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Endoscopic Ultrasound 2024Endobronchial ultrasound (EBUS) imaging is a valuable tool for predicting lymph node (LN) metastasis in lung cancer patients. This study aimed to develop a risk-scoring...
BACKGROUND AND OBJECTIVES
Endobronchial ultrasound (EBUS) imaging is a valuable tool for predicting lymph node (LN) metastasis in lung cancer patients. This study aimed to develop a risk-scoring model based on EBUS multimodal imaging (grayscale, Doppler mode, elastography) to predict LN metastasis in lung cancer patients.
PATIENTS AND METHODS
This retrospective study analyzed 350 metastatic LNs in 314 patients with lung cancer and 124 reactive LNs in 96 patients with nonspecific inflammation. The sonographic findings were compared with the final pathology results and clinical follow-up. Univariate and multivariate logistic regression analyses were performed to evaluate the independent risk factors of metastatic LNs. According to the coefficients of corresponding indicators in logistic regression analysis, a risk-scoring model was established. Receiver operating characteristic curve was applied to evaluate the predictive capability of model.
RESULTS
Multivariate analysis showed that short axis >10 mm, distinct margin, absence of central hilar structure, presence of necrosis, nonhilar vascularity, and elastography score 4 to 5 were independent predictors of metastatic LNs. Both short axis and margin were scored 1 point, and the rest of independent predictors were scored 2 points. The combination of 3 EBUS modes had the highest area under the receiver operating characteristic and accuracy of 0.884 (95% confidence interval, 0.846-0.922) and 87.55%, respectively. The risk stratification was as follows: 0 to 2 points, malignancy rate of 11.11%, low suspicion; 3 to 10 points, malignancy rate of 86.77%, high suspicion.
CONCLUSIONS
The risk-scoring model based on EBUS multimodal imaging can effectively evaluate metastatic LNs in lung cancer patients to support clinical decision making.
PubMed: 38947743
DOI: 10.1097/eus.0000000000000051 -
Health-Related Quality of Life in Pregnant Women With Gestational Hypertension: A Systematic Review.Cureus May 2024This review seeks to evaluate the levels of health-related quality of life (HRQoL) among pregnant women experiencing pregnancy-induced hypertension (PIH). It also aims... (Review)
Review
This review seeks to evaluate the levels of health-related quality of life (HRQoL) among pregnant women experiencing pregnancy-induced hypertension (PIH). It also aims to identify the specific aspects of HRQoL most impacted by PIH during pregnancy and determine the existence of effective interventions to enhance the HRQoL of these pregnant women. A systematic literature search was conducted in the following databases: PUBMED, SCOPUS, Google Scholar, and EMBASE using the following keywords: Health-related quality of life; pregnancy; pregnancy-induced hypertension; quality of life; gestational hypertension. Among the 32 studies assessed, only eight met the criteria for inclusion, exhibiting a good quality based on assessment with both AXIS (Appraisal Tool for Cross-Sectional Studies) and CASP (Critical Appraisal Skills Programme) checklists. The findings indicate a decline in HRQoL among pregnant women with gestational hypertension, notably affecting both physical and mental dimensions. Furthermore, some studies provided recommendations for interventions that healthcare professionals could employ to improve poor HRQoL levels. Limited research has focused on the HRQoL in pregnant women with PIH. Compared to their healthy counterparts, pregnant women experiencing PIH exhibit a decrease in their HRQoL. It's crucial for healthcare practitioners to proactively address the HRQoL of these pregnant women using effective strategies to mitigate this decline. This approach aims to safeguard both pregnant women and their fetuses from potential complications associated with lower HRQoL levels.
PubMed: 38947727
DOI: 10.7759/cureus.61340 -
Cureus May 2024The thyroid gland is an essential endocrine organ that secretes hormones to regulate homeostasis across multiple organ systems throughout the body. It is actively...
The thyroid gland is an essential endocrine organ that secretes hormones to regulate homeostasis across multiple organ systems throughout the body. It is actively regulated by the hypothalamic-pituitary-thyroid (HPT) axis, where negative feedback modulates the amounts of active hormone being released; thus, lesions that disrupt the proper functioning of this gland or its regulatory mechanisms can be destructive. Toxic thyroid adenomas are usually singular benign functioning nodules in the thyroid gland that cause thyrotoxicosis. Hyperthyroidism is commonly clinically silent, however, in most symptomatic cases, patients will be diagnosed based on abnormal laboratory findings and typical hyperthyroid symptoms. This case report examines an 81-year-old male with an extensive medical history who presented with complaints of new-onset generalized fatigue coupled with bilateral lower extremity muscle cramps. A positron emission tomography (PET) scan for other medical conditions incidentally noted mildly increased uptake in the thyroid gland, prompting a further investigation that resulted in a diagnosis of toxic thyroid adenoma. The patient responded well to treatment with methimazole and has remained in a euthyroid state.
PubMed: 38947590
DOI: 10.7759/cureus.61322 -
Heliyon Jun 2024Acne inversa (AI) is an inflammatory skin disease associated with nicastrin (NCSTN) mutations. Despite the dysregulated bacterial-host immune interactions being an...
Acne inversa (AI) is an inflammatory skin disease associated with nicastrin (NCSTN) mutations. Despite the dysregulated bacterial-host immune interactions being an essential event in AI, the interaction between bacteria and keratinocytes in AI pathophysiology remains unclear. In this study, the NCSTN gene was suppressed using short hairpin RNA in HaCaT cells. Using RNA sequencing, real-time polymerase chain reaction, and western blotting, the expression of IL-36 cytokines was analyzed. The impact of on AI keratinocyte inflammation and underlying regulatory molecules was investigated by exposing the HaCaT cells to . By stimulating NCSTN knockdown HaCaT cells with IFN-γ, the expression and regulatory mechanism of Cathepsin S (Cat S), an IL-36γ cleavage and activating protease, were investigated. After NCSTN knockdown, the IL-36α expression increased, and the IL-36Ra expression was downregulated. NCSTN/MEK/ERK impairment-induced Krüppel-like factor 4 (KLF4) up-regulation in concert with -induced nuclear factor kappa B elevation acts synergistically to promote IL-36γ production with the subsequent IL-8 activation in HaCaT cells. NCSTN/MEK/ERK impairment was also observed in familial AI lesions. IFN-γ-induced Cat S in keratinocytes was enhanced after NCSTN knockdown. The expression of IFN-II pathway molecules was significantly upregulated in both NCSTN knockdown HaCaT cells and familial AI lesions. The Cat S expression was significantly elevated in the patient's AI lesions. Our findings suggested a synergistic relationship between and NCSTN/MAPK/KLF4 axis in IL-36γ-induced familial AI keratinocytes.
PubMed: 38947455
DOI: 10.1016/j.heliyon.2024.e31509 -
Heliyon Jun 2024In this article, a dual-mode, dual-polarized antenna designed using characteristic mode analysis (CMA) is described. An elliptical-shaped patch radiator is chosen with...
In this article, a dual-mode, dual-polarized antenna designed using characteristic mode analysis (CMA) is described. An elliptical-shaped patch radiator is chosen with double slits on its minor axis. This design is based on mode separation from the circular patch into the elliptical patch. The suggested antenna geometry has a footprint of 60 mm × 60 mm × 1.6 mm. To design and fabricate the antenna, an FR-4 substrate with a relative permittivity of 4.3 is used, along with copper sheets 0.035 mm thick for the ground plane and the radiating plane. The circular patch has the resonating mode at 1.8 GHz, whereas the elliptical radiator gives different resonant modes at 1.8 GHz and 3.5 GHz. An orthogonal mode is excited with a 50-Ω coaxial feed line at 3.5 GHz by applying a full-wave approach. The antenna gives a -10dB bandwidth of 51 MHz (1.77-1.82 GHz) centered at 1.8 GHz and a bandwidth of 210 MHz (3.37-3.58 GHz) centered at 3.5 GHz. The working principle is explained through modal analysis and characteristic angles. This dual-band antenna covers a 1.8 GHz GSM band with horizontal polarization and a 3.5 GHz 5G service with vertical polarization. Peak gain attained with these bands is 5.9 dBi and 7.1 dBi, respectively. A CST full-wave simulator is used for the simulations. As a result of the antenna, radiation is stable and enhanced. Compared to measured results, simulation results are close to reality. The characteristic mode analysis (CMA) provides an in-depth look into different operating modes on the antenna in contrast with the conventional method, which relies on the simulated current distribution to verify functionality.
PubMed: 38947453
DOI: 10.1016/j.heliyon.2024.e32217 -
Heliyon Jun 2024To analyze the effect of allicin on the immunoreactivity of osteosarcoma (OS) cells and further explore whether its mechanism is related to the long non-coding...
OBJECTIVE
To analyze the effect of allicin on the immunoreactivity of osteosarcoma (OS) cells and further explore whether its mechanism is related to the long non-coding Ribonucleic Acid (lncRNA) CBR3-AS1/miR-145-5p/GRP78 axis, so as to provide clinical evidence.
METHODS
The human OS cell line Saos-2 was treated with allicin at 25, 50, and 100 μmol/L, respectively, to observe changes in cell biological behaviors. Subsequently, CBR3-AS1 abnormal expression vectors were constructed and transfected into Saos-2 to discuss their influence on OS. Furthermore, the regulatory relationship between allicin and the CBR3-AS1/miR-145-5p/GRP78 axis was validated by rescue experiments. Finally, a nude mice tumorigenesis experiment was carried out to analyze the effects of allicin and CBR3-AS1/miR-145-5p/GRP78 axis on the growth of living tumors. Alterations in T-lymphocyte subsets were also detected to assess the effect of allicin on OS immunoreactivity.
RESULTS
With the increase of allicin concentration, Saos-2 activity decreased and apoptosis increased (P < 0.05). In addition, the expression of CBR3-AS1 and GRP78 decreased after allicin intervention, while miR-145-5p increased (P < 0.05). Silencing CBR3-AS1 led to reduced Saos-2 activity, enhanced apoptosis, and activated mitophagy and endoplasmic reticulum stress (P < 0.05). In the rescue experiment, the effect of CBR3-AS1 on OS cells was reversed by silencing miR-145-5p, while the impact of miR-145-5p was reversed by GRP78. Finally, the tumorigenesis experiment in nude mice confirmed the regulatory effects of allicin and CBR3-AS1/miR-145-5p/GRP78 on tumor growth in vivo. Meanwhile, it was seen that allicin activated CD4CD8 in OS mice, confirming that allicin has the effect of activating OS immunoreactivity.
CONCLUSIONS
Allicin activates OS immunoreactivity and induces apoptosis through the CBR3-AS1/miR-145-5p/GRP78 molecular axis.
PubMed: 38947424
DOI: 10.1016/j.heliyon.2024.e31971 -
Journal of Cancer 2024Gastric cancer (GC) is one of the most common malignancies worldwide, with high incidence and mortality rate. Tripartite motif-containing 28 (TRIM28) is an important...
Gastric cancer (GC) is one of the most common malignancies worldwide, with high incidence and mortality rate. Tripartite motif-containing 28 (TRIM28) is an important molecule that affects the occurrence and development of tumors, but its function in GC has not been elucidated clearly. The purpose of this study is to explore the molecular mechanism by which TRIM28 affect the GC. TRIM28 expression was tested in RNA-seq data from TCGA database, tumor tissue samples from patients and GC cell lines. Genes were silenced or overexpressed by siRNA, lentivirus-mediated shRNA, or plasmids. Cell Counting Kit-8 (CCK-8) and colony formation assays were performed to explore the proliferation of GC cells after TRIM28 knockdown. RNA-seq and TCGA database were used to identify target genes. Luciferase report assay was employed to detect the possible mechanism between TRIM28 and Indoleamine 2,3-dioxygenase (IDO1). Tryptophan concentration in cell supernatant was measured using a fluorometric assay kit. MGC-803 and 746T cells were injected into mice to establish xenograft animal models. The expression of TRIM28 was positively correlated with tumor size and poorer prognosis. Upregulation of TRIM28 was observed in GC tissues and cells. , we proved that knockdown of TRIM28 significantly inhibited the proliferation of GC cells. Then TRIM28 was found to be positively correlated with the expression of IDO1 in GC cells. In accordance with this, tryptophan levels in cell supernatants were increased in TRIM28 knockdown GC cells and overexpression of IDO1 could reverse this phenotype. Serum response factor (SRF), a reported regulator of IDO1, was also regulated by TRIM28 in GC cells. And decreased expression of IDO1 induced by TRIM28 knockdown could be partly reversed through overexpression of serum response factor (SRF) in GC cells. Functional research demonstrated that the expression of IDO1 was increased in GC and IDO1 knockdown could also inhibited the proliferation of GC cells. Furthermore, overexpression of IDO1 could partly reverse proliferation inhibited by TRIM28 knockdown in GC cells. , knockdown of TRIM28 significantly inhibited the tumor growth and overexpression of IDO1 and SRF both could reverse proliferation inhibited by TRIM28 knockdown. TRIM28 is crucial in the development of GC, and may regulate IDO1 through SRF. TRIM28 promote GC cell proliferation through SRF/IDO1 axis.
PubMed: 38947391
DOI: 10.7150/jca.95094 -
Journal of Cancer 2024Ferroptosis has been characterized as non-apoptotic programmed cell death and is considered a novel strategy for antitumor treatment. The factor that binds to inducer of...
Ferroptosis has been characterized as non-apoptotic programmed cell death and is considered a novel strategy for antitumor treatment. The factor that binds to inducer of short transcripts-1 (FBI-1) is an important proto-oncogene playing multiple roles in human malignancies and the development of resistance to therapy. However, the roles of FBI-1 in ferroptosis of endocrine independent prostate carcinoma are still unknown. The results of this study showed that FBI-1 inhibited the ferroptosis of prostate carcinoma PC-3 cells (a typical endocrine-independent prostate carcinoma cell line) via the miR-324-3p/glutathione peroxidase 4 (miR-324-3p/GPX4) axis. Overexpression of FBI-1 enhanced the expression levels of GPX4. In contrast, knockdown of FBI-1 decreased the expression of GPX4 and induced the ferroptosis of PC-3 cells. The miR-324-3p decreased the expression of GPX4 by targeting the 3'-untranslated region of GPX4 to induce ferroptosis. Notably, FBI-1 increased the expression of GPX4 by repressing the levels of miR-324-3p. The transcription of miR-324-3p was mediated by specificity protein 1 (SP1), and FBI-1 repressed the expression of miR-324-3p by repressing the activation of SP1. In clinical specimens, the endogenous levels of FBI-1 were positively associated with Glutathione Peroxidase 4 (GPX4) and negatively related with the expression of miR-324-3p. Therefore, the results indicated that the miR-324-3p/GPX4 axis participates in the FBI-1-mediated ferroptosis of prostate carcinoma cells.
PubMed: 38947389
DOI: 10.7150/jca.96306 -
Journal of Cancer 2024[This corrects the article DOI: 10.7150/jca.31338.].
[This corrects the article DOI: 10.7150/jca.31338.].
PubMed: 38947382
DOI: 10.7150/jca.98604 -
Biomicrofluidics May 2024The low success rate of new drugs transitioning from animal testing to human clinical trials necessitates the development of more accurate and representative models.... (Review)
Review
The low success rate of new drugs transitioning from animal testing to human clinical trials necessitates the development of more accurate and representative models. Recent advances in multi-organ-on-a-chip technology offer promising avenues for studying complex organ-organ interactions. Gut-liver-on-a-chip systems hold particular promise for mimicking the intricate interplay between the gut and liver, which play crucial roles in nutrient absorption, drug metabolism, detoxification, and immune response. Here, we discuss the key components of the gut-liver axis, including the gut epithelium, liver cells, gut microbiota, and their roles in the organ functions. We then explore the potential of gut-liver-on-a-chip models to replicate the intricate interactions between the two organs for pharmacokinetic studies and their expansion to more complicated multi-organ models. Finally, we provide perspectives and future directions for developing more physiologically relevant gut-liver-axis models for more efficient drug development, studying liver diseases, and personalizing treatment strategies.
PubMed: 38947281
DOI: 10.1063/5.0206271