Decreased brain iron deposition based on quantitative susceptibility mapping correlates with reduced neurodevelopmental status in children with autism spectrum disorder.

To investigate potential correlations between the susceptibility values of certain brain regions and the severity of disease or neurodevelopmental status in children with autism spectrum disorder (ASD), 18 ASD children and 15 healthy controls (HCs) were recruited. The neurodevelopmental status was assessed by the Gesell Developmental Schedules (GDS) and the severity of the disease was evaluated by the Autism Behavior Checklist (ABC). Eleven brain regions were selected as regions of interest and the susceptibility values were measured by quantitative susceptibility mapping. To evaluate the diagnostic capacity of susceptibility values in distinguishing ASD and HC, the receiver operating characteristic (ROC) curve was computed. Pearson and Spearman partial correlation analysis were used to depict the correlations between the susceptibility values, the ABC scores, and the GDS scores in the ASD group. ROC curves showed that the susceptibility values of the left and right frontal white matter had a larger area under the curve in the ASD group. The susceptibility value of the right globus pallidus was positively correlated with the GDS-fine motor scale score. These findings indicated that the susceptibility value of the right globus pallidus might be a viable imaging biomarker for evaluating the neurodevelopmental status of ASD children.

Anti-collagenase, Anti-elastase, Anti-urease, and Anti-cancer Potentials of Isokaempferide as Natural Compound: In vitro and in silico Study.

One of the main goals of medicinal chemistry in recent years has been the development of new enzyme inhibitors and anti-cancer medicines. The isokaempferide' ability to inhibit the enzymes urease, elastase, and collagenase were also studied. The results showed that isokaempferide was the most effective compound against the assigned enzymes, with IC 50 values of 23.05 µM for elastase, 12.83 µM for urease, and 33.62 µM for collagenase respectively. It should be emphasized that natural compound was more effective at inhibiting some enzymes. Additionally, the compound was tested for their anti-cancer properties using colon, lung, breast cancer cell lines. The chemical activities of isokaempferide against urease, collagenase, and elastase were investigated utilizing the molecular docking study. The anti-cancer activities of the compound were evaluated against lung cancer cells such as SPC-A-1, SK-LU-1, 95D, breast cancer cells like MCF7, Hs 578Bst, Hs 319.T, and UACC-3133 cell lines, and colon cancer cell lines like CL40, SW1417, LS1034, and SW480. The chemical activities of isokaempferide against some of the expressed surface receptor proteins (EGFR, estrogen receptor, CD47, progesterone receptor, folate receptor, CD44, HER2, CD155, CXCR4, CD97, and endothelin receptor) in the mentioned cell lines were assessed using the molecular docking calculations. The results showed the probable interactions and their characteristics at an atomic level. The docking scores revealed that isokaempferide has a strong binding affinity to the enzymes and proteins. In addition, the compound formed powerful contact with the enzymes and receptors. Thus, isokaempferide could be potential inhibitor for enzymes and cancer cells.

Reduction mammoplasty and mastopexy for multiple bilateral fibroadenomas: a case report and literature review.

Treatment of multiple benign breast nodules is sometimes challenging with respect to establishing a surgical plan that achieves both therapeutic and cosmetic goals. Successful application of oncoplastic techniques has been reported in selected cases of benign breast lesions. In this case report, we present the surgical treatment and outcome of a patient with multiple fibroadenomas in ptotic and voluminous breasts. A combined procedure of extensive glandular resection and reduction mammoplasty using a modified vertical pedicle technique was performed on this patient, who desired complete lesion removal, volume reduction, and mastopexy. The cosmetic result was satisfactory at both the short- and mid-term follow-up. In addition, different techniques applied in the treatment of breast fibroadenoma are herein reviewed and discussed.

Osimertinib Covalently Binds to CD34 and Eliminates Myeloid Leukemia Stem/Progenitor Cells.

Osimertinib is a third-generation covalent EGFR inhibitor that is used in treating non-small cell lung cancer. First-generation EGFR inhibitors were found to elicit pro-differentiation effect on acute myeloid leukemia (AML) cells in preclinical studies, but clinical trials yielded mostly negative results. Here, we report that osimertinib selectively induced apoptosis of CD34+ leukemia stem/progenitor cells but not CD34- cells in EGFR-negative AML and chronic myeloid leukemia (CML). Covalent binding of osimertinib to CD34 at cysteines 199 and 177 and suppression of Src family kinases (SFK) and downstream STAT3 activation contributed to osimertinib-induced cell death. SFK and STAT3 inhibition induced synthetic lethality with osimertinib in primary CD34+ cells. CD34 expression was elevated in AML cells compared with their normal counterparts. Genomic, transcriptomic, and proteomic profiling identified mutation and gene expression signatures of patients with AML with high CD34 expression, and univariate and multivariate analyses indicated the adverse prognostic significance of high expression of CD34. Osimertinib treatment induced responses in AML patient-derived xenograft models that correlated with CD34 expression while sparing normal CD34+ cells. Clinical responses were observed in two patients with CD34high AML who were treated with osimertinib on a compassionate-use basis. These findings reveal the therapeutic potential of osimertinib for treating CD34high AML and CML and describe an EGFR-independent mechanism of osimertinib-induced cell death in myeloid leukemia. SIGNIFICANCE: Osimertinib binds CD34 and selectively kills CD34+ leukemia cells to induce remission in preclinical models and patients with AML with a high percentage of CD34+ blasts, providing therapeutic options for myeloid leukemia patients.

Environmental fate and risk evolution of calcium channel blockers from chlorine-based disinfection to sunlit surface waters.

Organic micropollutants present in disinfected wastewater and discharged to sunlit surface waters may be transformed by multiple processes, such as chlorination due to the presence of chlorine residuals, solar irradiation as well as solar-irradiated chlorine residues. This study reports, for the first time, the multi-scenario degradation kinetics, transformation products, and risk evolution of calcium channel blockers (CCBs), a class of emerging pharmaceutical contaminants with worldwide prevalence in natural waters and wastewater. It was found that the chlorination of the studied CCBs (amlodipine (AML) and verapamil (VER)) was dominated by the reaction of HOCl with their neutral species, with second-order rate constants of 6.15×104 M-1 s-1 (AML) and 7.93×103 M-1 s-1 (VER) at pH 5.0-11.0. Bromination is much faster than chlorination, with the measured kapp,HOBr values of 2.94×105 M-1 s-1 and 6.58×103 M-1 s-1 for AML and VER, respectively, at pH 7.0. Furthermore, both CCBs would undergo photolytic attenuations with hydroxyl and carbonate radicals as the dominant reactive species in water. Notably, free chlorine mainly contributed to their abatement during the solar/chlorine treatment. Additionally, the halogen addition on the aromatic ring was observed during chlorination and bromination of the two CCBs. Cyclization was observed under solar irradiation only, while the aromatic ring was opened in the solar/chlorine system. Some products generated by the three transformation processes exhibited non-negligible risks of high biodegradation recalcitrance and toxicity, potentially threatening the aquatic environment and public health. Overall, this study elucidated the environmental fate of typical CCBs under different transformation processes to better understand the resulting ecological risks in these environmental scenarios.

Beyond ENO1, emerging roles and targeting strategies of other enolases in cancers.

Aerobic glycolysis is a hallmark property of cancer metabolism. Enolase is a glycolytic enzyme that catalyzes the conversion of 2-phosphoglycerate into phosphoenolpyruvate. In mammals, enolases exist in three isoforms, encoded by the genes ENO1, ENO2, and ENO3. The altered expression of enolases is a common occurrence in various types of cancer. Although most published studies on enolases have predominantly focused on the role of ENO1 in cancer, ENO2 and ENO3 have recently emerged as crucial regulatory molecules in cancer development. Significant progress has been made in understanding their multifaceted roles in oncogenesis. In this comprehensive review, we provide an overview of the structure, subcellular localization, diagnostic and prognostic significance, biological functions, and molecular mechanisms of ENO2 and ENO3 in cancer progression. The importance of enolase in cancer development makes it a novel therapeutic target for clinical applications. Furthermore, we discuss anticancer agents designed to target enolases and summarize their anticancer efficacy in both in vitro and in vivo studies.

TSPO is a novel biomarker for prognosis that regulates cell proliferation through influencing mitochondrial functions in HCC.

The disorder of mitochondrial functions plays a key role in oncogenesis. It is known that TSPO (18-kDa translocator protein) lies in a peculiar location at the interface between the mitochondria and the cytosol. TSPO is found in many types of tissues and is associated with multiple cellular processes, including apoptosis, cell proliferation and the regulation of mitochondria. However, the involvement of TSPO in hepatocellular carcinoma (HCC) remains unclear. In this study, we found that TSPO is upregulated in HCC tissue and is associated with poor differentiation and poor survival. Multivariate analyses showed that TSPO was an independent predictive factor for poor prognosis in HCC patients. For the first time, we provided evidence that TSPO knockdown suppressed HCC cell proliferation in vitro. Hence, TSPO knockdown-induced apoptosis by disturbing mitochondrial function by enhancing the formation of reactive oxygen species (ROS) and decreasing the mitochondrial membrane potential (ΔΨm). An assay exploring the underlying mechanism revealed that TSPO knockdown modulated apoptotic regulatory proteins by regulating the ERK signaling pathway. Through a functional assay and an in vivo mouse model, the anti-cancer effect of PK11195, a specific ligand of TSPO, on HCC was revealed. In summary, TSPO may potentially serve as a prognostic biomarker, and TSPO might be a potential therapeutic target for HCC.

Chinese expert consensus on the management of patients with hematologic malignancies infected with SARS-CoV-2.

In December 2022, the Omicron variant of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) became dominant in China due to its high infectivity and lower mortality rate. The risk of critical illness and mortality among patients with hematologic malignancies who contracted SARS-CoV-2 was particularly high. The aim of this study was to draft a consensus to facilitate effective treatments for these patients based on the type and severity of the disease. Following the outbreak of the novel coronavirus in China, a steering committee consisting of experienced hematologists was formed by the Specialized Committee of Oncology and Microecology of the Chinese Anti-Cancer Association. The expert group drafted a consensus on the management and intervention measures for different types of hematologic malignancies based on the clinical characteristics of the Omicron variant of the SARS-CoV-2 infection, along with relevant guidelines and literature. The expert group drafted independent recommendations on several important aspects based on the epidemiology of the Omicron variant in China and the unique vulnerability of patients with hematologic malignancies. These included prophylactic vaccinations for those with hematologic malignancies, the use of plasma from blood donors who recovered from the novel coronavirus infection, the establishment of negative pressure wards, the use of steady-state mobilization of peripheral blood hematopoietic stem cells, the provision of psychological support for patients and medical staff, and a focus on maintaining a healthy intestinal microecology.

Analgesia quality index improves the quality of postoperative pain management: a retrospective observational study of 14,747 patients between 2014 and 2021.

BACKGROUND: The application of artificial intelligence patient-controlled analgesia (AI-PCA) facilitates the remote monitoring of analgesia management, the implementation of mobile ward rounds, and the automatic recording of all types of key data in the clinical setting. However, it cannot quantify the quality of postoperative analgesia management. This study aimed to establish an index (analgesia quality index (AQI)) to re-monitor and re-evaluate the system, equipment, medical staff and degree of patient matching to quantify the quality of postoperative pain management through machine learning. METHODS: Utilizing the wireless analgesic pump system database of the Cancer Hospital Affiliated with Nantong University, this retrospective observational study recruited consecutive patients who underwent postoperative analgesia using AI-PCA from June 1, 2014, to August 31, 2021. All patients were grouped according to whether or not the AQI was used to guide the management of postoperative analgesia: The control group did not receive the AQI guidance for postoperative analgesia and the experimental group received the AQI guidance for postoperative analgesia. The primary outcome was the incidence of moderate-to-severe pain (numeric rating scale (NRS) score ≥ 4) and the second outcome was the incidence of total adverse reactions. Furthermore, indicators of AQI were recorded. RESULTS: A total of 14,747 patients were included in this current study. The incidence of moderate-to-severe pain was 26.3% in the control group and 21.7% in the experimental group. The estimated ratio difference was 4.6% between the two groups (95% confidence interval [CI], 3.2% to 6.0%; P < 0.001). There were significant differences between groups. Otherwise, the differences in the incidence of total adverse reactions between the two groups were nonsignificant. CONCLUSIONS: Compared to the traditional management of postoperative analgesia, application of the AQI decreased the incidence of moderate-to-severe pain. Clinical application of the AQI contributes to improving the quality of postoperative analgesia management and may provide guidance for optimum pain management in the postoperative setting.

An overview of meta-analyses on radiomics: more evidence is needed to support clinical translation.

OBJECTIVE: To conduct an overview of meta-analyses of radiomics studies assessing their study quality and evidence level. METHODS: A systematical search was updated via peer-reviewed electronic databases, preprint servers, and systematic review protocol registers until 15 November 2022. Systematic reviews with meta-analysis of primary radiomics studies were included. Their reporting transparency, methodological quality, and risk of bias were assessed by PRISMA (Preferred Reporting Items for Systematic reviews and Meta-Analyses) 2020 checklist, AMSTAR-2 (A MeaSurement Tool to Assess systematic Reviews, version 2) tool, and ROBIS (Risk Of Bias In Systematic reviews) tool, respectively. The evidence level supporting the radiomics for clinical use was rated. RESULTS: We identified 44 systematic reviews with meta-analyses on radiomics research. The mean ± standard deviation of PRISMA adherence rate was 65 ± 9%. The AMSTAR-2 tool rated 5 and 39 systematic reviews as low and critically low confidence, respectively. The ROBIS assessment resulted low, unclear and high risk in 5, 11, and 28 systematic reviews, respectively. We reperformed 53 meta-analyses in 38 included systematic reviews. There were 3, 7, and 43 meta-analyses rated as convincing, highly suggestive, and weak levels of evidence, respectively. The convincing level of evidence was rated in (1) T2-FLAIR radiomics for IDH-mutant vs IDH-wide type differentiation in low-grade glioma, (2) CT radiomics for COVID-19 vs other viral pneumonia differentiation, and (3) MRI radiomics for high-grade glioma vs brain metastasis differentiation. CONCLUSIONS: The systematic reviews on radiomics were with suboptimal quality. A limited number of radiomics approaches were supported by convincing level of evidence. CLINICAL RELEVANCE STATEMENT: The evidence supporting the clinical application of radiomics are insufficient, calling for researches translating radiomics from an academic tool to a practicable adjunct towards clinical deployment.

A systematic review of radiomics in giant cell tumor of bone (GCTB): the potential of analysis on individual radiomics feature for identifying genuine promising imaging biomarkers.

PURPOSE: To systematically assess the quality of radiomics research in giant cell tumor of bone (GCTB) and to test the feasibility of analysis at the level of radiomics feature. METHODS: We searched PubMed, Embase, Web of Science, China National Knowledge Infrastructure, and Wanfang Data to identify articles of GCTB radiomics until 31 July 2022. The studies were assessed by radiomics quality score (RQS), transparent reporting of a multivariable prediction model for individual prognosis or diagnosis (TRIPOD) statement, checklist for artificial intelligence in medical imaging (CLAIM), and modified quality assessment of diagnostic accuracy studies (QUADAS-2) tool. The radiomic features selected for model development were documented. RESULTS: Nine articles were included. The average of the ideal percentage of RQS, the TRIPOD adherence rate and the CLAIM adherence rate were 26%, 56%, and 57%, respectively. The risk of bias and applicability concerns were mainly related to the index test. The shortness in external validation and open science were repeatedly emphasized. In GCTB radiomics models, the gray level co-occurrence matrix features (40%), first order features (28%), and gray-level run-length matrix features (18%) were most selected features out of all reported features. However, none of the individual feature has appeared repeatably in multiple studies. It is not possible to meta-analyze radiomics features at present. CONCLUSION: The quality of GCTB radiomics studies is suboptimal. The reporting of individual radiomics feature data is encouraged. The analysis at the level of radiomics feature has potential to generate more practicable evidence for translating radiomics into clinical application.

221S-1a inhibits endothelial proliferation in pathological angiogenesis through ERK/c-Myc signaling.

Pathological angiogenesis plays a major role in many disease processes, including cancer and diabetic retinopathy. Antiangiogenic therapy is a potential management for pathologic angiogenesis. The novel synthetic compound 221S-1a, derived from captopril, tanshinol and borneol, may have antiangiogenic properties. On the basis of MS, NMR and HPLC analysis, the structure of 221S-1a was identified. The cellular uptake and metabolism of this compound was also observed. Next, the antiangiogenic properties of 221S-1a were evaluated in tumor-xenograft and OIR models in vivo. The inhibitory properties of 221S-1a on endothelial cell proliferation, migration, tube formation and sprouting were detected in vitro. Furthermore, 221S-1a induced G1/S phase arrest was detected by PI staining flow cytometry analysis and Cyclin D, Cyclin E expression. 221S-1a inhibited ERK1/2 activation and nuclear translocation, in addition to downregulation of c-Myc, a transcription factor that regulates cell cycle progression. Molecular docking indicated the interaction of 221S-1a with the ATP-binding site of ERK2, leading to the inhibition of ERK2 phosphorylation and a concomitant inhibition of ERK1 phosphorylation. In conclusion, 221S-1a inhibited the G1/S phase transition by blocking the ERK1/2/c-Myc pathway to reduce tumor and OIR retinal angiogenesis. These novel findings suggest that 221S-1a is a potential pharmacologic candidate for treating pathological angiogenesis.

The Circadian System Is Essential for the Crosstalk of VEGF-Notch-mediated Endothelial Angiogenesis in Ischemic Stroke.

Ischemic stroke is a major public health problem worldwide. Although the circadian clock is involved in the process of ischemic stroke, the exact mechanism of the circadian clock in regulating angiogenesis after cerebral infarction remains unclear. In the present study, we determined that environmental circadian disruption (ECD) increased the stroke severity and impaired angiogenesis in the rat middle cerebral artery occlusion model, by measuring the infarct volume, neurological tests, and angiogenesis-related protein. We further report that Bmal1 plays an irreplaceable role in angiogenesis. Overexpression of Bmal1 promoted tube-forming, migration, and wound healing, and upregulated the vascular endothelial growth factor (VEGF) and Notch pathway protein levels. This promoting effect was reversed by the Notch pathway inhibitor DAPT, according to the results of angiogenesis capacity and VEGF pathway protein level. In conclusion, our study reveals the intervention of ECD in angiogenesis in ischemic stroke and further identifies the exact mechanism by which Bmal1 regulates angiogenesis through the VEGF-Notch1 pathway.

Oligomer-to-monomer transition underlies the chaperone function of AAGAB in AP1/AP2 assembly.

Assembly of protein complexes is facilitated by assembly chaperones. Alpha and gamma adaptin-binding protein (AAGAB) is a chaperone governing the assembly of the heterotetrameric adaptor complexes 1 and 2 (AP1 and AP2) involved in clathrin-mediated membrane trafficking. Here, we found that before AP1/2 binding, AAGAB exists as a homodimer. AAGAB dimerization is mediated by its C-terminal domain (CTD), which is critical for AAGAB stability and is missing in mutant proteins found in patients with the skin disease punctate palmoplantar keratoderma type 1 (PPKP1). We solved the crystal structure of the dimerization-mediating CTD, revealing an antiparallel dimer of bent helices. Interestingly, AAGAB uses the same CTD to recognize and stabilize the γ subunit in the AP1 complex and the α subunit in the AP2 complex, forming binary complexes containing only one copy of AAGAB. These findings demonstrate a dual role of CTD in stabilizing resting AAGAB and binding to substrates, providing a molecular explanation for disease-causing AAGAB mutations. The oligomerization state transition mechanism may also underlie the functions of other assembly chaperones.

Oncogenic role of microRNA-19b-3p-mediated SOCS3 in glioma through activation of JAK-STAT pathway.

The altered expression of microRNA (miRNA) has been implicated in glioma. Here, the current study aimed to clarify the oncogenic effects of miR-19b-3p on cellular processes of glioma and to elucidate the underlying mechanism associated with SOCS3 and the JAK-STAT signaling pathway. Differentially expressed genes related to glioma were initially identified via microarray analysis. Twenty-five glioma patients were selected for clinical data collection, while additional 12 patients with traumatic brain injuries were selected as controls. Cell senescence was assessed by ß-galactosidase staining, proliferation by MTT assay and apoptosis by flow cytometry following gain- and/or loss-of-function of miR-19b-3p or SOCS3. Glioma xenograft mouse model was developed through subcutaneous injection to nude mice to provide evidence in vivo. The glioma patients exhibited overexpressed miR-19b-3p and poorly-expressed SOCS3. SOCS3 was identified as a target gene of miR-19b-3p through dual-luciferase reporter gene assay. miR-19b-3p repressed SOCS3 expression and activated the JAK-STAT signaling pathway. Furthermore, miR-19b-3p inhibition promoted apoptosis and senescence, and suppressed cell proliferation through inactivation of the JAK-STAT signaling pathway and up-regulation of SOCS3. The reported regulatory axis was validated in nude mice as evidenced by suppressed tumor growth. Taken together, this study demonstrates that miR-19b-3p facilitates glioma progression via activation of the JAK-STAT signaling pathway by targeting SOCS3, highlighting a novel therapeutic target for glioma treatment.

Localized ablative immunotherapy drives de novo CD8+ T-cell responses to poorly immunogenic tumors.

BACKGROUND: Localized ablative immunotherapies hold great promise in stimulating antitumor immunity to treat metastatic and poorly immunogenic tumors. Tumor ablation is well known to release tumor antigens and danger-associated molecular patterns to stimulate T-cell immunity, but its immune stimulating effect is limited, particularly against metastatic tumors. METHODS: In this study, we combined photothermal therapy with a potent immune stimulant, N-dihydrogalactochitosan, to create a local ablative immunotherapy which we refer to as laser immunotherapy (LIT). Mice bearing B16-F10 tumors were treated with LIT when the tumors reached 0.5 cm3 and were monitored for survival, T-cell activation, and the ability to resist tumor rechallenge. RESULTS: We found that LIT stimulated a stronger and more consistent antitumor T-cell response to the immunologically 'cold' B16-F10 melanoma tumors and conferred a long-term antitumor memory on tumor rechallenge. Furthermore, we discovered that LIT generated de novo CD8+ T-cell responses that strongly correlated with animal survival and tumor rejection. CONCLUSION: In summary, our findings demonstrate that LIT enhances the activation of T cells and drives de novo antitumor T-cell responses. The data presented herein suggests that localized ablative immunotherapies have great potential to synergize with immune checkpoint therapies to enhance its efficacy, resulting in improved antitumor immunity.

Chlorination of methotrexate in water revisited: Deciphering the kinetics, novel reaction mechanisms, and unexpected microbial risks.

Chlorination of a typical anticancer drug with annually ascending use and global prevalence (methotrexate, MTX) in water has been studied. In addition to the analysis of kinetics in different water/wastewater matrices, high-resolution product identification and in-depth secondary risk evaluation, which were eagerly urged in the literature, were performed. It was found that the oxidation of MTX by free available chlorine (FAC) followed first-order kinetics with respect to FAC and first-order kinetics with respect to MTX. The pH-dependent rate constants (kapp) ranged from 170.00 M-1 s-1 (pH 5.0) to 2.68 M-1 s-1 (pH 9.0). The moiety-specific kinetic analysis suggested that 6 model substructures of MTX exhibited similar reactivity to the parent compound at pH 7.0. The presence of Br- greatly promoted MTX chlorination at pH 5.0-9.0, which may be ascribed to the formation of bromine with higher reactivity than FAC. Comparatively, coexisting I- or humic acid inhibited the degradation of MTX by FAC. Notably, chlorination effectively abated MTX in different real water matrices. The liquid chromatography-high resolution mass spectrometry analysis of multiple matrix-mediated chlorinated samples indicated the generation of nine transformation products (TPs) of MTX, among which seven were identified during FAC oxidation for the first time. In addition to the reported electrophilic chlorination of MTX (the major and dominant reaction pathway), the initial attacks on the amide and tertiary amine moieties with C-N bond cleavage constitute novel reaction mechanisms. No genotoxicity was observed for MTX or chlorinated solutions thereof, whereas some TPs were estimated to show multi-endpoint aquatic toxicity and higher biodegradation recalcitrance than MTX. The chlorinated mixtures of MTX with or without Br- showed a significant ability to increase the conjugative transfer frequency of plasmid-carried antibiotic resistance genes within bacteria. Overall, this work thoroughly examines the reaction kinetics together with the matrix effects, transformation mechanisms, and secondary environmental risks of MTX chlorination.

Correlation of magnetic resonance imaging quantitative parameters and apparent diffusion coefficient value with pathological breast cancer.

BACKGROUND: China ranks 120th worldwide for the incidence of breast cancer and 163rd for mortality. Early screening, diagnosis, and timely determination of the optimal treatment plan can help ensure clinical efficacy and prognosis. AIM: To investigate the relationship between quantitative magnetic resonance imaging parameters, apparent diffusion coefficient value, pathological immunohistochemical status, and patient prognosis. METHODS: A total of 108 patients with breast cancer (breast cancer group) and 110 patients with benign breast tumors (benign group) confirmed by pathological examination at our Hospital from September 2013 to August 2016 were selected. All patients had undergone preoperative magnetic resonance imaging (MRI) examinations, and the quantitative parameters of MRI and apparent diffusion coefficient (ADC) values for the two groups were compared. The MRI quantitative parameters and ADC values of patients with different estrogen receptor (ER), progesterone receptor, and human epidermal growth factor receptor-2 expression were statistically analyzed. The relationship between the quantitative parameters of MRI and ADC values and patient recurrence was analyzed using receiver operating curves. RESULTS: The measured values of the quantitative parameters of MRI- Ktrans, Kep, and Ve in the breast cancer group were higher than those in the benign group; the ADC value in the breast cancer group was lower than that in the benign group, and the difference was statistically significant (P < 0.05). The Ktrans, Ve, and ADC values in patients with ER-positive breast cancer were significantly lower than those in patients with negative ER expression (P < 0.05). After 5 years of follow-up, 22 patients with breast cancer experienced postoperative recurrence. The Kep, Ve, and ADC values of the recurrence group were significantly lower than those of the non-recurrence group, and the difference was statistically significant (P < 0.05). CONCLUSION: MRI quantitative parameters and ADC are related to the expression of breast cancer-related immunological receptor factors and have certain clinical value in assessing postoperative recurrence in patients.

Common carotid artery thrombosis and malignant middle cerebral artery infarction following ovarian hyperstimulation syndrome: A case report.

BACKGROUND: Arterial thrombosis is a serious and rare complication of ovarian hyperstimulation syndrome (OHSS). Herein, we describe a case of OHSS complicated by common carotid artery thrombosis and malignant middle cerebral artery infarction after egg retrieval and before embryo transfer. CASE SUMMARY: A 32-year-old female with a family history of thrombosis who was undergoing in vitro fertilization due to unexplained infertility, was admitted due to abdominal distension for 3 d and coma for 2 h. She received egg retrieval 7 d ago and embryo transfer had not yet been performed. Blood biochemical analysis showed estrogen of 15781 pmol/L. Gynecological examination showed palpable masses on both sides of the adnexal areas. Ultrasound observed enlarged ovaries and abdominal ascites. Imaging examination of the head and neck revealed fresh malignant middle cerebral artery infarction in the left side of brain and internal carotid artery as well as occlusion in the left carotid artery, internal carotid artery, and middle cerebral artery. The patient was finally diagnosed with severe OHSS, complicated by common carotid artery thrombosis and malignant middle cerebral artery infarction. Liquid replacement, anticoagulation, vascular endothelium protection, brain protection and decompressive craniectomy were carried out. Rehabilitation training was then performed for 6 mo. At present, she has poor speaking ability and decreased muscle strength on the right side. CONCLUSION: There is a risk of thrombosis during any period of OHSS. During in vitro assisted reproduction, for cases with a family history of thrombosis, hyperlipidemia and other high-risk factors, serum lipid levels should be controlled as soon as possible to improve metabolic dysfunction. When thrombosis occurs, timely and effective treatment should be performed to improve the prognosis.

An updated systematic review of radiomics in osteosarcoma: utilizing CLAIM to adapt the increasing trend of deep learning application in radiomics.

OBJECTIVE: To update the systematic review of radiomics in osteosarcoma. METHODS: PubMed, Embase, Web of Science, China National Knowledge Infrastructure, and Wanfang Data were searched to identify articles on osteosarcoma radiomics until May 15, 2022. The studies were assessed by Radiomics Quality Score (RQS), Transparent Reporting of a multivariable prediction model for Individual Prognosis Or Diagnosis (TRIPOD) statement, Checklist for Artificial Intelligence in Medical Imaging (CLAIM), and modified Quality Assessment of Diagnostic Accuracy Studies (QUADAS-2) tool. The evidence supporting radiomics application for osteosarcoma was rated according to meta-analysis results. RESULTS: Twenty-nine articles were included. The average of the ideal percentage of RQS, the TRIPOD adherence rate and the CLAIM adherence rate were 29.2%, 59.2%, and 63.7%, respectively. RQS identified a radiomics-specific issue of phantom study. TRIPOD addressed deficiency in blindness of assessment. CLAIM and TRIPOD both pointed out shortness in missing data handling and sample size or power calculation. CLAIM identified extra disadvantages in data de-identification and failure analysis. External validation and open science were emphasized by all the above three tools. The risk of bias and applicability concerns were mainly related to the index test. The meta-analysis of radiomics predicting neoadjuvant chemotherapy response by MRI presented a diagnostic odds ratio (95% confidence interval) of 28.83 (10.27-80.95) on testing datasets and was rated as weak evidence. CONCLUSIONS: The quality of osteosarcoma radiomics studies is insufficient. More investigation is needed before using radiomics to optimize osteosarcoma treatment. CLAIM is recommended to guide the design and reporting of radiomics research.