Jess, I can't imagine they would give no update tomorrow, Even they could not be that stupid, if there's no update tomorrow, You better pack your bags because this will be a long, long trip.
Exactly Jess, Way , Way to much excitement here, The BO numbers are pure fantasy, If there was a BO before this had a chance to put the Abbott Automated Assay out, TOP dollar would be $4.00 , And that's stretching it IMHO
We examine galectin-3 expression in CNS after EMCV inoculation.
Galectin-3 is up-regulated in several degenerated lesions 96 h after EMCV.
Iba-1 positive microglia was activated within and around the focus of infection.
Microlesions with a few galectin-3 positive cells were detected in cerebellum at 48 h.
Galectin-3 is a key mediator between viral infection and neuronal degeneration.
Galectin-3 is a β-galactosidase-binding lectin which is important in cell proliferation and apoptotic regulation. Encephalomyocarditis virus (EMCV), which includes the Enterovirus genus, can cause not only acute myocarditis but also neuronal degeneration of central nervous system in various animals including mice. The pathophysiological role of galectin-3 in central nervous system following acute viral infection is not fully understood. The goal of this study is to determine the localization and time-course of galectin-3 expression after acute viral inoculation with EMCV. Galectin-3 is up-regulated in degenerated lesions of brain area including cerebellum, hippocampus, thalamus and cerebral hemisphere, 96 h after EMCV inoculation. At the same time, Iba-1 positive microglia was morphologically activated within and around the focus of infection. Interestingly, in cerebellum, the microlesions containing a few galectin-3 cells were detected in the immediate-early phase of infection, as early as 48 h after EMCV inoculation. Thus, our results indicate that galectin-3 expression may be a key mediator between viral infection and neuronal degeneration in central nervous system including cerebellum. Furthermore, detection of galectin-3 might be an early diagnostic method for neuronal degeneration after virus infection.
That 4,106,071 Shares of Common Stock is based on the Number of shares outstanding at the time of the Agreement, The Agreement also states (( the number of shares which may be issued under the Purchase Agreement may not exceed an amount that would result in the Company breaching its obligations under the rules of the NASDAQ Global Market. In particular, the Company may not issue more than 4,106,071 shares, representing 19.99% of the total number of its outstanding shares on January 24, 2013 ))
What we dont know is will that 19.99% apply now with the OS at around 35M shares outstanding which would bring the total # shares to around 7M ?????
That would be great if it happens, But there is value beyond a Buyout, If I were only thinking Buyout, I would be very disappointed if it didn't happen.
Why don't you go away, Your contribution to this board is nonsense, You know nothing about investing or stocks, Your Investment plan is , GO GO GO ,GET LOST
I don't know who runs the IR at this company, But they don't know what they're doing and should have been let go with the rest of the employees on Sept 11
Jess, I believe some posters on this board have already reported this last week, As usual, BGMD is late on this, This has been out for a while
hellokimy310 • Mar 18, 2015 2:56 PM
Also Google (unrelated): Prevalence, Impact, and Predictive Value of Detecting Subclinical Coronary and Carotid Atherosclerosis in Asymptomatic Adults
First result. It's a summary of the BioImage study from JACC March 2015! This is very interesting. BG Medicine owns this study. So what does this mean for them? Less
Thats a first
Too many things could happen between this Wed and next Tuesday, If they don't inform investors as to what's going on with the 10K and Abbott, I'll get back in after earnings.
Go To OP - 87
could not post whole abstract, heres the link
No routine tests currently exist to objectively diagnose mild traumatic brain injury mTBI /concussion. Previously reported biomarkers for mTBI represented proteins released from the damaged neurons or glia. However, the low levels of these proteins and/or the complexity of assays used for their detection limits the implementation of these biomarkers in routine practice. Here we sought to identify proteins whose synthesis is altered after mTBI and whose blood levels could be measured using standard immunoassays. Adult patients sustaining a concussion within the past 24 h were enrolled. Controls were uninjured subjects and patients with orthopedic injur OI. Four candidate biomarkers were identified: copeptin, galectin 3 LGALS3, matrix metalloproteinase 9 MMP9, and occludin OCLN. A 3.4-fold decrease p
Huh, $7M WILL NOT fund this company for 2 years.
They just went through $6M in the last 6 months , just the GE loan by itself will cost approx 400k a month until Sept 2015, how you come up with figure is beyond me
Yeah I seen that last nite, That was a good find.
There was no money involved there it was a (( collaboration )) between these Hospitals and BG Medicine .
But it is always good to get your name out there, Just IMHO, The Bioimage study is BG Medicines most valuable asset of a company, To me that study is worth more then Gal 3.
BioImage Study Patient Cohort and Banked Specimens
We have exclusive rights to diagnostic inventions arising from our analysis of data generated from the BioImage Study, a proprietary observational and community-based cohort of over 6,800 individuals who have been followed since 2009. Baseline blood serum, plasma, and DNA and RNA samples collected from all participants have been stored and are available for our analysis. In addition, insurance claims data, including information regarding diagnoses, procedures, and therapies related to over 1,200 non-fatal cardiovascular events that were experienced by participants in the cohort over the more than four years since follow-up was initiated is available to us for data mining. We believe that this asset provides us with a unique and proprietary platform from which we may develop new diagnostic products.
treatment did not impair the prognostic value of Gal-3 assessed with a 17.8 ng/mL cut off. Gal-3 levels maintained its strong prognostic value in CHF also in patients treated with MRAs. The significance of the observed lack of an interaction between Gal-3 and treatment effect of MRAs remains to be elucidated.
Galectin-3 (Gal-3) is considered as a myocardial fibrosis biomarker with prognostic value in heart failure (HF). Since aldosterone is a neurohormone with established fibrotic properties, we aimed to investigate if mineralocorticoid receptor antagonists (MRAs) would modulate the prognostic value of Gal-3.
The IBLOMAVED cohort comprised 427 eligible chronic HF patients (CHF) with echocardiography and heart failure biomarkers assessments (BNP). After propensity score matching CHF patients for cardiovascular risk factors, to form balanced groups, Gal-3 levels were measured at baseline in plasma from patients treated with MRAs (MRA-Plus, n=101) or not (MRA-Neg, n=101). The primary end point was all-cause mortality with a follow-up of 3 years.
Gal-3 in plasma from these patients were similar with median values of 14.0 ng/mL [IQR, 9.9–19.3] and 14.4 ng/mL [IQR, 12.3–19.8] (P = 0.132) in MRA-Neg and MRA-Plus, respectively. Patients with Gal-3 ≤17.8 ng/mL had an HR of 1 (reference group) and 1.5 [0.4–5.7] in MRA-Neg and MRA-Plus, respectively (p=0.509). Patients with Gal-3 ≥ 17.8 ng/mL had an HR of 7.4 [2.2–24.6] and 9.0 [2.9–27.8] in MRA-Plus and MRA-Neg, respectively (p=0.539) and a median survival time of 2.4 years [95%CI,1.8–2.4]. Multivariate Cox proportional hazard analysis confirmed that MRA and the interaction term between MRA treatment and Gal-3 17.8 ng/mL were not factors associated with survival.