Brain abscess, a severe intracranial infectious disease, refers to the parenchyma abscess caused by local infection or remote spread. Recently, advancements in modern medicine, especially the wide application of antimicrobial drugs, have contributed to the gradual decrease in the prevalence of this disease. However, cases of cryptogenic brain abscess that feature an unknown origin and atypical symptoms are rising. In this retrospective study, we report and analyze two cases of cryptogenic brain abscess. The first patient was a 30-year-old healthy man who was admitted to our hospital due to 1 week of headache and 3 days of headache aggravation, accompanied by nausea and vomiting. Head MRI shows a circular space-occupying as well as apparently enhanced DWI signals were observed in the right parietal lobe, and the ring wall manifested an apparent increase in signal intensity after enhancement. The patient was diagnosed as a brain abscess before operation and given craniotomy. The postoperative pathology confirmed brain abscess and recovered well after surgery. The second patient was a 45-year-old healthy woman who was hospitalized in a local hospital due to symptoms of headache and right limb weakness for 1 week. Head MRI shows a circular space-occupying lesion in the left basal ganglia, and the ring wall manifested an apparent increase in signal intensity after enhancement. The patient was suspected of glioma at the local hospital and was transferred to our hospital. Twelve hours after hospitalization, the patient was suspected of developing cerebral palsy and thus underwent emergency surgery including lesion resection in the left basal ganglia, resection of the polus temporalis, and a decompressive craniotomy. Postoperative pathology confirmed brain abscess. The patient was eventually conscious, but left the right limb hemiplegia. Hence, when a patient develops the classical triad of fever, headache, and focal neurologic deficits, the possibility of brain abscess should be investigated. Early diagnosis and treatment are crucial to minimize various complications and the number of deaths.

Emerging evidence indicates that the cellular electromagnetic field regulates the fundamental physics of cell biology. The electromagnetic oscillations and synchronization of biomolecules triggered by the internal and external pulses serve as the physical basis of the cellular electromagnetic field. Recent studies have indicated that centrosomes, a small organelle in eukaryotic cells that organize spindle microtubules during mitosis, also function as a nano-electronic generator in cells. Additionally, cellular electromagnetic fields are defined by cell types and correlated to the epigenetic status of the cell. These interactions between tissue-specific electromagnetic fields and chromatin fibers of progenitor cells regulate cell differentiation and organ sizes. The same mechanism is implicated in the regulation of tissue homeostasis and morphological adaptation in evolution. Intercellular electromagnetic interactions also regulate the migratory behaviors of cells and the morphogenesis programs of neural circuits. The process is closely linked with centrosome function and intercellular communication of the electromagnetic fields of microtubule filaments. Clearly, more and more evidence has shown the importance of cellular electromagnetic fields in regulatory processes. Furthermore, a detailed understanding of the physical nature of the inter- and intracellular electromagnetic interactions will better our understanding of fundamental biological questions and a wide range of biological processes.

Emerging evidence indicates that intratumor bacteria exist as an active and specific tumor component in many tumor types beyond digestive and respiratory tumors. However, the biological impact and responsible molecules of such local bacteria–tumor direct interaction on cancer therapeutic response remain poorly understood. Trastuzumab is among the most commonly used drugs targeting the receptor tyrosine-protein kinase erbB-2 (ErbB2) in breast cancer, but its resistance is inevitable, severely limiting its clinical effectiveness. Here, we demonstrate that the quorum-sensing signaling molecule N-(3-oxo-dodecanoyl) homoserine lactone (3oc), a chemical compound released by Pseudomonas aeruginosa ( P. aeruginosa ), one tumor-resident bacteria with a relative high abundance in breast cancer, promotes breast cancer cell resistance to trastuzumab. Mechanically, 3oc directly leads to spontaneous dimerization of the transforming growth factor β (TGF-β) type II serine/threonine kinase receptor on the cell membrane in a ligand-independent manner. The 3oc-induced TGF-β signaling subsequently triggers ErbB2 phosphorylation and its downstream target activation, overcoming the inhibition effect of trastuzumab on ErbB2. With specific real-time qPCR, fluorescence in situ hybridization imaging, and liquid chromatography ionization tandem mass spectrometry analyses of clinical samples, we confirmed that P. aeruginosa and its signaling molecule 3oc exist in breast cancer tissues and there is a clinical correlation between P. aeruginosa colonization and trastuzumab resistance. This work expands the biological functions of intratumor bacteria in cancer treatment responsiveness and provides a unique perspective for overcoming trastuzumab resistance.

Numerous lines of evidence have shown that microRNAs (miRNAs) play a vital role in regulating the progression in many types of cancers, including T cell acute lymphoblastic leukemia (T-ALL). In this study, the potential underlying mechanism and functional role of miR-141-3p in T-ALL cells were determined. We found that the expression level of miR-141-3p was significantly downregulated, while that of tumor necrosis factor receptor-associated factor 5 (TRAF5) was strongly upregulated in tissues from patients with T-ALL compared with healthy controls. Subsequently, upregulation of miR-141-3p significantly repressed T-ALL cell proliferation and promoted cell apoptosis. Conversely, downregulation of miR-141-3p significantly inhibited cell apoptosis and enhanced T-ALL cell proliferation. We also verified that TRAF5 was the direct target of miR-141-3p in T-ALL cells. Additionally, TRAF5 overexpression significantly repressed cell apoptosis and increased T-ALL cell proliferation. In summary, miR-141-3p regulates T-ALL cell progression by directly targeting TRAF5, and may serve as a potential therapeutic target for T-ALL.