Capital Medical University

About: Capital Medical University is a education organization based out in Beijing, China. It is known for research contribution in the topics: Population & Medicine. The organization has 56150 authors who have published 47290 publications receiving 811249 citations.

Prevalence and characteristics of primary angle-closure diseases in a rural adult Chinese population: the Handan Eye Study.

Abstract: PURPOSE To investigate the prevalence and characteristics of primary angle-closure suspect (PACS), primary angle closure (PAC), and primary angle-closure glaucoma (PACG) in a rural population in China METHODS In all, 6716 Han Chinese 30 years of age and older (5480 subjects 40 years of age and older) from 13 villages in Handan were randomly selected and completed an ophthalmologic examination, including visual acuity, intraocular pressure (IOP), slit-lamp examination, gonioscopy and stereoscopic photography, and visual field PACS was defined as present if either eye had the posterior trabecular meshwork not visible for 180° or more on gonioscopy PAC was present in an eye with PACS and peripheral anterior synechiae (PAS) and/or IOP 21 mm Hg, but without glaucomatous neuropathy (GON) PACG was defined as PAC with evidence of GON RESULTS The standardized prevalences of PACG, PAC, and PACS were 05% (95% confidence interval [CI]: 03‐07%), 15% (95% CI: 12‐18%), and 104% (95% CI: 96‐112%) in those 40 years of age and older The prevalence of all three conditions increased with age (P 0001) Females had much higher rates of PACS, PAC, and PACG (P 005); 21 persons with PACG (65%) were blind in at least one eye: 13 were due to glaucoma and the other 8 likely had other causes CONCLUSIONS The prevalence of PACS, PAC, and PACG in this rural population is similar to what was previously reported in urban Chinese residents Two thirds of those with PACG were blind in at least one eye Strategies to detect and treat this preventable disease in rural China are needed (Invest Ophthalmol Vis Sci 2011;52:8672‐8679) DOI:101167/iovs11-7480

Plasmid-mediated quinolone resistance genes and antibiotic residues in wastewater and soil adjacent to swine feedlots: potential transfer to agricultural lands.

Abstract: Background: Inappropriate use of antibiotics in swine feed could cause accelerated emergence of antibiotic resistance genes, and agricultural application of swine waste could spread antibiotic resistance genes to the surrounding environment. Objectives: We investigated the distribution of plasmid-mediated quinolone resistance (PMQR) genes from swine feedlots and their surrounding environment. Methods: We used a culture-independent method to identify PMQR genes and estimate their levels in wastewater from seven swine feedlot operations and corresponding wastewater-irrigated farm fields. Concentrations of (fluoro)quinolones in wastewater and soil samples were determined by ultra-performance liquid chromatography–electrospray tandem mass spectrometry. Results: The predominant PMQR genes in both the wastewater and soil samples were qnrD, qepA, and oqxB, whereas qnrS and oqxA were present only in wastewater samples. Absolute concentrations of all PMQR genes combined ranged from 1.66 × 107 to 4.06 × 108 copies/mL in wastewater and 4.06 × 106 to 9.52 × 107 copies/g in soil. Concentrations of (fluoro)quinolones ranged from 4.57 to 321 ng/mL in wastewater and below detection limit to 23.4 ng/g in soil. Significant correlations were found between the relative abundance of PMQR genes and (fluoro)quinolone concentrations (r = 0.71, p = 0.005) and the relative abundance of PMQR genes in paired wastewater and agricultural soil samples (r = 0.91, p = 0.005). Conclusions: Swine feedlot wastewater may be a source of PMQR genes that could facilitate the spread of antibiotic resistance. To our knowledge, this is the first study to examine the occurrence of PMQR genes in animal husbandry environments using a culture-independent method.

Curcumin Protects against Ischemic Stroke by Titrating Microglia/Macrophage Polarization.

Abstract: Stroke is the most common type of cerebrovascular disease and is a leading cause of disability and death. Ischemic stroke accounts for approximately 80% of all strokes. The remaining 20% of strokes are hemorrhagic in nature. To date, therapeutic options for acute ischemic stroke are very limited. Recent research suggests that shifting microglial phenotype from the pro-inflammatory M1 state toward the anti-inflammatory and tissue-reparative M2 phenotype may be an effective therapeutic strategy for ischemic stroke. The dietary phytochemical curcumin has shown promise in experimental stroke models, but its effects on microglial polarization and long-term recovery after stroke are unknown. Here we address these gaps by subjecting mice to distal middle cerebral artery occlusion (dMCAO) and administering curcumin intraperitoneally (150 mg/kg) immediately after ischemia and 24 hours later. Histological studies revealed that curcumin post-treatment significantly reduced cerebral ischemic damage 3 days after dMCAO. Sensorimotor functions—as measured by the adhesive removal test and modified Garcia scores—were superior in curcumin-treated mice at 3, 5, 7, and 10 days after stroke. RT-PCR measurements revealed an elevation of M2 microglia/macrophage phenotypic markers and a reduction in M1 markers in curcumin-treated brains 3 days after dMCAO. Immunofluorescent staining further showed that curcumin treatment significantly increased the number of CD206+Iba1+ M2 microglia/macrophages and reduced the number of CD16+Iba1+ M1 cells 10 days after stroke. In vitro studies using the BV2 microglial cell line confirmed that curcumin inhibited lipopolysaccharide (LPS) and interferon-γ (IFN-γ)-induced M1 polarization. Curcumin treatment concentration-dependently reduced the expression of pro-inflammatory cytokines, including TNF-α, IL-6, and IL-12p70, in the absence of any toxic effect on microglial cell survival. In conclusion, we demonstrate that curcumin has a profound regulatory effect on microglial responses, promoting M2 microglial polarization and inhibiting microglia-mediated pro-inflammatory responses. Curcumin post-treatment reduces ischemic stroke-induced brain damage and improves functional outcomes, providing new evidence that curcumin might be a promising therapeutic strategy for stroke.

IFITM Genes, Variants, and Their Roles in the Control and Pathogenesis of Viral Infections.

Abstract: Interferon-induced transmembrane proteins (IFITMs) are a family of small proteins that localize in the plasma and endolysosomal membranes. IFITMs not only inhibit viral entry into host cells by interrupting the membrane fusion between viral envelope and cellular membranes, but also reduce the production of infectious virions or infectivity of progeny virions. Not surprisingly, some viruses can evade the restriction of IFITMs and even hijack the antiviral proteins to facilitate their infectious entry into host cells or promote the assembly of virions, presumably by modulating membrane fusion. Similar to many other host defense genes that evolve under the selective pressure of microorganism infection, IFITM genes evolved in an accelerated speed in vertebrates and many single-nucleotide polymorphisms (SNPs) have been identified in the human population, some of which have been associated with severity and prognosis of viral infection (e.g., influenza A virus). Here, we review the function and potential impact of genetic variation for IFITM restriction of viral infections. Continuing research efforts are required to decipher the molecular mechanism underlying the complicated interaction among IFITMs and viruses in an effort to determine their pathobiological roles in the context of viral infections in vivo.