General transcription factor IIIC subunit 2 (GTF3C2) is one of the polymerase III transcription-related factors. Previous studies have revealed that GTF3C2 is involved in regulating cell proliferation. However, the role of GTF3C2 in hepatocellular carcinoma (HCC) remains unclear. This study aimed to determine its expression, biological function, and mechanism in HCC.

The expression of GTF3C2 in HCC and non-tumor tissues, along with its clinical significance, was investigated using public databases and clinical samples. Reverse transcription-quantitative polymerase chain reaction and Western blot assays were performed to detect the expression of GTF3C2, ubiquitin specific peptidase 21 (USP21), mitogen-activated protein kinase 2 (MEK2), extracellular signal-regulated kinase 1/2 (ERK1/2), and p-ERK1/2 in cells. A luciferase reporter assay was conducted to explore the regulatory effect of GTF3C2 on USP21 transcription. Cell Counting Kit-8, 5-ethynyl-2′-deoxyuridine, and colony formation assays were performed to assess HCC cell proliferation. Subcutaneous injection of HCC cells into nude mice was used to evaluate tumor growth in vivo.

GTF3C2 expression was upregulated in HCC tissues and was positively correlated with advanced tumor stages and high tumor grades. HCC patients with high GTF3C2 expression had significantly worse survival outcomes. Knockdown of GTF3C2 suppressed the proliferation of Hep3B and HCCLM3 cells, while overexpression of GTF3C2 facilitated the proliferation of SNU449 and Huh7 cells. GTF3C2 promoted USP21 expression by activating its transcription, which subsequently increased the levels of MEK2 and p-ERK1/2 in HCC cells. Overexpression of both USP21 and MEK2 counteracted the GTF3C2 knockdown-induced inactivation of the ERK1/2 pathway. Moreover, GTF3C2 promoted HCC cell proliferation in vitro and tumor growth in vivo by regulating the USP21/MEK2/ERK1/2 pathway.

Upregulation of GTF3C2 is frequently observed in HCC tissues and predicts poor prognosis. GTF3C2 promotes HCC cell proliferation via the USP21/MEK2/ERK1/2 pathway.

This study investigates upper gastrointestinal tract (UGIT) involvement in patients with ulcerative colitis (UC), a condition traditionally considered limited to the colon. Although extra-colonic manifestations of UC are well recognized, UGIT issues have received less attention. This research aimed to document the clinical, endoscopic, and histopathological UGIT findings in adults with UC and assess their association with disease severity and extent.

This descriptive cross-sectional study was conducted at Ain Shams University over one year. A total of 78 UC patients underwent comprehensive clinical evaluations, including assessments of gastrointestinal complaints, medication history, disease progression, surgeries, and physical examinations. Endoscopic assessments of both the UGIT and colon were performed, accompanied by biopsies for histopathological analysis.

The study population had a mean age of 35.26 years, with a nearly equal gender distribution. Endoscopic findings revealed significant UGIT involvement: 64% of patients had esophagitis and/or gastroesophageal reflux disease, 93% had gastritis, and 80% had duodenitis. Histopathological findings showed notable inflammation, basal cell hyperplasia, and ulcerations in the esophagus, with 51.3% of patients exhibiting chronic gastritis and 38.5% testing positive for Helicobacter pylori infection. Statistical analysis demonstrated a strong association between colonic disease severity and UGIT endoscopic (p < 0.0001 and p < 0.001 in the esophagus and stomach, respectively) and histopathological (p < 0.004, p < 0.001, and p <0.005 in the esophagus, stomach, and duodenum, respectively) findings, particularly in patients with UGIT symptoms.

This study concludes that UGIT endoscopic and histopathological changes are prevalent among Egyptian UC patients, suggesting a significant link between UC and these UGIT findings.

Breast cancer remains one of the leading causes of cancer-related deaths worldwide. Early detection of breast cancer significantly improves outcomes and survival rates, minimizing treatments. Imaging techniques are critical in identifying abnormalities and diagnosing breast cancer at its earliest stages, often before clinical symptoms emerge. Mammography remains standard for screening in average-risk women, while supplementary methods like ultrasound, magnetic resonance imaging, and tomosynthesis enhance detection rates, particularly in women with dense breasts or those at high risk. Given that certain factors, such as family history, age, genetic mutations, and breast density, affect the risk of developing breast cancer, some women may benefit from earlier or more frequent screenings. Personalized screening protocols are becoming more common, tailoring the type and frequency of imaging to the individual’s risk profile. Newer technologies, such as molecular breast imaging and contrast-enhanced mammography show promise but require further validation for widespread use. In conclusion, imaging techniques including mammography, ultrasound, magnetic resonance imaging, and newer technologies like three-dimensional mammography and molecular breast imaging are essential tools in the early detection of breast cancer, leading to better outcomes for patients. This literature review provides an overview of current breast cancer imaging methods, their role in early diagnosis, and their effectiveness and limitations.

Patients with cirrhosis are at an increased risk of bacterial infection (BI), which is the most common precondition for acute-on-chronic liver failure (ACLF). In this study, we aimed to evaluate the ability of mitochondria-related indicators (mitochondrial mass and mitochondrial membrane potential (MMP)) of T cells in peripheral blood to predict BI and ACLF within 90 days in cirrhotic patients.

We prospectively studied mitochondria-related indicators in various T cells from 235 cirrhotic patients at the Second Hospital of Nanjing. The outcomes of interest were BI and ACLF.

The restricted cubic spline analysis showed that the MMP of CD8+ T cells had a linear relationship with the risk of BI and ACLF (both P < 0.001). Multivariable Cox regression analysis demonstrated that the MMP of CD8+ T cells was an independent risk factor for both BI and ACLF (BI: hazard ratio 0.96, 95% confidence interval 0.94–0.98; P < 0.001; ACLF: hazard ratio 0.94, 95% confidence interval 0.90–0.97; P < 0.001). The MMP of CD8+ T cells exhibited better diagnostic efficacy than traditional indices in predicting BI (C index: 0.75). The MMP of CD8+ T cells, when combined with traditional models (Child-Turcotte-Pugh and model for end-stage liver disease score), improved their diagnostic efficiency in predicting both BI and ACLF. Additionally, the MMP of CD8+ T cells showed a significant negative correlation with inflammation-related markers (P < 0.05). Mitochondrial damage and abnormally activated mitochondrial autophagy were observed in CD8+ T cells from cirrhotic patients with low MMP.

The MMP of CD8+ T cells could serve as a valuable predictor of BI and ACLF within 90 days in cirrhotic patients.

Balamuthia mandrillaris is a free-living amoeba that can cause granulomatous amoebic encephalitis, a lethal neurological condition in humans. This pathogen infects not only immunocompromised hosts but, more commonly, immunocompetent individuals. Balamuthia mandrillaris mainly infects the skin and nervous system. When it affects the nervous system, it can manifest as Balamuthia mandrillaris encephalitis (BAE). This article presents a case of BAE in central China, diagnosed through next-generation sequencing and histopathology. The patient is a 64-year-old male who was admitted to the Department of Neurosurgery with a one-week history of headache. Magnetic resonance imaging scans revealed a mass in the right temporal-occipital region, and postoperative pathological examination confirmed that the lesion was BAE. We will detail the clinical course of this disease in this patient, aiming to enhance clinicians’ understanding of Balamuthia mandrillaris infections.

Ferroptosis plays an essential role in chronic liver diseases, and cyclooxygenase-2 (COX-2) affects liver fibrosis through multiple mechanisms. However, research on COX-2 regulation of ferroptosis in chronic liver injury remains limited. This study aimed to investigate whether and how COX-2 regulates ferroptosis in chronic liver injury.

In vivo, a thioacetamide (TAA)-induced chronic liver injury model, characterized by significant liver lipid peroxidation and oxidative stress, was used. COX-2+/+ and COX-2–/– mice were treated with TAA or normal saline. In vitro, primary mouse hepatocytes were isolated and treated with dimethyl sulfoxide (DMSO), erastin+DMSO, etoricoxib+erastin+DMSO, and tBHQ+erastin+DMSO. Mitochondrial morphology, iron metabolism, lipid peroxidation, and oxidative stress were assessed to verify ferroptosis. The nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway was measured to investigate the relationship between COX-2 and ferroptosis.

TAA-treated COX-2–/– mice presented milder liver fibrosis, whereas TAA-treated COX-2–/– mice livers and etoricoxib+erastin+DMSO-treated primary hepatocytes exhibited alleviated mitochondrial damage compared with TAA-treated COX-2+/+ littermates and erastin+DMSO-treated primary hepatocytes, respectively. The knockout of COX-2 decreased ferrous ion concentration (p < 0.01) and mitigated lipid peroxidation in TAA-treated livers (p < 0.05). Furthermore, both COX-2 knockout and etoricoxib restored reduced glutathione (p < 0.05) and glutathione peroxidase 4 (p < 0.05), while decreasing malondialdehyde levels (p < 0.05). Additionally, COX-2 inhibition upregulated Nrf2, which helped alleviate erastin+DMSO-induced ferroptosis (p < 0.01).

Ferroptosis contributes to the progression of chronic liver injury. Inhibition of COX-2 upregulates Nrf2, mitigating hepatocyte ferroptosis in chronic liver injury.

The refusal of blood transfusions and blood derivatives compels surgeons to face clinical and ethical challenges. We reviewed our perioperative and long-term outcomes of Jehovah’s Witnesses undergoing colon cancer surgery to evaluate the feasibility of bloodless procedures.

We retrospectively analyzed data from patients with colon cancer and Jehovah’s Witnesses who underwent surgery between January 2014 and December 2023. A protocol was systematically followed to optimize hemoglobin levels and other parameters according to the Enhanced Recovery After Surgery guidelines.

Sixteen patients underwent colon surgery, with a median age of 69 years and an equal gender distribution. Thirty-seven and a half percent had preoperative anemia and were managed by a hematologist. All procedures were performed in accordance with oncological standards. Postoperative treatment included low molecular weight heparin, and hemoglobin levels temporarily decreased postoperatively. No blood transfusions were needed during hospitalization. Two patients required surgical intervention due to postoperative hemorrhage. Complications included anastomotic dehiscence and perforation, with an overall morbidity rate of 25% and no 90-day mortality.

This study highlights the challenges in managing patients who reject blood products during colon cancer surgeries; however, the outcomes show results comparable to those of the general population with appropriate protocols. Preoperative optimization is crucial to reduce blood loss. Treatment of postoperative hemorrhage requires a lower threshold for intervention due to limited alternatives to blood products. Despite the limitations of the study, the findings advocate for careful monitoring and intervention. Larger studies are needed to validate these findings and improve care for this group of patients.

Spinal cord injury (SCI) significantly impacts the central nervous system, with limited effective treatments available. Brain-derived neurotrophic factor (BDNF) plays a crucial role in neuronal growth, survival, and regeneration after SCI. MicroRNAs, particularly miR-124-3p, have been implicated in SCI pathophysiology. However, the relationship between miR-124-3p and BDNF in the context of SCI remains unclear. This study aimed to investigate the correlation between miR-124-3p expression and BDNF levels in a rat model of spinal cord injury and to assess how the timing of injury affects this relationship.

This study included 72 male Wistar rats divided into three groups: intact (n = 8), sham (n = 32), and SCI (n = 32). SCI diagnosis was confirmed through behavioral-motor function analysis using the Basso, Beattie & Brenham score and histological examination with crystal violet staining. The expression levels of miR-124-3p and BDNF were assessed using real-time polymerase chain reaction in all groups at four time points (one hour, one day, three days, and seven days post-injury).

In the SCI group, a marked reduction in miR-124-3p expression was observed relative to both the sham and intact groups. Conversely, there was a substantial elevation in BDNF expression within the SCI group in comparison to the sham and intact groups. The findings underscore a negative association between miR-124-3p expression and BDNF messenger RNA levels.

The downregulation of miR-124-3p and concurrent upregulation of BDNF suggest a potential regulatory role of miR-124-3p in modulating BDNF expression during SCI. These findings provide new insights into the molecular mechanisms underlying SCI and suggest that miR-124-3p and BDNF could serve as potential therapeutic targets. Further research is needed to explore the translational potential of these findings for developing novel diagnostic and therapeutic strategies for SCI.