Performance of DAPT Score and ESC Criteria for Predicting Clinical Outcomes in Chinese Patients with Acute Coronary Syndrome.

Purpose: The values of European Society of Cardiology (ESC) criteria and dual antiplatelet therapy (DAPT) score in the stratification of ischemic risk were assessed in this study. Methods: A total of 489 patients with acute coronary syndrome who received DAPT at discharge between June 2020 and August 2020 were enrolled. The primary endpoint was the occurrence of major adverse cardiovascular events (MACE), which included recurrent ACS or unplanned revascularization, all-cause death, or ischemic stroke during a 27-month follow-up period. Results: Patients with ESC-defined high-risk showed a significantly higher risk of MACE (HR 2.75, 95% CI 1.78-4.25), all-cause death (HR 2.49, 95% CI 1.14-5.43), and recurrent ACS or unplanned revascularization (HR 2.80, 95% CI 1.57-4.99) than those with ESC-defined low/medium-risk during follow-up. The results of landmark analysis showed that patients in the high-risk group had a significantly higher risk of MACE (HR 2.80,95 CI% 1.57-4.97), recurrent ACS or unplanned revascularization (HR 3.19,95 CI% 1.47-6.93) within one year, and a higher risk of MACE (HR 2.69,95 CI% 1.38-5.23) after one year. There was no significant difference in the incidence of MACE between patients with a DAPT score ≥2 and a DAPT score <2. The C-indices of ESC criteria and DAPT score for prediction of MACE were 0.63 (95% CI 0.57-0.70) and 0.54 (95% CI 0.48-0.61), respectively. The predictive value of ESC criteria for MACE was better than the DAPT score according to the DeLong test (z-statistic=2.30, P=0.020). Conclusion: Patients with ESC-defined high-risk had a higher risk of MACE compared to those with ESC-defined low/medium-risk. The discriminant ability of the ESC criteria was better than the DAPT score for MACE. The ESC criteria demonstrated moderate discriminatory capacity of MACE in ACS patients treated with DAPT.

Protective Effect of Nicorandil on Contrast-Induced Acute Kidney Injury After Emergency Percutaneous Coronary Intervention.

Objective: To investigate the protective effect of nicorandil on contrast-induced acute kidney injury (CIAKI) in patients with acute ST-segment elevation myocardial infarction (STEMI) after emergency percutaneous coronary intervention (PCI). Methods: This is a single-center, retrospective control study. A total of 156 patients with STEMI were divided into the nicorandil group (n = 55) and the control group (n = 101). The incidence of CIAKI, defined as an increase of >25% or absolute values > 44.2 µmol/L in serum creatinine (Scr) from baseline within 72 h of exposure to a contrast agent after exclusion of other causes, was the primary endpoint. The secondary endpoints were: (1) changes of Scr, estimated glomerular filtration rate (eGFR), uric acid, and ß2-microglobulin at 24/48/72 h and 5 to 7 days after PCI; (2) the peak value difference of creatine kinase isoenzymes (CK-MB) after PCI; (3) adverse events within 6 months after PCI. Results: The overall incidence of CIAKI was 21.8%; the incidence of CIAKI in the nicorandil group was significantly lower (12.7% [7/55]) than in the control group (26.7% [27/101]) (P = .043). Compared with the control group, Scr, uric acid, and ß2-microglobulin levels were lower, and the level of eGFR was higher in nicorandil group (P all < .05). The peak value of CK-MB in the nicorandil group was lower than that in the control group (105.30 [56.61, 232.04] vs 178.00 [77.08, 271.91]U/L, P = .042). There was no significant difference in adverse events between the 2 groups within 6 months after PCI. Moreover, multivariate logistic regression analysis showed that hypertension and diabetes were independent risk factors for CIAKI, while nicorandil treatment was a protective factor. Conclusion: Our data suggest that intravenous nicorandil after emergency PCI has a protective effect on the occurrence of CIAKI in STEMI patients.

Adherence with cardiovascular medications and the outcomes in patients with coronary arterial disease: "Real-world" evidence.

BACKGROUND: Cardiovascular medications are vital for the secondary prevention of coronary arterial disease (CAD). However, the effect of cardiovascular medication may depend on the optimal adherence of the patients. This meta-analysis aims to determine the magnitude of adherence to vascular medications that influences the absolute and relative risks (RRs) of mortality in patients with CAD in real-world settings. METHODS: The Cochrane Library, PubMed, and EMBASE databases were searched through March 1, 2022. Prospective studies reporting association as RR and 95% confidence interval between cardiovascular medication adherence and any cardiovascular events and/or all-cause mortality in patients with CAD were included. A one-stage robust error meta-regression method was used to summarize the dose-specific relationships. RESULTS: A total of 18 studies were included. There is a significant inverse linear association between cardiovascular medication adherence and cardiovascular events (pnonlinearity = .68) or mortality (pnonlinearity = .82). The exposure-effect analysis showed that an improvement of 20% cardiovascular medication adherence was associated with 8% or 12% lower risk of any cardiovascular events or mortality, respectively. In subgroup analysis, the benefit was observed in adherence of stain (RR: 0.90, for cardiovascular events, RR: 0.85, for mortality), angiotensin-converting enzyme inhibitors (ACEI)/angiotensin II receptor blockers (ARB)(RR: 0.90, for mortality), and antiplatelet agent (RR: 0.89 for mortality) but not in beta-blocker (RR: 0.90, p = .14, for cardiovascular events, RR: 0.97, p = .32 for mortality). Estimated absolute differences per 1 million individuals per year for mortality associated with 20% improvement were 175 cases for statin, 129 cases for antiplatelet, and 117 cases for ACEI/ARB. CONCLUSION: Evidence from the real word showed poor adherence to vascular medications contributes to a considerable proportion of all cardiovascular disease events and mortality in patients with CAD.

The effect of LncRNA SNHG16 on vascular smooth muscle cells in CHD by targeting miRNA-218-5p.

PURPOSE: To explore the role of SNHG16 in coronary heart disease (CHD) and its effect on vascular smooth muscle cells via miR-218-5p. METHODS: A quantitative real time polymerase chain reaction (qRT-PCR) assay was carried out to determine the expression of serum SNHG16 and miR-218-5p in the observation group before and after treatment and in the control group. Then, receiver operating characteristic (ROC) curves were drawn to analyze the value of SNHG16 and miR-218-5p in the diagnosis and prognosis prediction of CHD. Furthermore, purchased coronary artery smooth muscle cells (HCASMC) were transfected with SNHG16 mimics, SNHG16 inhibitor, miR-218-5p mimics, miR-218-5p inhibitor, or negative control, and then the cell proliferation, migration, apoptosis, and apoptosis-related proteins (Bax, Bcl-2, and Caspase-3) and Wnt/ß-catenin signaling pathway-related proteins (c-myc and ß-catenin) in the cells were detected. RESULTS: Both SNHG16 and miR-218-5 had good predictive value for the development and recurrence of CHD (P < 0.001). In addition, cell experiments showed that inhibition of SNHG16 weakened the proliferation and migration of HCASMC cells and intensified their apoptosis, SNHG16 and miR-218-5p had the same binding sites, and the dual luciferase reporter assay revealed that the fluorescence activity of HG16-WT was inhibited by transfected miR-mimics, but enhanced by transfected miR-inhibitor (both P < 0.050). Furthermore, the rescue experiment revealed that the effect of inhibiting SNHG16 on HCASMC cells was completely reversed by miR-218-5p (P > 0.050). CONCLUSIONS: Highly expressed SNHG16 targetedly regulates miR-218-5p and promotes the proliferation and migration of HCASMC via the Wnt/ß-catenin signaling pathway, giving rise to CHD.

Predictive value of electrocardiographic left ventricular hypertrophy in the general population: A meta-analysis.

BACKGROUND: Conflicting results have been reported on the predictive value of the electrocardiographic left ventricular hypertrophy (LVH) in the general population. This meta-analysis sought to compare the predictive value of different electrocardiographic criteria of LVH in the general population. METHODS: We comprehensively searched PubMed and Embase databases until May 9, 2020 to identify observational studies investigating the predictive value of different electrocardiographic criteria for LVH (Sokolow-Lyon voltage, Cornell voltage or Cornell product) in the general population. Outcome measures were major adverse cardiovascular events (MACEs), cardiovascular or all-cause mortality. RESULTS: Ten studies enrolling 58,400 individuals were included. Comparison with and without electrocardiographic LVH, the pooled risk ratio (RR) of MACEs was 1.62 (95% confidence interval [CI] 1.40-1.89) for the Sokolow-Lyon voltage criteria, 1.70 (95% CI 1.27-2.29) for the Cornell voltage criteria, and 1.56 (95% CI 1.17-2) for the Cornell product criteria. The pooled RR of all-cause mortality was 1.47 (95% CI 1.10-1.97) for the Sokolow-Lyon voltage criteria and 1.87 (95% CI 1.29-2.71) for the Cornell voltage criteria. Furthermore, the pooled RR of cardiovascular mortality was 1.38 (95% CI 1.19-1.60) for the Sokolow-Lyon criteria, 1.66 (95% CI 1.24-2.33) for the Cornell voltage criteria, and 1.82 (95% CI 0.65-5.09) for the Cornell product criteria. CONCLUSIONS: Different electrocardiographic criteria for evaluating LVH had a similar value in predicting MACEs among the general population. LVH detected by the Cornell voltage appeared to have a stronger predictive value in prediction of cardiovascular or all-cause mortality.

Human umbilical cord mesenchymal stem cells-derived exosomes transfers microRNA-19a to protect cardiomyocytes from acute myocardial infarction by targeting SOX6.

Exosomes secreted by human umbilical cord mesenchymal stem cells (hucMSCs) protect cardiomyocytes from anoxia-reoxygenation injury. But the mechanism of hucMSC-exo-microRNA (miR)-19a in acute myocardial infarction (AMI) remains unclear. For this study, cardiac function related indicators, inflammatory factors and markers of myocardial injury, cardiomyocyte injury, infarct size, and apoptosis were detected in vivo experiments. The gain-and loss-of function was performed to evaluate the effects of hucMSC-exo with down/upregulated miR-19a on AMI rats and hypoxic H9C2 cells. Western blot analysis was used to detect levels of AKT/JNK3/caspase-3 axis-related proteins. Consequently, hucMSC-exo alleviated AMI and inhibited cardiomyocyte apoptosis. miR-19a was downregulated in AMI tissues and cells, and increased after hucMSC-exo treatment. miR-19a knockdown in hucMSC-exo impaired the protective role of hucMSC-exo alone in the AMI damage. SOX6 is a target gene of miR-19a and its inhibition lightened hypoxic damage of H9C2 cells. SOX6 knockdown together with miR-19a inhibition in hucMSC-exo activated AKT and inhibited JNK3/caspase-3 axis. Taken together, hucMSC-exo protected cardiomyocytes from AMI injury by transferring miR-19a, targeting SOX6, activating AKT, and inhibiting JNK3/caspase-3 activation. This study may provide new understanding for AMI treatment.

A Comparative Study of High-Resolution Chemical-Shift-Eliminated Magnetic Resonance Imaging of Finger Specimens with Microcomputed Tomography.

OBJECTIVE: High-resolution images of finger joints with chemical-shift elimination can be obtained using an interleaved water-fat (IWF) sequence. This study assessed IWF imaging of finger joints in the delineation of bone structures by comparing images of cadaver fingers with those of microcomputed tomography (CT) that served as a standard reference. MATERIALS AND METHODS: IWF images with spatial resolution of 176 µ × 176 µ × 300 µ were obtained from the distal and proximal interphalangeal joints of two cadaver finger specimens using a custom-built radiofrequency receive coil at 1.5T. Regular three-dimensional gradient-echo (GRE) images were also acquired with similar parameters and compared with the IWF images to evaluate the effects of chemical shift. Micro-CT scans were obtained and served as the standard reference. The image data were reviewed by two experienced musculoskeletal radiologists in consensus. The delineation of normal joint structures and abnormalities in the finger specimens as revealed by the magnetic resonance imaging (MRI) and micro-CT images were compared. The IWF and regular GRE images were assigned scores 0-3 for the depiction of apparent marginal bone defects, with zero being the same in appearance to the micro-CT image and three as having minimal resemblance to it. Statistical analysis of the scoring results was conducted to compare the two MRI techniques. RESULTS: The high-resolution IWF images provided accurate delineation of bone and calcified structures as seen in micro-CT. The thickness of subchondral bone was depicted similarly on the IWF water + fat and the micro-CT images but not on the regular GRE images. The regular GRE sequence showed false marginal bone defects not observed with IWF and micro-CT. In addition, the IWF water-only images facilitated the identification of bone cyst by revealing its water content. CONCLUSION: High-resolution IWF imaging should be useful for the early diagnosis and treatment assessment of arthritis and should also benefit basic research in the pathophysiology of the disease.

Effect of milrinone on cardiac functions in patients undergoing coronary artery bypass graft: a meta-analysis of randomized clinical trials.

BACKGROUND AND AIM: Inotropes are commonly used to treat myocardial dysfunction, which is the major complication after coronary artery bypass graft (CABG). Milrinone, a phosphodiesterase 3 inhibitor, is one of these inotropes. Recently, a number of clinical studies have been carried out to evaluate the effects of milrinone on cardiac function in patients with low ventricular ejection fraction undergoing CABG. However, it has been inconclusive because of the inconsistent results. In addition, some studies found that milrinone increased the incidence of postoperative atrial arrhythmias and did not show any long-term beneficial effects on survival. Therefore, it is very important to perform a meta-analysis to summarize the results so as to determine the clinical efficacy and safety of milrinone. METHOD: Several databases and websites for clinical trials were searched until October 2015 for prospective clinical studies comparing milrinone versus placebo on cardiac functions in patients undergoing CAGB. RESULTS: Four articles were identified by our search strategy. 1) Milrinone decreased incidence of myocardial ischemia and myocardial infarction (15.6% versus 44.4%; 4.7% versus 18% in milrinone and control group, respectively). 2) Milrinone decreased duration of inotropic support (95% confidence interval [CI]: -6.52 to -1.68; P=0.0009) and mechanical ventilation (h) support (95% CI -5.00 to -0.69; P=0.010), but did not decrease the requirement for intra-aortic balloon pump or inotropic support (P>0.05). 3) Milrinone did not decrease the overall mortality or morbidity, intensive care unit stay (P>0.05). CONCLUSION: Perioperative continuous infusion of milrinone is effective to lower incidence of myocardial ischemia and myocardial infarction in patients post-CABG, but it was unable to improve the overall morbidity and mortality or decreased duration of intensive care unit stay. The available sample size is small; therefore, future studies should be directed toward a better understanding of the benefit of milrinone to CABG patients.

TNF is required for the induction but not the maintenance of compression-induced BME signals in murine tail vertebrae: limitations of anti-TNF therapy for degenerative disc disease.

While bone marrow edema (BME) is diagnostic of spondyloarthropathy, its nature remains poorly understood. In contrast, BME in ankylosing spondylitis is caused by tumor necrosis factor (TNF)-induced vascular and cellular changes. To investigate the relationship between chronic compression and TNF signaling in compression-induced BME we utilized a tail vertebrae compression model with WT, TNF-Tg, and TNFR1&2-/- mice to evaluate: (i) healing following release of chronic compression, (ii) induction of BME in the absence of TNFR, and (iii) efficacy of anti-TNF therapy. Compression-induced normalized marrow contrast enhancement (NMCE) in WT was significantly decreased threefold (p < 0.01) within 2 weeks of release, while the NMCE values in TNF-Tg vertebrae remained elevated, but had a significant decrease (p < 0.05) by 6 weeks after the release of compression. TNFR1&2-/- mice were resistant to compression-induced BME. Anti-TNF therapy did not affect NMCE versus placebo. Histological examination revealed that NMCE values significantly correlated with marrow vascularity and cellularity (p < 0.05), which account for 76% of the variability of NMCE. Collectively, these data demonstrate a critical role for TNF in the induction of chronic compression-induced BME, but not in its maintenance. Amelioration of BME is achieved through biomechanical stability, but is not affected by anti-TNF therapy.

High-resolution interleaved water-fat MR imaging of finger joints with chemical-shift elimination.

PURPOSE: To study the use of an interleaved water-fat (IWF) sequence with a custom-made radiofrequency (RF) coil for high-resolution imaging of arthritic finger joints. MATERIALS AND METHODS: High-resolution finger magnetic resonance imaging (MRI) was performed using a custom-made dedicated RF receiver coil and an IWF sequence. A phantom, a cadaver finger specimen, and the fingers of two normal controls and six arthritic subjects were imaged with a resolution of 156 × 156 × 600 µm. The appearance of anatomic structures on the IWF images were compared with images acquired with a regular sequence. The images were reviewed by two musculoskeletal radiologists for the depiction of anatomical structures and for the presence of abnormalities. RESULTS: The high-resolution images revealed detailed structures of the finger joints not detectable using typical clinical resolution. The IWF sequence gave more realistic depiction of subchondral bone thickness, and avoided false bone erosions displayed in the regular sequence. It also allowed better visualization of ligaments and tendons. CONCLUSION: This pilot study shows the feasibility and the potential usefulness of high-resolution IWF imaging for finger joint evaluation. This technique may be useful for the diagnosis and treatment assessment of arthritis, and for the study of joint disease pathogenesis.

Chronic axial compression of the mouse tail segment induces MRI bone marrow edema changes that correlate with increased marrow vasculature and cellularity.

Magnetic resonance imaging (MRI) of bone marrow edema (BME) has been found to be helpful in the diagnosis of back pain attributed to degenerative disk disease (DDD) and spondyloarthropathy (SA), but its interpretation is limited by a lack of knowledge of its nature and natural history. We assessed effects of compressive forces to mouse tail segments of WT and TNF-Tg mice with SA, via contrast enhanced-MRI and histology. Normalized marrow contrast enhancement (NMCE) of uninstrumented WT vertebrae significantly decrease, threefold (p < 0.01) from 8 to 12 weeks of age, while the NMCE of TNF-Tg vertebrae remained elevated. Compressive loading (6x body weight) increased NMCE twofold (p < 0.02) within 2 weeks in WT tails, which was equal to 6x loaded TNF-Tg tails within 4 weeks. Histology confirmed degenerative changes and that load-induced NMCE corresponded to increased vascular sinus tissue (35 +/- 3% vs. 19 +/- 3%; p < 0.01) and cellularity (4,235 +/- 886 vs.1,468 +/- 320 cells/mm(2); p < 0.01) for the loaded versus unloaded WT, respectively. However, micro-computed tomography (CT) analyses failed to detect significant load-induced changes to bone. While the bone marrow of loaded WT and TNF-Tg vertebrae were similar, histology demonstrated mild cellular infiltrate and increased osteoclastic resorption in the WT tails versus severe inflammatory-erosive arthritis in TNF-Tg joints. Significant (p < 0.05) decreases in cortical and trabecular bone volume in uninstrumented TNF-Tg versus WT vertebrae were confirmed by micro-CT. Thus, chronic load-induced DDD causes BME signals in vertebrae similar to those observed from SA, and both DDD and SA signals correlate with a conversion from yellow to red marrow, with increased vascularity.

High-resolution uniform MR imaging of finger joints using a dedicated RF coil at 3T.

PURPOSE: To develop a dedicated radiofrequency (RF) coil for high-resolution magnetic resonance imaging (MRI) of finger joints at 3T to improve diagnostic evaluation of arthritic diseases. MATERIALS AND METHODS: A dedicated cylindrical RF receive coil was developed for imaging finger joints at 3T. A planar coil, a saddle coil, and a 1.5T coil with similar design as the dedicated coil were also constructed to compare imaging performance with the dedicated coil. A phantom was used for quantitative evaluation. Three-dimensional images were obtained on four subjects and a cadaver finger specimen using isotropic resolution of 160 mum in 9:32 minutes. The images were reviewed by two musculoskeletal radiologists. RESULTS: The dedicated finger coil provided higher signal-to-noise and greater signal uniformity than the other coils. It supported high-resolution imaging that demonstrated anatomical details of the entire finger joint, and in the subject study revealed abnormalities not detectable by traditional clinical resolution. CONCLUSION: The dedicated finger coil optimizes the potential advantages of 3T scanners compared to lower field magnets. Use of this coil should facilitate early diagnosis, improve assessment of treatment response, and provide better understanding of basic mechanisms that underlie arthritis.

Elucidating bone marrow edema and myelopoiesis in murine arthritis using contrast-enhanced magnetic resonance imaging.

OBJECTIVE: While bone marrow edema (BME) detected by magnetic resonance imaging (MRI) is a biomarker of arthritis, its nature remains poorly understood due to the limitations of clinical studies. In this study, MRI of murine arthritis was used to elucidate its cellular composition and vascular involvement. METHODS: BME was quantified using normalized bone marrow intensity (NBMI) from precontrast MRI and normalized marrow contrast enhancement (NMCE) following intravenous administration of gadopentate dimeglumine. Wild-type (WT) and tumor necrosis factor (TNF)-transgenic mice were scanned from 2 to 5 months of age, followed by histologic or fluorescence-activated cell sorting (FACS) analysis of marrow. In efficacy studies, TNF-transgenic mice were treated with anti-TNF or placebo for 8 weeks, and then were studied using bimonthly MRI and histologic analysis. RESULTS: NBMI values were similar in WT and TNF-transgenic mice at 2 months. The values in WT mice steadily decreased thereafter, with mean values becoming significantly different from those of TNF-transgenic mice at 3.5 months (mean +/- SD 0.29 +/- 0.08 versus 0.46 +/- 0.13; P < 0.05). Red to yellow marrow transformation occurred in WT but not TNF-transgenic mice, as observed histologically at 5 months. The marrow of TNF-transgenic mice that received anti-TNF therapy converted to yellow marrow, with lower NBMI values versus placebo at 6 weeks (mean +/- SD 0.26 +/- 0.07 versus 0.61 +/- 0.22; P < 0.05). FACS analysis of bone marrow revealed a significant correlation between NBMI values and CD11b+ monocytes (R2 = 0.91, P = 0.0028). Thresholds for "normal" red marrow versus pathologic BME were established, and it was also found that inflammatory marrow is highly permeable to contrast agent. CONCLUSION: BME signals in TNF-transgenic mice are caused by yellow to red marrow conversion, with increased myelopoiesis and increased marrow permeability. The factors that mediate these changes warrant further investigation.

Longitudinal assessment of synovial, lymph node, and bone volumes in inflammatory arthritis in mice by in vivo magnetic resonance imaging and microfocal computed tomography.

OBJECTIVE: To develop longitudinal 3-dimensional (3-D) measures of outcomes of inflammation and bone erosion in murine arthritis using contrast-enhanced magnetic resonance imaging (CE-MRI) and in vivo microfocal computed tomography (micro-CT) and, in a pilot study, to determine the value of entry criteria based on age versus synovial volume in therapeutic intervention studies. METHODS: CE-MRI and in vivo micro-CT were performed on tumor necrosis factor-transgenic (TNF-Tg) mice and their wild-type littermates to quantify the synovial and popliteal lymph node volumes and the patella and talus bone volumes, respectively, which were validated histologically. These longitudinal outcome measures were used to assess the natural history of erosive inflammatory arthritis. We also performed anti-TNF versus placebo efficacy studies in TNF-Tg mice in which treatment was initiated according to either age (4-5 months) or synovial volume (3 mm(3) as detected by CE-MRI). Linear regression was performed to analyze the correlation between synovitis and focal erosion. RESULTS: CE-MRI demonstrated the highly variable nature of TNF-induced joint inflammation. Initiation of treatment by synovial volume produced significantly larger treatment effects on the synovial volume (P = 0.04) and the lymph node volume (P < 0.01) than did initiation by age. By correlating the MRI and micro-CT data, we were able to demonstrate a significant relationship between changes in synovial and patellar volumes (R(2) = 0.75, P < 0.01). CONCLUSION: In vivo CE-MRI and micro-CT 3-D outcome measures are powerful tools that accurately demonstrate the progression of erosive inflammatory arthritis in mice. These methods can be used to identify mice with arthritis of similar severity before intervention studies are initiated, thus minimizing heterogeneity in outcome studies of chronic arthritis seen between genetically identical littermates.

MRI and quantification of draining lymph node function in inflammatory arthritis.

While erosion and tissue necrosis are the end-stage result of inflammatory arthritis, factors that can predict their initiation and severity are unknown. In an effort to identify these prognostic factors we developed contrast-enhanced (CE)-magnetic resonance imaging (MRI) for the mouse knee to assess the pathogenesis of inflammatory arthritis. Using this approach to study synovitis and draining lymph node (LN) function we first demonstrated that the LNs of TNF-Tg mice at 5 months are significantly larger and have greater enhancement in comparison to wild-type (WT) mice. This difference correlated with the abundance of dilated LYVE-1+ sinuses in the draining LNs. Dynamic CE-MRI further demonstrated differences between TNF-Tg and WT mice in the kinetics of LN enhancement. We established an LN capacity (LNcap) measurement that is a function of both volume and CE. We demonstrated that TNF-Tg mice have a 15-fold increase over WT levels at 5 months age (P < 0.001). Amelioration of arthritis with anti-TNF therapy resulted in a significant decrease in LNcap (P < 0.0001) that approached WT levels within 4 weeks. Interestingly, this functional decrease was not associated with a reduction of lymphatic vessels, which persist after therapy in both LNs and synovium. To assess the relationship between draining LN function and synovitis, a regression analysis was performed that demonstrated a significant negative correlation (R(2) = 0.63, P = 0.01) between LNcap and synovial volume. TNF-Tg mice with a lower LNcap display an accelerated progression of arthritis. These results indicate a protective function of enhanced lymphatic drainage in inflammatory arthritis.

In vivo MRI using liquid nitrogen cooled phased array coil at 3.0 T.

A liquid nitrogen (LN2) cooled dual-channel array coil was designed and built for use on a 3.0-T whole-body scanner. In vivo imaging of a volunteer's fingers and imaging of a deceased mouse and oil phantom were performed using the LN2 cooled array and a similar room-temperature coil. Imaging results showed that the LN2 cooled array provides a signal-to-noise ratio gain of up to 240% as compared with its room-temperature counterpart. LN2 cooled arrays may be useful for high-resolution clinical imaging of joints, skin, eyes and peripheral vessels as well as for biomedical imaging of small animals in human disease modeling.

A four-element phased array coil for high resolution and parallel MR imaging of the knee.

A four-element phased array coil for MR imaging of the knee was designed, built and tested for clinical use at 1.5 Tesla. In routine imaging, it provides over twofold increase in signal-to-noise (SNR) compared to two commercially available knee coils, and supports higher spatial image resolution. The phased array knee coil was also tested for its compatibility with parallel MR imaging that reduces imaging time by several folds over conventional MR technique. Results obtained using SiMultaneous Acquisition of Spatial Harmonics (SMASH) technique shows that our phased array knee coil can be used with parallel MR imaging. These improvements may enhance knee diagnosis with higher image quality and reduced scan time.