Single-portal-phase low-tube-voltage dual-energy CT for short-term follow-up of acute pancreatitis: evaluation of CT severity index,interobserver agreement and radiation dose

Objectives

To intra-individually compare single-portal-phase low-tube-voltage (100-kVp) computed tomography (CT) with 120-kVp images for short-term follow-up assessment of CT severity index (CTSI) of acute pancreatitis, interobserver agreement and radiation dose.

Methods

We retrospectively analysed 66 patients with acute pancreatitis who underwent initial dual-contrast-phase CT (unenhanced, arterial, portal phase) at admission and short-term (mean interval 11.4 days) follow-up dual-contrast-phase dual-energy CT. The 100-kVp and linearly blended images representing 120-kVp acquisition follow-up CT images were independently evaluated by three radiologists using a modified CTSI assessing pancreatic inflammation, necrosis and extrapancreatic complications. Scores were compared with paired t test and interobserver agreement was evaluated using intraclass correlation coefficients (ICC).

Results

Mean CTSI scores on unenhanced, portal- and dual-contrast-phase images were 4.9, 6.1 and 6.2 (120 kVp) and 5.0, 6.0 and 6.1 (100 kVp), respectively. Contrast-enhanced series showed a higher CTSI compared to unenhanced images (P?P?>?0.7). CTSI scores were comparable for 100-kVp and 120-kVp images (P?>?0.05). Interobserver agreement was substantial for all evaluated series and subcategories (ICC 0.67–0.93). DLP of single-portal-phase 100-kVp images was reduced by 41 % compared to 120-kVp images (363.8 versus 615.9 mGy cm).

Conclusions

Low-tube-voltage single-phase 100-kVp CT provides sufficient information for follow-up evaluation of acute pancreatitis and significantly reduces radiation exposure.

Key Points

? Single-portal-phase CT provides sufficient evaluation for follow-up of acute pancreatitis. ? Follow-up CT does not benefit from unenhanced or arterial-phase acquisition. ? CT severity index scores are equal for dual-contrast-phase 100-/120-kVp acquisition (P?>?0.05). ? 100-kVp single-portal-phase follow-up CT of acute pancreatitis significantly reduces radiation exposure.     

Transcutaneous electrical stimulation of urinary bladder in patients with spinal cord injuries

Introduction  The treatment of neurogenic dysfunctions of micturition, both surgical and conservative, aims primarily to protect upper urinary tract function. This goal can be achieved by lowering intravesical pressure and increasing urinary bladder capacity in the urine collection phase or by facilitating bladder emptying. Objective  The objective of this paper was to assess the outcome of transcutaneous stimulation of the urinary bladder in the treatment of neurogenic disorders of micturition. Materials and methods  The effect of urinary bladder stimulation was assessed in 22 patients (4 females, 18 males) with spinal injuries (19 with injuries to the lumbo-sacral spine and 3 with cervical spine injuries) treated at the Department of Rehabilitation of the Military Hospital in Bydgoszcz, Poland, in 2006 and 2007. The treatment consisted of 30 procedures of transcutaneous electrical stimulation of the urinary bladder. A pulsed sinusoid current was used with a pulse duration of 200 ms, break duration of 1,000 ms, intensity of 15–20 mA, frequency of 50 Hz, and duration of stimulation of 15 min. A urodynamic study was carried out in each patient at baseline and on completion of the electrical stimulation therapy (immediately and after 2 months). Results  Electrical stimulation of the neurogenic urinary bladder produced increases in the cystometric bladder capacity and reduction in the amount of residual urine (72% of patients), with reduction of intravesical pressure at peak urine flow (59% of the patients). The dynamic aspects of micturition also improved with increased peak voiding velocity in 77.3% of the patients. More than half of the patients (57%) still had elevated intravesical pressures during micturition that posed a risk to the function of the upper urinary tract despite significant decreases following the stimulation therapy. Micturition, which was absent at baseline, was restored in three patients. No local complications were observed. Conclusions  Transcutaneous electrical stimulation of the urinary bladder in patients with neurogenic bladder dysfunction improves lower urinary tract function. Urodynamic studies executed 2 months after finishing TES show persistent results.     

Increased Bone Resorption Is Associated With Increased Risk of Cardiovascular Events in Men: The MINOS Study

Better assessment of the association between cardiovascular disease and osteoporosis in older men may help identify shared etiologies for bone and heart health in this population. We assessed the association of BMD and bone turnover markers (BTMs) with risk of cardiovascular events (myocardial infarction or stroke) in 744 men ≥50 yr of age. During the 7.5‐yr prospective follow‐up, 43 strokes and 40 myocardial infarctions occurred in 79 men. After adjustment for confounders (age, weight, height, smoking, education, physical activity, self‐reported history of diabetes, hypertension, and prevalent ischemic heart disease), men in the lowest quartile of BMD at the spine, whole body, and forearm had a 2‐fold increased risk of cardiovascular events. Men in the highest quartile of bone resorption markers (deoxypyridinoline [DPD], C‐telopeptide of type I collagen) had a 2‐fold increased risk of cardiovascular events (e.g., multivariable‐adjusted hazard ratio [including additional adjustment for BMD] was 2.11 [95% CI: 1.26–3.56], for the highest quartile of free DPD relative to the lowest three quartiles). The results were similar for men without prevalent ischemic heart disease and for myocardial infarction and stroke analyzed separately. Our data suggest that men with low BMD or high bone resorption may be at increased risk of myocardial infarction and stroke in addition to fracture. Thus, men with osteoporosis may benefit from screening for cardiovascular disease. Further study to elucidate the biological mechanism shared by bone and vascular disease may help efforts to identify men at risk or develop treatment.     

Renovascular hypertension – simultaneous aortic and renal artery reconstruction

Despite the enormous progress that has been madein the fields of vascular surgery and intensive care, reconstructive surgery of renal arteries in the presence of arteriosclerosis of the abdominal aorta remains a serious therapeutic problem and is associated with a high rate of complications. The purpose of this study was to analyze the results of treatment of patients with renovascular hypertension and so-called difficult aorta. Surgery was carried out in 68 patients with a critically stenosed renal artery and severe arteriosclerosis of the abdominal aorta. In 53 patients an aortobifemoral prosthetic graft was implanted together with endarterectomy of the renal artery in 23 patients, an aortorenal venous graft in 23 patients and a prosthetic graft in 7 patients. In the remaining 15 patients extra-anatomic anastomoses were performed between the splenic artery and the renal artery (7 patients), hepatic artery and renal artery (6) and between the superior mesenteric and renal artery (2). Postoperatively, the hypertension was cured in 55% of patients, improved in 38% and remained unchanged in 7%. After 1 year the results were respectively 47, 36, and 17%. The patients with an aortorenal prosthetic graft demonstrated a greater tendency for hypertension to recur.     

Impaired bone microarchitecture at the distal radius in older men with low muscle mass and grip strength: The STRAMBO study

The aim was to study the association between bone microarchitecture and muscle mass and strength in older men. Volumetric bone mineral density (vBMD) and bone microarchitecture were assessed in 810 men aged ≥60 years at the distal radius by high‐resolution peripheral computed tomography (HR‐pQCT). Areal bone mineral density (aBMD) and appendicular muscle mass (ASM) were assessed by dual‐energy X‐ray absorptiometry (DXA). Relative ASM of the upper limbs (RASM‐u.l.) was calculated as ASM of the upper limbs/(height)². Grip strength was measured by dynanometry. In multivariable models, men in the lowest RASM‐u.l. quartile had lower cross‐sectional area (CSA), cortical area (Ct.Ar), cortical thickness (Ct.Th), and trabecular area (Tb.Ar) at distal radius compared with men in the highest quartile. The trends remained significant after adjustment for grip strength. Men in the lowest quartile of the normalized grip strength (grip strength/[height]²) had lower aBMD, total vBMD, Ct.Ar, Ct.Th, Tb.vBMD, and Tb.N, and higher Tb.Sp and Tb.Sp.SD. The associations for Ct.Ar, total vBMD, Ct.Th, Tb.vBMD, and Tb.Sp remained significant after adjustment for RASM‐u.l. In the models including RASM‐u.l. and normalized grip strength, CSA and Tb.Ar were associated with RASM‐u.l. but not with the strength. Lower Ct.Th, Tb.vBMD, and Tb.N were associated with lower grip strength but not with RASM‐u.l. Lower Ct.Ar was associated with lower grip strength and with lower RASM‐u.l. In conclusion, in older men, low RASM‐u.l. and low grip strength are associated with poor cortical and trabecular microarchitecture partly independently of each other, after adjustment for confounders. © 2013 American Society for Bone and Mineral Research     

Enhanced Dopamine-Dependent Hippocampal Plasticity after Single MK-801 Application

Dopaminergic hyperfunction and N-methyl-D-aspartate receptor (NMDAR) hypofunction have both been implicated in psychosis. Dopamine-releasing drugs and NMDAR antagonists replicate symptoms associated with psychosis in healthy humans and exacerbate symptoms in patients with schizophrenia. Though hippocampal dysfunction contributes to psychosis, the impact of NMDAR hypofunction on hippocampal plasticity remains poorly understood. Here, we used an NMDAR antagonist rodent model of psychosis to investigate hippocampal long-term potentiation (LTP). We found that single systemic NMDAR antagonism results in a region-specific, presynaptic LTP at hippocampal CA1-subiculum synapses that is induced by activation of D1/D5 dopamine receptors and modulated by L-type voltage-gated Ca²⁺ channels. Thereby, our findings may provide a cellular mechanism how NMDAR antagonism can lead to an enhanced hippocampal output causing activation of the hippocampus-ventral tegmental area-loop and overdrive of the dopamine system.     

Impairment of the septal cholinergic neurons in MPTP-treated A30P α-synuclein mice

Dementia in Parkinson's disease (PDD) and dementia with Lewy bodies (DLB) are characterized by loss of acetylcholine (ACh) from cortical areas. Clinical studies report positive effects of acetylcholine esterase (AChE) inhibitors in PDD and dementia with Lewy bodies. We here report that the number of neurons expressing a cholinergic marker in the medial septum-diagonal band of Broca complex decreases in A30P α-synuclein-expressing mice during aging, paralleled by a lower AChE fiber density in the dentate gyrus and in the hippocampal CA1 field. After inducing dopamine depletion by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP), no acute but a delayed loss of cholinergic neurons and AChE-positive fibers was observed, which was attenuated by L-3,4-dihydroxyphenylalanine (DOPA) treatment. Expression of nerve growth factor (NGF) and tyrosine receptor kinase A (TrkA) genes was upregulated in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride-treated wild type mice, but not in A30P α-synuclein expressing animals. In contrast, upregulation of sortilin and p75^NTR genes was found in the A30P α-synuclein-expressing mice. These results suggest that dopamine deficiency may contribute to the impairment of the septohippocampal system in patients with PDD and that L-3,4-dihydroxyphenylalanine may not only result in symptomatic treatment of the akinetic-rigid syndrome but may also alleviate the degeneration of basal forebrain cholinergic system and the cognitive decline.     

Amyloid beta and the longest-lived rodent: the naked mole-rat as a model for natural protection from Alzheimer's disease

Amyloid beta (Aβ) is implicated in Alzheimer's disease (AD) as an integral component of both neural toxicity and plaque formation. Brains of the longest-lived rodents, naked mole-rats (NMRs) approximately 32 years of age, had levels of Aβ similar to those of the 3xTg-AD mouse model of AD. Interestingly, there was no evidence of extracellular plaques, nor was there an age-related increase in Aβ levels in the individuals examined (2–20+ years). The NMR Aβ peptide showed greater homology to the human sequence than to the mouse sequence, differing by only 1 amino acid from the former. This subtle difference led to interspecies differences in aggregation propensity but not neurotoxicity; NMR Aβ was less prone to aggregation than human Aβ. Nevertheless, both NMR and human Aβ were equally toxic to mouse hippocampal neurons, suggesting that Aβ neurotoxicity and aggregation properties were not coupled. Understanding how NMRs acquire and tolerate high levels of Aβ with no plaque formation could provide useful insights into AD, and may elucidate protective mechanisms that delay AD progression.     

Renal Mechanisms of Association between Fibroblast Growth Factor 1 and Blood Pressure

The fibroblast growth factor 1 (FGF1) gene is expressed primarily in the kidney and may contribute to hypertension. However, the biologic mechanisms underlying the association between FGF1 and BP regulation remain unknown. We report that the major allele of FGF1 single nucleotide polymorphism rs152524 was associated in a dose-dependent manner with systolic BP (P=9.65×10⁻⁵) and diastolic BP (P=7.61×10⁻³) in a meta-analysis of 14,364 individuals and with renal expression of FGF1 mRNA in 126 human kidneys (P=9.0×10⁻³). Next-generation RNA sequencing revealed that upregulated renal expression of FGF1 or of each of the three FGF1 mRNA isoforms individually was associated with higher BP. FGF1-stratified coexpression analysis in two separate collections of human kidneys identified 126 FGF1 partner mRNAs, of which 71 and 63 showed at least nominal association with systolic and diastolic BP, respectively. Of those mRNAs, seven mRNAs in five genes (MME, PTPRO, REN, SLC12A3, and WNK1) had strong prior annotation to BP or hypertension. MME, which encodes an enzyme that degrades circulating natriuretic peptides, showed the strongest differential coexpression with FGF1 between hypertensive and normotensive kidneys. Furthermore, higher level of renal FGF1 expression was associated with lower circulating levels of atrial and brain natriuretic peptides. These findings indicate that FGF1 expression in the kidney is at least under partial genetic control and that renal expression of several FGF1 partner genes involved in the natriuretic peptide catabolism pathway, renin-angiotensin cascade, and sodium handling network may explain the association between FGF1 and BP.