From technique mastery to scientific thinking: how open-ended experiments shape medical students' perception of laboratory course roles in China.

Background: Basic science education is universally acknowledged as a pivotal component of medical education. In China, medical students undergo significant preclinical training but often lack scientific thinking. As China transitions to a knowledge-intensive nation, addressing this gap is crucial.

Dust event identification and characterization with one-year online observations in Beijing.

Dust storms have a profound impact on air quality, atmospheric chemistry, and human well-being by carrying vast amounts of particles over distances of thousands of kilometers. However, the overall characteristics of these dust events and their influence on secondary pollution in the northern China region are not yet well understood, due to a lack of long-term, comprehensive observations and objective identification techniques. Based on principal component analysis combined with high-time-resolution observations of particulate matter components, here we developed a robust method to identify dust storm events and identified 14 dust events in Beijing in 2019.

IL-1β mediates Candida tropicalis-induced immunosuppressive function of MDSCs to foster colorectal cancer.

Background: There is increasing evidence that gut fungi dysbiosis plays a crucial role in the development and progression of colorectal cancer (CRC). It has been reported that gut fungi exacerbate the severity of CRC by regulating tumor immunity. Our previous studies have shown that the opportunistic pathogenic fungal pathogen, Candida tropicalis (C.

MSCs promote the efferocytosis of large peritoneal macrophages to eliminate ferroptotic monocytes/macrophages in the injured endometria.

Background: Endometria are one of the important components of the uterus, which is located in the peritoneal cavity. Endometrial injury usually leads to intrauterine adhesions (IUA), accompanied by inflammation and cell death. We previously reported that both the endometrial ferroptosis was increased and monocytes/macrophages were involved in endometrial injury of IUA.

Mitochondria-mediated ferroptosis induced by CARD9 ablation prevents MDSCs-dependent antifungal immunity.

Background: Caspase Recruitment Domain-containing protein 9 (CARD9) expressed in myeloid cells has been demonstrated to play an antifungal immunity role in protecting against disseminated candidiasis. Hereditary CARD9 ablation leads to fatal disseminated candidiasis. However, the myeloid cell types and molecular mechanisms implicated in CARD9 protecting against disseminated candidiasis remain wholly elusive.

2bRAD-M reveals the difference in microbial distribution between cancerous and benign ovarian tissues.

The development of ovarian cancer is closely related to various factors, such as environmental, genetic and microbiological factors. In previous research, bacteria were identified in human tumors by 16S rRNA sequencing. However, the microbial biomass in tumor tissue is too low and cannot be accurately identified by 16S rRNA sequencing.

promotes CRC by down-regulating tumor cell-intrinsic PD-1 receptor via autophagy.

The programmed cell death 1 (PD-1) receptor is an immune checkpoint molecule that induces immune tolerance and mediates the immune escape of tumor cells. It is mainly expressed in immune cells such as T cells, B cells and monocytes. In recent years, studies have shown that tumor cell-intrinsic PD-1 plays different roles in the development of melanoma, Liver cancer and lung cancer.

Quxie Capsule Alleviates Colitis-associated Colorectal Cancer Through Modulating the Gut Microbiota and Suppressing -induced Aerobic Glycolysis.

Aim: Quxie capsule (QX), a compound of 21 kinds of Traditional Chinese Medicine (TCM) herbs, has been used to treat patients with metastatic colorectal cancer (mCRC) and could suppress the growth of colon cancer. However, the mechanisms of QX inhibiting colorectal cancer remain unclear. In current study, we attempted to determine the anti-colorectal cancer (CRC) effects of QX and the mechanisms of QX in alleviating colorectal cancer.

Candida tropicalis induces NLRP3 inflammasome activation via glycogen metabolism-dependent glycolysis and JAK-STAT1 signaling pathway in myeloid-derived suppressor cells to promote colorectal carcinogenesis.

Our previous studies showed that Candida tropicalis promoted colorectal cancer (CRC) by activating the function of MDSCs. However, underlying molecular mechanisms remains to be further investigated. In the present study, we indicated that C.

Gut fungi enhances immunosuppressive function of myeloid-derived suppressor cells by activating PKM2-dependent glycolysis to promote colorectal tumorigenesis.

Background: Accumulating evidence implicates that gut fungi are associated with the pathogenesis of colorectal cancer (CRC). Our previous study has revealed that Candida tropicalis (C. tropicalis) promotes colorectal tumorigenesis by enhancing immunosuppressive function of myeloid-derived suppressor cells (MDSCs) and increasing accumulation of MDSCs, but the underlying mechanisms remain unestablished.

Local and systemic inflammation triggers different outcomes of tumor growth related to infiltration of anti-tumor or pro-tumor macrophages.

Background: Previous evidence suggests inflammation may be a double-edged sword with cancer-promoting and cancer suppressing function. In this study, we explore the impact of local and systemic inflammation on cancer growth.

Methods: Female BALB/C mice were subcutaneously implanted with foreign body (plastic plates) to build up a local inflammation and intraperitoneally injected with PolyIC or lipopolysaccharides (LPS) to build up a systemic inflammation, followed by subcutaneous injection of 5  × 10 5 colon cancer cells.

Melatonin-Primed MSCs Alleviate Intrauterine Adhesions by Affecting MSC-Expressed Galectin-3 on Macrophage Polarization.

Intrauterine adhesion (IUA) is characterized by the presence of fibrosis in the uterine cavity. It is mainly caused by infection or trauma to the endometrium, and it imposes a great challenge to female reproductive health. Mesenchymal stem cells (MSCs) have been used to regenerate the human endometrium in patients with IUA, but stem cell therapy is not curative in some patients.

Card9 protects fungal peritonitis through regulating Malt1-mediated activation of autophagy in macrophage.

Fungal peritonitis is an inflammatory condition of the peritoneum which occurs secondary to peritoneal dialysis. Most cases of peritonitis are caused by microbial invasion into the peritoneal cavity, resulting in high morbidity and mortality. Unlike bacterial peritonitis, little is known on fungal peritonitis.

Card9 protects sepsis by regulating Ripk2-mediated activation of NLRP3 inflammasome in macrophages.

Sepsis is characterized by systemic inflammation, it's caused by primary infection of pathogenic microorganisms or secondary infection of damaged tissue. In this study, we focus on sepsis-induced intestine barrier functional disturbalice, presenting as increased permeability of intestinal epithelium. We observed that the phenotype of LPS-induced sepsis was exacerbated in Card9 mice, especially displaying more serious intestinal inflammation and gut barrier dysfunction.

Citric acid of ovarian cancer metabolite induces pyroptosis via the caspase-4/TXNIP-NLRP3-GSDMD pathway in ovarian cancer.

Malignant tumors display profound changes in cellular metabolism, yet how these altered metabolites affect the development and growth of tumors is not fully understood. Here, we used metabolomics to analyze the metabolic profile differences in ovarian cancer and found that citric acid (CA) is the most significantly downregulated metabolite. Recently, CA has been reported to inhibit the growth of a variety of tumor cells, but whether it is involved in pyroptosis of ovarian cancer and its potential molecular mechanisms still remains to be further investigated.

Inflammation and cancer: paradoxical roles in tumorigenesis and implications in immunotherapies.

Chronic inflammation caused by persistent infections and metabolic disorders is thought to contribute to the increased cancer risk and the accelerated cancer progression. Oppositely, acute inflammation induced by bacteria-based vaccines or that is occurring after cancer selectively inhibits cancer progression and metastasis. However, the interaction between inflammation and cancer may be more complex than the current explanations for the relationship between chronic and acute inflammation and cancer.

s promotes chemotherapy resistance in colon cancer through increasing lactate production to regulate the mismatch repair system.

Due to chemotherapeutic drug resistance, tumor recurrence is common in patients with colorectal cancer (CRC) and chemo-resistant patients are often accompanied by defects in the mismatch repair system (MMR). Our previous study has shown that () is closely related to the occurrence and development of colorectal cancer, but whether this conditional pathogenic fungus is involved in chemotherapy needs further investigation. Here we found that promoted chemotherapy resistance of colon cancer to oxaliplatin.

Fungal-induced glycolysis in macrophages promotes colon cancer by enhancing innate lymphoid cell secretion of IL-22.

Incorporation of microbiome data has recently become important for prevention, diagnosis, and treatment of colorectal cancer, and several species of bacteria were shown to be associated with carcinogenesis. However, the role of commensal fungi in colon cancer remains poorly understood. Here, we report that mice lacking the c-type lectin Dectin-3 (Dectin-3 ) show increased tumorigenesis and Candida albicans burden upon chemical induction.

The adaptor protein CARD9, from fungal immunity to tumorigenesis.

The adaptor protein CARD9 is in charge of mediating signals from PRRs of myeloid cells to downstream transcription factor NF-κB. CARD9 plays an indispensable role in innate immunity. Both mice and humans with CARD9 deficiency show increased susceptibility to fungal and bacterial infections.

The mycobiota of the human body: a spark can start a prairie fire.

Mycobiota are inseparable from human health, shaking up the unique position held by bacteria among microorganisms. What is surprising is that this seemingly small species can trigger huge changes in the human body. Dysbiosis and invasion of mycobiota are confirmed to cause disease in different parts of the body.

C-type lectin receptor-mediated immune recognition and response of the microbiota in the gut.

C-type lectin receptors (CLRs) are powerful pattern-recognition receptors that discern 'self' and 'non-self' in our body and protect us from invasive pathogens by mediating immune recognition and response. The gastrointestinal tract is very important for the maintenance of homeostasis; it is the largest shelter for the billions of microorganisms in the body and CLRs play a crucial regulatory role in this system. This study focuses on several CLRs, including Dectin-1, Dectin-2, Dectin-3 and Mincle.

CARD9 prevents lung cancer development by suppressing the expansion of myeloid-derived suppressor cells and IDO production.

Caspase recruitment domain-containing protein 9 (CARD9) is an adaptor protein and highly expressed in myeloid cells. Our previous study demonstrates a critical protective effect of CARD9 in the development of colitis-associated colon cancer. Nevertheless, the effect of CARD9 in lung cancer remains unclear.

Cancer Immunotherapy: A Focus on the Regulation of Immune Checkpoints.

In recent years, the role of cancer immunotherapy has become increasingly important compared to traditional cancer treatments, including surgery, chemotherapy and radiotherapy. Of note, the clinical successes of immune checkpoint blockade, such as PD-1 and CTLA-4, represent a landmark event in cancer immunotherapy development. Therefore, further exploration of how immune checkpoints are regulated in the tumor microenvironment will provide key insights into checkpoint blockade therapy.

FC-99 ameliorates sepsis-induced liver dysfunction by modulating monocyte/macrophage differentiation via Let-7a related monocytes apoptosis.

Background: The liver is a vital target for sepsis-related injury, leading to inflammatory pathogenesis, multiple organ dysfunction and high mortality rates. Monocyte-derived macrophage transformations are key events in hepatic inflammation. N-[(4-methoxy)methyl]-4-methyl-1,2-benzenediamine (FC-99) previously displayed therapeutic potential on experimental sepsis.