Jewish Hospital

About: Jewish Hospital is a healthcare organization based out in Cincinnati, Ohio, United States. It is known for research contribution in the topics: Antigen & Population. The organization has 3881 authors who have published 3414 publications receiving 123044 citations.

Metformin-diet ameliorates coronary heart disease risk factors and facilitates resumption of regular menses in adolescents with polycystic ovary syndrome.

Abstract: Background: In 35 adolescent females (17 ± 2 years) with polycystic ovary syndrome (PCOS), median body mass index (BMI) 30.8 kg/m 2 , we assessed effeicacy of metformin-diet for 1 year for reduction of weight, insulin, HOMA insulin resistance (IR), cholesterol, triglycerides, and resumption of regular menses. Methods: Calories (26% protein, 44% carbohydrate) were targeted to 1,500-1,800/day if BMI was <25 or to 1,200-1,500/day if BMI was ≥25, along with 2,550 mg metformin. Results: Median weight fell from 82.7 to 79.1 kg (p = 0.009), insulins 16.7 to 13.3 μU/ml (p <0.0001), HOMA IR 3.41 to 2.74 (p = 0.0004), total cholesterol 164 to 151 mg/dl (p = 0.002), and triglyceride 103 to 85 mg/dl (p = 0.006). The percentage of cycles with normal menses rose from a pre-treatment mean of 22% to 74%, p < 0.0001. Conclusions: In adolescents with PCOS, metformin-diet reduces weight, insulin, IR, cholesterol, and triglycerides, and facilitates resumption of regular menses.

Fluorescent markers for studying phagosome-lysosome fusion

Abstract: Lysosomotropic fluorescent aminoacridines such as acridine orange and quinacrine have achieved prominence as markers for studying lysosome-phagosomes fusion, especially in macrophages. Experiments described demonstrate that because the aminoacridines traverse biological membranes with facility, they diffuse throughout the system, and ultimately accumulate intra- or extracellularly where they are most efficiently bound. Their presence or absence in phagosomes is therefore not unequivocally indicative of fusion or nonfusion. Alternative fluorescent lysosomal markers are described, and systems defined for which the aminoacridines may probably be used with confidence.

Involvement of cell-cell adhesion molecules in liver colonization by metastatic murine lymphoma/lymphosarcoma variants

Abstract: Metastatic variant sublines of the murine RAW117 large cell lymphoma or lymphosarcoma have been established in vitro by sequential cycles of harvesting of liver tumor nodules after intravenous inoculation of tumor cell suspensions into syngeneic BALB/c mice. After five and tenin vivo selections for liver colonization, variant sublines RAW117-H5 and -H10, respectively, were established, and these formed significantly more surface liver tumors than the parental RAW117-P line. RAW117 sublines were tested for their abilities to adhere to embryonic mouse liver or brain cells in anin vitro cell-cell adhesion assay. Liver colonizing RAW117-H10 cells adhered with greater selectivity to liver cells than to brain cells. Parental RAW 117-P cells were more homotypically adhesive, but they were nonselective in their organ cell adhesion properties. We examined RAW117 cells for the presence of liver cross-reactive antigens using polyclonal xenoantibody preparations directed against embryonic murine liver cells. These antibody preparations block organ-specific homotypic adhesion of embryonic murine liver cellsin vitro. The amount of fetal liver antigen(s) expressed on RAW117 sublines correlated with liver colonization potentials (H10 > H5 > P) in quantitative absorption assays. Treatment of the highly metastatic RAW117-H10 subline with polyclonal anti-embryonic murine liver F(ab′)2 or Fab′ antibody fragments had no effect on RAW117-H10 cell viability or growthin vitro orin vivo, but inhibited liver colonization (median liver tumor colonies reduced from > 200 to 0) and prolonged life expectancy. In contrast, pretreatment of RAW 117-H 10 cells with polyclonal anti-H-2 did not modify thein vivo biologic properties of these metastatic cells.

Familial deficiency of two subunits of the first component of complement. C1r and C1s associated with a lupus erythematosus-like disease.

Abstract: Complete absence of C1r and almost complete absence of C1s were found in 4 of 8 living siblings. Two of the 4 suffer from a syndrome that combines discoid lupus erythematosus and nondeforming rheumatoid-like arthritis; one of the siblings has mild nephritis. The other 2 C1 deficient family members are clinically well. Evidence from this and other families suggests that deficiency of C1 components or C4 is associated with higher risk of developing a lupus-like disease than is deficiency of C2.