Salvia miltiorrhiza suppresses cardiomyocyte ferroptosis after myocardial infarction by activating Nrf2 signaling.

ETHNOPHARMACOLOGICAL RELEVANCE: Ferroptosis, a recently identified non-apoptotic form of cell death reliant on iron, is distinguished by an escalation in lipid reactive oxygen species (ROS) that are iron-dependent. This phenomenon has a strong correlation with irregularities in iron metabolism and lipid peroxidation. Salvia miltiorrhiza Bunge (DS), a medicinal herb frequently utilized in China, is highly esteemed for its therapeutic effectiveness in enhancing blood circulation and ameliorating blood stasis, particularly during the treatment of cardiovascular diseases (CVDs). Numerous pharmacological studies have identified that DS manifests antioxidative stress effects as well as inhibits lipid peroxidation. However, ambiguity persists regarding the potential of DS to impede ferroptosis in cardiomyocytes and subsequently improve myocardial damage post-myocardial infarction (MI). AIM OF THE STUDY: The present work focused on investigating whether DS could be used to prevent the ferroptosis of cardiomyocytes and improve post-MI myocardial damage. MATERIALS AND METHODS: In vivo experiments: Through ligation of the left anterior descending coronary artery, we constructed both a wild-type (WT) and NF-E2 p45-related factor 2 knockout (Nrf2-/-) mouse model of MI. Effects of DS and ferrostatin-1 (Fer-1) on post-MI cardiomyocyte ferroptosis were examined through detecting ferroptosis and myocardial damage-related indicators as well as Nrf2 signaling-associated protein levels. In vitro experiments: Erastin was used for stimulating H9C2 cardiomyocytes to construct an in vitro ferroptosis cardiomyocyte model. Effects of DS and Fer-1 on cardiomyocyte ferroptosis were determined based on ferroptosis-related indicators and Nrf2 signaling-associated protein levels. Additionally, inhibitor and activator of Nrf2 were used for confirming the impact of Nrf2 signaling on DS's effect on cardiomyocyte ferroptosis. RESULTS: In vivo: In comparison to the model group, DS suppressed ferroptosis in cardiomyocytes post-MI and ameliorated myocardial damage by inducing Nrf2 signaling-related proteins (Nrf2, xCT, GPX4), diminishing tissue ferrous iron and malondialdehyde (MDA) content. Additionally, it enhanced glutathione (GSH) levels and total superoxide dismutase (SOD) activity, effects that are aligned with those of Fer-1. Moreover, the effect of DS on alleviating cardiomyocyte ferroptosis after MI could be partly inhibited through Nrf2 knockdown. In vitro: Compared with the erastin group, DS inhibited cardiomyocyte ferroptosis by promoting the expression of Nrf2 signaling-related proteins, reducing ferrous iron, ROS, and MDA levels, but increasing GSH content and SOD activity, consistent with the effect of Fer-1. Additionally, Nrf2 inhibition increased erastin-mediated ferroptosis of cardiomyocytes through decreasing Nrf2 signaling-related protein expressions. Co-treatment with DS and Nrf2 activator failed to further enhance the anti-ferroptosis effect of DS. CONCLUSION: MI is accompanied by cardiomyocyte ferroptosis, whose underlying mechanism is probably associated with Nrf2 signaling inhibition. DS possibly suppresses ferroptosis of cardiomyocytes and improves myocardial damage after MI through activating Nrf2 signaling.

Nonlinear Association of Glycosylated Hemoglobin With Single Intracranial Aneurysm Rupture in Patients With Diabetes Mellitus: A Cross-Sectional Study.

Background: The published literature linking diabetes mellitus (DM) to intracranial aneurysm (IA) ruptured has been controversial and limited by methodology. Thus, this study was performed to examine whether hyperglycemia control status is independently associated with single IA rupture in patients with DM. Methods: We conducted a cross-sectional study on two Chinese hospitals between January 2010 and November 2017. Medical records of 223 patients with single IA and DM were reviewed and analyzed. We used glycosylated hemoglobin (GHB) as the independent variable of interest, and the outcome variable was ruptured status of IA. Covariates included data on demographics, morphological parameters, lifestyle habits, clinical features, and comorbidities. Results: Multivariable adjusted binary logistic regression and sensitivity analyses indicated that GHB was not associated with IA rupture (odds ratio OR, = 1.07, 95% CI 0.84-1.35). A nonlinear association between GHB and IA rupture was observed, whose inflection points were 5.5 and 8.9. The OR values (95% confidence intervals) were 0.38 (0.16-0.9) at the range of 1.88-5.5% of GHB, 1.6 (1.03, 2.5) at the range of 5.5-8.9%, and 0.56 (0.06-5.34) at the range of 8.9-10.1, respectively. Conclusion: The independent correlation between GHB and risk of IA rupture presented is nonlinear. The good glycemic control in single IA patients with DM can reduce the risk of IA rupture, and vice versa.

U-Shaped Association of Aspect Ratio and Single Intracranial Aneurysm Rupture in Chinese Patients: A Cross-Sectional Study.

Background: Previous studies have analyzed the association of aspect ratio (AR) on the ruptured intracranial aneurysm (IA), but the findings are inconclusive and controversial. Therefore, the study aimed to derive a more detailed estimation of this association between AR and ruptured IA in Chinese IA patients. Methods: The present work was a cross-sectional study. We retrospectively collected 1,588 Chinese patients with a single IA from January 2010 to November 2017. The relationship was examined between AR at diagnosis and ruptured IA. Covariates included data of demographics, morphological parameters, lifestyle habits, clinical features, and comorbidities. Binary logistic regression and two-piecewise linear models were used to analyze independent associations of AR with ruptured IA. Results: The results suggest that the association between AR and IA rupture was U-shaped. In the AR range of 1.08-1.99, the prevalence of IA rupture was 13% lower for each 0.1-unit increment in AR [odds ratio 0.87, 95% confidence interval (CI) 0.80-0.98]. Conversely, for every 0.1-unit increase in AR, the prevalence of IA rupture increased by ~3% (odds ratio 1.03, 95% CI 1.01-1.06) in the AR range of 3.42-4.08. Conclusion: The relationship between AR and ruptured IA was U-shaped, with the negative association at AR of 1.08-1.99 and positive association at AR of 3.42-4.08.

Efficacy of Integrated Traditional Chinese and Western Medicine for Treating COVID-19: A Systematic Review and Meta-Analysis of RCTs.

Background: Integrated Chinese and Western medicine (integrated medicine) is routinely used in the treatment of coronavirus disease 2019 (COVID-19) in China. In this study, we undertook a systematic review and meta-analysis of published randomized controlled trials (RCTs) to evaluate the efficacy of integrated medicine therapy for patients with COVID-19. Methods: In this meta-analysis, we searched PubMed, Embase, Web of Science, SinoMed, China National Knowledge Infrastructure (CNKI), Chongqing VIP (CQVIP), and Wanfang databases from inception to April 12, 2021, to identify RCTs of integrated medicine in the treatment of COVID-19. The quality of RCTs was assessed by the Cochrane risk of bias tool. RevMan v5.3 and Stata software packages were used for statistical analysis. Results: Nineteen RCTs involving 1,853 patients met our inclusion criteria. Compared with patients treated by conventional Western medicine (CWM), patients treated by integrated medicine have a higher overall effective rate [RR = 1.17, 95% CI: (1.10, 1.26), p < 0.00001], fever disappearance rate [RR = 1.25, 95% CI: (1.04, 1.50), p = 0.02], fatigue disappearance rate [RR = 1.28, 95% CI: (1.00, 1.63), p = 0.05], and chest CT improvement rate [RR = 1.24, 95% CI: (1.14, 1.34), p < 00001]. Beneficial effects of the integrated medicine therapy were also seen in C-reactive protein (CRP) level [WMD = -4.14, 95% CI: (-6.38, -1.91), p = 0.0003] and white blood cell (WBC) count [WMD = 0.35, 95% CI: (0.11, 0.58), p = 0.004]. Subgroup analyses showed that, when the treatment time is <2 weeks, the effect of integrated medicine treatment is more obvious in improving the overall effective rate, clinical symptoms (fever, fatigue, and cough), the CRP level, and WBC count compared with that of the CWM treatment. For patients with severe and non-severe COVID-19, integrated medicine is more effective in improving fever and cough symptoms and WBC count than using CWM alone. Conclusion: The results of the current meta-analysis suggested that the integrated medicine can improve the clinical symptoms, chest CT and infection indicators of COVID-19 patients. Even if the treatment time is <2 weeks, the effect of integrated medicine in improving symptoms is more obvious compared with the treatment of CWM. However, the results should be interpreted cautiously due to the heterogeneity among the studies.

Molecular Mechanism of the Effect of Huanglian Jiedu Decoction on Type 2 Diabetes Mellitus Based on Network Pharmacology and Molecular Docking.

BACKGROUND: Huanglian Jiedu Decoction (HLJDD) is a Traditional Chinese Medicine (TCM) formula comprising four herbal medicines. This decoction has long been used in China for clinically treating T2DM. However, the molecular mechanism of HLJDD treat for T2DM is still not fully known. Hence, this study was designed to reveal the synergistic mechanism of HLJDD formula in the treatment of T2DM by using network pharmacology method and molecular docking. METHODS: Retrieving and screening of active components of different herbs in HLJDD and corresponding T2DM-related target genes across multiple databases. Subsequently, STRING and Cytoscape were applied to analysis and construct PPI network. In addition, cluster and topological analysis were employed for the analysis of PPI networks. Then, the GO and KEGG enrichment analysis were performed by using ClueGO tool. Finally, the differentially expressed analysis was used to verify whether the expression of key target genes in T2DM and non-T2DM samples was statistically significant, and the binding capacity between active components and key targets was validated by molecular docking using AutoDock. RESULTS: There are 65 active components involved in 197 T2DM-related targets that are identified in HLJDD formula. What is more, 39 key targets (AKT1, IL-6, FOS, VEGFA, CASP3, etc.) and 3 clusters were obtained after topological and cluster analysis. Further, GO and KEGG analysis showed that HLJDD may play an important role in treating T2DM and its complications by synergistically regulating many biological processes and pathways which participated in signaling transduction, inflammatory response, apoptotic process, and vascular processes. Differentially expressed analysis showed that AKT1, IL-6, and FOS were upregulated in T2DM samples and a significant between sample differential expression. These results were validated by molecular docking, which identified 5 high-affinity active components in HLJDD, including quercetin, wogonin, baicalein, kaempferol, and oroxylin A. CONCLUSION: Our research firstly revealed the basic pharmacological effects and relevant mechanisms of the HLJDD in the treatment of T2DM and its complications. The prediction results might facilitate the development of HLJDD or its active compounds as alternative therapy for T2DM. However, more pharmacological experiments should be performed for verification.

The role of ginsenoside Rb1, a potential natural glutathione reductase agonist, in preventing oxidative stress-induced apoptosis of H9C2 cells.

BACKGROUND: Oxidative stress-induced cardiomyocytes apoptosis is a key pathological process in ischemic heart disease. Glutathione reductase (GR) reduces glutathione disulfide to glutathione (GSH) to alleviate oxidative stress. Ginsenoside Rb1 (GRb1) prevents the apoptosis of cardiomyocytes; however, the role of GR in this process is unclear. Therefore, the effects of GRb1 on GR were investigated in this study. METHODS: The antiapoptotic effects of GRb1 were evaluated in H9C2 cells by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, annexin V/propidium iodide staining, and Western blotting. The antioxidative effects were measured by a reactive oxygen species assay, and GSH levels and GR activity were examined in the presence and absence of the GR inhibitor 1,3-bis-(2-chloroethyl)-1-nitrosourea. Molecular docking and molecular dynamics simulations were used to investigate the binding of GRb1 to GR. The direct influence of GRb1 on GR was confirmed by recombinant human GR protein. RESULTS: GRb1 pretreatment caused dose-dependent inhibition of tert-butyl hydroperoxide-induced cell apoptosis, at a level comparable to that of the positive control N-acetyl-L-cysteine. The binding energy between GRb1 and GR was positive (-6.426 kcal/mol), and the binding was stable. GRb1 significantly reduced reactive oxygen species production and increased GSH level and GR activity without altering GR protein expression in H9C2 cells. Moreover, GRb1 enhanced the recombinant human GR protein activity in vitro, with a half-maximal effective concentration of ≈2.317 µM. Conversely, 1,3-bis-(2-chloroethyl)-1-nitrosourea co-treatment significantly abolished the GRb1's apoptotic and antioxidative effects of GRb1 in H9C2 cells. CONCLUSION: GRb1 is a potential natural GR agonist that protects against oxidative stress-induced apoptosis of H9C2 cells.

Effects and mechanism of action of Huang-Lian-Jie-Du-Tang in atopic dermatitis-like skin dysfunction in vivo and in vitro.

ETHNOPHARMACOLOGICAL RELEVANCE: Atopic dermatitis (AD), a disorder prevalent during childhood and adulthood, seriously affects the patient's quality of life. Although Huang-Lian-Jie-Du-Tang (HLJDT) has shown anti-inflammatory effects in previous studies, its effects and mechanism of action underlying AD disorder are still largely unknown. OBJECTIVE: This study explored the anti-inflammatory and immunomodulatory effects of HLJDT on the AD-like dermal disorder, induced in vitro by lipopolysaccharide (LPS)-triggered inflammation, and in vivo by 2,4-dinitrochlorobenzene (DNCB). MATERIALS AND METHODS: In vivo HLJDT effects were investigated by determining the severity of dermatitis, which consisted of observing signs of skin lesions, visually and through haematoxylin and eosin (HE) staining, in mouse ears and dorsal skin, measuring serum levels of interleukin (IL)-1α, IL-1ß, IL-2, IL-4, IL-5, IL-6, interferon (IFN)-γ, the tumour necrosis factor (TNF)-α, and determining the splenic index, number of splenic CD4+/CD8+ T-lymphocytes, as well as the phosphorylation levels of mitogen-activated protein kinases (including MAPKs-p38, ERK, and JNK), IκB-α, and nuclear factor kappa B (NF-κB) (p65) within dermal lesions. Morphological changes in LPS-induced inflammation were observed under a microscope, and ELISA and qPCR assays were used to measure IL-1α, IL-1ß, IL-6, and TNF-α expression levels. The protein expression levels of P-ERK/ERK, P-p38/p38, P-JNK/JNK, P-IKß-α, and P-p65 were measured through western blotting. Additionally, p65 expression was assessed by immunofluorescence, and LPS binding to RAW264.7 cell membrane was studied with laser confocal microscopy. RESULTS: HLJDT could remarkably mitigate DNCB-induced AD-like lesion symptoms, alleviating inflammatory mediator infiltration in mouse ears and dorsal skin tissue, down-regulating serum expression levels of IL-1α, IL-1ß, IL-2, IL-4, IL-5, IL-6, IFN-γ, and TNF-α, normalising the splenic CD4+/CD8+ T-lymphocyte ratio, and inactivating MAPKs (including p38, ERK, and JNK), IκB-α, and NF-κB (p65) in dorsal skin. Furthermore, HLJDT inhibited LPS-induced differentiation of RAW264.7 cells, as evidenced by the decreased protein and mRNA expression of IL-1α, IL-1ß, IL-6, and TNF-α. Additionally, it decreased ERK, p38, JNK, IKß-α, and p65 phosphorylation levels in the MAPKs/NF-κB pathway, inhibited p65 nuclear translocation, and reduced LPS binding to the RAW264.7 cell membrane. CONCLUSIONS: HLJDT significantly improved AD-like symptoms via inhibition of the MAPKs/NF-κB pathway. Therefore, administration of HLJDT might be a potential treatment for AD in the clinical setting.

Tanshinone I inhibits vascular smooth muscle cell proliferation by targeting insulin-like growth factor-1 receptor/phosphatidylinositol-3-kinase signaling pathway.

Vascular smooth muscle cell (VSMC) proliferation plays a critical role in arterial remodeling during various vascular diseases including atherosclerosis and hypertension. Tanshinone I, a major component of Salvia miltiorrhiza, exerts protective effects against cardiovascular diseases. In this study, we investigated the effects of tanshinone I on VSMC proliferation, as well as the underlying mechanisms. We found that this compound inhibited the proliferation of VSMCs in a dose-dependent manner, based on 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) and 5-ethynyl-2'-deoxyuridine (EdU) assays. Western blotting demonstrated that tanshinone I inhibited the expression of proliferation-related proteins, including cyclin-dependent kinase 4 (CDK4), cyclin D3, and cyclin D1, in a dose-dependent manner. Molecular docking showed that this compound docked to the inhibitor-binding site of the insulin-like growth factor 1 (IGF-1) receptor (IGF-1R), and the binding energy between tanshinone I and IGF-1R was -9.021 kcal/mol. Molecular dynamic simulations showed that the IGF-1R-tanshinone I binding was stable. We also found that tanshinone I dose-dependently inhibited IGF-1R activation and its downstream molecules, insulin receptor substrate (IRS)-1, phosphatidylinositol-3-Kinase (PI3K), Akt, glycogen synthase kinase-3 beta (GSK3ß), mammalian target of rapamycin (mTOR), 70S6K, and ribosomal protein S6 (RPS6). Notably, activation of IGF-1R by recombinant IGF-1 rescued the activity of IGF-1R and its downstream molecules, and the proliferation of tanshinone I-treated VSMC. In addition, blocking PI3K signaling with LY294002 showed the important role of this pathway in tanshinone I-mediated suppression of VSMC proliferation. Collectively, these data demonstrated that tanshinone I might inhibit VSMC proliferation by inhibiting IGF-1R/PI3K signaling.

Rheum palmatum extract exerts anti-hepatocellular carcinoma effects by inhibiting signal transducer and activator of transcription 3 signaling.

ETHNOPHARMACOLOGICAL RELEVANCE: Hepatocellular carcinoma (HCC) is among the most common malignancies. Signal transducer and activator of transcription 3 (STAT3), with abnormal expression and constitutive activation, has been reported to promote proliferation, metastasis, survival and angiogenesis of HCC cells. Rheum palmatum (RP), a traditional Chinese medicinal herb, exhibited tumor-suppressing effects in multiple human cancers, but its potential functions in HCC remain unexplored. AIM OF THE STUDY: This study aimed to examine the involvement of STAT3 signaling in the anti-HCC effects of RP extract. MATERIALS AND METHODS: SMMC-7721 and HepG2 HCC cell lines were treated with RP extract for 24 h, and then viability, migration, and invasion of HCC cells and angiogenesis of human umbilical vein endothelial cells (HUVECs) were analyzed using MTS, wound-healing, Transwell invasion and tube formation assays, respectively. Western blotting and immunohistochemistry (IHC) were used to examine the activation of key molecules in STAT3 signaling, including STAT3, JAK2, and Src. Additionally, we explored the in vivo antitumor effects of RP extract in a xenograft tumor nude mouse model of HCC. RESULTS: The result showed that RP extract reduced viability, migration, and invasion of SMMC-7721 and HepG2 cells and angiogenesis of HUVECs. It suppressed the phosphorylation of STAT3 and its upstream kinases including JAK2 and Src. In addition, RP extract treatment downregulated STAT3 target genes, including survivin, Bcl-xL, Mcl-1, Bcl-2, MMP-2, MMP-9, Cyclin D1, CDK4, c-Myc, and VEGF-C. Furthermore, RP extract suppressed the xenograft tumor growth and activation of STAT3 in xenograft tumor mice. CONCLUSION: Collectively, the results showed that RP extract prevented HCC progression by inhibiting STAT3, and might be useful for the treatment of HCC.

3,5-Dicaffeoylquinic acid protects H9C2 cells against oxidative stress-induced apoptosis via activation of the PI3K/Akt signaling pathway.

BACKGROUND: Oxidative stress-induced apoptosis plays an important role in the development of heart failure. 3,5-Dicaffeoylquinic acid (3,5-diCQA), a phenolic compound, has shown protective effects against oxidative stress in many diseases. OBJECTIVE: The objective of this study was to investigate the anti-apoptosis potential of 3,5-diCQA in cardiomyocyte cells under oxidative stress and explore its underlying mechanisms. DESIGN: A model of tert-butyl hydroperoxide (TBHP)-induced apoptosis in a cardiomyocyte cell line (H9C2) was established. Cell viabilities on cell lines were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium (MTT) assay. The apoptosis was measured by hoechst33342 and propidium iodide (PI) fluorescent staining. PI (in red) stained the regions of cell apoptosis; Hoechet33342 (in blue) stained the nuclei. The Western blot was used to determine the expressions of related proteins such as p-PI3K: phosphorylated phosphatidylinositol-3-kinase (p-PI3K), phosphorylated Serine and Threonine kinase AKT (p-AKT), p-PTEN, Bcl-2, Bax, and caspase-3. Afterward, a PI3K inhibitor, LY294002, was applied to confirm the influence of the PI3K/Akt pathway on TBHP-treated cells of 3,5-diCQA. Then, H9C2 cells were pre-incubated with 3,5-diCQA alone to determine if the expression of activated PI3K/Akt signaling was mediated by 3,5-diCQA in H9C2 cells. RESULTS: The results showed that TBHP resulted in an increase in cardiomyocyte apoptosis, whereas 3,5-diCQA treatment protected cells from TBHP-induced apoptosis in a dose-dependent manner. Moreover, 3,5-diCQA decreased expressions of Bax and caspase-3 but increased the phosphorylation levels of PI3K and Akt in TBHP-treated cells, which are the key molecules mediating cell survival, whereas phosphatase and tensin homologue deleted on chromosome 10 (PTEN) phosphorylation was unchanged. Importantly, pre-incubation with a PI3K inhibitor (LY294002) partly abolished the anti-apoptosis effects of 3,5-diCQA. Further, 3,5-diCQA enhanced the phosphorylation levels of PI3K and Akt in H9C2 cells directly, while LY294002 attenuated the effects of 3,5-diCQA on PI3K and Akt. CONCLUSION: This study suggested that 3,5-diCQA rescued myocardium from apoptosis by increasing the activation of the PI3K/Akt signaling pathway.

Anti-inflammatory and immune response regulation of Si-Ni-San in 2,4-dinitrochlorobenzene-induced atopic dermatitis-like skin dysfunction.

ETHNOPHARMACOLOGICAL RELEVANCE: Si-Ni-San (SNS) is a well-known decoction in traditional Chinese medicine. Although studies have indicated that the anti-inflammatory and anti-allergic properties of SNS and its components can account for their therapeutic effects, the role and mechanism of SNS in treating skin dysfunction remain unclear. AIM OF THE STUDY: Atopic dermatitis (AD), a disorder known for its prevalence in infants and adults, severely influences the quality of life of affected patients. In this study, we aimed to investigate the anti-inflammatory and immune response modulations of SNS in 2,4-dinitrochlorobenzene (DNCB)-induced AD-like skin dysfunction. MATERIALS AND METHODS: Dermatitis was induced in Kunming mice by the topical application of DNCB. SNS or dexamethasone (positive control) was topically applied every day over the course of the 21-day study. The following were assessed: dermatitis severity scores; ear and dorsal skin haematoxylin and eosin staining; interleukin (IL)- 1α, IL-1ß, IL-2, IL-4, IL-6, and tumour necrosis factor (TNF)-α cytokine levels in the serum; spleen index; spleen CD4 + /CD8 + T lymphocyte ratio; and phosphorylation levels of mitogen-activated protein kinases (MAPKs- p38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK)), IκB-α, and nuclear factor (NF)-κB (p65) in skin lesions. RESULTS: SNS significantly alleviated the symptoms of AD-like lesions induced by DNCB, decreased the infiltration of inflammatory cells in the ear and dorsal tissues, suppressed the increased cytokine levels in the serum, reduced the CD4 + /CD8 +T lymphocyte ratio in the spleen, and downregulated the activation of MAPKs, IκB-α, and NF-κB (p65) in the dorsal skin. The effects were similar to those of dexamethasone. CONCLUSIONS: SNS alleviated the DNCB-induced AD-like skin dysfunction in mice through anti-inflammatory and immune system modulation, indicating that SNS shows potential for AD treatment in clinical settings.

A Model-Based Temperature-Prediction Method by Temperature-Induced Spectral Variation and Correction of the Temperature Effect.

In the present paper, a new model-based method was proposed for temperature prediction and correction. First, a temperature prediction model was obtained from training samples; then, the temperature of test samples were predicted; and finally, the correction model was used to reduce the nonlinear effects of spectra from temperature variations. Two experiments were used to verify the proposed method, including a water-ethanol mixture experiment and a ternary mixture experiment. The results show that, compared with classic method such as continuous piecewise direct standardization (CPDS), our method is efficient for temperature correction. Furthermore, the temperatures of test samples are not necessary in the proposed method, making it easier to use in real applications.

[Cone-beam pseudo lambda tomography under FDK framework].

The medical CT scanner is rapidly evolving from the fan-beam mode to the cone-beam geometry mode. In this paper, a new cone-beam pseudo Lambda tomography was proposed based on the Noo's fan beam super-short scan formula and FDK framework. The proposed pseudo-LT algorithm, which avoids the computation of any PI line and any differential operation, has a significant practical implementation, thus leading to the images with quality improvement and reduced artifacts. The results in the simulation studies confirm the observation that the new algorithm can improve the image resolution over the traditional algorithms with noise projection data.