. The transversal relaxivities of the Gd3+-doped zeolites are comparable in magnitude to the longitudinal ones at low magnetic fields (<60 MHz). However at higher fields, the transversal relaxivities steeply increased, whereas the longitudinal relaxivities decreased as field strength increased. Therefore, these materials have potential as T1 MRI contrast agents at low field, and as T2 agents at higher fields.