Shear-wave elastography in renal stiffness in children with hematuria and/or proteinuria.

BACKGROUND: We sought to evaluate renal stiffness in children with hematuria and/or proteinuria using shear wave elastography (SWE) and to investigate the clinical value of renal stiffness in children with hematuria and/or proteinuria. METHODS: According to the results of urinary occult blood and urinary protein tests, 349 pediatric patients were categorized into one of four groups: pure hematuria (HU), pure proteinuria (PU), concomitant hematuria and proteinuria (HUPU), or control (non-HUPU). Patient demographic data, laboratory test results, and renal ultrasound data were collected. RESULTS: There were significant differences in cortical/medullary elasticity among the four groups (the most sensitive cutoff value between HU and PU was 1.72) (P < 0.05). We found that hematuria and proteinuria interacted with renal cortical elasticity (P < 0.05) but that hematuria and proteinuria did not interact with renal medullary elasticity or cortical/medullary elasticity (P > 0.05). Renal elasticity values correlated with sex, age, body surface area, body mass index, qualitative urinary protein, urine N-acetyl-ß-D-glucosaminidase, 24-hour urinary protein quantity, renal volume, and renal cortical thickness (P < 0.05). CONCLUSIONS: SWE can be used to detect changes in renal stiffness in children with hematuria and/or proteinuria. SWE is beneficial for the early detection of glomerular disease in children with abnormal urine test results. IMPACT: This study evaluated the utility of shear wave elastography for the assessment of renal elasticity in pediatric patients presenting with hematuria and/or proteinuria. Children with pure proteinuria had significantly higher renal cortical/medullary elasticity values than those with pure hematuria. An interaction effect between hematuria and proteinuria on renal cortical stiffness was observed. Shear wave elastography can be used as a tool to assess early renal injury in children with urinalysis abnormalities.

Sound touch elastography of Achilles tendons in patients with type 2 diabetes mellitus versus healthy adults.

BACKGROUND: The studies of the effect of diabetes on the stiffness of Achilles tendon (AT) tissue remain inconclusive, we believe it is necessary to find a reliable method which can be used to detect the stiffness changes of the AT in the diabetic state. The objective of the present study was to investigate the effectiveness of sound touch elastography (STE) as a tool for detecting diabetic Achilles tendinopathy. METHODS: We conducted a retrospective review of 180 participants, consisting of 82 patients with type 2 diabetes mellitus (T2DM) and 98 healthy adults, who had undergone AT ultrasonography. Young 's modulus (E) values of the distal, middle, and proximal segments of bilateral ATs of all participants were measured using STE technique. The E values of each AT segment between the case and control group were compared. RESULTS: The E values of the three segments of ATs in T2DM patients were lower than the healthy controls (P < 0.05). In both groups, the E values of the distal segments were lower than those of the middle segments, and the latter were lower than those of the proximal segments (P < 0.05). The E value of each segment of AT was inversely related to FPG, HbA1c, and diabetes duration (P < 0.05). The best cut-off points for the E values of the three segments of the AT for detecting diabetic tendinopathy were 347.44 kPa (AUC, 0.779), 441.57 kPa (AUC, 0.692), and 484.35 kPa (AUC, 0.676), respectively. CONCLUSION: STE can be used as a complementary diagnostic tool for the diagnosis of diabetic Achilles tendinopathy.

OTUD1 promotes pathological cardiac remodeling and heart failure by targeting STAT3 in cardiomyocytes.

Rationale: Understanding the molecular mechanisms of deleterious cardiac remodeling is important for the development of treatments for heart failure. Recent studies have highlighted a role of deubiquitinating enzymes in cardiac pathophysiology. In the present study, we screened for alteration of deubiquitinating enzymes in experimental models of cardiac remodeling, which indicated a potential role of OTU Domain-Containing Protein 1 (OTUD1). Methods: Wide-type or OTUD1 knockout mice with chronic angiotensin II infusion and transverse aortic constriction (TAC) were utilized to develop cardiac remodeling and heart failure. We also overexpressed OTUD1 in mouse heart with AAV9 vector to validate the function of OTUD1. LC-MS/MS analysis combined with Co-IP was used to identify the interacting proteins and substrates of OTUD1. Results: We found that OTUD1 is elevated in mouse heart tissues following chronic angiotensin II administration. OTUD1 knockout mice were significantly protected against angiotensin II-induced cardiac dysfunction, hypertrophy, fibrosis and inflammatory response. Similar results were obtained in the TAC model. Mechanistically, OTUD1 bounds to the SH2 domain of STAT3 and causes deubiquitination of STAT3. Cysteine at position 320 of OTUD1 exerts K63 deubiquitination to promote STAT3 phosphorylation and nuclear translocation, thereby increasing STAT3 activity to induce inflammatory responses, fibrosis, and hypertrophy in cardiomyocytes. Finally, OTUD1 overexpression by AAV9 vector increases Ang II-induced cardiac remodeling in mice and OTUD1-regulated responses can be inhibited by blocking STAT3. Conclusion: Cardiomyocyte OTUD1 promotes pathological cardiac remodeling and dysfunction by deubiquitinating STAT3. These studies have highlighted a novel role of OTUD1 in hypertensive heart failure and identified STAT3 as a target of OTUD1 in mediating these actions.

Sclareol attenuates angiotensin II-induced cardiac remodeling and inflammation via inhibiting MAPK signaling.

Chronic inflammation plays an important role in hypertensive heart failure. Suppressing angiotensin II (Ang II)-induced cardiac inflammation may contribute to the treatment of hypertension-associated heart failure. Sclareol, a natural product initially isolated from the leaves and flowers of Salvia sclarea, possesses antiinflammatory and immune-regulation activity in various systems. However, its effect on Ang II-induced cardiac remodeling remains unknown. In this study, we have explored the potential effects of sclareol on Ang II-induced heart failure. In vivo experiments were conducted in mice with Ang II-pump infusion for 28 days. Sclareol administration at 5 mg·kg-1 ·d-1 significantly reduced the expression of myocardial injury markers. Sclareol also exerts protective effects against Ang II-induced cardiac dysfunction in mice which is associated with alleviated cardiac inflammation and fibrosis. Transcriptome analysis revealed that inhibition of the Ang II-activated mitogen-activated protein kinase (MAPK) pathway contributed to the protective effect of sclareol. Sclareol inhibits Ang II-activated MAPKs pathway to reduce inflammatory response in mouse hearts and cultured cardiomyocytes. Blockage of MAPKs in cardiomyocytes abolished the antiinflammatory effects of sclareol. In conclusion, we show that sclareol protects hearts against Ang II-induced injuries through inhibiting MAPK-mediated inflammation, indicating the potential use of sclareol in the prevention of hypertensive heart failure.

Blockage of MyD88 in cardiomyocytes alleviates cardiac inflammation and cardiomyopathy in experimental diabetic mice.

Hyperglycemia-associated inflammation contributes to diabetic cardiomyopathy. Myeloid differentiation primary-response protein 88 (MyD88) is an adapter protein of many Toll-like receptors (TLRs) and is recruited to TLRs to initiate inflammatory response in endotoxin-activated innate immunity. However, the role of MyD88 in diabetic cardiomyopathy is unknown. We examined the role and mechanism of MyD88 in inflammatory heart injuries in diabetes and identified MyD88 as a potential target for the treatment of diabetic cardiomyopathy. In this study, we first found that MyD88 expression was increased in cardiomyocytes of diabetic mouse hearts. In cultured cardiomyocytes, MyD88 inhibition either by siRNA or by small-molecular inhibitor LM8 markedly blocked TLR4-MyD88 complex formation, reduced pro-inflammatory mitogen-activated protein kinases/nuclear factor-κB (MAPKs/NF-κB) cascade activation and decreased pro-inflammatory cytokine expression under high glucose condition. Moreover, pharmacologic inhibition of MyD88 by LM8 showed significantly anti-inflammatory, anti-hypertrophic and anti-fibrotic effects in the hearts of both type 1 and type 2 diabetic mice. These beneficial effects of MyD88 inhibition were correlated to the reduced activation of TLR4-MyD88-MAPKs/NF-κB signaling pathways in the hearts. Taken together, MyD88 in cardiomyocytes mediates diabetes-induced cardiac inflammatory injuries and pharmacological inhibition of MyD88 shows significantly cardioprotective effects, indicating MyD88 as a potential therapeutic target for diabetic cardiomyopathy.

Diacerein alleviates Ang II-induced cardiac inflammation and remodeling by inhibiting the MAPKs/c-Myc pathway.

BACKGROUND: Heart failure is a common event in the course of hypertension. Recent studies have highlighted the key role of the non-hemodynamic activity of angiotensin II (Ang II) in hypertension-related cardiac inflammation and remodeling. A naturally occurring compound, diacerein, exhibits anti-inflammatory activities in various systems. HYPOTHESIS/PURPOSE: In this study, we have examined the potential effects of diacerein on Ang II-induced heart failure. METHODS: C57BL/6 mice were administered Ang II by micro-osmotic pump infusion for 4 weeks to develop hypertensive heart failure. Mice were treated with diacerein by gavage for final 2 weeks. RNA-sequencing analysis was performed to explore the potential mechanism of diacerein. RESULTS: We found that diacerein could inhibit inflammation, myocardial fibrosis, and hypertrophy to prevent heart dysfunction, without the alteration of blood pressure. To explore the potential mechanism of diacerein, RNA-sequencing analysis was performed, indicating that MAPKs/c-Myc pathway is involved in that cardioprotective effects of Diacerein. We further confirmed that diacerein inhibits Ang II-activated MAPKs/c-Myc pathway to reduce inflammatory response in mouse hearts and cultured cardiomyocytes. Deficiency of MAPKs or c-Myc in cardiomyocytes abolished the anti-inflammatory effects of diacerein. CONCLUSION: Our results indicate that diacerein protects hearts in Ang II-induced mice through inhibiting MAPKs/c-Myc-mediated inflammatory responses, rendering diacerein a potential therapeutic candidate agent for hypertensive heart failure.

Preparation and evaluation of the anti-cancer properties of RGD-modified curcumin-loaded chitosan/perfluorohexane nanocapsules in vitro.

Curcumin (Cur) encapsulation in nanocapsules (NCs) could improve its availability and therapeutic antitumor efficacy. Cur-loaded chitosan/perfluorohexane (CS/PFH) nanocapsules (CS/PFH-Cur-NCs) were thus synthesized via a nanoemulsion process. To further enhance the selective tumor targeting ability of Cur-loaded NCs, a novel CS/PFH-Cur-NCs with conjugation of Arg-Gly-Asp (RGD) peptide (RGD-CS/PFH-Cur-NCs) were prepared in this study. The properties of these NCs were then explored through in vitro release experiments and confocal laser scanning microscopy-based analyses of the ability of these NCs to target MDA-MB-231 breast cancer cells. In addition, an MTT assay-based approach was used to compare the relative cytotoxic impact of CS/PFH-Cur-NCs and RGD-CS/PFH-Cur-NCs on these breast cancer cells. It was found that both CS/PFH-Cur-NCs and RGD-CS/PFH-Cur-NCs were smooth, relatively uniform, spheroid particles, with the latter being 531.20 ± 68.97 nm in size. These RGD-CS/PFH-Cur-NCs can be ideal for contrast imaging studies, and were better able to target breast cancer cells in comparison to CS/PFH-Cur-NCs. In addition, RGD-CS/PFH-Cur-NCs were observed to induce cytotoxic MDA-MB-231 cell death more swiftly in comparison to CS/PFH-Cur-NCs. These findings suggest that NC encapsulation and RGD surface modification can remarkably improve the anti-tumor efficacy of Cur. These novel NCs may thus manifest a significant potential value in the realm of image-guided cancer therapy, underscoring an important direction for future research.

Can virtual touch tissue imaging quantification be a reliable method to detect anterior talofibular ligament type I injury at the acute, subacute, and chronic stages?

BACKGROUND: Anterior talofibular ligament (ATFL) injury affects ankle joint stability. To date, very few studies have examined tissue stiffness changes inside injured ligaments. Virtual touch tissue imaging quantification (VTIQ) allows for the non-invasive quantitative measurement of tissue stiffness. The present study aimed to examine the efficacy of VTIQ as a method for detecting ligament injury. METHODS: A total of 206 patients diagnosed with unilateral ATFL type I injury (81 acute cases, 69 subacute cases, and 56 chronic cases) were reviewed retrospectively. Shear wave velocity (SWV) values were collected from both the injured and non-affected sides of the ATFL using a virtual touch tissue imaging quantification technique (ACUSON Oxana 2, Siemens Medical Solutions USA, Inc.). RESULTS: The average SWV of injured ATFL was 4.09±1.15 m/s in the acute group, 5.60±1.39 m/s in the subacute group, and 7.74±1.44 m/s in the chronic group (P<0.001). The SWV values of the ATFL on the non-affected side were almost identical (acute 7.50±1.12 m/s, subacute 7.53±1.06 m/s, and chronic 7.61±1.30 m/s; P>0.05). The injured ATFL had a significantly lower SWV value than the non-affected ATFL in the acute and subacute groups (P<0.001); however, there was no significant difference in the chronic group (P>0.05). Concerning the validity of SWV as a predictor of acute and subacute ATFL injury, the receiver operator characteristics curve analysis showed that the best cut-off point for SWV was 6.165 m/s, with 84.3% sensitivity, 88.5% specificity, and an area under the curve of 0.93 (95% CI, 0.90-0.95). CONCLUSIONS: VTIQ is a reliable sonographic method for detecting acute and subacute ATFL type I injury.

Combination CTLA-4 immunoglobulin treatment and ultrasound microbubble-mediated exposure improve renal function in a rat model of diabetic nephropathy.

OBJECTIVE: This study explored the therapeutic impact of combined cytotoxic T lymphocyte-associated antigen 4 immunoglobulin (CTLA-4-Ig) treatment and microbubble-mediated exposure in a rat model of diabetic nephropathy (DN). METHOD: We treated rats using CTLA-4-Ig and/or microbubble exposure. At 8 weeks post-intervention, key parameters were evaluated including blood biochemistry, damage to renal tissue, renal parenchymal elasticity, ultrastructural changes in podocytes, and renal parenchymal expression of CD31, CD34, IL-6, Fn, Collagen I, Talin, Paxillin, α3ß1, podocin, nephrin, and B7-1. RESULT: We found that renal function in the rat model of DN can be significantly improved by CTLA-4-Ig and CTLA-4-Ig + ultrasound microbubble treatment. Treatment efficacy was associated with reductions in renal parenchymal hardness, decreases in podocyte reduction, decreased IL-6, Fn and Collagen I expression, increased Talin, Paxillin and α3ß1 expression, elevated podocin and nephrin expression, and decreased B7-1 expression. In contrast, these treatments did not impact CD31 or CD34 expression within the renal parenchyma. CONCLUSION: These findings clearly emphasize that CTLA-4-Ig can effectively prevent podocyte damage, inhibiting inflammation and fibrosis, and thereby treating and preventing DN. In addition, ultrasound microbubble exposure can improve the ability of CTLA-4-Ig to pass through the glomerular basement membrane in order to access podocytes such that combination CTLA-4-Ig + microbubble exposure treatment is superior to treatment with CTLA-4-Ig only.

Review on experimental study and clinical application of low-intensity pulsed ultrasound in inflammation.

Low-intensity pulsed ultrasound (LIPUS), as physical therapy, is widely used in both research and clinical settings. It induces multiple bioeffects, such as alleviating pain, promoting tissue repair, and shortening disease duration. LIPUS can also mediate inflammation. This paper reviews the application of LIPUS in inflammation and discusses the underlying mechanism. In basic experiments, LIPUS can regulate inflammatory responses at the cellular level by affecting some signaling pathways. In a clinical trial, LIPUS has been shown to alleviate inflammatory responses efficiently. As a cheap, safe, and convenient physical method, LIPUS is promising as anti-inflammatory therapy.

Myeloid differentiation protein 2 mediates angiotensin II-induced inflammation and mesenchymal transition in vascular endothelium.

Angiotensin II (Ang II)-induced vascular inflammation and injury entails endothelial to mesenchymal transition (EndMT). Recent studies have shown that Ang II engages toll-like receptor 4 (TLR4) in the vasculature to mediate adverse effects. Here, we aimed to investigate whether myeloid differentiation protein 2 (MD2), an extracellular molecule indispensable for TLR4 activation, mediates Ang II-induced vascular injury and EndMT. We utilized MD2 knockout mice and wildtype mice treated with a specific MD2 inhibitor to decipher its role in aortas of Ang II-challenged mice. To confirm our results and to provide mechanistic insights, we exposed cultured endothelial cells to Ang II, with or without MD2 silencing. We show that Ang II causes deleterious remodeling and EndMT in aortas of mice within two weeks. These Ang II effects were largely absent in MD2 knockout mice and in wildtype mice treated with a MD2 inhibitor. MD2 silencing in cultured endothelial cells confirmed the essential role of MD2 in Ang II-induced inflammatory factor induction, and EndMT-associated phenotypic change. We also found that Ang II-MD2-EndMT axis involves the activation of nuclear factor-κB. Our studies highlight an essential role of MD2 in Ang II-induced vascular inflammation and EndMT contributing to vascular injury. These results also imply that MD2 may be targeted to dampen inflammatory cardiovascular and EndMT-associated diseases.

Assessment of real-time three-dimensional echocardiography as a tool for evaluating left atrial volume and function in patients with type 2 diabetes mellitus.

OBJECTIVE: To assess the value of real-time three-dimensional echocardiography (RT-3DE) in evaluating changes in left atrial volume and function in type 2 diabetes mellitus (DM) and type 2 diabetic nephropathy (DN) patients. METHOD: 104 control subjects, 109 DN patients, and 111 DM patients were recruited and underwent RT-3DE. Data pertaining to the left atrium were analyzed using the 3DQA software in order to determine left atrial maximum volume index (LAVImax), left atrial pre-systolic volume index (LAVIp), left atrial minimum volume index (LAVImin), total left atrial ejection fraction (LAEFt), passive left atrial ejection fraction (LAEFp), and active left atrial ejection fraction (LAEFa). Differences between these three groups and correlations between individual index values and E/e' ratios were additionally assessed. RESULT: LAVImax, LAVIp, and LAVImin were higher in the DN and DM groups relative to controls, whereas LAEFt and LAEFp were higher in controls relative to DM and DN patients (P < 0.05). LAVImax, LAVIp, and LAVImin in the DN group were significantly higher than those in the DM group, while LAEFt, LAEFp were higher in DM patients relative to DN patients (P < 0.05). The E/e' ratio was also found to be significantly correlated with LAVImax, LAVIp, and LAVImin. CONCLUSION: Our results indicate that RT-3DE can be used to assess changes in left atrial volume and function in patients with diabetes and can be used to monitor disease progression-related damage to such left atrial functionality.

A novel salviadione derivative, compound 15a, attenuates diabetes-induced renal injury by inhibiting NF-κB-mediated inflammatory responses.

Diabetic nephropathy is the leading cause of renal failure worldwide. Elevated inflammatory signaling has been shown to lead to deterioration of renal function in human and experimental diabetes. We recently developed a salviadione derivative (compound 15a) that prevented microbial lipopolysaccharide-induced inflammatory responses, which are largely driven by nuclear factor-κB (NF-κB). In the present study, we have tested the hypothesis that 15a will protect kidneys from diabetes-induced dysfunction by suppressing NF-κB activation and inflammatory signaling. Treatment of diabetic mice with 15a inhibited diabetes-induced renal fibrosis, NF-κB activation, and upregulation of proinflammatory cytokines. Histologically, kidney specimens from diabetic mice treated with 15a were indistinguishable from non-diabetic controls. We confirmed our findings in cultured renal tubular epithelial cells exposed to high levels of glucose. In these cultured cells, 15a pretreatment prevented high glucose-induced NF-κB activation and expression of inflammatory cytokines. These protective effects were also reflected in reduced levels of proteins involved in matrix expansion. Overall, our studies show that a salviadione derivative, 15a, is effective in suppressing diabetes-induced NF-κB activation and inflammatory signaling.

The value of 2D speckle-tracking strain echocardiography in evaluating the relationship between carotid elasticity and left ventricular systolic function in patients with diabetic nephropathy.

OBJECTIVE: To investigate the relationship between the elasticity of the carotid artery and the LV (left ventricle) systolic function in patients with diabetic nephropathy (DN) by using two-dimensional speckle-tracking strain echocardiography (2D-STE). METHODS: DN patients (n = 108) and control subjects (n = 112), all of whom underwent echocardiography and carotid ultrasound. Analysis of LV GLS (global longitudinal strain) from the apical two-chamber (2C), three-chamber (3C), and four-chamber (4C) views. Meanwhile, the circumferential strain (CS) of the carotid artery was obtained from the view of the short-axis right common carotid artery. The differences between the two groups were compared, and a correlation analysis between CS and GLS was performed. RESULTS: The 4CGLS, 2CGLS, 3CGLS, and CS of the DN group were significantly lower at significant levels in contrast to the control group (p < 0.05). There was a significantly positive correlation of CS with 4CGLS, 2CGLS, and 3CGLS in all subjects (r = 0.809, p = 0.000; r = 0.830, p = 0.000; r = 0.830, p = 0.000, respectively). CONCLUSION: 2D-STE is a relatively new technique for assessing the mechanical characteristics of the carotid artery in patients with DN. Reduced values of CS correlate with reduced LV systolic function as evaluated by strain measurements, which can predict the risk of systolic dysfunction of LV.

Uniaxial Tensile Strain Induced the Enhancement of Thermoelectric Properties in n-Type BiCuOCh (Ch = Se, S): A First Principles Study.

It is well known that the performance of thermoelectric measured by figure of merit ZT linearly depends on electrical conductivity, while it is quadratic related to the Seebeck coefficient, and the improvement of Seebeck coefficient may reduce electrical conductivity. As a promising thermoelectric material, BiCuOCh (Ch = Se, S) possesses intrinsically low thermal conductivity, and comparing with its p-type counterpart, n-type BiCuOCh has superior electrical conductivity. Thus, a strategy for increasing Seebeck coefficient while almost maintaining electrical conductivity for enhancing thermoelectric properties of n-type BiCuOCh is highly desired. In this work, the effects of uniaxial tensile strain on the electronic structures and thermoelectric properties of n-type BiCuOCh are examined by using first-principles calculations combined with semiclassical Boltzmann transport theory. The results indicate that the Seebeck coefficient can be enhanced under uniaxial tensile strain, and the reduction of electrical conductivity is negligible. The enhancement is attributed to the increase in the slope of total density of states and the effective mass of electron, accompanied with the conduction band near Fermi level flatter along the Γ to Z direction under strain. Comparing with the unstrained counterpart, the power factor can be improved by 54% for n-type BiCuOSe, and 74% for n-type BiCuOS under a strain of 6% at 800 K with electron concentration 3 × 1020 cm-3. Furthermore, the optimal carrier concentrations at different strains are determined. These insights point to an alternative strategy for superior thermoelectric properties.

Assessment of early damage of endometrium after artificial abortion by shear wave elastography.

OBJECTIVES: This study aimed to investigate the application of shear wave elastography (SWE) in the early damage detection through assessing the endometrial elasticity after artificial abortion. METHODS: A total of nulliparous women (20-30 years) who received ultrasonography in our hospital were recruited between January 2017 and December 2017. These women were divided into normal control group (NC; n = 65), after once artificial abortion group (AOAA; n = 68), after twice artificial abortion group (ATAA; n = 61), and after three times or more (range, 3-6) artificial abortion group (ATTMAA; n = 60). SWE was performed to evaluate the endometrium; Young's modulus of the endometrium was determined and then the endometrial thickness was measured. RESULTS: Young's modulus of the endometrium increased in the order of NC group, AOAA group, ATAA group, and ATTMAA group, and Young's modulus increased with the increase in the number of artificial abortions (p < 0.05). The endometrial thickness in the ATTMAA group was significantly lower than in the NC group, AOAA group, and ATAA group (p < 0.05), but there was no marked difference among the NC group, AOAA group, and ATAA group (p > 0.05). CONCLUSIONS: SWE increases with increasing number of abortions, which may indicate the damage that is done to the endometrium earlier than measurement of the endometrial thickness do.

The Diagnostic Value of Ultrasound in Medullary Thyroid Carcinoma: A Comparison With Computed Tomography.

PURPOSE: To explore the clinical value of ultrasound in the diagnosis of medullary thyroid carcinoma by comparing with enhanced computed tomography. METHODS: This retrospective study was performed on 62 patients with pathologically confirmed medullary thyroid carcinoma. All patients underwent ultrasound and enhanced computed tomography examinations before surgery. The findings of the pathologic examination of resected specimens were considered as gold standard and were compared with the results of these 2 methods. RESULTS: There were 73 medullary thyroid carcinoma lesions and 29 benign lesions in 62 patients. In all, 55 of 73 medullary thyroid carcinoma lesions and 27 of 29 benign lesions were correctly diagnosed by ultrasound; and 45 of 73 medullary thyroid carcinoma lesions and 24 of 29 benign lesions were correctly diagnosed by enhanced computed tomography. The accuracy of ultrasound and enhanced computed tomography was 80.4% and 67.6%, respectively. There was significant difference between 2 methods (P < .05). CONCLUSIONS: Ultrasound can be used to observe the location, number, size, shape, border, internal echo, calcification, and blood flow of the lesion. It is a convenient, inexpensive, and nonradiative method with higher accuracy than enhanced computed tomography.

Effects of Cytotoxic T Lymphocyte-Associated Antigen 4 Immunoglobulin Combined with Microbubble-Mediated Irradiation on Hemodynamics of the Renal Artery in Rats with Diabetic Nephropathy.

Cytotoxic T lymphocyte-associated antigen 4 immunoglobulin (CTLA-4-Ig) can inhibit the effect of B7-1 and improve renal hemodynamics in rats with diabetic nephropathy (DN). Nevertheless, a strategy that could increase the permeation of CTLA-4-Ig through endothelial cells and basement membrane remains to be discovered. We investigated the effect of CTLA-4-Ig combined with microbubble-mediated irradiation on the hemodynamics of renal arteries in DN rats. Rats were treated with CTLA-4-Ig and/or microbubble exposure. After 8 wk of intervention, color Doppler ultrasonography was used to detect peak systolic velocity (PSV), end-diastolic velocity (EDV), mean velocity (MV), systolic acceleration (SAC), pulsatility index (PI) and resistance index (RI) of the renal artery trunk. The CTLA-4-Ig + microbubble exposure group exhibited significantly higher PSV, EDV and MV than the CTLA-4-Ig group, which had significantly higher values than the non-intervention group. The CTLA-4-Ig + microbubble exposure group exhibited significantly lower SAC, PI and RI than the CTLA-4-Ig group, which had significantly lower values than the non-intervention group. Our results indicate that both CTLA-4-Ig and CTLA-4-Ig + microbubble exposure can reduce the blood flow resistance and improve the blood flow velocity of renal arteries in rats. Moreover, the effect of CTLA-4-Ig + microbubble exposure is better than that of CTLA-4-Ig alone. Our study provides a new, effective and non-invasive strategy for the treatment of DN.