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Spatial dataflow architectures such as reconfigurable dataflow accelerators (RDA) can provide much higher performance and efficiency than CPUs and GPUs. In particular, vectorized reconfigurable dataflow accelerators (vRDA) in recent literature represent a design point that enhances the efficiency of dataflow architectures with vectorization. Today, vRDAs can be exploited using either hardcoded kernels or MapReduce languages like Spatial, which cannot vectorize data-dependent control flow. In contrast, CPUs and GPUs can be programmed using general-purpose threaded abstractions. The ideal combination would be the generality of a threaded programming model coupled with the efficient execution model of a vRDA. We introduce Revet: a programming model, compiler, and execution model that lets threaded applications run efficiently on vRDAs. The Revet programming language uses threads to support a broader range of applications than Spatial's parallel patterns, and our MLIR-based compiler lowers this language to a generic dataflow backend that operates on streaming tensors. Finally, we show that mapping threads to dataflow outperforms GPUs, the current state-of-the-art for threaded accelerators, by 3.8x.

Despite the availability of a protective vaccine for over 3 decades, the number of persons with chronic HBV infection remains high. These persons are at risk for complications of cirrhosis and hepatocellular carcinoma (HCC). Current treatment is effective at inhibiting viral replication and reducing complications of chronic HBV infection, but is not curative, and in the case of nucleos(t)ide analogues must be administered long-term, if not indefinitely, due to persistence of the covalently closed circular (cccDNA) in the hepatocyte. Thus, there is a need for novel, finite therapy that can cure chronic HBV infection. A number of agents are in early phase development and can be broadly viewed as direct acting antiviral agents that either target key viral or host proteins important for the viral life cycle or immunemodulators that boost or restore an ineffective host immune response. This review will highlight key developments in antiviral/immunomodulatory therapy, the rationale for choosing these approaches and possible therapeutic regimens.

T cells play a critical role in viral infection. We examined whether T-cell effector and regulatory responses can define clinical stages of chronic hepatitis B (CHB).We enrolled 200 adults with CHB who participated in the National Institutes of Health-supported Hepatitis B Research Network from 2011 through 2013 and 20 uninfected individuals (controls). Peripheral blood lymphocytes from these subjects were analyzed for T-cell responses (proliferation and production of interferon gamma and interleukin 10) to overlapping hepatitis B virus (HBV) peptides (preS, S, preC, core, and reverse transcriptase), influenza matrix peptides, and lipopolysaccharide. T-cell expression of regulatory markers FOXP3, programmed death-1, and cytotoxic T lymphocyte-associated antigen-4 was examined by flow cytometry. Immune measures were compared with clinical parameters, including physician-defined immune-active, immune-tolerant, or inactive CHB phenotypes, in a blinded fashion.Compared with controls, patients with CHB had weak T-cell proliferative, interferon gamma, and interleukin 10 responses to HBV, with increased frequency of circulating FOXP3(+)CD127(-) regulatory T cells and CD4(+) T-cell expression of programmed death-1 and cytotoxic T lymphocyte-associated antigen-4. T-cell measures did not clearly distinguish between clinical CHB phenotypes, although the HBV core-specific T-cell response was weaker in hepatitis B e antigen (HBeAg)(+) than HBeAg(-) patients (percent responders: 3% vs 23%; P = .00008). Although in vitro blockade of programmed death-1 or cytotoxic T lymphocyte-associated antigen-4 increased T-cell responses to HBV, the effect was weaker in HBeAg(+) than HBeAg(-) patients. Furthermore, T-cell responses to influenza and lipopolysaccharide were weaker in CHB patients than controls.HBV persists with virus-specific and global T-cell dysfunction mediated by multiple regulatory mechanisms, including circulating HBeAg, but without distinct T-cell-based immune signatures for clinical phenotypes. These findings suggest additional T-cell-independent or regulatory mechanisms of CHB pathogenesis that warrant further investigation.

Chronic hepatitis B virus (HBV) infection is an important cause of cirrhosis and hepatocellular carcinoma worldwide; populations that migrate to the US and Canada might be disproportionately affected. The Hepatitis B Research Network (HBRN) is a cooperative network of investigators from the United States and Canada, created to facilitate clinical, therapeutic, and translational research in adults and children with hepatitis B. We describe the structure of the network and baseline characteristics of adults with hepatitis B enrolled in the network.

A47-year-old woman reported an 18-month-old pretibial rash on her left shin during a routine office visit. She had a history of type 1 diabetes mellitus (DM) and has been on insulin therapy for the past 13 years. She did not complain of any itching, pain, or bleeding from the rash. On examination, an 8x3 cm elongated indurated plaque with telangiectases, central atrophy, and yellow pigmentation was noted. Reddishbrown pigmentation was present peripherally along the margins. No ulcerations were present. Patient was diagnosed to have necrobiosis lipoidica on the basis of history and typical features on examination.(Published: 17 December 2013)Citation: Journal of Community Hospital Internal Medicine Perspectives 2013, 3-4: 22627 - http://dx.doi.org/10.3402/jchimp.v3i3-4.22627

Additional file 1 . Supplemental methods, figures and tables. SM 1.1. Mapping of the O-glycosylation sites. SM 1.2. Beta elimination and mass spectrometric analysis of HPX O-glycans. Table S1. Basic characteristics of disease-free controls and HALT-C participants. Table S2. The impact of IFN treatment on S-HPX. Groups of fibrotic and cirrhotic participants in the HALT-C trial were separated into the IFN treated and control arms. Table S3. Model estimates for logistic regression model in discovery set. Table S4. S-HPX measurement in the discovery and validation sets of participants. Figure S1. Precursor mass spectra confirmation of complete desialylation of HPX using 2M Acetic acid. Figure S2. ETD spectra of sialidase-treated O-glycopeptides corresponding to HILIC fractions of mono- (top), bis- (middle), and triply-glycosylated (bottom) O-glycopeptide of HPX. Figure S3. Direct quantification of S-HPX at progressing stages of liver disease divided by gender (left) and race (right; CA Caucasian, AA African-American). Figure S4. Significant associations of S-HPX and other clinical variables. Figure S5. Quantification of detected N-glycopeptides at three different N-glycosylation sequons (N64, N187 and N453) of HPX.

Additional file 1 . Supplemental methods, figures and tables. SM 1.1. Mapping of the O-glycosylation sites. SM 1.2. Beta elimination and mass spectrometric analysis of HPX O-glycans. Table S1. Basic characteristics of disease-free controls and HALT-C participants. Table S2. The impact of IFN treatment on S-HPX. Groups of fibrotic and cirrhotic participants in the HALT-C trial were separated into the IFN treated and control arms. Table S3. Model estimates for logistic regression model in discovery set. Table S4. S-HPX measurement in the discovery and validation sets of participants. Figure S1. Precursor mass spectra confirmation of complete desialylation of HPX using 2M Acetic acid. Figure S2. ETD spectra of sialidase-treated O-glycopeptides corresponding to HILIC fractions of mono- (top), bis- (middle), and triply-glycosylated (bottom) O-glycopeptide of HPX. Figure S3. Direct quantification of S-HPX at progressing stages of liver disease divided by gender (left) and race (right; CA Caucasian, AA African-American). Figure S4. Significant associations of S-HPX and other clinical variables. Figure S5. Quantification of detected N-glycopeptides at three different N-glycosylation sequons (N64, N187 and N453) of HPX.