Cell membrane derived liposomes loaded with DNase I target neutrophil extracellular traps which inhibits colorectal cancer liver metastases.

Neutrophil extracellular traps (NETs) are web-like chromatin structures that are coated with granule proteins and trap microorganisms. However, NETs can damage the host tissue, contribute to the development of autoimmunity and lead to other dysfunctional outcomes in noninfectious diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), diabetes, atherosclerosis, vasculitis, thrombosis, and cancer. As a potential therapeutic approach, targeted ablation of neutrophil extracellular traps is of utmost importance for the treatment of NET-associated diseases. Here, the specific interaction between CCDC25 and NETs was exploited to produce biomimetic CCDC25-overexpressing cell membrane hybrid liposomes capable of targeting NETs in NET-associated diseases. The hybrid liposomes were constructed by fusing cell membrane nanovesicles derived from genetically engineered cells, which stably express CCDC25, and the resulting cell membrane hybrid liposomes exhibited enhanced affinity for NETs in two different NET-associated disease models. Furthermore, after encapsulation of DNase I in the liposomes, the nanoformulation efficiently eliminated NETs and significantly suppressed the recruitment of neutrophils. Overall, we present a bionic nanocarrier that specifically targets NETs in vivo and successfully inhibits colorectal cancer liver metastases; importantly, this could be a promising therapeutic approach for the treatment of NET-associated diseases.

Trojan Horse Nanocapsule Enabled In Situ Modulation of the Phenotypic Conversion of Th17 Cells to Treg Cells for the Treatment of Multiple Sclerosis in Mice.

Th17/Treg imbalance is closely related to the occurrence and development of multiple sclerosis (MS), and the transdifferentiation of Th17 cells into Treg cells may contribute to the resolution of inflammation, presenting a therapeutic strategy for MS. To modulate this phenotypic shift in situ, a "Trojan horse"-like hybrid system, nanocapsule-coupled Th17 cells, is reported for MS treatment. Following intravenous injection into MS mice, the hybrid system efficiently transmigrates across the blood-brain barrier and homes to the inflamed MS niche. (Aminooxy)-acetic acid, a transdifferentiation inducer, is locally released upon the production of ROS and in turn taken up by Th17 cells. It is demonstrated that the Trojan horse hybrid system enables in situ phenotypic transdifferentiation of Th17 cells into anti-inflammatory Treg cells. This phenotypic conversion leads to a domino-like immune response that is conducive to MS therapy. Overall, this work highlights a new pathway for accurate modulation of the phenotypes of adoptively transferred cells in situ, from proinflammatory to anti-inflammatory for MS therapy, and may be broadly applicable for patients suffering from other autoimmune diseases.

[Research progress of autofluorescence imaging of parathyroid glands].

The main causes of hypoparathyroidism are unintentional parathyroidectomy and/or impaired blood supply. Therefore, accurate identification and preservation of parathyroid glands in situ during thyroid or parathyroid surgery has become one of the problems that plague endocrine surgeons. In recent years, near-infrared autofluorescence imaging technology has gradually attracted more and more attention from surgeons because of its simplicity, safety, accuracy, real-time, no-contrast agent, and non-invasiveness. This article reviews the development history, clinical application, and application prospects of the parathyroid gland autofluorescence imaging technology in recent years.

The Relationship Between Hemoglobin Glycation Variation Index and Vitamin D in Type 2 Diabetes Mellitus.

OBJECTIVE: This study aimed to investigate the relationship between hemoglobin glycation variation index (HGI) and vitamin D in patients with type 2 diabetes mellitus (T2DM). MATERIALS AND METHODS: This is a cross-sectional study that recruited 347 patients with T2DM. The subjects were divided into no vitamin D deficiency group (25(OH)D ≥20 ng/mL) and vitamin D deficiency group (25(OH)D < 20 ng/mL). HGI was calculated as the difference between the measured and predicted values of HbA1c using the linear relationship between HbA1c level and fasting plasma glucose levels. All study participants were divided into high HGI and low HGI groups using the median of HGI as the boundary. At last, the subjects were divided into male group and female group, and these groups were further subdivided into vitamin D deficiency group and no vitamin D deficiency group. RESULTS: The levels of HGI were significantly higher in the vitamin D deficiency group compared with the no vitamin D deficiency group for all patients. The same was true for female patients but not for male patients. The prevalence of vitamin D deficiency in the high HGI group was higher than that in the low HGI group. The high HGI group had lower vitamin D levels compared to the low HGI group. Compared to the male group, the female group had lower vitamin D levels but higher HGI levels. A negative correlation existed between 25(OH) D and HGI in all subjects, as well as in the female-only subgroups. In the male-only subgroups, there was no correlation between them, and this positive correlation still existed after adjusting for other factors in multilinear regression analysis. CONCLUSION: Our study showed for the first time that HGI is inversely associated with vitamin D in all patients with T2DM, and the correlation was also found in female patients, but not in male patients.