Miracle-dz/UniFAR-FTUs huggingface dataset:
Classification of LSB and MLSB stego images via shift and pixel pairs irrelevance

For distinguish the LSB (Least significant bit) replacement stego image from MLSB (Multiple least significant bits) stego image, which are two typical kinds of steganographical methods of image spatial domain and have been applied widely, a classification algorithm based on the shift of pixel value and irrelevance of pixel pairs is proposed. In this algorithm, a shift operator is adopted for each pixel value of test image, and then the irrelevance of a kind of special adjoint pixels is extracted as the feature, at last the BP (Back-Propagation) neural network is designed to classify LSB replacement and MLSB replacement images. Results of experiments show that the proposed method can distinguish the MLSB replacement stego images from LSB replacement stego images reliably.
Nondenaturing two‐dimensional electrophoretic analysis of loop‐sheet polymerization of serpin, squamous cell carcinoma antigen‐2

Two homologous serine proteinase inhibitors (serpins), squamous cell carcinoma (SCC) antigen‐1 and ‐2 were separated by nondenaturing two‐dimensional electrophoresis combined with immunostaining to acquire further information on these proteins under physiological conditions. Polymers of SCC antigen‐2 were detected in cytosolic extracts prepared from tumor tissues. The polymer formation of SCC antigen‐2 was apparently decreased and the SCC antigen‐2‐synthetic peptide binary complexes were newly formed by the addition of synthetic peptide with sequences corresponding to residues from P14 to P2 in the reactive center loop of SCC antigen‐2. On the other hand, the incubation with synthetic peptides having the sequence of the reactive center loop of SCC antigen‐1 or antithrombin had no effect on polymerization of SCC antigen‐2. These data suggest that the polymerization of SCC antigen‐2 may occur spontaneously in vivo by the loop‐sheet mechanism of serpin.
Characterization of Virulence Factor Regulation by SrrAB, a Two-Component System in Staphylococcus aureus

ABSTRACT Workers in our laboratory have previously identified the staphylococcal respiratory response AB (SrrAB), a Staphylococcus aureus two-component system that acts in the global regulation of virulence factors. This system down-regulates production of agr RNAIII, protein A, and toxic shock syndrome toxin 1 (TSST-1), particularly under low-oxygen conditions. In this study we investigated the localization and membrane orientation of SrrA and SrrB, transcription of the srrAB operon, the DNA-binding properties of SrrA, and the effect of SrrAB expression on S. aureus virulence. We found that SrrA is localized to the S. aureus cytoplasm, while SrrB is localized to the membrane and is properly oriented to function as a histidine kinase. srrAB has one transcriptional start site which results in either an srrA transcript or a full-length srrAB transcript; srrB must be cotranscribed with srrA. Gel shift assays of the agr P2, agr P3, protein A (spa), TSST-1 (tst), and srr promoters revealed SrrA binding at each of these promoters. Analysis of SrrAB-overexpressing strains by using the rabbit model of bacterial endocarditis demonstrated that overexpression of SrrAB decreased the virulence of the organisms compared to the virulence of isogenic strains that do not overexpress SrrAB. We concluded that SrrAB is properly localized and oriented to function as a two-component system. Overexpression of SrrAB, which represses agr RNAIII, TSST-1, and protein A in vitro, decreases virulence in the rabbit endocarditis model. Repression of these virulence factors is likely due to a direct interaction between SrrA and the agr, tst, and spa promoters.
Ubiquitin Regulates GGA3-mediated Degradation of BACE1*

BACE1 (β-site amyloid precursor protein-cleaving enzyme 1) is a membrane-tethered member of the aspartyl proteases, essential for the production of β-amyloid, a toxic peptide that accumulates in the brain of subjects affected by Alzheimer disease. The BACE1 C-terminal fragment contains a DXXLL motif that has been shown to bind the VHS (VPS27, Hrs, and STAM) domain of GGA1–3 (Golgi-localized γ-ear-containing ARF-binding proteins). GGAs are trafficking molecules involved in the transport of proteins containing the DXXLL signal from the Golgi complex to endosomes. Moreover, GGAs bind ubiquitin and traffic synthetic and endosomal ubiquitinated cargoes to lysosomes. We have previously shown that depletion of GGA3 results in increased BACE1 levels and activity because of impaired lysosomal degradation. Here, we report that the accumulation of BACE1 is rescued by the ectopic expression of GGA3 in H4 neuroglioma cells depleted of GGA3. Accordingly, the overexpression of GGA3 reduces the levels of BACE1 and β-amyloid. We then established that mutations in the GGA3 VPS27, Hrs, and STAM domain (N91A) or in BACE1 di-leucine motif (L499A/L500A), able to abrogate their binding, did not affect the ability of ectopically expressed GGA3 to rescue BACE1 accumulation in cells depleted of GGA3. Instead, we found that BACE1 is ubiquitinated at lysine 501 and is mainly monoubiquitinated and Lys-63-linked polyubiquitinated. Finally, a GGA3 mutant with reduced ability to bind ubiquitin (GGA3L276A) was unable to regulate BACE1 levels both in rescue and overexpression experiments. These findings indicate that levels of GGA3 tightly and inversely regulate BACE1 levels via interaction with ubiquitin sorting machinery.
Vascular Smooth Muscle Cell Peroxisome Proliferator–Activated Receptor-&ggr; Mediates Pioglitazone-Reduced Vascular Lesion Formation

Objective—Peroxisome proliferator–activated receptor-&ggr; (PPAR&ggr;) has been reported to decrease vascular lesion formation. However, the critical role of vascular smooth muscle cell (VSMC) PPAR&ggr; in vascular lesion formation following transplantation is not well understood. In this study, we investigated the role of VSMC PPAR&ggr;-mediated signaling in transplantation-associated vascular lesion formation. Methods and Results—Carotid arteries from smooth muscle cell-selective PPAR&ggr; knockout (SMPG KO) and wild-type mice were transplanted to CBA/CaJ recipient mice. The recipient mice received a control diet or pioglitazone-containing diet. Pioglitazone reduced vascular lesion formation in transplanted wild-type, but not in SMPG KO carotid arteries. Histological analysis suggested that PPAR&ggr; attenuates vascular lesion formation through antiinflammatory signaling, as evidenced by the increase of intimal inflammatory cells and tumor necrosis factor-&agr; expression in SMPG KO allografts. Intravital microscopy revealed increased inflammatory cell rolling and attachment to endothelial cells in small blood vessels of SMPG KO mice following cytokine stimulation. SMPG KO mice, as shown by Western blotting, have elevated vascular cell adhesion molecule-1 (VCAM-1) expression. Furthermore, immunohistochemistry demonstrated SMPG KO allografts have increased VCAM-1. Conclusion—Loss of PPAR&ggr; in VSMC promotes transplantation-associated vascular lesion formation through increased VCAM-1 expression. VSMC PPAR&ggr; also mediates pioglitazone-reduced vascular lesion formation.
PU.1 and NFATc1 mediate osteoclastic induction of the mouse β3 integrin promoter

Expression of the αvβ3 integrin is required for normal osteoclast function. We previously showed that an evolutionary conserved NFATc1 binding site is required for RANKL induction and NFATc1 transactivation of the human β3 promoter. The mechanism conferring specificity for RANKL induction and NFATc1 transduction of the β3 gene in osteoclast differentiation is unclear since NFATc1 is expressed and activated in numerous cell types that do not express the β3 gene. PU.1 is an ETS family transcription factor in myeloid cells associated with expression of various osteoclast genes. The present study investigates the role of NFATc1 in concert with PU.1 in osteoclast‐specific transcription of the mouse β3 integrin gene. The mouse β3 promoter was transactivated by NFATc1 in RAW264.7 cells and deletion or mutation of either of the conserved NFAT and PU.1 binding sites abrogated transactivation. NFATc1 transactivation of the mouse β3 promoter was specifically dependent on co‐transfected PU.1 in HEK293 cells, to the exclusion of other ETS family members. Direct binding of NFATc1 and PU.1 to their cognate sequences was demonstrated by EMSA and NFATc1 and PU.1 occupy their cognate sites in RANKL‐treated mouse marrow precursors in chromatin immuno‐precipitation (ChIP) assays. TAT‐mediated transduction with dominant‐negative NFATc1 dose‐dependently blocked endogenous expression of the mouse β3 integrin and the formation of TRAP positive multinucleated cells in RANKL‐treated mouse macrophages. These data provide evidence that NFATc1, in concert with PU.1, are involved in regulation of β3 integrin expression during osteoclast differentiation and suggest that PU.1 confers specificity to the NFATc1 response to macrophage lineage cells. J. Cell. Physiol. 215: 636–644, 2008. © 2008 Wiley‐Liss, Inc.
Instantaneous interactions between brain sites can distinguish movement from rest but are relatively poor at resolving different movement types

Classification of finger movements from brain signals is an important problem in emerging neural prosthetics research. Current techniques have focused primarily on aggregating data from different brain sites independently, without regard to the interaction between different brain sites. We performed a very simple experiment classifying finger movements during electrocorticographic recording from motor cortex. Unlike previous experiments of this type, we examined whether the most-simple type of instantaneous interactions between brain regions could improve classification. We focused on two simple, but salient markers: phase coherence of the 12-20 Hz beta range, and simple correlation in broadband spectral change. We compared behavioral classification using these interactions with simple amplitude changes in beta and broadband magnitude. We found that inter-electrode phase coherence and cross-correlation, were relatively poor at distinguishing between finger movements, and only mediocre at identifying null/rest periods.
Enterotoxigenic Escherichia coli in a population of infants with diarrhea in Chile

The incidence of enterotoxigenic Escherichia coli (ETEC) was investigated in 95 E. coli strains isolated from 48 infants with diarrhea in Santiago, Chile. By using standard biological assays and DNA-DNA hybridization procedures, ETEC was found in 31.2% of the cases: 14 strains produced heat-stable enterotoxin (ST) only, three strains produced heat-labile enterotoxin (LT) and ST, and two strains produced LT only. DNA probes detected all enterotoxin producers except one ST-producing strain. The ST strains hybridized with one or both of the human ST probes (ST Ib and ST A2). Two of the LT-ST strains hybridized with the ST Ia and ST Ib probes, and the third strain did not hybridize with any of the ST probes. Only the ST group expressed multiple resistance (85.7%) and colonization factor antigen I (CFA I) (92.8%); CFA II was found in two of three LT-ST strains. The O153:H45 serotype was found in 10 of 14 ST strains, and O6:K15:H16 was found in one LT strain and in two LT-ST strains. These findings suggest that ETEC, especially strains that produce ST, may be an important cause of diarrhea among Chilean infants.
Knowledge Discovery on Functional Disabilities: Clustering Based on Rules versus other Approaches

In Europe senior citizens are a fast growing part of population, increasing proportion of disabled persons and that of persons with reduced quality of life. The concept of disability itself is not always precise and quantifiable. To improve agreement on it, the World Health Organization (WHO) developed the clinical test WHO Disability Assessment Schedule, (WHO-DASII) that includes physical, mental, and social well-being, as a generic measure of functioning. From the medical point of view, the purpose of this work is to extract knowledge about performance of the WHO-DASII using a sample of patients from an italian hospital.This Knowledge Discovery problem has been faced by using clustering based on rules, an hybrid AI and Statistics technique introduced by Gibert (1994), which combines some Inductive Learning (from AI) with clustering (from Statistics) to extract knowledge from certain complex domains in form of tipical profiles. In this paper, the results of applying this technique to the WHO-DASII results is presented together with a comparison of other more classical analysis approaches.
Therapy Failure Resulting from Superinfection by a Drug-Resistant HIV Variant

Background HIV-1-infected patients can be superinfected with additional HIV-1 variants. Therapy failure can be the consequence of an infection with a resistant strain. Methods A patient was diagnosed with a recent HIV-1 infection in April 2005 and subsequently clinically monitored. HIV-1 evolution was studied by population sequencing of the first 984 bases of the pol gene as well as 454 ultra-deep pyrosequencing (UDPS) of parts of the pol and env genes. Results The patient was diagnosed with a wild-type HIV-1 strain, but experienced rapid virological failure after initiating a non-nucleoside reverse transcriptase inhibitor (NNRTI)-based treatment regimen 3 years later. Population sequencing and UDPS revealed the presence of a second HIV-1 strain with a Y188L NNRTI resistance mutation in a sample obtained shortly prior to initiation of therapy. Phylogenetic analyses showed that the two HIV-1 strains were genetically distinct, providing evidence for superinfection. Conclusions The virological treatment failure in this patient was probably due to the superinfection with an NNRTI-resistant HIV-1 variant. Superinfection with drug-resistant strains can undermine HIV-1 treatment regimens selected on the basis of resistance testing at diagnosis. Patients, especially in high-risk groups, as well as their clinicians, should be aware of the risks and dangers of superinfections.
Short-term retention of lexical-semantic representations: Implications for speech production

Patients with semantic STM deficits have difficulty comprehending sentences that require the retention of several lexical-semantic representations prior to their integration into higher-level propositions (Martin, 1995; Martin & Romani, 1994). In Experiment 1, patients with a semantic retention deficit had difficulty with the same type of constructions in speech production, namely noun phrases with one or two prenominal adjectives. Their performance improved when they could produce the nouns and adjectives in sentence form, which placed smaller demands on lexical-semantic retention. In Experiment 2 these patients were better able to produce syntactically complex sentences than the prenominal adjective phrases having an equal number of content words, indicating that the findings in Experiment 1 could not be attributed to syntactic complexity. These patients produced more pauses in the sentence constructions in Experiments 1 and 2, suggesting that the timing of such productions is abnormal. In contrast, patient EA, with a phonological retention deficit, performed better than the patients with a semantic retention deficit on the AN phrases despite having a smaller STM span. She showed no significant benefit of producing sentence compared to phrase constructions, and also made fewer and shorter pauses than the other patients. These findings support the multiple capacities view of verbal working memory and suggest that the same semantic retention capacity used in language comprehension is used in speech production.
Coordinate Regulation of DNA Damage and Type I Interferon Responses Imposes an Antiviral State That Attenuates Mouse Gammaherpesvirus Type 68 Replication in Primary Macrophages

ABSTRACT DNA damage response (DDR) is a sophisticated cellular network that detects and repairs DNA breaks. Viruses are known to activate the DDR and usurp certain DDR components to facilitate replication. Intriguingly, viruses also inhibit several DDR proteins, suggesting that this cellular network has both proviral and antiviral features, with the nature of the latter still poorly understood. In this study we show that irradiation of primary murine macrophages was associated with enhanced expression of several antiviral interferon (IFN)-stimulated genes (ISGs). ISG induction in irradiated macrophages was dependent on type I IFN signaling, a functional DNA damage sensor complex, and ataxia-telangiectasia mutated kinase. Furthermore, IFN regulatory factor 1 was also required for the optimal expression of antiviral ISGs in irradiated macrophages. Importantly, DDR-mediated activation of type I IFN signaling contributed to increased resistance to mouse gammaherpesvirus 68 replication, suggesting that the coordinate regulation of DDR and type I IFN signaling may have evolved as a component of the innate immune response to virus infections.
Reconstruction of Total Maxillectomy Defects with Preservation of the Orbital Contents

&NA; Reconstruction after total maxillectomy with preservation of the orbital contents is technically more challenging than when the maxillectomy is combined with orbital exenteration. Reconstruction of such defects should (1) provide support to the orbital contents, (2) obliterate any communication between the orbit and nasopharynx, (3) reconstruct the palatal surface, and (4) achieve facial symmetry and a good aesthetic result. We report our experience in performing reconstructive surgery on 14 patients who had a total maxillectomy and preservation of the orbital contents using nonvascu‐larized bone grafts for reconstruction of the orbital floor and maxilla, in conjunction with a soft‐tissue free flap or pedicled muscle flap. The orbital floor was reconstructed using split ribs in six cases (42.9 percent), split calvaria in six cases (42.9 percent), and iliac crest graft in two cases (14.3 percent). A myocutaneous rectus abdominis free flap was used for soft‐tissue reconstruction and resurfacing of the palatal mucosa in twelve patients (85.7 percent), and a temporalis muscle transposition was used in two elderly patients (14.3 percent). One patient died 2 days after surgery. Mean follow‐up and aesthetic and functional results were assessed in the remaining 13 patients a minimum of 6 months postoperatively. In 9 of these 13 patients (69.2 percent), postoperative radiotherapy was administered. No reexplorations or free flap failures were observed. One rectus flap developed partial necrosis of the skin island intraorally without affecting the final result. All patients had adequate functional vision. One patient had a mild vertical dystopia; there were no cases of enoph‐thalmos. Ectropion was the most common undesirable result and was present in 10 of 13 cases (76.9 percent). It was graded as mild in four cases (40.0 percent), moderate in four cases (40.0 percent), and severe in the remaining two cases (20.0 percent). Speech was considered normal in six cases (46.2 percent), near normal in six cases (46.2 percent), and intelligible in one case (7.7 percent). Chewing function was considered good (soft to unrestricted diet) in all cases except for one patient who was only able to eat a puréed diet. Aesthetic results after immediate reconstruction were considered good in nine cases (69.2 percent) and fair in four cases (30.8 percent). Primary reconstruction of total maxillectomy defects with orbital content preservation remains a complex problem without a perfect solution. The combination of nonvascularized bone grafts for orbital/maxillary reconstruction with a soft‐tissue free flap is a safe, reliable, and effective method of maximizing postoperative functional and aesthetic results. (Plast. Reconstr. Surg. 102: 1874, 1998.)
Left main coronary artery dissection during percutaneous coronary intervention treated by stenting.

AIM Outcome after stenting for iatrogenic left main coronary artery (LMCA) dissection during percutaneous coronary intervention (PCI). METHODS From our database all patients with a PCI complicated by an LMCA dissection, between 1996 and 2001, were selected and medical records were reviewed. RESULTS Eighteen patients out of 7199 (0.25%) were found with an LMCA dissection during a PCI for unstable (n=14) and stable angina (n=4). Antegrade dissections were caused by guiding catheters (n=6). Retrograde dissections were caused by stent implantation (n=7) and balloon angioplasty (n=5). All patients were treated by stent implantation in the LMCA. Three patients died (17%) within ten days of the procedure. Emergency surgery was performed in four patients (22%) because of persistent ischaemia due to low coronary flow. One patient was operated one day later because of unstable angina and a failed attempt to recanalise the left descending coronary artery. The other ten patients (56%) with a stent in the LMCA were free of cardiac complaints after a follow-up period of 3.0 years (range 1.9-5.0). Cardiac catheterisation in six patients between three and eight months did not show stenosis of the LMCA stent. CONCLUSION LMCA dissection during a PCI can be treated by stent implantation, especially when the dissection is limited to the LMCA. When flow cannot be restored adequately, resulting in ischaemia and haemodynamic instability, LMCA stenting may serve as a bridge to emergency CABG.
Whole‐body hypothermia has central and peripheral influences on elbow flexor performance

The superimposed twitch technique was used to study the effect of whole‐body hypothermia on maximal voluntary activation of elbow flexors. Seven subjects [26.4 ± 4 years old (mean ± SD)] were exposed to 60 min of either immersion in 8°C water (hypothermia) or sitting in 22°C air (control). Voluntary activation was assessed during brief (3 s) maximal voluntary contractions (MVCs) and then during a 2 min fatiguing sustained MVC. Hypothermia (core temperature 34.8 ± 0.9°C) decreased maximal voluntary torque from 98.2 ± 1.0 to 82.8 ± 5.8% MVC (P < 0.001) and increased central conduction time from 7.9 ± 0.4 to 9.1 ± 0.7 ms (P < 0.05). Hypothermia also decreased maximal resting twitch amplitude from 17.6 ± 4.0 to 10.0 ± 1.7% MVC (P < 0.005) and increased the time‐to‐peak twitch tension from 55.4 ± 4.0 to 79.0 ± 11.7 ms (P < 0.001). During the 2 min contraction, hypothermia decreased initial torque (P < 0.01) but attenuated the subsequent rate of torque decline (control from 95.5 ± 4 to 29.4 ± 8% MVC; and hypothermia from 85.3 ± 8 to 37.3 ± 5% MVC; P < 0.01). Cortical superimposed twitches increased as fatigue developed but were always lower in the hypothermic conditions. Cortical superimposed twitches increased from a value of 0.4 ± 0.3% MVC prefatigue to 3.9 ± 1.4% MVC postfatigue (P < 0.001) in the hypothermic conditions and from 1.7 ± 0.9 to 5.5 ± 2.3% MVC in control conditions. Our results suggest that hypothermia decreases MVCs primarily via peripheral mechanisms and attenuates the rate of fatigue development by reducing central fatigue.
Biodistribution and Radiation Dosimetry in Humans of a New PET Ligand, 18F-PBR06, to Image Translocator Protein (18 kDa)

As a PET biomarker for inflammation, translocator protein (18 kDa) (TSPO) can be measured with an 18F-labeled aryloxyanilide, 18F-N-fluoroacetyl-N-(2,5-dimethoxybenzyl)-2-phenoxyaniline (18F-PBR06), in the human brain. The objective of this study was to estimate the radiation absorbed doses of 18F-PBR06 based on biodistribution data in humans. Methods: After the injection of 18F-PBR06, images were acquired from head to thigh in 7 healthy humans. Urine was collected at various time points. Radiation absorbed doses were estimated by the MIRD scheme. Results: Moderate to high levels of radioactivity were observed in organs with high densities of TSPO and in organs of metabolism and excretion. Bone had low levels of radioactivity. The effective dose was 18.5 μSv/MBq. Conclusion: The effective dose of 18F-PBR06, compared with other 18F radioligands, was moderate. This radioligand had negligible defluorination, as indirectly assessed by bone radioactivity. Doses to the gallbladder wall and spleen may limit the amount of permissible injected radioactivity.