Excessive aggregation of fine particles may play a crucial role in adolescent spontaneous pneumothorax pathogenesis.

Background: The pathogenesis of primary spontaneous pneumothorax (PSP) is unclear. Fine particles aggregated in the lung can be phagocytosed by alveolar macrophages (AMs) to induce an inflammatory reaction and damage local pulmonary tissue, which could be a mechanism of PSP. This project aimed to explore the pathological association between fine particulate matter and PSP. Methods: Thirty pulmonary bullae tissues were obtained from surgery of PSP patients (B group). The adjacent normal tissues of the lungs were defined as the control S group. Another 30 normal lung tissues with nonpneumothorax disease (NPD) were applied as the control N group. Hematoxylin and eosin (H & E), Wright-Giemsa (W-G), Victoria blue, and immunohistochemical (IHC) staining experiments were performed to measure the levels of fine particulate matter, alveolar macrophages (AMs), pulmonary elastic fibers, monocyte chemoattractant protein-1 (MCP-1), and matrix metalloproteinase-9 (MMP-9) in the lung tissues. The serum levels of MCP-1 and MMP-9 were prospectively analyzed as well. Results: Histopathological examinations revealed obvious deposition of fine particulate matter and inflammatory reactions (proliferation of AMs) in the B group, compared with those in the S group and the N group. These alterations were significantly associated with PSP. The numbers of AMs and pulmonary elastic fibers, the positive area of the H-score, as well as the concentrations of MCP-1 and MMP-9 in the lungs of the experimental group were obviously raised compared with the controls (P < 0.05). Conclusions: Fine particulate matter aggregation, inflammation (macrophage hyperplasia), and overexpression of MCP-1 and MMP-9 may contribute to the pathogenesis of PSP. The overaccumulation of fine particulate matter may play a crucial part in the occurrence of adolescent and young adult PSP. Trial registration: This project was enrolled on the Chinese Clinical Trial Registry: ChiCTR2100051460.

Establishment of a prediction algorithm for the Honghe minority group based on warfarin maintenance dose.

Background:CYP2C9 and VKORC1 are important factors in warfarin metabolism. The authors explored the effects of these genetic polymorphisms and clinical factors on a warfarin maintenance dose and then established the prediction algorithm for Honghe minorities in China. Materials & methods: Quantitative fluorescence PCR determined the mutation frequency of CYP2C9 and VKORC1-1639 G>A alleles. The authors collected the relevant clinical factors, including age, gender, body surface area (BSA), international normalized ratio value, daily warfarin dose, comorbidity and concomitant prescriptions. Results: The mean values of BSA and international normalized ratio in Honghe minorities were lower than in Han Chinese (p = 0.00). The genotype of CYP2C9*1/*1 and VKORC1-1639 AA was the main allele, the mutationfrequency of VKORC1-1639 AA and the number of male of Honghe minorities were lower than that of Han Chinese (p = 0.013 and p = 0.04). The significances of the effect on actual warfarin dose value were gender, VKORC1 AA mutant, CYP2C9*1/*1, age, hypertension and BSA sequentially. Conclusion: By multiple linear regression analysis with genetic and clinical factors, the authors determined a prediction algorithm for adjusting individual dosing of warfarin in this population. Clinical trial registration number: ChiCTR2100051778.

Role of ultrasound and CT in the early diagnosis and surgical treatment of primary sternal osteomyelitis caused by Salmonella: Case reports.

Primary sternal osteomyelitis (PSO) caused by Salmonella is a rare condition and most commonly associated with sickle cell disease. Only one such case has been previously reported in an infant (age, <1 year) worldwide. The present study reported on two infantile cases of PSO caused by Salmonella in the absence of any hematological diseases. A total of two male infants (age, ≤1 year) were referred to our hospital for fever and rapid breathing accompanied by a chest wall mass involving the lower end of the sternum. Imaging findings on CT and ultrasound, which included sternal segment dislocation, lytic destruction and periosteal elevation, confirmed the diagnosis of PSO. Blood and purulent material cultures confirmed that the causative pathogen was Salmonella. The infants were completely cured by sequential intravenous and oral antibiotics followed by surgical debridement. The infants remained symptom-free and local recurrence of PSO was not detected at follow-up. PSO caused by Salmonella in the absence of any hematological diseases is a rare condition. Unfamiliarity with this disease may lead to a delay in diagnosis and serious complications. The current case report presents two cases of PSO along with a brief overview of the characteristics and management modalities for this condition, and it provides a comprehensive reference for pediatricians regarding this rare disease, particularly in infants.

The integrative regulatory network of circRNA and microRNA in keloid scarring.

Circular RNA (circRNA), a novel type of non-coding RNA that consists of a circular loop, has been demonstrated to act as a "sponge" for microRNAs (miRNAs). However, the role of circRNAs in keloid remains unknown. In this study, we investigated circRNA expression profiles in keloid to identify potential diagnostic and therapeutic circRNAs. We performed a circRNA microarray assay to determine circRNA expression in keloid and paired normal skin tissues. Quantitative reverse transcription polymerase chain reaction was used to evaluate the expression levels of candidate circRNAs. The most significantly over-expressed circRNA was used to predict putative miRNA targets and the binding sites of miRNAs with this circRNA. Finally, we constructed a circRNA-miRNA interaction network and carried out gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. We found 52 significantly upregulated and 24 downregulated circRNAs in keloid compared with normal skin tissue. We confirmed that hsa_circ_0057452, hsa_circ_0007482, hsa_circ_0020792, hsa_circ_0057342, and hsa_circ_0043688 were significantly upregulated in keloid tissues. Analysis of the circRNA-miRNA interaction network revealed that circRNAs could interact with miRNAs, including miRNA-29a, miRNA-23a-5p and miRNA-1976. GO and KEGG analyses indicated that these target genes were involved in biological functions and signaling pathways that may play vital roles in the pathogenesis of keloid. This study revealed that circRNAs are potentially implicated in the development of keloid and could serve as novel diagnostic and therapeutic targets.