The formation of brain vasculature is an essential step during central nervous system development. The molecular mechanism underlying brain angiogenesis remains incompletely understood. The role of Atg7, an autophagy-related protein, in brain angiogenesis was investigated in this study. We found that the microvessel density in mice brains with endothelial-specific knockout of Atg7 (Atg7 EKO) was significantly decreased compared to wild-type control. Consistently, in vitro angiogenesis assays showed that Atg7 knockdown impaired angiogenesis in brain microvascular endothelial cells. Further results indicated that knockdown of Atg7 reduced interleukin-6 (IL-6) expression in brain microvascular endothelial cells, which is mediated by NF-κB-dependent transcriptional control. Interestingly, exogenous IL-6 restored the impaired angiogenesis and reduced cell motility caused by Atg7 knockdown. These results demonstrated that Atg7 has proangiogenic activity in brain angiogenesis which is mediated by IL-6 production in a NF-κB-dependent manner.

Chlamydia pecorum is a zoonotic pathogen. Here, we report the first case of human infection with C. pecorum. A man aged 51 years with high fever and dry cough was diagnosed with severe community-acquired pneumonia and respiratory failure. C. pecorum was found responsible for the infection, which was detected from bronchoalveolar lavage fluid through metagenomic next-generation sequencing. C. pecorum infection was further identified by quantitative polymerase chain reaction and complement fixation test. The patient's condition improved rapidly after targeted treatment. He was a farmer with diabetes mellitus and had a history of close contact with sheep, which might result in C. pecorum infection. Our report could provide a direction for the diagnosis and treatment of human C. pecorum pneumonia.

Background: China has a double burden of diabetes mellitus and tuberculosis. Diabetes mellitus and tuberculosis are both important risk factors for Aspergillus infection. Aspergillus lentulus is an emerging fungal pathogen in China and invasive aspergillosis due to A. lentulus is associated with high mortality. Case presentation: A 79-year-old man was admitted to our hospital, complaining of a 7-day history of fever. Five days before admission, he was diagnosed with pulmonary infection at a local hospital, but his symptoms did not relieve after antibiotic therapy. The patient was diagnosed with diabetes mellitus two months ago. About 20 days ago, he began to present chest tightness and shortness of breath after physical activity. After admission, he developed continuous fever and rapid respiratory deterioration, and finally died after his family abandoned treatment. Pulmonary coinfection with M. tuberculosis and A. lentulus was identified by metagenome next-generation sequencing (mNGS) from bronchoalveolar lavage fluid. Conclusions: Clinicians and laboratories should be alert to the emerging A. lentulus infection in China due to its drug-resistance and high mortality. In comparison with conventional methods, mNGS has a great advantage for the diagnosis of mixed pulmonary infection.

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease caused by SFTS virus (SFTSV). SFTS patients were prone to invasive pulmonary aspergillosis (IPA), which was directly related to increased mortality. Here, we present a critical case of SFTS complicated by IPA in a previously healthy 58-year-old woman. On day 1, SFTSV and three different Aspergillus species were both detected in the patient's bronchoalveolar lavage fluid and blood through metagenomic next-generation sequencing (mNGS). After 17 days of treatment, the patient was still in poor condition and A. fumigatus was once again detected in her blood through mNGS. Then her family decided to give up treatment because of financial problems and grave prognosis. She was discharged home and died the next day. Medical personnel should be alter to the possibility of IPA in SFTS patients due to its high mortality. mNGS may be used as an auxiliary diagnostic tool and efficacy-monitoring method for suspected SFTS complicated by IPA.

Objective: Diabetic retinopathy (DR) is a prevalent and serious complication among individuals with diabetes, significantly compromising their visual acuity and overall quality of life. Lysine acetyltransferase 5 (KAT5), an essential catalytic subunit of the nucleosome acetyltransferase of the H4 complex, is implicated in the development of various diseases, including neurological disorders, breast cancer, and lung cancer. However, the function of KAT5 in DR remains poorly understood. This study aims to investigate the influence of KAT5 on autophagy (Atg) during DR. Material and Methods: Experiments were conducted using streptozotocin (STZ)-treated rats to induce diabetes and observe changes in KAT5 expression and its effect on Atg. Retinal tissues and RF/6A cells were utilized to analyze the expression levels of various proteins and their involvement in Atg and apoptosis. KAT5 depletion and Atg7 knockdown were performed to further understand their roles in the process. Results: The eyeballs of STZ-treated rats showed increased expression of KAT5. Depletion of KAT5 attenuated STZ-induced DR injury in rats. The retinal tissues of STZ-treated rats exhibited reduced expression of B-cell lymphoma-2 (Bcl-2) and increased levels of BCL-2-associated X protein and cleaved caspase 3, which could be reversed by KAT5 depletion. STZ treatment induced expression of Beclin-1 and microtubule-associated protein 1 light chain 3B in retinal tissues, and KAT5 knockdown blocked this effect. In monkey retinal choroidal endothelial ( RF/6A) cells, high glucose (HG) treatment decreased 5-ethynyl-2’-deoxyuridine-positivecells and increased terminal deoxynucleotidyl transferase dUTP nick-end labeling-positive cells, which were reversed by KAT5 depletion. KAT5 depletion also attenuated HG-induced apoptosis and Atg in RF/6A cells. Mechanistically, KAT5 depletion reduced histone H3 lysine 27 acetylation and ribonucleic acid ( RNA) polymerase II enrichment on the Atg7 promoter, leading to a decrease in the messenger RNA ( mRNA) and protein expression of Atg7. Atg7 knockdown suppressed Atg in RF/6A cells under HG conditions and reversed the effect of KAT5 depletion on cell apoptosis and Atg. Conclusion: The findings suggest that KAT5 contributes to DR by modulating Atg through epigenetic regulation of Atg7. KAT5 emerges as a valuable target for DR treatment, providing a fresh perspective on the disease’s pathogenesis and laying the foundation for the development of potential therapeutic strategies.