Feasibility study on the clinical application of CT-based synthetic brain T1-weighted MRI: comparison with conventional T1-weighted MRI.

OBJECTIVES: This study aimed to examine the equivalence of computed tomography (CT)-based synthetic T1-weighted imaging (T1WI) to conventional T1WI for the quantitative assessment of brain morphology. MATERIALS AND METHODS: This prospective study examined 35 adult patients undergoing brain magnetic resonance imaging (MRI) and CT scans. An image synthesis method based on a deep learning model was used to generate synthetic T1WI (sT1WI) from CT data. Two senior radiologists used sT1WI and conventional T1WI on separate occasions to independently measure clinically relevant brain morphological parameters. The reliability and consistency between conventional and synthetic T1WI were assessed using statistical consistency checks, comprising intra-reader, inter-reader, and inter-method agreement. RESULTS: The intra-reader, inter-reader, and inter-method reliability and variability mostly exhibited the desired performance, except for several poor agreements due to measurement differences between the radiologists. All the measurements of sT1WI were equivalent to that of T1WI at 5% equivalent intervals. CONCLUSION: This study demonstrated the equivalence of CT-based sT1WI to conventional T1WI for quantitatively assessing brain morphology, thereby providing more information on imaging diagnosis with a single CT scan. CLINICAL RELEVANCE STATEMENT: Real-time synthesis of MR images from CT scans reduces the time required to acquire MR signals, improving the efficiency of the treatment planning system and providing benefits in the clinical diagnosis of patients with contraindications such as presence of metal implants or claustrophobia. KEY POINTS: • Deep learning-based image synthesis methods generate synthetic T1-weighted imaging from CT scans. • The equivalence of synthetic T1-weighted imaging and conventional MRI for quantitative brain assessment was investigated. • Synthetic T1-weighted imaging can provide more information per scan and be used in preoperative diagnosis and radiotherapy.

Retroperitoneoscopic enucleation adrenalectomy: a viable surgical option for small nonsecreting adrenal tumors with low potential of malignancy.

Laparoscopic total adrenalectomy has become the standard treatment for adrenal mass. Meanwhile, there has been a growing trend toward laparoscopic adrenal-sparing surgery worldwide to avoid the risk and potential complications of adrenal insufficiency. The objectives of this study were to describe a retroperitoneoscopic adrenal tumor enucleation technique, to assess the clinical outcomes of this technique in the treatment of 20-40 mm nonsecreting adrenal tumor (NAT) with low potential of malignancy, and to provide a feasible choice for patients who have preference on resection. This study was a retrospective analysis of 61 patients with low potential of malignancy in 20-40 mm NAT identified at the first imaging examination or during follow-up. All patients were scheduled for planned enucleation adrenalectomy by a single surgeon between July 2016 and December 2020 in Xuanwu Hospital, Beijing, China. In all patients, retroperitoneoscopic surgery was performed via a retroperitoneoscopic process for all the patients. The crucial techniques of enucleation are presented in the video. Safety and feasibility factors of enucleation technique were measured for this study. No blood transfusion or organ injury was registered during the operation. The median operation time was 75 min, and the median blood loss was 35 mL. All operations were successfully performed without open conversion. A total of 58 patients received successful enucleation surgery. Three cases were converted to retroperitoneoscopic total adrenalectomy. In this study, surgical outcomes of retroperitoneoscopic enucleation adrenalectomy as a method to remove adrenal tumors were assessed. This procedure is a feasible and safe technique with the added benefit of preserving the remaining functional adrenal tissue.

Imaging diagnostic features of intracranial primary extranodal Rosai-Dorfman disease: Two case reports and literature review.

In this report, we describe 2 cases of rare intracranial extranodal Rosai-Dorfman disease. The occurrence of this type of non-Langerhans cell histiocytosis in the central nervous system is infrequent, with less than 5% of cases. The first patient was a 35-year-old male who presented with recurring headaches, and the second patient was a 50-year-old male who reported sudden onset of dizziness and vomiting. Computed tomography scans were performed in both cases, but magnetic resonance imaging played a crucial role in the characterization of the lesions and their locations in the thalamus, third ventricle, lateral ventricles, and cerebellopontine angle area. The final diagnosis was confirmed through pathological examination and immunohistochemistry following brain tumor resection. These cases underscore the significance of magnetic resonance imaging in the early diagnosis of intracranial extranodal Rosai-Dorfman disease.

ERCC6L promotes cell growth and metastasis in gastric cancer through activating NF-κB signaling.

ERCC6L has been reported to act as a potential oncogenic protein in various cancers. However, the role of ERCC6L in the progression of gastric cancer (GC) remains to be elucidated. Herein, we aimed to assess the clinical significance, the role, and the underlying mechanism of ERCC6L in GC progression. In this study, the mRNA and protein expression levels of ERCC6L were measured in GC specimens by quantitative real-time PCR (qRT-PCR), Western blot, and immunohistochemistry, and its clinical significance was assessed. The effect of ERCC6L overexpression or knockdown on GC cell growth, migration, and invasion was explored by functional experiments. Notably, the possible mechanisms underlying the action of ERCC6L were also investigated. We found that ERCC6L was upregulated in GC tissues, and its expression was associated with tumor size, clinical stage, and poor prognosis in GC patients. Besides, ERCC6L facilitated GC cell proliferation and metastasis in vitro and in vivo. Mechanically, ERCC6L modulated GC cell behavior via activation of NF-κB signaling. Our results indicated that ERCC6L played a critical role in GC progression and metastasis. In addition, ERCC6L promoted GC cell growth and metastasis via activation of NF-κB signaling, thus possibly providing a target for GC.

An imbalance between blood CD4+CXCR5+Foxp3+ Tfr cells and CD4+CXCR5+Tfh cells may contribute to the immunopathogenesis of rheumatoid arthritis.

BACKGROUND: Follicular helper T (Tfh) cells are a subgroup of activated CD4+ T cells which can assist the formation and maintenance of germinal centers. Follicular regulatory T (Tfr) cells are a new class of regulatory T cells which play a major role in suppressing cells in humoral immunity. In contrast to the role of Tfh cells, Tfr cells can inhibit the function of Tfh cells and B cells. Imbalance of blood Tfr/Tfh ratio resulted in the expansion of auto-reactive B cells and auto-antibody production (). However, the effect of Tfr cells and Tfh cells in the pathogenesis of RA (rheumatoid arthritis) is unclear. The purpose of this study was to investigate the function of Tfr cells and Tfh cells in the pathogenesis of RA. METHODS: We recruited 20 patients fulfilled the the American College of Rheumatology diagnosis criteria and 20 healthy controls (HCs). The number of CD4+CXCR5+Foxp3+ Tfr cells and CD4+CXCR5+ Tfh cells in 20 RA patients were measured by flow cytometry analysis. Furthermore, the correlations between the Tfr/Tfh ratio and the characteristic clinical parameters were assessed. The serum levels of IL-21(interleukin-21), CXCL13 (chemokine (C-X-C motif) ligand 13) and TGF-ß (Transforming growth factor-ß) were measured by ELISA. The formation of ectopic germinal center (GC) of synovial membrane was examined by H&E staining. The transcriptional levels of CXCR5 (C-X-C chemokine receptor type 5), CXCL13, ICOS (inducible co-stimulater) and TGF-ß mRNA were also analyzed. In addition, the expression of Bcl-6 (B-cell lymphoma 6), CXCR5, CXCL13 and ICOS in synovial membrane were examined by immunohistochemistry. RESULTS: RA patients had more Tfh cells in peripheral blood, conversely, the frequency of blood Tfr cells (p < 0.05) and the ratio of Tfr/Tfh were significantly decreased compared to healthy controls (p < 0.05, p < 0.01). Furthermore, the ratio of Tfr/Tfh was negatively correlated with values of ESR (r=-0.57, p < 0.05), RF (r=-0.5275, p < 0.001), CRP (r=-0.4486, p < 0.001), IgG (r=-0.4631, p < 0.05), DAS28 scores (r=-0.5645, p < 0.01), as well as the levels of IL-21(r=-0.7398, p < 0.01), CXCL13 (r=-0.4832, p < 0.05). However, the ratio of Tfr/Tfh was positively with the serum level of TGF-ß (r=0.5115, p < 0.05). Higher mRNA expression of CXCR5, CXCL13, ICOS and lower TGF-ß mRNA expression were observed in RA patients. The serum expression level of IL-21, CXCL13 was significantly increased and expression of TGF-ß was significantly decreased in RA patients. Furthermore, ectopic germinal center formation and higher expression of Bcl-6, CXCR5, ICOS, CXCL13 in the synovial membrane of the joints in RA patients were observed. CONCLUSIONS: The decreased blood CD4+CXCR5+Foxp3+ Tfr cells/CD4+CXCR5+ Tfh cells may be responsible for the immunopathogenesis of RA.

High versus low ligation of inferior mesenteric artery during laparoscopic radical resection of rectal cancer: A retrospective cohort study.

Laparoscopic radical resection is standard treatment for resectable rectal cancer. However, whether high or low inferior mesenteric artery (IMA) ligation should be performed remains controversial. This retrospective cohort study compared the advantages and disadvantages of low vs high IMA ligation in patients undergoing laparoscopic total mesorectal excision for rectal cancer.Rectal cancer patients (n = 322) undergoing total mesorectal excision at our institution in 2010 to 17 were enrolled; 174 underwent high IMA ligation group and 148 low IMA ligation (LIMAL group). Baseline data on patients, operative indices, economic indices, pathology findings, perioperative complications, and survival in the 2 groups were analyzed retrospectively.The low IMA ligation group had significantly higher anus retention ratio (P = .022), shorter hospital stay (P = .025), lower medical expenses (P = .032), fewer cases of anastomotic leakage (P = .023) and anastomotic stricture (P < .001), and lower incidence of postoperative genitourinary dysfunction (P = .003). Cox regression analysis indicated that local recurrence, distant metastasis, tumor differentiation, and tumor-node-metastasis stage were independently associated with survival.Low ligation of the IMA during laparoscopic radical resection of rectal cancer appears to be associated with a lower risks for anastomotic leakage, anastomotic stricture, and genitourinary dysfunction, a shorter hospital stay, and lower costs. In contrast, the rate of lymph node harvest, tumor recurrence rate, metastasis, or mortality was not found to be related with the level of IMA ligation.

TYRO3 facilitates cell growth and metastasis via activation of the Wnt/ß-catenin signaling pathway in human gastric cancer cells.

It has become increasingly important to identify valuable therapeutic targets to improve the prognosis of cancer patients. Although emerging evidence has suggested TYRO3 as a potential therapeutic target in various types of cancers, less is known about its role in gastric cancer (GC) development. Herein, we investigated the functional and molecular mechanisms by which TYRO3 influenced GC. TYRO3 mRNA and protein were evaluated by quantitative real-time PCR (qRT-PCR), western blotting, and immunohistochemistry. Other methods including stable transfection of TYRO3 into GC cells, wound healing, Transwell assays, CCK-8 assays, colony formation assays, immunocytochemistry in vitro, and tumorigenesis in vivo were also conducted. Our results indicated that high levels of TYRO3 significantly correlated with clinical metastasis and poor prognoses in patients with GC. In addition, TYRO3 silencing distinctively suppressed GC cell growth, invasion, and metastasis both in vitro and in vivo. Conversely, TYRO3 overexpression led to the opposite effects. Mechanistic analyses revealed that the Wnt/ß-catenin signaling pathway might be involved in TYRO3-facilitated GC cell behavior. Collectively, we demonstrated that elevated TYRO3 expression contributed to GC cell growth and metastasis via the Wnt/ß-catenin pathway, suggesting a novel therapeutic target for GC.

Relationship between intracranial pressure and phase-contrast cine MRI-derived measures of cerebrospinal fluid parameters in communicating hydrocephalus.

BACKGROUND: To explore the correlation between intracranial pressure (ICP) and cerebrospinal fluid (CSF) parameters assessed by phase-contrast cine MRI (PC-MRI). METHODS: Fifteen normal people and 80 subjects with communicating hydrocephalus who underwent PC-MRI examinations from a single center were included in this cross-sectional study. In addition to recording patient's age, heart rate, blood pressure and body mass index (BMI), ICP and CSF hemodynamic parameters, such as flow velocity and aqueduct diameter, were measured for correlation analysis. RESULTS: The mean ICP and CSF aqueduct diameter in hydrocephalus patients were 151.05 mmH2O and 2.877 mm, respectively, and the maximum (6.938 cm/s) and mean (0.845 cm/s) CSF flow velocities were significantly higher in these patients compared with the controls (P<0.05). After adjusting for age, heart rate, blood pressure, and BMI, there was no significant relationship between peak velocity and ICP (P>0.05). Furthermore, a nonlinear relationship was observed between the ICP and the average velocity of CSF, and the ICP and aqueduct diameter. The ICP increased with the average velocity above 1.628 cm/s (P≤0.01), and the aqueduct diameter increased more than 3.6 mm (P<0.001). CONCLUSIONS: This study found significant correlations between ICP and average velocity and aqueduct diameter. These findings can be useful in assisting clinicians in predicting ICP more effectively, thus improving patient management.

A-kinase-interacting protein 1 facilitates growth and metastasis of gastric cancer cells via Slug-induced epithelial-mesenchymal transition.

A-kinase-interacting protein 1 (AKIP1) has previously been reported to act as a potential oncogenic protein in various cancers. The clinical significance and biological role of AKIP1 in gastric cancer (GC) is, however, still elusive. Herein, this study aimed to investigate the functional and molecular mechanism by which AKIP1 influences GC. AKIP1 mRNA and protein expressions in GC tissues were examined by quantitative real-time PCR (qRT-PCR), Western blot and immunohistochemistry. Other methods including stably transfected against AKIP1 into gastric cancer cells, wound healing, transwell assays, CCK-8, colony formation, qRT-PCR and Western blot in vitro and tumorigenesis in vivo were also performed. The up-regulated expression of AKIP1 in GC specimens significantly correlated with clinical metastasis and poor prognosis in patients with GC. AKIP1 knockdown markedly suppressed GC cells proliferation, invasion and metastasis both in vitro and in vivo. In contrast, AKIP1 overexpression resulted in the opposite effects. Moreover, mechanistic analyses indicated that Slug-induced epithelial-mesenchymal transition (EMT) might be responsible for AKIP1-influenced GC cells behaviour. Our findings demonstrated that high AKIP1 expression significantly correlated with clinical metastasis and unfavourable prognosis in patients with GC. Additionally, AKIP1 promoted GC cells proliferation, migration and invasion by activating Slug-induced EMT.

CD4+CXCR5+PD-1+ T Follicular Helper Cells Play a Pivotal Role in the Development of Rheumatoid Arthritis.

BACKGROUND T follicular helper (Tfh) cells are a subgroup of activated CD4+ T cells in the germinal centers of secondary lymphoid organs, they play critical roles in the development of many chronic autoimmune inflammatory diseases. The aim of this study was to investigate whether circulating Tfh cells contribute to the development of rheumatoid arthritis (RA). MATERIAL AND METHODS Thirty patients fulfilled the diagnosis criteria that was established by the American College of Rheumatology and 30 healthy controls were recruited. The frequency of Tfh cells in patients and collagen-induced arthritis (CIA) in DBA/1J mice were analyzed by flow cytometry. The serum IL-21 level was examined by enzyme-linked immunosorbent assay (ELISA). The mRNA expression of Blimp-1 and Bcl-6 were detected by qRT-PCR. RESULTS RA patients had more CD4⁺PD-1⁺CXCR5⁺ Tfh cells in peripheral blood compared with healthy controls, and CIA in DBA/1J mice showed similar results. Higher mRNA expression of Bcl-6 and lower Blimp-1 mRNA expression were observed in patients with RA compared to healthy controls, and the expression level of IL-21 was higher in RA patients, which was also seen in CIA mice. Furthermore, the spleen CD4⁺ICOS⁺CXCR5⁺ Tfh cells in CIA mice show significantly higher frequency than that in the control mice. The percentage of CD4⁺PD-1⁺CXCR5⁺ Tfh cells was correlated positively with the values of erythrocyte sedimentation rate (ESR) (r=0.968, P<0.001), rheumatoid factor (RF) (r=0.962, P<0.001), C-reactive protein (CRP) (r=0.953, P<0.001), and anti-cyclic citrullinated peptide antibodies (ACPA) (r=0.966, P<0.001), and the level of serum interleukin (IL)-21 in RA patients showed positive correlation with ESR (r=0.982, P<0.001), RF (r=0.959, P<0.001), CRP (r=0.951, P<0.001), and ACPA (r=0.971, P<0.001) as well. CONCLUSIONS The activated Tfh cells in the peripheral blood may be responsible for the development of RA.

TRIM37 promotes cell invasion and metastasis by regulating SIP1-mediated epithelial-mesenchymal transition in gastric cancer.

BACKGROUND: Tripartite motif containing 37 (TRIM37) has been demonstrated to function importantly during the progression of various cancers. However, the role of TRIM37 in gastric cancer (GC) remains elusive. MATERIALS AND METHODS: TRIM37 mRNA and protein expressions were determined by qRT-PCR, Western blot, and immunohistochemical staining in GC specimens. The effects of TRIM37 on GC cells behavior were evaluated by transwell assays in vitro and metastasis assay in vivo, respectively. Besides, qRT-PCR, Western blot, and immunofluorescence staining were employed to detect the expressions of TRIM37 and epithelial-mesenchymal transition (EMT)-related markers. RESULTS: The present study revealed that TRIM37 mRNA or protein expression was significantly increased in GC tissues compared with that in paracancerous control tissues, and its aberrant overexpression was closely associated with clinical metastasis and poor prognosis in patients with GC. TRIM37 knockdown significantly suppressed GC cells migration and invasion in vitro, as well as metastasis in vivo. Inversely, TRIM37 overexpression exerted the opposite effects. Mechanistic studies suggested that SIP1-mediated EMT might be responsible for TRIM37-facilitated GC cells migration and invasion. CONCLUSION: Our findings revealed that high TRIM37 expression was associated with clinical metastasis and poor survival in patients with GC. TRIM37 promoted GC cells migration and invasion via EMT, mediated by the transcription factor SIP1, thus providing a candidate target for GC treatment.

CPEB4 promotes growth and metastasis of gastric cancer cells via ZEB1-mediated epithelial- mesenchymal transition.

BACKGROUND: Cytoplasmic polyadenylation element-binding protein 4 (CPEB4) has previously been reported to be associated with biological malignancy in various cancers. However, its function in tumor growth and metastasis in gastric cancer (GC) remains obscure. Here, we explored the functional and molecular mechanisms by which CPEB4 influences GC. MATERIALS AND METHODS: The expression of CPEB4 was assessed using Western blot and immunohistochemistry in GC specimens. The roles of CPEB4 in GC cell proliferation, migration, and invasion were investigated by cell-counting kit-8 (CCK-8), colony formation, and EdU assay; wound-healing assay; and transwell assay, respectively. Quantitative real-time PCR (qRT-PCR), Western blot, and immunofluorescence staining were performed to detect the expressions of CPEB4 and epithelial-mesenchymal transition (EMT)-related markers. The function of CPEB4 on GC cell growth and metastasis was also determined in vivo through establishing subcutaneous xenograft tumor and lung metastatic mice model. RESULTS: The results revealed that the expression of CPEB4 was increased in GC tissues compared with matched normal tissues. High expression level of CPEB4 was significantly associated with clinical metastasis and unfavorable prognosis in patients with GC. Furthermore, CPEB4 silencing remarkably inhibited GC cells' proliferation, invasion, and metastasis in vitro and in vivo. Conversely, CPEB4 overexpression achieved the opposite effects. Mechanically, we proved that ZEB1-mediated EMT might be involved in CPEB4-facilitated GC cells' proliferation, invasion, and metastasis. CONCLUSION: Our findings implied that CPEB4 expression predicted a worse prognosis in patients with GC. Besides, CPEB4 contributed to GC cells' proliferation, migration, and invasion via ZEB1-mediated EMT.

Alpha B-crystallin promotes the invasion and metastasis of gastric cancer via NF-κB-induced epithelial-mesenchymal transition.

Alpha B-crystallin (CRYAB) is overexpressed in a variety of cancers. However, little is known about its specific function and regulatory mechanism in gastric cancer. Here, we first explore the role of CRYAB in gastric cancer progression and metastasis. The expression of CRYAB was determined by western blot and immunohistochemistry in gastric cancer tissues. Besides, methods including stably transfected against CRYAB into gastric cancer cells, western blot, migration and invasion assays in vitro and metastasis assay in vivo were also conducted. The expression of CRYAB is up-regulated in gastric cancer tissues compared with matched normal tissues. High expression level of CRYAB is closely correlated with cancer metastasis and shorter survival time in patients with gastric cancer. Additionally, CRYAB silencing significantly suppresses epithelial-mesenchymal transition (EMT), migration and invasion of gastric cancer cells in vitro and in vivo, whereas CRYAB overexpression dramatically reverses these events. Mechanically, CRYAB facilitates gastric cancer cells invasion and metastasis via nuclear factor-κ-gene binding (NF-κB)-regulated EMT. These findings suggest that CRYAB expression predicts a poor prognosis in patients with gastric cancer. Besides, CRYAB contributes to gastric cancer cells migration and invasion via EMT, mediated by the NF-κB signalling pathway, thus possibly providing a novel therapeutic target for gastric cancer.

SPOCK1 promotes the invasion and metastasis of gastric cancer through Slug-induced epithelial-mesenchymal transition.

Metastasis is a crucial impediment to the successful treatment for gastric cancer. SPOCK1 has been demonstrated to facilitate cancer metastasis in certain types of cancers; however, the role of SPOCK1 in the invasion and metastasis of gastric cancer remains elusive. SPOCK1 and epithelial-mesenchymal transition (EMT)-related biomarkers were detected by immunohistochemistry and Western blot in gastric cancer specimens. Other methods including stably transfected against SPOCK1 into gastric cancer cells, Western blot, migration and invasion assays in vitro and metastasis assay in vivo were also performed. The elevated expression of SPOCK1 correlates with EMT-related markers in human gastric cancer tissue, clinical metastasis and a poor prognosis in patients with gastric cancer. In addition, knockdown of SPOCK1 expression significantly inhibits the invasion and metastasis of gastric cancer cells in vitro and in vivo, inversely, SPOCK1 overexpression results in the opposite effect. Interestingly, SPOCK1 expression has no effect on cell proliferation in vitro and in vivo. Regarding the mechanism(s) of SPOCK1-induced cells invasion and metastasis, we prove that Slug-induced EMT is involved in SPOCK1-facilitating gastric cancer cells invasion and metastasis. The elevated SPOCK1 expression is closely correlated with cancer metastasis and patient survival, and SPOCK1 promotes the invasion and metastasis of gastric cancer through Slug-mediated EMT, thereby possibly providing a novel therapeutic target for gastric cancer.