PENGARUH BOBOT TELUR TETAS ITIK TERHADAP PERKEMBANGAN EMBRIO, FERTILITAS DAN BOBOT TETAS

EFFECT OF DUCK EGG WEIGHT ON FERTILITY, EMBRYO DEVELOPMENT AND HATCHING WEIGHT OF DAY OLD DUCK. This study was done to evaluate embryonic development for determination of egg fertility and hatching weight of day old duck (DOD). This study involved 160 eggs of duck with the average egg weight (EW) classified into 55g ≤  EW < 60g, 61g ≤ EW < 65g, 65g ≤ EW < 70g and 71g ≤ EW < 75g. Data collection was conducted over 28 days, as long as the period of hatching process. The design method used in this study was completely randomized design. Existing data were analyzed using analysis of variance. Treatments in this study were 4 treatments and 4 replications at each treatment. The variables measured were the percentage of egg fertility, embryo development and hatching weight. Results showed that duck embryo development during the hatching process was in good condition process. The results of variance analysis showed that treatments of egg weight did not affect significantly the percentages of egg fertility. The percentages of fertility were ranging between 85 – 95%. Hatching weights were ranging between 31g – 51g per DOD. Based on the results of this study, it can be concluded that egg weight had no effect on the process of embryonic development and fertility, except those for the hatching weight of DOD. Key words: Duck egg weight, embryonic development, fertility, hatching weight

Proteoglycan-4 Regulates Fibroblast to Myofibroblast Transition and Expression of Fibrotic Genes in the Synovium

Background: Synovial tissue fibrosis is common in advanced OA with features including the presence of stress fiber-positive myofibroblasts and deposition of cross-linked collagen type-I. Proteoglycan-4 (PRG4) is a mucinous glycoprotein secreted by synovial fibroblasts and is a major component of synovial fluid. PRG4 is a ligand of the CD44 receptor. Our objective was to examine the role of PRG4-CD44 interaction in regulating synovial tissue fibrosis in vitro and in vivo. Methods: OA synoviocytes were treated with TGF-β ± PRG4 for 24h and α-SMA content was determined using immunofluorescence. Rhodamine-labeled rhPRG4 was incubated with OA synoviocytes ± anti-CD44 or isotype control antibodies and cellular uptake of rhPRG4 was determined following a 30-min incubation and α-SMA expression following a 24-h incubation. HEK-TGF-β cells were treated with TGF-β ± rhPRG4 and Smad3 phosphorylation was determined using immunofluorescence and TGF-β/Smad pathway activation was determined colorimetrically. We probed for stress fibers and focal adhesions (FAs) in TGF-β-treated murine fibroblasts and fibroblast migration was quantified ± rhPRG4. Synovial expression of fibrotic markers: α-SMA, collagen type-I, and PLOD2 in Prg4 gene-trap (Prg4GT) and recombined Prg4GTR animals were studied at 2 and 9 months of age. Synovial expression of α-SMA and PLOD2 was determined in 2-month-old Prg4GT/GT&Cd44−/− and Prg4GTR/GTR&Cd44−/− animals. Results: PRG4 reduced α-SMA content in OA synoviocytes (p \u3c 0.001). rhPRG4 was internalized by OA synoviocytes via CD44 and CD44 neutralization attenuated rhPRG4’s antifibrotic effect (p \u3c 0.05). rhPRG4 reduced pSmad3 signal in HEKTGF- β cells (p \u3c 0.001) and TGF-β/Smad pathway activation (p \u3c 0.001). rhPRG4 reduced the number of stress fiberpositive myofibroblasts, FAs mean size, and cell migration in TGF-β-treated NIH3T3 fibroblasts (p \u3c 0.05). rhPRG4 inhibited fibroblast migration in a macrophage and fibroblast co-culture model without altering active or total TGF-β levels. Synovial tissues of 9-month-old Prg4GT/GT animals had higher α-SMA, collagen type-I, and PLOD2 (p \u3c 0.001) content and Prg4 re-expression reduced these markers (p \u3c 0.01). Prg4 re-expression also reduced α-SMA and PLOD2 staining in CD44-deficient mice. Conclusion: PRG4 is an endogenous antifibrotic modulator in the joint and its effect on myofibroblast formation is partially mediated by CD44, but CD44 is not required to demonstrate an antifibrotic effect in vivo

Sentinel node biopsy stands the test of time and the proof of time

International audienceObservational studies conducted in the 1970s, including that by Bernard Guerrier, cited by Bocca et al. [1], and subsequent studies published in the literature [2], have shown that neck dissection must be systematically performed in operable stage T1-T2N0 oral and oropharyngeal squamous cell carcinoma (OC) in order to diagnose and treat occult micrometastases [3]

An exploratory, open-label, randomized, multicenter study to investigate the pharmacodynamics of a glycoengineered antibody (imgatuzumab) and cetuximab in patients with operable head and neck squamous cell carcinoma

Background: In addition to inhibiting epidermal growth factor receptor (EGFR) signaling, anti-EGFR antibodies of the IgG1 subtype can induce a complementary therapeutic effect through the induction of antibody-dependent cell-mediated cytotoxicity (ADCC). Glycoengineering of therapeutic antibodies increases the affinity for the Fc-gamma receptor, thereby enhancing ADCC.Patients and methods: We investigated the changes in immune effector cells and EGFR pathway biomarkers in 44 patients with operable, advanced stage head and neck squamous cell carcinoma treated with two pre-operative doses of either glycoengineered imgatuzumab (GA201; 700 or 1400 mg) or cetuximab (standard dosing) in a neoadjuvant setting with paired pre- and post-treatment tumor biopsies.Results: Significant anti-tumor activity was observed with both antibodies after just two infusions. Metabolic responses were seen in 23 (59.0%) patients overall. One imgatuzumab-treated patient (700 mg) achieved a pathological complete response. An immediate and sustained decrease in peripheral natural killer (NK) cells was consistently observed with the first imgatuzumab infusion but not with cetuximab. The functionality of the remaining peripheral NK cells was maintained. Similarly, a pronounced increase in circulating cytokines was seen following the first infusion of imgatuzumab but not cetuximab. Overall, tumor-infiltrating CD3+ cell counts increased following treatment with both antibodies. A significant increase from baseline in CD3+/perforin+ cytotoxic T-cells occurred only in the 700 mg imgatuzumab group (median 95% increase, p &lt; 0.05). The most prominent decrease of EGFR-expressing cells was recorded after treatment with imgatuzumab (700 mg: –34.6%; 1400 mg: –41.8%). The post-treatment inflammatory tumor microenvironment was strongly related to baseline tumor-infiltrating immune cell density, and baseline levels of EGFR and pERK in tumor cells most strongly predicted therapeutic response.Conclusions: These pharmacodynamic observations and relationship with efficacy are consistent with the proposed mode of action of imgatuzumab combining efficient EGFR pathway inhibition with ADCC-related immune anti-tumor effects.Clinical trial registration number: NCT01046266 (ClinicalTrials.gov).</p