Miracle-dz/UniFAR-FTUs huggingface dataset:
Analysis of Host Cells Associated with the Spv-Mediated Increased Intracellular Growth Rate of Salmonella typhimurium in Mice

ABSTRACT The 90-kb virulence plasmid of Salmonella typhimuriumencodes five spv genes which increase the growth rate of the bacteria within host cells within the first week of systemic infection of mice (P. A. Gulig and T. J. Doyle, Infect. Immun. 61:504–511, 1993). The presently described study was aimed at identifying the host cells associated with Spv-mediated virulence by manipulating the mouse host and the salmonellae. To test the effects of T cells and B cells on the Spv phenotype, salmonellae were orally inoculated into nude and SCID BALB/c mice. Relative to normal BALB/c mice, nude and SCID BALB/c mice were unaffected for splenic infection with either the Spv+ or Spv−S. typhimurium strains at 5 days postinoculation. When mice were pretreated with cyclophosphamide to induce granulocytopenia, there was a variable increase in total salmonella infection, but the relative splenic CFU of Spv+ versus Spv−S. typhimurium was not changed after oral inoculation. In contrast, depletion of macrophages from mice by treatment with cyclophosphamide plus liposomes containing dichloromethylene diphosphate resulted in equivalent virulence of Spv+ and Spv−salmonellae. To examine if the spv genes affected the growth of salmonellae in nonphagocytic cells, aninvA::aphT mutation was transduced into Spv+ and Spv−S. typhimuriumstrains. InvA− Spv+ salmonellae were not significantly affected for splenic infection after subcutaneous inoculation compared with the wild-type strain, and InvA−Spv− salmonellae were only slightly attenuated relative to InvA+ Spv− salmonellae. Invasion-defective salmonellae still exhibited the Spv phenotype. Therefore, infection of nonphagocytes is not involved with the Spv virulence function. Taken together, these data demonstrate that macrophages are essential for suppressing the infection by Spv−S. typhimurium, by serving as the primary host cell for Spv-mediated intracellular replication and possibly by inhibiting the replication of salmonellae within other macrophages.
Adaptive Query Routing on Distributed Context - The COSINE Framework

Context-awareness has become a desired key feature of today's mobile systems, yet, its realization still remains a challenge. On the one hand, mobile computing provides great potential for adaptations based on sensed contextual information. On the other hand, the lack of dependability in mobile networks hampers an efficient provision of this information to requesting clients. In this paper we present COSINE, a context management framework for mobile environments. COSINE has been developed on the principles of peer-to-peer computing and establishes context sharing infrastructures consisting of loosely coupled Web services. The services represent modular entities of the applied context model and manage the retrieval, aggregation, query, and provision of context data. Clients access the distributed information transparently via proxies and a self-adaptive routing of queries provides increased fault-tolerance, which is essential in mobile environments.
[Immortalization of human fetal esophageal epithelial cells induced by E6 and E7 genes of human papilloma virus 18].

OBJECTIVE For studying the relationship between HPV and esophageal carcinoma, an immortalized human fetal esophageal epithelial cell line (SHEE) was established. METHODS The human fetal esophageal tissues were cultured and infected with HPV 18 E6E7 AAV. It was examined by light- and electron-microscope for morphological changes, by PCR and FISH for detection of HPV E6E7 and by soft agar culture and nude mice inoculatior for dectecting tumor transformation. RESULTS The cell line has become immortal and has propagated cntinuously for more than 50 passages. After a long-term culture, the phenotype keeps the characteristics of primary epithelial cells. They showed as monolayer growth and anchorage dependent growth without forming colonies in softagar. They were nontumorigenic in nude mice. SHEE cells contained tonofilaments in its cytoplasm by electron microscopic examination and showed cytokeratin positive in immunohistochemical procedure. So it shows that the cells are squamous epithelium in origin. The cell line contained the HPV 18 E6 and E7 genes by FISH and PCR assay. CONCLUSION Establishment of the esophageal epithelial cell line SHEE successfully immortalized with HPV 18, E6E7, supports that the HPV18 may be related to the etiology of esophageal carcinoma. It will facilitate further research on etiology and pathogenesis of esophageal carcinoma.
Heat‐Transport Mechanisms in Superlattices

The heat transport mechanisms in superlattices are identified from the cross‐plane thermal conductivity Λ of (AlN)x–(GaN)y superlattices measured by time‐domain thermoreflectance. For (AlN)4.1 nm–(GaN)55 nm superlattices grown under different conditions, Λ varies by a factor of two; this is attributed to differences in the roughness of the AlN/GaN interfaces. Under the growth condition that gives the lowest Λ, Λ of (AlN)4 nm–(GaN)y superlattices decreases monotonically as y decreases, Λ = 6.35 W m−1 K−1 at y = 2.2 nm, 35 times smaller than Λ of bulk GaN. For long‐period superlattices (y > 40 nm), the mean thermal conductance G of AlN/GaN interfaces is independent of y, G ≈ 620 MW m−2 K−1. For y < 40 nm, the apparent value of G increases with decreasing y, reaching G ≈ 2 GW m−2 K−1 at y < 3 nm. MeV ion bombardment is used to help determine which phonons are responsible for heat transport in short period superlattices. The thermal conductivity of an (AlN)4.1 nm–(GaN)4.9 nm superlattice irradiated by 2.3 MeV Ar ions to a dose of 2 × 1014 ions cm−2 is reduced by <35%, suggesting that heat transport in these short‐period superlattices is dominated by long‐wavelength acoustic phonons. Calculations using a Debye‐Callaway model and the assumption of a boundary scattering rate that varies with phonon‐wavelength successfully capture the temperature, period, and ion‐dose dependence of Λ.
JNK and PTEN cooperatively control the development of invasive adenocarcinoma of the prostate

The c-Jun NH2-terminal kinase (JNK) signal transduction pathway is implicated in cancer, but the role of JNK in tumorigenesis is poorly understood. Here, we demonstrate that the JNK signaling pathway reduces the development of invasive adenocarcinoma in the phosphatase and tensin homolog (Pten) conditional deletion model of prostate cancer. Mice with JNK deficiency in the prostate epithelium (ΔJnk ΔPten mice) develop androgen-independent metastatic prostate cancer more rapidly than control (ΔPten) mice. Similarly, prevention of JNK activation in the prostate epithelium (ΔMkk4 ΔMkk7 ΔPten mice) causes rapid development of invasive adenocarcinoma. We found that JNK signaling defects cause an androgen-independent expansion of the immature progenitor cell population in the primary tumor. The JNK-deficient progenitor cells display increased proliferation and tumorigenic potential compared with progenitor cells from control prostate tumors. These data demonstrate that the JNK and PTEN signaling pathways can cooperate to regulate the progression of prostate neoplasia to invasive adenocarcinoma.
Analysis of switching in a DC circuit

This paper presents an analysis of the static switching in a DC circuit. Power semiconductor devices are used in various electrical switchgear with static switching because they are very fast and do not require maintenance. In the static switchgear there is not the electric arc as in the case of electromechanical switchgear. By the simulations performed in this work were obtained the waveforms of currents and voltages that occur during the switching. The analysis conducted in this paper highlights the advantages and disadvantages of static switching in a DC circuit.
Carotid Body Ablation Abrogates Hypertension and Autonomic Alterations Induced by Intermittent Hypoxia in Rats

Chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnea, enhances carotid body (CB) chemosensory responses to hypoxia and produces autonomic dysfunction, cardiac arrhythmias, and hypertension. We tested whether autonomic alterations, arrhythmogenesis, and the progression of hypertension induced by CIH depend on the enhanced CB chemosensory drive, by ablation of the CB chemoreceptors. Male Sprague–Dawley rats were exposed to control (Sham) conditions for 7 days and then to CIH (5% O2, 12/h 8 h/d) for a total of 28 days. At 21 days of CIH exposure, rats underwent bilateral CB ablation and then exposed to CIH for 7 additional days. Arterial blood pressure and ventilatory chemoreflex response to hypoxia were measured in conscious rats. In addition, cardiac autonomic imbalance, cardiac baroreflex gain, and arrhythmia score were assessed during the length of the experiments. In separate experimental series, we measured extracellular matrix remodeling content in cardiac atrial tissue and systemic oxidative stress. CIH induced hypertension, enhanced ventilatory response to hypoxia, induced autonomic imbalance toward sympathetic preponderance, reduced baroreflex gain, and increased arrhythmias and atrial fibrosis. CB ablation normalized blood pressure, reduced ventilatory response to hypoxia, and restored cardiac autonomic and baroreflex function. In addition, CB ablation reduced the number of arrhythmias, but not extracellular matrix remodeling or systemic oxidative stress, suggesting that reductions in arrhythmia incidence during CIH were related to normalization of cardiac autonomic balance. Present results show that autonomic alterations induced by CIH are critically dependent on the CB and support a main role for the CB in the CIH-induced hypertension.
Phenotypic and molecular characterization of chickpea rhizobia isolated from different areas of Morocco

Aims: To determine the biodiversity of rhizobial strains nodulating Cicer arietinum L. in representative soils from various areas of Morocco. Methods and Results: Symbiotic traits, utilization of 49 carbohydrate sources, resistance to antibiotics and heavy metals, tolerance to salinity, to extreme temperatures and pH were studied as phenotypic markers. In addition, restriction fragment length polymorphism (RFLP) of PCR‐amplified 16S rDNAs were compared with those of reference strains. Numerical analysis of the phenotypic characteristics showed that the 48 strains studied fell into three distinct groups. RFLP analysis of 16S rRNA genes revealed an additional heterogeneity and four ribotypes were identified. Conclusions: Chickpea rhizobia isolated from Moroccan soils are both phenotypically and genetically diverse. Most of these rhizobia belong to the Mesorhizobium genus. However, some strains originating from a particular soil appeared to have 16S rRNA genes similar to Sinorhizobium as well as very distinct auxanographic characteristics compared with Mesorhizo‐ bium isolates. Significance and Impact of the Study: A well characterized collection of chickpea‐nodulating rhizobia in representative soils of Morocco has been generated, which can be used to develop efficient inoculants for this crop. This is the first report evidencing that chickpeas may be nodulated by bacteria from the Sinorhizobium genus.
Mitochondrial metabolic regulation by GRP78

ER chaperone GRP78 is the central regulator of adrenals and gonadal steroid synthesis for mammalian survival. Steroids, essential for mammalian survival, are initiated by cholesterol transport by steroidogenic acute regulatory protein (StAR). Appropriate protein folding is an essential requirement of activity. Endoplasmic reticulum (ER) chaperones assist in folding of cytoplasmic proteins, whereas mitochondrial chaperones fold only mitochondrial proteins. We show that glucose regulatory protein 78 (GRP78), a master ER chaperone, is also present at the mitochondria-associated ER membrane (MAM), where it folds StAR for delivery to the outer mitochondrial membrane. StAR expression and activity are drastically reduced following GRP78 knockdown. StAR folding starts at the MAM region; thus, its cholesterol fostering capacity is regulated by GRP78 long before StAR reaches the mitochondria. In summary, GRP78 is an acute regulator of steroidogenesis at the MAM, regulating the intermediate folding of StAR that is crucial for its activity.
Folliculin encoded by the BHD gene interacts with a binding protein, FNIP1, and AMPK, and is involved in AMPK and mTOR signaling

Birt–Hogg–Dubé syndrome, a hamartoma disorder characterized by benign tumors of the hair follicle, lung cysts, and renal neoplasia, is caused by germ-line mutations in the BHD(FLCN) gene, which encodes a tumor-suppressor protein, folliculin (FLCN), with unknown function. The tumor-suppressor proteins encoded by genes responsible for several other hamartoma syndromes, LKB1, TSC1/2, and PTEN, have been shown to be involved in the mammalian target of rapamycin (mTOR) signaling pathway. Here, we report the identification of the FLCN-interacting protein, FNIP1, and demonstrate its interaction with 5′ AMP-activated protein kinase (AMPK), a key molecule for energy sensing that negatively regulates mTOR activity. FNIP1 was phosphorylated by AMPK, and its phosphorylation was reduced by AMPK inhibitors, which resulted in reduced FNIP1 expression. AMPK inhibitors also reduced FLCN phosphorylation. Moreover, FLCN phosphorylation was diminished by rapamycin and amino acid starvation and facilitated by FNIP1 overexpression, suggesting that FLCN may be regulated by mTOR and AMPK signaling. Our data suggest that FLCN, mutated in Birt–Hogg–Dubé syndrome, and its interacting partner FNIP1 may be involved in energy and/or nutrient sensing through the AMPK and mTOR signaling pathways.
The effect of periodontal treatment on serum leptin, interleukin-6, and C-reactive protein.

BACKGROUND Previous studies suggest that periodontitis is closely related to obesity and metabolic syndrome. Leptin, a pleiotrophic hormone produced by adipose tissue, has been reported to be related to periodontitis. This study investigates the effects of periodontal treatment on the serum levels of leptin and other cytokines in patients with chronic periodontitis (CP). METHODS Serum samples were taken from 33 CP patients (22 non-smokers, 11 smokers) and 18 healthy subjects. The serum leptin, adiponectin, tumor necrosis factor-alpha, interleukin (IL)-6, and C-reactive protein (CRP) levels were measured before and after non-surgical periodontal treatment. RESULTS Significant differences between healthy and CP patients were found in serum leptin, IL-6, and CRP levels (P = 0.0018, P = 0.0064, and P = 0.0095, respectively). The serum leptin level was associated with mean probing depth, mean clinical attachment level, mean alveolar bone loss, and body mass index. There were significant associations between serum leptin levels and IL-6 and CRP levels. After non-surgical periodontal treatment, serum leptin, IL-6, and CRP levels were significantly decreased (mean +/- SD before and after, P value, respectively: leptin, 8.02 +/- 5.5, 7.10 +/- 4.4, P = 0.015; IL-6, 1.73 +/- 1.02, 1.36 +/- 0.73, P = 0.048; and CRP, 802.0 +/- 1065, 491.2 +/- 479.3, P = 0.047). CONCLUSIONS Periodontal treatment is effective in reducing serum leptin, IL-6, and CRP levels. The results suggest that leptin, IL-6, and CRP could be mediating factors that connect metabolic syndrome and periodontitis.
Effects of Methyl Eugenol Feeding on Mating Compatibility of Asian Population of Bactrocera dorsalis (Diptera: Tephritidae) with African Population and with B. carambolae

Abstract Males of some species included in the Bactrocera dorsalis complex are strongly attracted to methyl eugenol (ME) (1,2-dimethoxy-4-(2-propenyl) benzene), a natural compound occurring in a variety of plant species. ME feeding of males of the B. dorsalis complex is known to enhance their mating competitiveness. Within B. dorsalis, recent studies show that Asian and African populations of B. dorsalis are sexually compatible, while populations of B. dorsalis and Bactrocera carambolae are relatively incompatible. The objectives of this study were to examine whether ME feeding by males affects mating compatibility between Asian and African populations of B. dorsalis and ME feeding reduces male mating incompatibility between B. dorsalis (Asian population) and B. carambolae. The data confirmed that Asian and African populations of B. dorsalis are sexually compatible for mating and showed that ME feeding only increased the number of matings. Though ME feeding also increased the number of matings of B. dorsalis (Asian population) and B. carambolae males but the sexual incompatibility between both species was not reduced by treatment with ME. These results conform to the efforts resolving the biological species limits among B. dorsalis complex and have implications for fruit fly control programs in fields and horticultural trade.
Controlling spatiotemporal chaos in excitable media using an array of control points

The dynamics of activation waves in excitable media can give rise to spiral turbulence, the resulting spatiotemporal chaos being associated with empirical biological phenomena such as life-threatening disturbances in the natural rhythm of the heart. In this paper, we propose a spatially extended but non-global scheme using an array of control points for terminating such spatiotemporally chaotic excitations. A low-amplitude control signal is applied sequentially at each point on the array, resulting in a traveling wave of excitation in the underlying medium which drives away the turbulent activity. Our method is robust even in the presence of significant heterogeneities in the medium, which have often been an impediment to the success of other control schemes.
Morphine phase-shifts circadian rhythms in mice: role of behavioural activation

The effect of morphine on circadial wheel-running rhythms of C57BL/6j mice was examined. Mice received morphine (25 mg kg−1, i.p.) or saline at eight different circadian phases in constant dark. Morphine injections in the middle of the inactive period induced significant advance phase shifts, whereas injections at other times induced small delay shifts or no responses. This phase–response relationship was not altered by optic enucleation. Morphine also induced hyperactivity. Restriction of activity prevented phase shifts. The results indicate that morphine shifts circadian rhythms by its effects on behaviour, rather than by a direct action on the circadian pacemaker. Morphine may represent a useful tool for further study of behaviourally induced phase-resetting in this species.
Deglaciation of the Norwegian fjords

Melting glaciers and ice sheets are perhaps the most visible signs of a warming climate. Glaciers are retreating on every continent, ice sheets are shedding icebergs into a warming ocean at an accelerating rate, and the atmosphere melts more ice as temperatures rise. Despite these lines of evidence, and a growing scientific and public attention to melting ice; we are still not able to present robust numbers of future sea level rise. While the overall picture is one of retreat and meltdown, complex patterns arise when we zoom in within a certain region. The geologic record testaments both collapse and periods of growth, and provides important clues to future mass loss. However, these records show that variable responses were present within regions exposed to the same climate forcing. This is also found in Greenland and Antarctica today, where observations reveal that neighbouring glaciers respond differently to the same climate warming. Caution is therefore needed when explaining the responses of these glaciers. The instrumental record helps us to improve process understanding, yet is unable to assess changes over time scales longer than a few decades. The geologic record provides a longer perspective, but is not able to resolve short-lived variations. This time scale issue is critical because we need to understand both the short-term and longterm response to improve understanding of glacier and ice sheet dynamics and their sensitivity to climate change. In this thesis, we use a suite of numerical model tools combined with geological data to assess how external forcing triggers and drives shortand long-term change. Equally important, we study how site-specific factors such as topography can prevent, delay, dampen, amplify, and override the ambient forcing. We assess theoretical cases as well as past and present glaciers in Norway and Greenland, with the goal to answer the overarching question: how do glaciers and ice sheets respond to climate change? We move from the sensitivity of a Norwegian ice cap to Holocene climate change in Paper I, via the impact of fjord geometry on grounding line stability in Paper II, to the abrupt retreat of the nearby Hardangerfjorden glacier during the Younger Dryas cold period in Paper III. We continue with the most active glacier in Greenland in Paper IV, and finish with a comprehensive study of the triggers and drivers of the deglaciation of the Norwegian fjords in Paper V. For marine-terminating glaciers, we find that grounding line dynamics and iceocean interactions are fundamental over time scales up to a century or two. Beyond this time frame, changes to the surface mass balance are likely to drive widespread, multi-centennial to millennial scale deglaciation. Based on the results presented in this thesis, we also suggest that topography is a factor that cannot be ignored. Once triggered, the response to climate change is to a large degree controlled by the underlying bed topography of ice caps (Paper I), and by the fjord bathymetry and width of marine-terminating glaciers (Papers II–V).
Lipoproteins Containing Apo B Extracted from Human Aortas Structure and Function a

We have isolated, by anti-LDL affinity chromatography, apo B-containing lipoproteins from homogenates of atherosclerotic plaques excised from the human aorta. This fraction, called A-LP, has similarities with plasma LDL, such as having similar size and relative lipid composition, along with containing apo B. However, the fraction also contains some particles larger than LDL, it is more electronegative than LDL, the relative protein content is less than in LDL, and its apo B is highly degraded. A-LP is recognized by a high affinity binding site on mouse peritoneal macrophages (MPM), as suggested by dose-response curves of stimulation of cholesterol esterification. The interaction is inhibited by negatively-charged carbohydrates such as fucoidin, but excess A-LP did not inhibit the degradation of labeled acetyl-LDL by MPM, suggesting that the binding site recognizing A-LP may not be the scavenger receptor. Finally, stimulation of cholesterol esterification by A-LP in MPM is unregulated over a 48 hr time interval, leading to massive accumulations of cholesteryl esters and a transition of these MPM to a morphology characteristic of foam cells. It is possible that when monocytes enter the arterial intima at specific sites and become tissue macrophages, they internalize A-LP in an unregulated fashion. This, in turn, would make the monocyte-macrophage lipid-laden, and could explain the etiology of foam cells in fatty streak lesions. The modification in A-LP relative to P-LDL responsible for the enhanced recognition still needs to be elucidated.