Radiation Dose and Image quality of coronary CT angiography performed with whole-heart coverage CT scanner with 0.25s rotation time in patients with irregular heart rhythm.

Objectives: To evaluate radiation exposure, image quality, and diagnostic performance of coronary CT angiography (CCTA) using the invasive coronary angiography (ICA) as the reference standard in patients with irregular heart rhythm on a 0.25 s rotation time, 16 cm coverage, single-beat, CT scanner with AI-assisted motion correction. Methods: CCTA data-sheets of 427 patients using a CT scanner with an ECG monitoring system and motion correction algorithm were collected retrospectively. All the patients were divided into two groups: regular heart rhythm (357 patients) and irregular heart rhythm (70 patients). 22 patients in irregular heart rhythm underwent ICA. Image quality and effective dose in both groups were evaluated and compared. Image quality was evaluated on 5-point scales. The diagnostic performance of CCTA in irregular heart rhythm group was compared with the results of ICA. Results: The image quality in both groups was similar (4.34 ± 0.47 vs 4.37 ± 0.48, p > 0.05). No significant difference was observed in effective dose between two groups (2.7 ± 0.7 vs 2.9 ± 1.3, p > 0.05). The diagnostic accuracy was 90.91% in a patient-based analysis, 96.97% in a vessel-based analysis, and 98.61% in a segment-based analysis. In irregular heart rhythm group, gender was an important factor affecting the number of CCTA scans in a single examination and the radiation dose exposed to the patient. Conclusions: For patients with irregular heart rhythm, a CT scanner with an ECG monitoring system and motion correction algorithm can not only reduce the radiation dose to the same level as patients with normal heart rhythms, but also ensure that the images with high diagnostic accuracy.

Applying a CT texture analysis model trained with deep-learning reconstruction images to iterative reconstruction images in pulmonary nodule diagnosis.

OBJECTIVE: To investigate the feasibility and accuracy of applying a computed tomography (CT) texture analysis model trained with deep-learning reconstruction images to iterative reconstruction images for classifying pulmonary nodules. MATERIALS AND METHODS: CT images of 102 patients, with a total of 118 pulmonary nodules (52 benign, 66 malignant) were retrospectively reconstructed with a deep-learning reconstruction (artificial intelligence iterative reconstruction [AIIR]) and a hybrid iterative reconstruction (HIR) technique. The AIIR data were divided into a training (n = 96) and a validation set (n = 22), and the HIR data were set as the test set (n = 118). Extracted texture features were compared using the Mann-Whitney U test and t-test. The diagnostic performance of the classification model was analyzed with the receiver operating characteristic curve (ROC), the area under ROC (AUC), sensitivity, specificity, and accuracy. RESULTS: Among the obtained 68 texture features, 51 (75.0%) were not influenced by the change of reconstruction algorithm (p > 0.05). Forty-four features were significantly different between benign and malignant nodules (p < 0.05) for the AIIR dataset, which were selected to build the classification model. The accuracy and AUC of the classification model were 92.3% and 0.91 (95% confidence interval [CI], 0.74-0.90) with the validation set, which were 80.0% and 0.80 (95% CI, 0.68-0.86) with the test set. CONCLUSION: With the CT texture analysis model trained with deep-learning reconstruction (AIIR) images showing favorable diagnostic accuracy in discriminating benign and malignant pulmonary nodules, it also has certain applicability to the iterative reconstruction (HIR) images.

Knockout of the Cannabinoid Receptor 2 Gene Promotes Inflammation and Hepatic Stellate Cell Activation by Promoting A20/Nuclear Factor-κB (NF-κB) Expression in Mice with Carbon Tetrachloride-Induced Liver Fibrosis.

BACKGROUND This study aimed to investigate the effect of deleting the cannabinoid receptor 2 (CB2) gene on the development of hepatic fibrosis induced by carbon tetrachloride (CCl4) in mice via regulating inflammation. MATERIAL AND METHODS The DNA was extracted from the tails of mice to identify whether the cannabinoid receptor 2 gene was successfully knocked out. A liver fibrosis model was established by an intraperitoneal injection of CCl4 into mice. Hepatic damage and hepatic fibrosis were evaluated by detecting serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and staining paraffin sections of liver tissue with hematoxylin-eosin (HE). The secretion and distribution of collagen in liver tissue were observed by Masson staining. Western blot analysis was performed to detect the expression of a-smooth muscle actin (alpha-SMA), transforming growth factor-ß1 (TGF-ß1), tumor necrosis factor alpha-induced protein 3 (A20), phosphorylated nuclear factor-kB p65 (p-NF-kappaB p65), tumor necrosis factor alpha (TNF-alpha), and interleukin-6 (IL-6) in liver tissue. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression of IL-6 and TNF-alpha mRNA in liver tissue. RESULTS Compared with the control mice, the mice with CB2 knockout that were exposed to CCl4 exhibited increased liver damage, liver fibrosis, and upregulated alpha-SMA, TGF-ß1, A20, and p-NF-kappaB p65 protein levels. IL-6 and TNF-alpha protein levels and mRNA levels were upregulated. CONCLUSIONS The deletion of the CB2 gene promoted the activation of hepatic stellate cells in mice with liver fibrosis and aggravated liver fibrosis by up-regulating the protein expression of A20 and p-NF-kappaB p65 and inducing inflammatory response, potentially providing new insight into the treatment of liver fibrosis.

A Preclinical Porcine Model of Portal Vein Thrombosis in Liver Cirrhosis.

BACKGROUND: This study aimed at presenting a novel method of developing a porcine model of portal vein thrombosis (PVT) in cirrhosis by intravenous administration of thrombin and insertion of a fibered coil. We further investigated changes of biochemical parameters, coagulation, and proinflammatory cytokine expression in the cirrhosis-PVT group. METHODS: Twelve male pigs were randomized into the control group (n = 3) and cirrhosis group (n = 9). In cirrhotic pigs, three were randomly selected to establish PVT by ultrasound-guided percutaneous puncture of the main portal vein (MPV) followed by intravenous thrombin administration and fibered coil insertion. Thrombosis in the MPV was detected by abdominal enhanced computer tomography (CT). The changes of hepatic function, coagulation system, and inflammation cytokines were compared among normal, cirrhosis, and cirrhosis with PVT groups. RESULTS: As manifested by the presence of a filling defect in MPV on portal venous-phase CT angiography, fibrin thrombi were formed in the MPV in cirrhotic pigs within one week and persisted for four weeks. Five weeks after surgery, abnormal liver functions occurred in association with PVT formation in cirrhosis. Both coagulation and thromboelastography parameters showed that cirrhosis-PVT pigs exhibited a procoagulant state through hyperfunction of platelets and clotting factors. Interleukin 6 (IL-6) as a potential inflammatory marker stimulated PVT-mediated inflammation activation in cirrhosis. CONCLUSIONS: Our study provides in vivo evidence that intravenous injection of a coil and thrombin into MPV under interventional guided devices enables a feasible method in thrombus creation. Further exploration and validation of large-sample cases are required to characterize utilities of this model.

[Cannabinoid receptor 2 deletion promotes proliferation and activation of hepatic macrophages in mice with acute liver injury induced by concanavalin A].

Objective To investigate the effect of cannabinoid receptor 2 (CB2) gene deletion on liver macrophages in mice with acute liver injury induced by concanavalin A (ConA). Methods The mice with gene deletion were identified by PCR. Twenty 8-week-old wild-type C57BL/6J male mice were randomly divided into control group and model group. Twenty C57BL/6J male mice with the deletion of CB2 were divided into CB2-/- control group and CB2-/- model group. The wild-type and CB2-/- mouse model groups were injected with ConA 20 mg/kg via tail vein to replicate the model of acute liver injury, and the control groups were injected with the same amount of PBS. Nine hours after modeling, the serum was taken for the detection of alanine aminotransferase (ALT); the degree of liver injury in each group was observed by HE staining; the expression levels of CD68 and TNF-alpha proteins related to liver macrophages were detected by Western blotting; and the positive level of F4/80 in the liver tissue was detected by immunohistochemistry. Results Compared with the two control groups, the liver injury degree of mice in the model groups were serious; the serum ALT level significantly increased; the positive expression of F4/80 in the liver tissue; and the expression of CD68 and TNF-alpha proteins were significantly enhanced. Compared with the WT model group, the CB2-/- model group had an increase in the degree and area of liver injury, the serum ALT, the positive expression of F4/80 in the liver tissue, and the expression of CD68 and TNF-alpha proteins. Conclusion The deletion of CB2 gene increases the proliferation and activation of macrophages in the mice with ConA-induced acute liver injury.

Aberrant methylation-induced dysfunction of p16 is associated with osteoblast activation caused by fluoride.

Chronic exposure to fluoride continues to be a public health problem worldwide, affecting thousands of people. Fluoride can cause abnormal proliferation and activation of osteoblast and osteoclast, leading to skeletal fluorosis that can cause pain and harm to joints and bones and even lead to permanent disability. Nevertheless, there is no recognized mechanism to explain the bone lesions of fluorosis. In this work, we performed a population study and in vitro experiments to investigate the pathogenic mechanism of skeletal fluorosis in relation to methylation of the promoter of p16. The protein coded by the p16 gene inhibits cdk (cyclin-dependent kinase) 4/cdk6-mediated phosphorylation4 of retinoblastoma gene product and induces cell cycle arrest. The results showed that hypermethylation of p16 and reduced gene expression was evident in peripheral blood mononuclear cells of patients with fluorosis and correlated with the level of fluoride exposure. Studies with cell cultures of osteoblasts revealed in response to sodium fluoride (NaF) treatment, there was an induction of p16 hypermethylation and decreased expression, leading to increased cell proliferation, a longer S-phase of the cell cycle, and development of skeletal fluorosis. Further, the methylation inhibitor, 5-aza-2-deoxycytidine, reversed the p16 hypermethylation and expression in response to NaF. These results reveal a regulatory role of p16 gene methylation on osteoblasts activation during the development of skeletal fluorosis.

Malignant obstructive jaundice treated with intraluminal placement of Iodine-125 seed strands and metal stents: An analysis of long-term outcomes and prognostic features.

PURPOSE: The purpose of this study was to analyze the long-term outcomes, including safety, efficacy, and prognostic features, of intraluminal brachytherapy with Iodine-125 (125I) seed strand and stent placement for treatment of patients with malignant obstructive jaundice (MOJ). METHODS AND MATERIALS: From January 2009 to December 2013, 107 consecutive patients with MOJ were treated with intraluminal placement of 125I seed strands and metal stents. A retrospective evaluation of therapeutic outcomes, including overall survival (OS), stent patency rate, complications, and prognostic features, was conducted in 101 patients. RESULTS: 125I seed strands and stents were all successfully implanted. The median followup time was 231 (45-1015) days, and the median OS was 394.0 (95% confidence interval: 319.1-468.9) days. The cumulative OS rates at 3, 6, 12, and 24 months were 95%, 77%, 53%, and 20%, respectively. The median stent patency period was 278.0 (95% confidence interval: 164.1-391.9) days, and cumulative patency rates at 3, 6, 12, and 24 months were 92%, 69%, 45%, and 13%, respectively. Multivariate analysis indicated that the serum conjugated/total bilirubin ≥88% before procedure (p = 0.032) and whether the patient receiving further treatment (p = 0.041) appear to be the prognostic factors of OS. There is no statistical prognostic factor for stent patency. CONCLUSIONS: The intraluminal placement of 125I seed strands and stents appears to be a safe and efficient therapy on MOJ. The patient with serum conjugated/total bilirubin ≥88% before procedure and receiving further treatment seems to live longer.

Treatment of Hepatocellular Carcinoma with Tumor Thrombus with the Use of Iodine-125 Seed Strand Implantation and Transarterial Chemoembolization: A Propensity-Score Analysis.

PURPOSE: To evaluate the safety and efficacy of iodine-125 (125I) seed strand implantation in combination with transarterial chemoembolization for the treatment of hepatitis B-related unresectable hepatocellular carcinoma (HCC) with portal vein invasion. MATERIALS AND METHODS: From January 2013 to June 2016, 76 HCC patients with type II tumor thrombus were included in this single-center retrospective study. Twenty patients underwent 125I seed strand implantation combined with transarterial chemoembolization (group A; n = 20), while 56 patients underwent transarterial chemoembolization alone (group B; n = 56). The procedure-related and radiation complications were assessed. Overall survivals were compared by propensity-score analysis. RESULTS: The technique was successfully performed in all patients. The mean intended dose (r = 10 mm; z = 0; 240 days) was 62.6 ± 1.8 Gy. No grade 3 or 4 adverse events related to the procedure occurred in either group. After propensity-score-matching analysis, 19 patients were selected into each group, respectively. In the propensity-matching cohort, the median overall survival time was significantly longer in group A than in the group B (19 pairs; 28.0 ± 2.4 vs 8.7 ± 0.4 mo; P = .001). Treatment strategy, arterioportal shunt, and number of transarterial chemoembolization sessions were significant predictors of favorable overall survival time. CONCLUSIONS: 125I seed strand implantation combined with transarterial chemoembolization is a safe and effective treatment for HCC patients with portal vein invasion.

The tumor necrosis factor receptor superfamily member 1B polymorphisms predict response to anti-TNF therapy in patients with autoimmune disease: A meta-analysis.

Numerous published data on the tumor necrosis factor receptor superfamily member 1B (TNFRSF1B) gene polymorphisms are shown to be associated with response or non-response to anti-TNF therapy in autoimmune diseases such as rheumatoid arthritis (RA), psoriasis and Crohn's Disease (CD). The aim of this study is to investigate whether the TNFRSF1B rs1061622 T/G or TNFRSF1A A/G rs767455 polymorphisms can predict the response to anti-TNF-based therapy in patients with autoimmune diseases. We conducted a meta-analysis of studies on the association between TNFRSF1B rs1061622 T/G polymorphism or TNFRSF1A A/G rs767455 polymorphism and non-responsiveness to anti-TNF therapy in autoimmune diseases. A total of 8 studies involving 929 subjects for TNFRSF1B rs1061622 and 564 subjects for TNFRSF1A rs767455 were finally considered. These studies consisted of seven studies on the TNFRSF1B polymorphism and four studies on the TNFRSF1A polymorphism. Meta-analysis showed significant association between the TNFRSF1B rs1061622 allele and non-responders to anti-TNF therapy [T/G odds ratio (OR) 0.72, 95% confidence interval (CI) 0.57-0.93, p=0.01]. Stratification by disease type indicated an association between the TNFRSF1B rs1061622 allele and non-responders to TNF antagonist in RA (T/G OR 0.69, 95% CI 0.48-0.99, p<0.05) and psoriasis (T/G OR 0.39, 95% CI 0.23-0.67, p<0.001), but not in CD (T/G OR 1.14, 95% CI 0.57-0.93, p=0.57). And there was no association between TNFRSF1A rs767455 genotype and non-responders to the anti-TNF therapy (A/G OR 0.93, 95% CI 0.70-1.23, p=0.59). This meta-analysis demonstrates that TNFRSF1B T allele carriers show a better response to anti-TNF therapy, and individuals carrying TNFRSF1A A allele have no relationship with the response to anti-TNF therapy for autoimmune diseases. The genotyping of this polymorphism could help to optimize the treatment by identifying patients with a likely poor response to biological drugs.

Kimura disease accompanied with nephrotic syndrome in a 45-year-old male.

Kimura disease (KD) is an uncommon chronic inflammatory disorder of unknown etiology, occurs mainly in Asian young males, presenting as subcutaneous growing masses, with a predilection for head and neck, with or without satellite lymphadenopathy. Herein, we report a case of an atypical manifestation of KD accompanied with NS in a middle-aged man, though the patient was clinically misdiagnosed previously. The diagnosis of KD can be difficult and misleading, so we must explore the main points of KD so as to prevent misdiagnosis.

Disruption of circulating CD4+ T-lymphocyte subpopulations in psoriasis patients is ameliorated by narrow-band UVB therapy.

Narrow-band UVB (NB-UVB) therapy is widely used in the treatment of psoriasis; however, its precise mechanism is still unclear. To investigate the circulating CD4(+) T-lymphocyte subpopulations in psoriasis patients before and after NB-UVB, thus providing new insights into the mechanism of NB-UVB in the treatment of psoriasis. We performed NB-UVB treatments for psoriasis patients (n = 30) and used flow cytometry, real-time PCR, and ELISA for the detection of circulating CD4(+) T-lymphocyte subpopulations. The results were compared with healthy controls (n = 20) as well. We found increased circulating T helper 1 (Th1) and Th17 cell levels as well as decreased circulating regulatory T cells (Treg) levels compared to healthy controls. Additionally, there was a positive correlation between the percentage of circulating Th17 cells and Psoriasis Area and Severity Index (PASI) score. Furthermore, the percentage of circulating Th17 cells was negatively correlated with the Treg cells which led to an imbalance of Th17/Treg. NB-UVB therapy significantly reduced circulating Th1and Th17 cell levels while increasing Treg cell levels. These findings indicate that the overexpression of Th1 and Th17 cells together with the imbalance of Th17/Treg cells may play an important role in the pathogenesis of psoriasis. The mechanism of NB-UVB in the treatment of psoriasis may be through the inhibition of Th1 and Th17 cell immune response as well as the promotion of Treg cell immune response, thus ameliorating the disorder of circulating CD4(+) T-lymphocyte subsets.

Needle-free injection of 5-aminolevulinic acid in photodynamic therapy for the treatment of condylomata acuminata.

The external application of 5-aminolevulinic acid (ALA) in photodynamic therapy (PDT) results in a shallow penetration depth in thick or extensive condylomata acuminata (CA) lesions, thus demonstrating a poor therapeutic effect for those patients. To compare the efficacy of needle-free injection with external application of ALA in PDT for the treatment of CA, 160 CA patients with thick or extensive warts received ALA-PDT by means of external application or needle-free injection of ALA, respectively. The complete response (CR) rate and recurrence rate in the two groups were analyzed. The CR rate after the first treatment in the needle-free injection group (68.8%) was significantly higher compared with that in the external application group (52.5%; P=0.035). The recurrence rates in the needle-free injection group and external application group were 4.1 and 15.4%, respectively (P=0.022). The needle-free injection of ALA increases the therapeutic effect of PDT for CA patients with thick or extensive lesions. It shortens the treatment time and reduces the recurrence rate, and has great potential in the treatment of CA.

Effects of cadmium on absorption, excretion, and distribution of nickel in rats.

The effects of cadmium (Cd (II)) on absorption, excretion, and distribution of nickel (Ni (II)) were studied in rats using (63)Ni-NiCl(2) as radiotracer in the presence and absence of CdCl(2), through intraperitoneal injection (i.p.). The time-concentration curves in the blood were fitted with a two-compartment model. The peak time (t ((peak))) is 0.31 h in the absence of Cd (II), and it is 5.5 h in the presence of Cd (II). The levels of nickels were higher at 3 h and lower (close to zero) at 24 h in all organs of interest, except kidneys, in the absence of Cd (II). There still residue Ni (II) at 72 h post-injection in the presence of Cd (II). The Cd (II) did effect the total Ni (II) excretion 24 h post-injection. Our study showed that cadmium has a competitive effect on the absorption of nickel and an inhibitory effect on the elimination of it, so cadmium may induce the bioaccumulation of nickel in the body.