Bacterial pathogens employ a number of genetic strategies to cause infection and, occasionally, disease in their hosts. Many of these virulence factors and their regulatory elements can be divided into a smaller number of groups based on the conservation of similar mechanisms. These common themes are found throughout bacterial virulence factors. For example, there are only a few general types of toxins, despite a large number of host targets. Similarly, there are only a few conserved ways to build the bacterial pilus and nonpilus adhesins used by pathogens to adhere to host substrates. Bacterial entry into host cells (invasion) is a complex mechanism. However, several common invasion themes exist in diverse microorganisms. Similarly, once inside a host cell, pathogens have a limited number of ways to ensure their survival, whether remaining within a host vacuole or by escaping into the cytoplasm. Avoidance of the host immune defenses is key to the success of a pathogen. Several common themes again are employed, including antigenic variation, camouflage by binding host molecules, and enzymatic degradation of host immune components. Most virulence factors are found on the bacterial surface or secreted into their immediate environment, yet virulence factors operate through a relatively small number of microbial secretion systems. The expression of bacterial pathogenicity is dependent upon complex regulatory circuits. However, pathogens use only a small number of biochemical families to express distinct functional factors at the appropriate time that causes infection. Finally, virulence factors maintained on mobile genetic elements and pathogenicity islands ensure that new strains of pathogens evolve constantly. Comprehension of these common themes in microbial pathogenicity is critical to the understanding and study of bacterial virulence mechanisms and to the development of new "anti-virulence" agents, which are so desperately needed to replace antibiotics.

/pdf/common-themes-in-microbial-pathogenicity-revisited-5g424sp8ag.pdf

Common themes in microbial pathogenicity revisited.

Amyloid is associated with debilitating human ailments including Alzheimer's and prion diseases. Biochemical, biophysical, and imaging analyses revealed that fibers produced by Escherichia coli called curli were amyloid. The CsgA curlin subunit, purified in the absence of the CsgB nucleator, adopted a soluble, unstructured form that upon prolonged incubation assembled into fibers that were indistinguishable from curli. In vivo, curli biogenesis was dependent on the nucleation-precipitation machinery requiring the CsgE and CsgF chaperone-like and nucleator proteins, respectively. Unlike eukaryotic amyloid formation, curli biogenesis is a productive pathway requiring a specific assembly machinery.

/pdf/role-of-escherichia-coli-curli-operons-in-directing-amyloid-5g4vw9r2sg.pdf

Role of Escherichia coli Curli Operons in Directing Amyloid Fiber Formation

Magnetic flux can penetrate a type-II superconductor in the form of Abrikosov vortices (also called flux lines, flux tubes, or fluxons) each carrying a quantum of magnetic flux phi 0=h/2e. These tiny vortices of supercurrent tend to arrange themselves in a triangular flux-line lattice (FLL), which is more or less perturbed by material inhomogeneities that pin the flux lines, and in high-Tc superconductors (HTSCs) also by thermal fluctuations. Many properties of the FLL are well described by the phenomenological Ginzburg-Landau theory or by the electromagnetic London theory, which treats the vortex core as a singularity. In Nb alloys and HTSCs the FLL is very soft mainly because of the large magnetic penetration depth lambda . The shear modulus of the FLL is c66~1/ lambda 2, and the tilt modulus c44(k)~(1+k2 lambda 2)-1 is dispersive and becomes very small for short distortion wavelengths 2 pi /k<< lambda . This softness is enhanced further by the pronounced anisotropy and layered structure of HTSCs, which strongly increases the penetration depth for currents along the c axis of these (nearly uniaxial) crystals and may even cause a decoupling of two-dimensional vortex lattices in the Cu-O layers. Thermal fluctuations and softening may `melt` the FLL and cause thermally activated depinning of the flux lines or ofthe two-dimensional `pancake vortices` in the layers. Various phase transitions are predicted for the FLL in layered HTSCs. Although large pinning forces and high critical currents have been achieved, the small depinning energy so far prevents the application of HTSCs as conductors at high temperatures except in cases when the applied current and the surrounding magnetic field are small.

https://iopscience.iop.org/article/10.1088/0034-4885/58/11/003/pdf

The flux-line lattice in superconductors

Curli are the major proteinaceous component of a complex extracellular matrix produced by many Enterobacteriaceae. Curli were first discovered in the late 1980s on Escherichia coli strains that caused bovine mastitis, and have since been implicated in many physiological and pathogenic processes of E. coli and Salmonella spp. Curli fibers are involved in adhesion to surfaces, cell aggregation, and biofilm formation. Curli also mediate host cell adhesion and invasion, and they are potent inducers of the host inflammatory response. The structure and biogenesis of curli are unique among bacterial fibers that have been described to date. Structurally and biochemically, curli belong to a growing class of fibers known as amyloids. Amyloid fiber formation is responsible for several human diseases including Alzheimer's, Huntington's, and prion diseases, although the process of in vivo amyloid formation is not well understood. Curli provide a unique system to study macromolecular assembly in bacteria and in vivo amyloid fiber formation. Here, we review curli biogenesis, regulation, role in biofilm formation, and role in pathogenesis.

/pdf/curli-biogenesis-and-function-4itudh7izj.pdf

Curli Biogenesis and Function

Bacteria have evolved a remarkable array of sophisticated nanomachines to export various virulence factors across the bacterial cell envelope. In recent years, considerable progress has been made towards elucidating the structural and molecular mechanisms of the six secretion systems (types I-VI) of Gram-negative bacteria, the unique mycobacterial type VII secretion system, the chaperone-usher pathway and the curli secretion machinery. These advances have greatly enhanced our understanding of the complex mechanisms that these macromolecular structures use to deliver proteins and DNA into the extracellular environment or into target cells. In this Review, we explore the structural and mechanistic relationships between these single- and double-membrane-embedded systems, and we briefly discuss how this knowledge can be exploited for the development of new antimicrobial strategies.

Secretion systems in Gram-negative bacteria: structural and mechanistic insights

Gram-negative bacteria are known to produce two types of surface organelles: flagella, which are required for motility and chemotaxis, and pili (fimbriae), which play a part in the interaction of bacteria with other bacteria and with eukaryotic host cells. Here we report a third class of E. coli surface organelles for which we propose the name curli. Curli are coiled surface structures composed of a single type of subunit, the curlin, which differs from all known pilin proteins and is synthesized in the absence of a cleavable signal peptide. Although the gene encoding this structural subunit, crl, is present and transcribed in most natural isolates of E. coli, only certain strains are able to assemble the subunit protein into curli. This assembly process occurs preferentially at growth temperatures below 37 degrees C. The ability of curli to mediate binding to fibronectin may be a virulence-associated property for wound colonization and for the colonization of fibronectin-coated surfaces.

Fibronectin binding mediated by a novel class of surface organelles on Escherichia coli.

The exponent $a$ for the nonlinear $\mathrm{IV}$ characteristics, $V\ensuremath{\sim}{I}^{a}$, is obtained from a critical scaling argument for a two dimensional superconductor below ${T}_{c}$. The scaling assumption is supported by numerical simulations. The $\mathrm{IV}$ characteristics for the resistively shunted-juction model is simulated numerically, and excellent agreement with the predicted exponent is found. The new scaling exponent differs from the generally accepted Ambegaokar-Halperin-Nelson-Siggia result. The reason for this discrepancy is discussed.

New Exponent for the Nonlinear IV Characteristics of a Two Dimensional Superconductor

Aims: Glomerular filtration rate is an important factor in management of heart failure (HF). Our objective was to validate eight creatinine-based equations for estimating glomerular filtration rate ...

/pdf/comparison-of-creatinine-based-methods-for-estimating-2wedo9621p.pdf

Comparison of creatinine-based methods for estimating glomerular filtration rate in patients with heart failure.

Simulations on the two-dimensional XY model are performed. The results are compared to experiments on a Josephson junction array for the case of a triangular lattice well below the Kosterlitz-Thouless temperature in a weak perpendicular magnetic field. Comparisons between experiments, existing theories and the simulations suggest that the characteristic features of the complex impedance seen in the experiments are due to vortex correlations induced by the presence of vortices with opposite vorticity.

Complex impedance of a two-dimensional Josephson junction array

A new critical dynamics close to the Kosterlitz-Thouless transition for two-dimensional vortex fluctuations is determined from simulations of $\mathrm{XY}$-type models with time-dependent Ginzburg-Landau dynamics. The critical divergence of the conductivity is $\ensuremath{\sigma}\ensuremath{\propto}{\ensuremath{\omega}}^{\ensuremath{-}y}$ with $y\ensuremath{\approx}0.83$. This result is translated into a prediction for the flux noise.

Critical Dynamics of Two-Dimensional Vortex Fluctuations.

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