This paper introduces the perioperative nursing of 20 cases of branchial cysts in newborn with cyst extraction. The nursing care focused on body position,respiratory care,diet management and wound care,which alleviated the patients' dyspnea,prevented respiratory aspiration and promoted wound healing. All the 20 newborn recovered well without recurrence in the four years after the operation.

Primary biliary cholangitis （PBC） is a persistent inflammatory autoimmune liver disease characterized by inflammatory injury and cholestasis in the small intrahepatic bile ducts. At present， the exact pathogenesis of PBC remains unknown， but a consensus has been reached on the fact that PBC is the result of the synergistic effect of various factors. In the cascade of immune and inflammatory reactions associated with PBC， macrophages appear as essential immune cells and actively participate in the damage to bile duct epithelial cells. This article introduces the origin and heterogeneity of macrophages in PBC and reviews the potential role of macrophages in the pathogenesis of PBC.

RNA interference (RNAi) has become a gold standard for validating gene function in basic life science research and provides a promising therapeutic modality for cancer and other diseases. This mini-review focuses on the potential of small interfering RNAs (siRNAs) in anticancer treatment, including the establishment and screening of cancer-associated siRNA libraries and their applications in anticancer drug target discovery and cancer therapy. This article also describes the current delivery approaches of siRNAs using lipids, polymers, and, in particular, gold nanoparticles to induce significant gene silencing and tumor growth regression.
Animals ; Clinical Trials as Topic ; Drug Carriers ; Drug Evaluation, Preclinical ; Gene Targeting ; Genetic Therapy ; methods ; Gold ; chemistry ; Humans ; Nanoparticles ; Neoplasms ; genetics ; therapy ; RNA Interference ; RNA, Small Interfering ; genetics

Hepatocellular carcinoma （HCC）， an insidious malignant tumor with high incidence and lethality， poses a major threat to physical and mental health of human beings. The pathological mechanism needs to be further studied. Surgery， radiotherapy， chemotherapy， and targeted drugs are effective but induce many adverse reactions. Traditional Chinese medicine （TCM） has unique advantages and abundant clinical experience in the treatment of HCC. There has been an explosion of research on the pathways， targets， and mechanism of TCM against HCC from the perspective of molecular biology. According to previous research， Chinese medicinals or compound Chinese medicine prescriptions， directly or indirectly prevent the occurrence and progression of HCC through multiple pathways and targets， which is closely related to the pathophysiological processes such as cell proliferation， metastasis， apoptosis， autophagy， inflammatory response， and immune response. This paper summarizes and analyzes research on the action pathways and mechanisms of Chinese medicine against HCC. Specifically， isoliquiritigenin， dendrobium candidum and Yexiazhu compound Ⅱ regulate phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt） signaling pathway to inhibit the growth， proliferation and metastasis of tumor cells. Toad venom and dioscorea zingiberensis induce and enhance HCC autophagy by modulating mammalian target of rapamycin （mTOR） signaling pathway. Myricetin， asparagus， and Biejiajian Wan regulate mitogen-activated protein kinase （MAPK） signaling pathway to promote HCC cell cycle arrest， inhibit angiogenesis， and induce apoptosis. Polygonum odoratum， tetragonum， and plantainoside modulate nuclear factor-kappa B （NF-κB） to inhibit inflammatory response and HCC metastasis and reduce drug resistance. Quercetin and erigeron breviscapus control the Janus kinase 2/signal transducer and activator of transcription 3 （JAK2/STAT3） signaling pathway to suppress epithelial-mesenchymal transition （EMT） and remodel cytoskeleton. This paper is expected to lay a theoretical basis for the in-depth research on and clinical application of Chinese medicine in the treatment of HCC.

Psoriasis is considered as an inflammatory disease driven by T cells, and its pathogenesis is closely related to the imbalance of intestinal bacteria flora. It has been reported that Bacteroides fragilis could play an anti-inflammatory role by regulating the expression of cytokines in T cells. To date, there is no report using B. fragilis to treat psoriasis. In this study, we explored the therapeutic effect of B. fragilis BF839 on psoriasis. We selected 27 psoriasis patients who were treated in the Second Affiliated Hospital of Guangzhou Medical University from April to October 2019. The patients were given B. fragilis BF839 orally for 12 weeks while maintaining the original treatment. The psoriasis area and severity index (PASI) score was evaluated before and after the treatment. The rate of drug withdrawal and reduction after 12 weeks of treatment were calculated. Our results showed that the rate of 12-week trial completion was 96.3% (26/27). We used PASIN to define the proportion of people whose PASI score decreased more than or equal to N% after treatment. At 12 weeks, PASI30, PASI50, and PASI75 were 65.4%, 42.3%, and 19.2%, respectively. The PASI score was 9.1±5.9 and 5.8±4.9 before and after 12 weeks of treatment respectively, and the difference was statistically significant (P<0.01). The effective rate of the visual analog scale (VAS) score was 42.3% at 12 weeks, and the VAS score was 2.9±2.2 and 2.3±2.1 before and after 12 weeks of treatment, respectively, which had no statistically significant difference (P>0.05). The adverse reaction rate of patients was 3.8% (1/26) within 12 weeks of treatment, including 1 case of constipation, and the rate of drug withdrawal and reduction was 60.0%. The above results suggest that B. fragilis BF839 may be functional on the treatment of psoriasis by reducing the PASI score and the drug usage rate with few side effect, which deserves further study.
Anti-Inflammatory Agents ; Bacteroides fragilis ; Cytokines ; Humans ; Psoriasis/drug therapy* ; Severity of Illness Index ; Treatment Outcome

Objective: To report on clinical characteristics and genetic findings in 15 Chinese patients with methylmalonic acidemia (MMA). Methods: For the 15 MMA patients detected by tandem mass spectrometry, genetic analysis was carried out in twelve pedigrees. Clinical characteristics, genetic finding, treatment and outcomes were retrospectively analyzed. Results: The main features of the patients included poor feeding, recurrent vomiting, lethargy, seizure and development retardation. Blood propionylcarnitine (except for 3 patients), its ratio with acetylcarnitine, and urine methylmalonic acid were increased in all patients. Twelve patients were diagnosed genetically, which included 7 with MUT variants, 4 with MMACHC variants, and 1 with MMAB variant. Nine MUT variants were detected, among which c. 1159A>C, 753+ 1delGinsTGGTTATTA and c. 504del were novel. Six known pathogenic MMACHC variants and two novel MMAB variants (c.289_290delGG, c. 566G>A) were also detected. Seven patients died of metabolic crises within a year, others had improved effectively following the treatment, but had mild to severe growth delay and/or developmental retardation. Conclusion The clinical manifestation of MMA are complex. Most patients have variants of the MUT and MMACHC genes. High mortality may occur before one year of age.

Increased intestinal barrier permeability, leaky gut, has been reported in patients with autism. However, its contribution to the development of autism has not been determined. We selected dextran sulfate sodium (DSS) to disrupt and metformin to repair the intestinal barrier in BTBR T⁺tf/J autistic mice to test this hypothesis. DSS treatment resulted in a decreased affinity for social proximity; however, autistic behaviors in mice were improved after the administration of metformin. We found an increased affinity for social proximity/social memory and decreased repetitive and anxiety-related behaviors. The concentration of lipopolysaccharides in blood decreased after the administration of metformin. The expression levels of the key molecules in the toll-like receptor 4 (TLR4)-myeloid differentiation factor 88 (MyD88)-nuclear factor kappa B (NF-κB) pathway and their downstream inflammatory cytokines in the cerebral cortex were both repressed. Thus, "leaky gut" could be a trigger for the development of autism via activation of the lipopolysaccharide-mediated TLR4-MyD88-NF-κB pathway.
Mice ; Animals ; NF-kappa B ; Myeloid Differentiation Factor 88/metabolism* ; Lipopolysaccharides/pharmacology* ; Toll-Like Receptor 4/metabolism* ; Autistic Disorder/metabolism* ; Signal Transduction/physiology*