Identification of hub biomarkers and immune cell infiltration characteristics of polymyositis by bioinformatics analysis.

Background: Polymyositis (PM) is an acquirable muscle disease with proximal muscle involvement of the extremities as the main manifestation; it is a category of idiopathic inflammatory myopathy. This study aimed to identify the key biomarkers of PM, while elucidating PM-associated immune cell infiltration and immune-related pathways. Methods: The gene microarray data related to PM were downloaded from the Gene Expression Omnibus database. The analyses using Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes, gene set enrichment analysis (GSEA), and protein-protein interaction (PPI) networks were performed on differentially expressed genes (DEGs). The hub genes of PM were identified using weighted gene co-expression network analysis (WGCNA) and least absolute shrinkage and selection operator (LASSO) algorithm, and the diagnostic accuracy of hub markers for PM was assessed using the receiver operating characteristic curve. In addition, the level of infiltration of 28 immune cells in PM and their interrelationship with hub genes were analyzed using single-sample GSEA. Results: A total of 420 DEGs were identified. The biological functions and signaling pathways closely associated with PM were inflammatory and immune processes. A series of four expression modules were obtained by WGCNA analysis, with the turquoise module having the highest correlation with PM; 196 crossover genes were obtained by combining DEGs. Subsequently, six hub genes were finally identified as the potential biomarkers of PM using LASSO algorithm and validation set verification analysis. In the immune cell infiltration analysis, the infiltration of T lymphocytes and subpopulations, dendritic cells, macrophages, and natural killer cells was more significant in the PM. Conclusion: We identified the hub genes closely related to PM using WGCNA combined with LASSO algorithm, which helped clarify the molecular mechanism of PM development and might have great significance for finding new immunotherapeutic targets, and disease prevention and treatment.

Optical weak measurement for the precise thickness determination of an ultra-thin film.

A total internal reflection system based on the weak value amplification principle is set up for the precise measurement of the thickness of an ultra-thin film. In this system, the film thickness is derived from the change of the double-peak pointer caused by the effective refractive index of the film, which is correlated to its thickness. The sensitivity and resolution of this system reached 2727.21 nm/RIU and 7.2×10-6 R I U, respectively, determined by using a sodium chloride solution with a refractive index of 1.331911. The growth process of TA/Fe(III) assembled films with thicknesses in the few nanometers range is monitored using the as-set-up system, and the experimental results are consistent with a theoretical calculation based on the Maxwell Garnett effective medium. Additionally, we theoretically calculated the detection limit for the thickness measurement of the film as 22 pm. We clearly provide a potential method for the precise measurement of the thickness of an ultra-thin film.

Multiple cardiac arrests induced by pulmonary embolism in a traumatically injured patient: A case report and review of the literature.

RATIONALE: Pulmonary embolism-induced cardiac arrest should not be given up arbitrarily, knowing that the etiology of pulmonary embolism is reversible in most cases. PATIENT CONCERNS: We present a case of continuous resuscitation lasting approximately 4 hours, during which 21 episodes of cardiac arrest occurred in a 46-year-old man who sustained high-level paraplegia after a road traffic accident. DIAGNOSES: Multiple cardiac arrests induced by pulmonary embolism. INTERVENTIONS: The patient received cardiopulmonary resuscitation and thrombolytic therapy. OUTCOMES: The patient was discharged in 2 weeks when his condition turned for the better. LESSONS: Cardiopulmonary resuscitation of patients with pulmonary embolism-induced cardiac arrest should not be given up arbitrarily, knowing that the etiology of pulmonary embolism is reversible in most cases. Effective external cardiac compression can not only save the patient's life but also attenuate neurological sequelae. Thrombolytic therapy is the key to the final success of resuscitation.

[Allelopathic effects of phenolic compounds of melon root exudates on Fusarium oxysporum f. sp. melonis].

In this study, the phenolic compounds of melon root exudates were identified by HPLC and seven phenolic compounds including gallic acid, phthalic acid, syringic acid, salicylic acid, ferulic acid, benzoic acid and cinnamic acid were observed. The laboratory experiment showed that ferulic acid, benzoic acid and cinnamic acid of 0.1 and 0.25 mmol x L(-1) could significantly promote the germination of Fusarium oxysporum f. sp. melonis spore while salicylic acid inhibited the spore germination to some degree. Syringic acid and ferulic acid significantly promoted the mycelium growth at the late stage of incubation. The pot experiments demonstrated that cinnamic acid, benzoic acid and ferulic acid enhanced melon infection at concentrations of 0.5, 0.1 and 0.5 mmol x L(-1).

Pyelonephritis Caused Solely by Escherichia hermanii.

INTRODUCTION: In contrast with Escherichia coli, the association of E. hermanii with urinary tract infections has not been described. CASE PRESENTATION: In this case, E. hermanii was the sole isolate recovered from urine specimens of a pyelonephritis patient. The organism was found to be susceptible to piperacillin-tazobactam, ceftazidime, cefazolin, cefixime, aztreonam, gentamicin, tobramycin, imipenem, meropenem and amikacin, and resistant to amoxicillin. Antibiotic treatment was initiated with oral cefixime (400 mg every 24 hours). The symptoms were relieved within 72 hours after therapy. A urine sample was taken seven days after antibiotic therapy. E. hermanii was no longer isolated. DISCUSSION: The present case demonstrates that the uropathogenic E. hermanii clone can cause destruction of the kidneys. During asymptomatic bacteriuria or cystitis, the bacteria remain in the urinary tract. Even when pyelonephritis develops, inflammatory response of the host is still restricted to the urinary tract. These signs mean that uropathogenic E. hermanii may be not very virulent.

Characterization of a water-soluble polysaccharide from Boletus edulis and its antitumor and immunomodulatory activities on renal cancer in mice.

A polysaccharide (BEP, Mw=113,432Da) was purified from Boletus edulis, which had a backbone consisting of (1→6)-linked-α-d-glucopyranosyl, (1→2,6)-linked-α-d-galactopyranosyl, (1→6)-linked-α-d-galactopyranosyl, and (1→3)-linked-α-d-rhamnopyranosyl residues, which were branched at O-2 position of (1→2,6)-linked-α-d-galactopyranosyl residue with a single terminal (1→)-linked-α-l-arabinofuranosyl residue. After 32 days' BEP administration to Renca tumor bearing mice, the tumor mass of Renca transplanted in mice was significantly repressed. Furthermore, BEP could significantly increase the spleen and thymus indices, stimulate splenocytes proliferation, augment NK cell and CTL activities in spleen, and promote the secretion of the cytokines IL-2 and TNF-α in Renca tumor bearing mice. Meanwhile oral administration of BEP (100 and 400mg/kg) restored all the altered hematological and biochemical parameters of tumor-bearing mice to normal levels. Thus, these data demonstrate that BEP possesses potential immunomodulatory activity and might be employed as effective therapeutic agents for the prevention of renal caner.

Suppression of SCIN inhibits human prostate cancer cell proliferation and induces G0/G1 phase arrest.

SCIN is a calcium regulated actin severing and capping protein. Its homologue in zebrafish is found to be related with cell death. In the present study, we found that SCIN is highly expressed in human prostate cancer specimens. However, the functions of SCIN in human prostate carcinoma cells are largely unknown. To address the function of SCIN in prostate carcinoma cells, we used lentivirus-mediated RNAi to knock down SCIN expression in PC3 cells, a prostate carcinoma cell line. We found that in vitro silencing of SCIN could inhibit the proliferation and colony formation ability of PC3 cells. Furthermore, cell cycle analysis showed that reduced SCIN expression lead to G0/G1 cell cycle arrest through the regulation of cell cycle-related genes, such as p21Waf1/Cip1, cyclin-dependent kinase inhibitor 2A (CDKN2A, p16Ink4A) and cyclin A2. These results suggest that SCIN plays an important role in the proliferation of prostate cancer cells and lentivirus-mediated inhibition of SCIN expression may be a potential therapeutic method for the treatment of prostate cancer.