Miracle-dz/UniFAR-FTUs huggingface dataset:
A low-complexity stopping criterion for the decoder of parallel concatenated LDPC codes

In this paper, we propose a novel stopping criteria that based on the mean of the magnitude of the extrinsic information in the iterative decoder of parallel concatenated LDPC (low- density parity-check) codes. The proposed criterion has low computation complexity and few storage requirements. Simulations results proved that the MEM (mean of extrinsic information magnitude) rules outperforms the other existing criterions in terms of BER and average number of super iterations.
Hormonal Regulation of a-Amylase Expression in Barley Aleurone Layers' THE EFFECTS OF GIBBERELLIC ACID REMOVAL AND ABSCISIC ACID AND PHASEIC ACID TREATMENTS

The expression of a-amylase isozymes in barley (Hordeum vulgare L.) aleurone layers is known to be maximally induced between 12 and 20 hours after addition of the phytohormone, gibberellic acid (GA3). Addition of another hormone, abscisic acid (ABA), or its metabolite, phaseic acid, during this time period resulted in reduced a-amylase expression. Expres- sion of the high isoelectric point a-amylase isozyme group was affected much more by both of these treatments than was expression of the low isoelectric point a-amylase isozyme group. Addition of either the translation inhibitor cycloheximide or the transcription inhibitor cordycepin prevented the decrease in a-amylase mRNA levels after ABA treatment. Cordycepin also prevented the decreases in a-amylase expression that result from phaseic acid treatment. Midcourse GA3 removal experiments were performed to determine whether ABA treatment and the removal of GA3 have analogous effects on a-amylase expression. It was found that cordycepin treatment also prevented decreases in a-amylase mRNA levels resulting from GA3 removal. We conclude that the suppression of a-amylase expression caused by ABA or midcourse GA3 removal is dependent on continuous RNA and protein synthesis. protease inhibitor.
Angiogenesis and ER / PR status in primary breast cancer patients : an analysis of 158 needle core biopsies

Formation of new blood vessels from a preexisting vascular bed (angiogenesis) is a complex multistep process, which may also permit metastasis. Estrogen and progesterone are important in breast tumorigenesis, and their effects on the breast are mediated by their respective receptors, the estrogen receptor (ER) and the progesterone receptor (PR). To investigate how tumor angiogenesis correlates with ER/PR status in breast carcinoma diagnosed on core biopsy, microvessels were counted (and graded the density of microvessels) within the initial invasive carcinomas of 158 patients. Using light microscopy, the number of microvessels was counted manually in a subjectively selected hot spot (in the most active areas of neovascularization per 400× field), and their values were separated as above or below median (low and high), without knowledge of the outcome in the patient or any other pertinent variable. When the mean values of MVD of the various groups defined by ER/PR status were compared, significant difference was noted (P = 1.57E-05). When tumors were classified as high or low MVD, based on a cut-off value (30.70175 microvessels/mm2), cases with high MVD were significantly more numerous in patients with ER+/PRstatus. MVD did show a relationship with groups defined by ER/PR status (P = 0.000801). Assessment of tumor angiogenesis may therefore prove valuable in selecting patients with early breast carcinoma for therapeutic hormonal therapy.
Aggregation and fibrillization of the recombinant human prion protein huPrP90-231.

According to the "protein-only" hypothesis, the critical step in the pathogenesis of prion diseases is the conformational transition between the normal (PrP(C)) and pathological (PrP(Sc)) isoforms of prion protein. To gain insight into the mechanism of this transition, we have characterized the biophysical properties of the recombinant protein corresponding to residues 90-231 of the human prion protein (huPrP90-231). Incubation of the protein under acidic conditions (pH 3.6-5) in the presence of 1 M guanidine-HCl resulted in a time-dependent transition from an alpha-helical conformation to a beta-sheet structure and oligomerization of huPrP90-231 into large molecular weight aggregates. No stable monomeric beta-sheet-rich folding intermediate of the protein could be detected in the present experiments. Kinetic analysis of the data indicates that the formation of beta-sheet structure and protein oligomerization likely occur concomitantly. The beta-sheet-rich oligomers were characterized by a markedly increased resistance to proteinase K digestion and a fibrillar morphology (i.e., they had the essential physicochemical properties of PrP(Sc)). Contrary to previous suggestions, the conversion of the recombinant prion protein into a PrP(Sc)-like form could be accomplished under nonreducing conditions, without the need to disrupt the disulfide bond. Experiments in urea indicate that, in addition to acidic pH, another critical factor controlling the transition of huPrP90-231 to an oligomeric beta-sheet structure is the presence of salt.
JNK phosphorylates the HSF1 transcriptional activation domain: Role of JNK in the regulation of the heat shock response

The role of c‐Jun NH2‐terminal kinase (JNK) signaling cascade in the stress‐inducible phosphorylation of heat shock factor 1 (HSF1) was investigated using known agonists and antagonists of JNK. We showed that treatment of HeLa cells with MG132, a proteasome inhibitor and known JNK activator, caused the transcriptional activation domain of HSF1 to be targeted and phosphorylated by JNK2 in vivo. Dose‐response and time course studies of the effects of heat shock and anisomycin treatment showed a close correlation of the activation of JNK and hyperphosphorylation of HSF1. SB203580 inhibited JNK at the 100 μM concentration and significantly reduced the amount of hyperphosphorylated HSF1 upon heat shock or anisomycin treatment. SB203580 and dominant‐negative JNK suppress hsp70 promoter‐driven reporter gene expression selectively at 45°C but not at 42°C heat stress, suggesting that JNK would be preferentially associated with the protective heat shock response against severe heat stress. The possibility that JNK‐mediated phosphorylation of HSF1 may selectively stabilize the HSF1 protein and confers protection to cells under conditions of severe stress is discussed. J. Cell. Biochem. 82: 326–338, 2001. © 2001 Wiley‐Liss, Inc.
A comparative biochemical and ultrastructural study of proteoglycan-collagen interactions in corneal stroma. Functional and metabolic implications.

1. Corneas of mouse, rat, guinea pig, rabbit, sheep, cat, dog, pig and cow were quantitatively analysed for water, hydroxyproline, nucleic acid, total sulphated polyanion, chondroitin sulphate/dermatan sulphate and keratan sulphate, several samples or pools of tissue from each species being used. Ferret cornea was similarly analysed for water and hydroxyproline on one pool of eight corneas. Pooled frog (38) and ferret (eight) corneas and a single sample of human cornea were qualitatively examined for keratan sulphate and chondroitin sulphate/dermatan sulphate by electrophoresis on cellulose acetate membranes. Nine species (mouse, frog, rat, guinea pig, rabbit, sheep, cat, pig and cow) were examined by light microscopy and six (mouse, frog, rat, guinea pig, rabbit and cow) by electron microscopy, with the use of Alcian Blue or Cupromeronic Blue in critical-electrolyte-concentration (CEC) methods to stain proteoglycans. 2. Water (% of wet weight), hydroxyproline (mg/g dry wt.) and chondroitin sulphate (mg/g of hydroxyproline) contents were approximately constant across the species, except for mouse. 3. Keratan sulphate contents (mg/g of hydroxyproline) increased with corneal thickness, whereas dermatan sulphate contents decreased. The oversulphated domain of keratan sulphate was absent from mouse and frog corneas, increasing as percentage of total keratan sulphate with increasing corneal thickness. Sulphation of dermatan sulphate was essentially complete (i.e. one sulphate group per disaccharide unit). 4. Chondroitin sulphate/dermatan sulphate proteoglycans were present at the d bands of the collagen fibrils of all species examined, orthogonally arrayed, with high frequency, and occasionally at the e bands. Keratan sulphate proteoglycans were present at the a and c bands of all species examined, but with far higher frequency in the thicker corneas, where keratan sulphate contents were high. 5. Alcian Blue CEC staining showed much higher sulphation of keratan sulphate in thick corneas, e.g. that of cow, than in thin corneas, e.g. that of mouse, in keeping with biochemical analyses. 6. It is suggested that the constancy of interfibrillar volumes is regulated via the swelling and osmotic pressure of the interfibrillar polyanions, by adjustment of the extent of sulphation in two independent proteoglycan populations, to achieve an 'average sulphation' of the total polyanion similar to that of fully sulphated chondroitin sulphate/dermatan sulphate. 7. The balance of synthesis of the two kinds of proteoglycans may be determined by the O2 supply to the avascular cornea. O2 supply may also determine the conversion of chondroitin sulphate into dermatan sulphate.
Built in self test for RAM using VHDL

This project emphasized mainly on software analysis. Modelsim-Altera 6.4a is the software that used to generate every single module of the Built-in-Self-Test (BIST) for Random access Memory (RAM) architecture. There are three key things to be concern in the BIST for RAM which is the Test Pattern Generator (TPG), Output Response Analysis (ORA) and RAM. The output of counter which is a type of TPG is analyzed to provide a pattern for March test algorithm. At the mean time, the ORA compare the output from decoder and the RAM output itself which modeled under the theory of numerical autonomy of error vectors from the circuit under test. The output of ORA, the comparator, will show pass or fail for faulty detection of RAM. The system has been successfully developed and vector waveform is used to examine the result of the system. From the result obtained, it showed that the system is working as expected with satisfactory result.
Does dysregulated expression of a deregulated viral GPCR trigger Kaposi's sarcomagenesis?

In 1994, the Kaposi's sarcoma‐associated herpesvirus (KSHV/HHV‐8) was identified as the etio¬logie agent of Kaposi's sarcoma (KS). KSHV has since been associated with two additional AIDS‐related ma¬lignancies: primary effusion lymphomas (PEL) and multicentric Castleman's disease (MCD). Although mo¬lecular characterization of the KSHV genome has re¬vealed several candidate oncogenes, infection with KSHV alone is not sufficient to cause KS, suggestive of an accomplice in KS initiation. Recent experimental evidence supports a key role for a particular KSHV gene, a constitutively‐active G‐protein‐coupled receptor (vGPCR), in the development of KS. However, it is unclear how a lytic gene expressed in cells destined to die can cause cancer. Here we propose that dysregulation of the viral gene program may lead to nonlytic vGPCR expression. Several candidate cofactors (e.g., HIV‐1 Tat, inflammation, aborted lytic cycle progres¬sion) are identified that may trigger vGPCR dysregulation, enabling oncogenic signaling pathways up‐regu¬lated by vGPCR, combined with the paracrine secretions from vGPCR‐expressing cells, to promote the initiation of KS. If KS is indeed dependent on vGPCR dysregulation, then the development of new therapeutic modalities specifically targeting this viral protein or its downstream targets may ultimately prove to be the most effective treatment strategy for this enigmatic disease. —Sodhi, A. , Montaner, S. , Gutkind, J. S. Does dysregulated expression of a deregulated viral GPCR trigger Kaposi's sarcomagenesis?
NOD2/CARD15 does not influence response to infliximab in Crohn's disease.

BACKGROUND & AIMS NOD2/CARD15 was recently identified as the first gene underlying Crohn's disease (CD) susceptibility. Monoclonal antibodies to tumor necrosis factor (TNF)-alpha (infliximab) are a potent treatment for CD, with about 70% of patients responding. It is not clear which factors influence treatment outcome. We assessed whether variants in NOD2/CARD15 are predictive for differences in clinical response. METHODS Two hundred forty-five CD patients (86 fistulizing, 159 luminal) receiving infliximab in an expanded access program were genotyped for the 3 main associated variants of NOD2/CARD15, without knowledge of the treatment response. Short-term clinical response was assessed at 4 weeks (refractory) or 10 weeks (fistulizing) after first infliximab infusion, and the mean duration of response was calculated. In a subgroup of patients, production of TNF in response to lipopolysaccharide (LPS) in mucosal biopsy tissue was also determined by means of immunoassay, and results were related to the different NOD2/CARD15 genotypes. RESULTS In total, 32.6% of patients carried mutations in NOD2/CARD15 (18.8% R702W, 8.6% G908R, and 10.2% 1007fs) compared with 15% in controls (P < 0.001). Despite observed differences in TNF production in mucosal biopsy tissue, there was no relationship between the overall presence of a mutation in NOD2/CARD15 or of any of the mutations separately and short-term infliximab response or response duration. Furthermore, multivariate analysis could not identify clinical characteristics that, in combination with NOD2/CARD15 mutations, were associated with response to infliximab. CONCLUSIONS In this cohort of CD patients, the frequency of NOD2/CARD15 mutations was significantly greater than that of healthy controls. However, NOD2/CARD15 was not predictive of treatment outcome with infliximab in CD.
Opa binding to cellular CD66 receptors mediates the transcellular traversal of Neisseria gonorrhoeae across polarized T84 epithelial cell monolayers

We have analysed the capacity of the 11 phase‐variable, opacity‐associated (Opa) proteins encoded by Neisseria gonorrhoeae MS11 to mediate traversal across polarized monolayers of the human colonic carcinoma T84 cell line. Gonococci expressing either the heparan sulphate proteoglycan (HSPG) binding Opa protein (Opa50) or no Opa protein (Opa−) did not interact with the apical pole of T84 monolayers, whereas the 10 variant Opa proteins previously shown to bind CD66 receptors were found to mediate efficient gonococcal adherence and transepithelial traversal. Consistent with this, T84 cells were shown by reverse transcriptase–polymerase chain reaction (RT–PCR) and immunoblotting to co‐express CD66a (BGP), CD66c (NCA) and CD66e (CEA). The recruitment of CD66 receptors by Opa‐expressing gonococci indicates their involvement in mediating adherence to the surface of T84 cells, and these bacterial interactions could be inhibited completely using polyclonal antibodies cross‐reacting with all of the CD66 proteins co‐expressed on T84 cells. Consistent results were obtained when Opa proteins were expressed in Escherichia coli, suggesting that the Opa–CD66 interaction is sufficient to mediate bacterial traversal. Transcytosis of Opa‐expressing N. gonorrhoeae or E. coli did not disrupt the barrier function of infected monolayers, as indicated by a sustained transepithelial electrical resistance (TEER) throughout the course of infection, and confocal laser scanning and electron microscopy both suggest a transcellular rather than a paracellular route of traversal across the monolayers. Parallels between the results seen here and previous work done with organ cultures confirm that T84 monolayers provide a valid model for studying neisserial interactions with the mucosal surface, and suggest that CD66 receptors contribute to this process in vivo.
Metabolic Fate of Unsaturated Glucuronic/Iduronic Acids from Glycosaminoglycans

Background: Some streptococci target host extracellular matrix glycosaminoglycans for infection. Results: The streptococcal metabolic pathway of glycosaminoglycan-derived unsaturated uronates was identified. The crystal structures of its isomerase and dehydrogenase were determined. Conclusion: Streptococci include an assembled genetic cluster for depolymerization, import, degradation, and metabolism of glycosaminoglycans. Significance: This study contributes to understanding of the streptococcal degradation/metabolism mechanism of glycosaminoglycans. Glycosaminoglycans in mammalian extracellular matrices are degraded to their constituents, unsaturated uronic (glucuronic/iduronic) acids and amino sugars, through successive reactions of bacterial polysaccharide lyase and unsaturated glucuronyl hydrolase. Genes coding for glycosaminoglycan-acting lyase, unsaturated glucuronyl hydrolase, and the phosphotransferase system are assembled into a cluster in the genome of pathogenic bacteria, such as streptococci and clostridia. Here, we studied the streptococcal metabolic pathway of unsaturated uronic acids and the structure/function relationship of its relevant isomerase and dehydrogenase. Two proteins (gbs1892 and gbs1891) of Streptococcus agalactiae strain NEM316 were overexpressed in Escherichia coli, purified, and characterized. 4-Deoxy-l-threo-5-hexosulose-uronate (Dhu) nonenzymatically generated from unsaturated uronic acids was converted to 2-keto-3-deoxy-d-gluconate via 3-deoxy-d-glycero-2,5-hexodiulosonate through successive reactions of gbs1892 isomerase (DhuI) and gbs1891 NADH-dependent reductase/dehydrogenase (DhuD). DhuI and DhuD enzymatically corresponded to 4-deoxy-l-threo-5-hexosulose-uronate ketol-isomerase (KduI) and 2-keto-3-deoxy-d-gluconate dehydrogenase (KduD), respectively, involved in pectin metabolism, although no or low sequence identity was observed between DhuI and KduI or between DhuD and KduD, respectively. Genes for DhuI and DhuD were found to be included in the streptococcal genetic cluster, whereas KduI and KduD are encoded in clostridia. Tertiary and quaternary structures of DhuI and DhuD were determined by x-ray crystallography. Distinct from KduI β-barrels, DhuI adopts an α/β/α-barrel structure as a basic scaffold similar to that of ribose 5-phosphate isomerase. The structure of DhuD is unable to accommodate the substrate/cofactor, suggesting that conformational changes are essential to trigger enzyme catalysis. This is the first report on the bacterial metabolism of glycosaminoglycan-derived unsaturated uronic acids by isomerase and dehydrogenase.
Aseptic meningitis occurring during anti-TNF-alpha therapy in rheumatoid arthritis and ankylosing spondylitis.

OBJECTIVES Aseptic meningitis is a rare and aggressive complication of rheumatoid arthritis (RA), usually histologically characterised by rheumatoid nodules and lymphocytic aggregates in leptomeninges. The aim of this study was to describe the clinical onset and evolution of aseptic meningitis occurring during anti-TNF-alpha (TNF-α) therapy. METHODS we retrospectively analysed the clinical records of patients with RA or ankylosing apondylitis (AS) treated by TNF-α drugs in the last 10 years. RESULTS Four out of 718 patients, treated with TNF-α, developed meningitis after a mean of 5 years (SD: 3.7) of TNF-α exposure (0.55%). Three subjects were affected by long-standing RA (median: 11 years, IQR:8.5-25), one patient by active AS of 8 years' duration. RA patients were treated with etanercept (2 cases) and infliximab (1 case), in association with methotrexate and prednisone. The AS patient was treated with adalimumab. Neurological onset was focal epilepsy (3 cases) and dysarthria (1 case). RM showed leptomeningeal enhancement of basal nuclei (1 case) or fronto-parietal zone (3 cases), associated in one patient with cerebritis. Bacterial, viral or parasitic infections were excluded. One patient underwent cerebral biopsy showing T and B lymphocytes' aggregates. All patients discontinued TNF-α drugs and were treated with high dose of steroids, added to methotrexate in two cases. Neurological symptoms resolved without residuals, and meningeal enhancement showed resolution with high latency. CONCLUSIONS Meningeal inflammation is a rare manifestation occurring in long-standing RA and AS in clinical remission. TNF-α therapy did not prevent this extra-articular complication.
Effect of a mobile unit on changes in knowledge and use of cervical cancer screening among rural Thai women.

BACKGROUND A large proportion of women in most developing countries, particularly in rural areas, have never had cervical cancer screening. This paper reports the effect of a cervical cancer screening programme using a mobile unit on changes in knowledge and use of Papanicolaou (Pap) smear screening among rural Thai women. METHODS Health education and collection of Pap smears were carried out by the mobile unit throughout the 54 rural villages in Mae Sot District, Tak Province, between January and February 1993. To determine the extent of changes, we compared the results of two interview surveys of women 18-65 years old in the villages selected by systematic sampling for each survey, first in January 1991 and then in January 1994. RESULTS A total of 1603 and 1369 women participated in each survey respectively. The proportion of women who knew of the Pap smear test increased from 20.8% in the first survey sample to 57.3% in the second survey sample. The proportion of those who had even been screened increased from 19.9% in the first survey sample to 58.1% in the second survey sample. These increases were observed solely among ever-married women and there were no significant changes among single women, most of whom remained unscreened. Of ever-married women, the magnitude of increase was highest in the age group 25-34 years, and declined with increasing age. CONCLUSIONS Greater efforts should be made to encourage the use of screening among the older women. The use of mobile units may be helpful for rapid achievement of higher screening coverage in rural areas, where existing screening services cannot effectively cover the female population at risk.
Ferritinophagy drives uropathogenic Escherichia coli persistence in bladder epithelial cells

ABSTRACT Autophagy is a cellular recycling pathway, which in many cases, protects host cells from infections by degrading pathogens. However, uropathogenic Escherichia coli (UPEC), the predominant cause of urinary tract infections (UTIs), persist within the urinary tract epithelium (urothelium) by forming reservoirs within autophagosomes. Iron is a critical nutrient for both host and pathogen, and regulation of iron availability is a key host defense against pathogens. Iron homeostasis depends on the shuttling of iron-bound ferritin to the lysosome for recycling, a process termed ferritinophagy (a form of selective autophagy). Here, we demonstrate for the first time that UPEC shuttles with ferritin-bound iron into the autophagosomal and lysosomal compartments within the urothelium. Iron overload in urothelial cells induces ferritinophagy in an NCOA4-dependent manner causing increased iron availability for UPEC, triggering bacterial overproliferation and host cell death. Addition of even moderate levels of iron is sufficient to increase and prolong bacterial burden. Furthermore, we show that lysosomal damage due to iron overload is the specific mechanism causing host cell death. Significantly, we demonstrate that host cell death and bacterial burden can be reversed by inhibition of autophagy or inhibition of iron-regulatory proteins, or chelation of iron. Together, our findings suggest that UPEC persist in host cells by taking advantage of ferritinophagy. Thus, modulation of iron levels in the bladder may provide a therapeutic avenue to controlling UPEC persistence, epithelial cell death, and recurrent UTIs.