Breast Carcinoma with a Special Histological Pattern of Sebaceous Differentiation and High-Frequency Microsatellite Instability: A Case Report and Review of the Literature.

The World Health Organization in its 2019 Classification of Breast Tumors termed breast sebaceous carcinoma as invasive breast carcinoma of no special type (IBC-NST), with a sebaceous pattern. Approximately 30 cases of IBC-NST with a sebaceous pattern have been reported in the literature, and in all cases the expression of mismatch repair proteins in tumors was normal. Here, we report a case of IBC-NST with a sebaceous pattern and high-frequency microsatellite instability (MSI-H). This case was a sporadic sebaceous pattern of IBC-NST with MSI-H and was unrelated to Muir-Torre syndrome. Its histopathological characteristics were similar to those of MSI-H-associated triple-negative breast carcinoma (TNBC) with a high histological grade but were without tumor-infiltrating lymphocytes (TILs). The tumor did not recur after 20 months of follow-up.

Ethylparaben induces subconjunctival fibrosis via the Wnt/ß-catenin signaling pathway.

The aim of the present study was to explore the etiology of subconjunctival fibrosis (SCF) induced by ethylparaben, the most prevalent preservative in Chinese eye drops. Ethylparaben was administered to the left eyes of male Sprague-Dawley rats in the experimental group twice daily for 1 month, whereas the control group received PBS. Experimental group rats displayed a mild promotion in density of fibroblasts and a tighter deposition of collagen in the bulbar subepithelial connective tissue compared with the control group. Furthermore, the present findings revealed that extracellular matrix expression was promoted in murine bulbar conjunctival tissues in the experimental group. In primary conjunctival fibroblasts, expression of ECM triggered by ethylparaben was suppressed by XAV-939. Furthermore, stimulation of the Wnt/ß-catenin axis triggered by ethylparaben was impaired by XAV-939. In conclusion, SCF triggered by ethylparaben results from extra ECM generation of conjunctival fibroblasts via the Wnt/ß-catenin axis.

MicroRNA-598 acts as an inhibitor in retinoblastoma through targeting E2F1 and regulating AKT pathway.

Recently, microRNAs (miRNAs) receive more attention due to their role in the pathogenesis of malignancies. Retinoblastoma (RB) is the most serious and harmful malignant tumor in infants and young children with eye diseases, which often endangers the lives of children. This study was designed to determine how miR-598 is involved in RB progression. In this study, quantitative reverse transcription-polymerase chain reaction, Western blot, dual-luciferase reporter, Cell Counting Kit-8, and Transwell assays were adopted to detect miR-598 expression and function in RB. The decreased expression of miR-598 was identified in RB. Overexpression of miR-598 suppressed the viability and metastasis of RB cells. Further, E2F transcription factor 1 (E2F1) is verified as a direct target of miR-598. Furthermore, E2F1 recovered miR-598-mediated-inhibition of cell viability and metastasis in RB. In addition, miR-598 was found to promote cell apoptosis and inactivate the protein kinase B (AKT) pathway in RB. miR-598 suppressed RB cell viability and metastasis through inhibiting E2F1 and inactivating AKT pathway, which may provide a new perspective for RB treatment.

A study on the protective effects of CpG oligodeoxynucleotide-induced mucosal immunity against lung injury in a mouse acute respiratory distress syndrome model.

This study aims to determine the feasibility of using oligodeoxynucleotides with unmethylated cytosine-guanine dinucleotide sequences (CpG ODN) as an immunity protection strategy for a mouse model of acute respiratory distress syndrome (ARDS). This is a prospective laboratory animal investigation. Twenty-week-old BALB/c mice in Animal research laboratory were randomized into groups. An ARDS model was induced in mice using lipopolysaccharides (LPSs). CpG ODN was intranasally and transrectally immunized before or after the 3rd and 7th days of establishing the ARDS model. Mice were euthanized on Day 7 after the second immunization. Then, retroorbital bleeding was carried out and the chest was rapidly opened to collect the trachea and tissues from both lungs for testing. CpG ODN significantly improved the pathologic impairment in mice lung, especially after the intranasal administration of 50 µg. This resulted in the least severe lung tissue injury. Furthermore, interleukin-6 (IL-6) and IL-8 concentrations were lower, which was second to mice treated with the rectal administration of 20 µg CpG ODN. In contrast, the nasal and rectal administration of CpG ODN in BALB/c mice before LPS immunization did not appear to exhibit any significant protective effects. The intranasal administration of CpG ODN may be a potential treatment approach to ARDS. More studies are needed to further determine the protective mechanism of CpG ODN.

Transforming growth factor-ß blocks glucose-induced inflammation and apoptosis in corneal epithelial cells.

Diabetic retinopathy is the most important ocular complication associated with diabetes. Corneal defects due to diabetes mellitus (DM) may cause severe vision impairments. This study aimed to identify the effect of transforming growth factor-ß (TGF-ß) on biological events, such as apoptosis and inflammation, in the diabetic cornea. High-glucose treatment induced reactive oxygen species (ROS) production and several biological events, including apoptosis and inflammatory cytokine secretion, in human corneal epithelial cells. However, administration of TGF-ß significantly decreased ROS production, Annexin V-positive cells, and levels of inflammatory cytokines. Sprague Dawley rats were injected with streptozotocin (STZ) as a model of DM. Inflammatory cytokine secretion, apoptosis, and inflammation were all increased by STZ treatment. However, apoptosis and inflammation were markedly reduced following TGF-ß treatment. In conclusion, TGF-ß can ameliorate the enhancement of apoptosis and inflammation in diabetic cornea in in vivo and in vitro.

Spontaneous splenic rupture in an acute leukemia patient with splenic tuberculosis: A case report.

Spontaneous splenic rupture, also referred to as atraumatic splenic rupture, is a rare but life-threatening emergency condition. Without timely diagnosis and treatment, the mortality rate of splenic rupture approaches 100%. The etiology of atraumatic splenic rupture varies; it is reportedly associated with neoplasms or splenic infection, but is rarely encountered in patients with both conditions. We herein report the case of a 58-year-old male patient with acute myeloid leukemia (AML) complicated by splenic tuberculosis (TB), who presented with spontaneous rupture of the spleen. Pathological examination of the resected spleen revealed multifocal granulomatosis with caseous necrosis. However, with timely diagnosis and surgical intervention, the patient recovered successfully and is currently on consolidation therapy. To the best of our knowledge, this is the first case of spontaneous splenic rupture in AML with splenic TB. The relevant literature on spontaneous splenic rupture was also reviewed and the potential etiology and treatment were discussed.