Efferocytosis is a physiologic phagocytic clearance of apoptotic cells, which modulates inflammatory responses and the immune environment and subsequently facilitates immune escape of cancer cells, thus promoting tumor development and progression. Efferocytosis is an equilibrium formed by perfect coordination among “find-me”, “eat-me” and “don’t-eat-me” signals. These signaling pathways not only affect the proliferation, invasion, metastasis, and angiogenesis of tumor cells but also regulate adaptive responses and drug resistance to antitumor therapies. Therefore, efferocytosis-related molecules and pathways are potential targets for antitumor therapy. Besides, supplementing conventional chemotherapy, radiotherapy and other immunotherapies with efferocytosis-targeted therapy could enhance the therapeutic efficacy, reduce off-target toxicity, and promote patient outcome.

Nanobiotechnology plays an important role in drug delivery, and various kinds of nanoparticles have demonstrated new properties, which may provide opportunities in clinical treatment. Nanoparticle-mediated drug delivery systems have been used in anti-inflammatory therapies. Diseases, such as inflammatory bowel disease, rheumatoid arthritis, and osteoarthritis have been widely impacted by the pathogenesis of inflammation. Efficient delivery of anti-inflammatory drugs can reduce medical dosage and improve therapeutic effect. In this review, we discuss nanoparticles with potential anti-inflammatory activity, and we present a future perspective regarding the application of nanomedicine in inflammatory diseases.

Traumatic brain injury (TBI) is an important cause of human mortality and morbidity, which can induce serious neurological damage. At present, clinical treatments for neurological dysfunction after TBI include hyperbaric oxygen, brain stimulation and behavioral therapy, but the therapeutic effect is not satisfactory. Recent studies have found that exogenous stem cells can migrate to damaged brain tissue, then participate in the repair of damaged brain tissue by further differentiation to replace damaged cells, while releasing anti-inflammatory factors and growth factors, thereby significantly improving neurological function. This article will mainly review the effects, deficiencies and related mechanisms of different types of stem cells in TBI.

The aim of this study was to compare the sensitivity of mammography (MG), ultrasound (US), magnetic resonance imaging (MRI), and combinations of these imaging modalities for the detection of small (≤2 cm) breast cancer and to evaluate the benefit of preoperative breast MRI after performing conventional imaging techniques for small breast cancer. This was an observational retrospective review of 475 patients with pathologically confirmed breast cancer. We reviewed the medical records; assessed the preoperative reports of MG, US, and MRI; and categorized them as benign features (BI-RADS 1–3) or malignant features (BI-RADS 4 or 5). The criterion standard for detection was the pathologic assessment of the surgical specimen. The sensitivities of the different techniques were compared using the McNemar test. Among the 475 women, the sensitivity of MG was significantly greater in patients with low breast density than in those with high breast density (84.5% vs 65.8%, P < .001). US had higher sensitivity than MG (P < .001), and the combination of MG + US showed better sensitivity than MG or US alone (P < .001). Further addition of MRI to the combination of MG and US statistically contributed to the sensitivity yield (from 93.3% to 98.2%; P < .001) but did not significantly increase the mastectomy rate (from 48.2% to 49.3%; P = .177). MG has limited diagnostic sensitivity in patients with small breast cancer, especially in those with dense breast tissue. US is better than MG at detecting small breast cancer, regardless of breast density. The addition of MRI to MG and US could increase sensitivity without increasing the mastectomy rate. This study suggests performing MRI routinely on the basis of MG and US for small (≤2 cm) breast cancer.

Somatostatin receptor (SSTR) 2, widely expressed in meningioma, is a G-protein-coupled receptor and can be activated by somatostatin or its synthetic analogs. SSTR2 is therefore extensively studied as a marker and target for the diagnosis and treatment of meningioma. Accumulating studies have revealed the crucial clinical significance of SSTR2 in meningioma. Summarizing the progress of these studies is urgently needed as it may not only provide novel and better management for patients with meningioma but also indicate the direction of future research. Pertinent literature is reviewed to summarize the recent collective knowledge and understanding of SSTR2’s clinical significance in meningioma in this review. SSTR2 offers novel ideas and approaches in the diagnosis, treatment, and prognostic prediction for meningioma, but more and further studies are required.

Many different treatments may affect the serum lipid profiles of breast cancer patients. This study analyzed serum lipid levels at different periods during treatment to observe the changes in lipid profiles during and after chemotherapy and to compare the different effects of different chemotherapy regimens on serum lipid profiles. A total of 805 patients were included in this study. We measured the lipid profiles of patients who received surgery without chemotherapy prior to the operation and at 3, 6 and 12 months after operation. In addition, in patients who underwent chemotherapy, the lipid profiles were measured prior to chemotherapy, prior to the last cycle of chemotherapy and 6 months after chemotherapy. Lipid profile measurements included total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), homocysteine (HCY), and uric acid (UA). (Neo)Adjuvant chemotherapy exerted an adverse temporary effect on lipid levels (manifested as increased TG and LDL-C levels, and decreased HDL-C levels, particularly in the adjuvant chemotherapy group) during the chemotherapy periods. However, this influence was not sustained, as the lipid profiles levels were generally restored to baseline levels 6 months after chemotherapy completion. Different age groups showed different changes in lipid levels that were influenced by chemotherapy. The younger group (20–40 years old) showed a greater increase in TC and LDL-C levels during chemotherapy than the 41-65-year-old group. Chemotherapy exerts an adverse temporary effect, and the effects of different regimens on lipid levels are similar. Furthermore, lipid profiles in younger women may be more sensitive to chemotherapy.