Axisymmetric Slow Rotation of Coaxial Soft/Porous Spheres.

The steady low-Reynolds-number rotation of a chain of coaxial soft spheres (each with an impermeable hard core covered by a permeable porous layer) about the axis in a viscous fluid is analyzed. The particles may be unequally spaced, and may differ in the permeability and inner and outer radii of the porous surface layer as well as angular velocity. By using a method of boundary collocation, the Stokes and Brinkman equations for the external fluid flow and flow within the surface layers, respectively, are solved semi-analytically. The particle interaction effect increases as the relative gap thickness between adjacent particles or their permeability decreases, which can be significant as the gap thickness approaches zero. A particle's hydrodynamic torque is reduced (its rotation is enhanced) when other particles rotate in the same direction at equivalent or greater angular velocities, but increases (its rotation is hindered) when other particles rotate in the opposite direction at arbitrary angular velocities. For particles with different radii or permeabilities, the particle interaction has a greater effect on smaller or more permeable particles than on larger or less permeable particles. For the rotation of three particles, the presence of the third particle can significantly affect the hydrodynamic torques acting on the other two particles. For the rotation of numerous particles, shielding effects between particles can be substantial. When the permeability of porous layers is low, relative fluid motion is barely felt by the hard cores of the soft particles. The insights gained from this analysis on the effects of interactions among rotating soft particles may be of great importance in many physicochemical applications of colloidal suspensions.

Sedimentation of a Charged Soft Sphere within a Charged Spherical Cavity.

The sedimentation of a soft particle composed of an uncharged hard sphere core and a charged porous surface layer inside a concentric charged spherical cavity full of a symmetric electrolyte solution is analyzed in a quasi-steady state. By using a regular perturbation method with small fixed charge densities of the soft sphere and cavity wall, a set of linearized electrokinetic equations relevant to the fluid velocity field, electrical potential profile, and ionic electrochemical potential energy distributions are solved. A closed-form formula for the sedimentation velocity of the soft sphere is obtained as a function of the ratios of core-to-particle radii, particle-to-cavity radii, particle radius-to-Debye screening length, and particle radius-to-porous layer permeation length. The existence of the surface charge on the cavity wall increases the settling velocity of the charged soft sphere, principally because of the electroosmotic enhancement of fluid recirculation within the cavity induced by the sedimentation potential gradient. When the porous layer space charge and cavity wall surface charge have the same sign, the particle velocity is generally enhanced by the presence of the cavity. When these fixed charges have opposite signs, the particle velocity will be enhanced/reduced by the presence of the cavity if the wall surface charge density is sufficiently large/small relative to the porous layer space charge density in magnitude. The effect of the wall surface charge on the sedimentation of the soft sphere increases with decreases in the ratios of core-to-particle radii, particle-to-cavity radii, and particle radius-to-porous layer permeation length but is not a monotonic function of the ratio of particle radius-to-Debye length.

CSK may be a potential prognostic biomarker reflecting the immune status of gastric cancer.

OBJECTIVE: C-terminal Src kinase (CSK), a sarcoma (Src) homologous family kinase, is one of the most important negative regulators. It acts as a tumor suppressor by inhibiting the activity of Src family tyrosine kinases. Paradoxically, CSK is highly expressed in a variety of common tumors. Therefore, we report the expression profile of CSK in pan-cancer patients, focusing on the prognostic value, immune infiltration pattern, and biological function of CSK in gastric cancer. MATERIALS AND METHODS: We used the TCGA database to analyze CSK expression, clinical relevance, prognostic significance, assessment of the tumor immune microenvironment, and GO and Kegg enrichment analysis based on co-expressed genes using a bioinformatics approach. RESULTS: CSK is a protective factor in gastric cancer, and its expression correlates with the level of immune cell infiltration and immune checkpoint molecules. CONCLUSIONS: Our findings suggest that CSK is an independent prognostic factor in gastric cancer and may predict molecular targeting and immunotherapy and provide ideas for its therapeutic strategy.

Syntenin-1-mediated arthritogenicity is advanced by reprogramming RA metabolic macrophages and Th1 cells.

OBJECTIVES: Syntenin-1, a novel endogenous ligand, was discovered to be enriched in rheumatoid arthritis (RA) specimens compared with osteoarthritis synovial fluid and normal synovial tissue (ST). However, the cellular origin, immunoregulation and molecular mechanism of syntenin-1 are undescribed in RA. METHODS: RA patient myeloid and lymphoid cells, as well as preclinical models, were used to investigate the impact of syntenin-1/syndecan-1 on the inflammatory and metabolic landscape. RESULTS: Syntenin-1 and syndecan-1 (SDC-1) co-localise on RA ST macrophages (MΦs) and endothelial cells. Intriguingly, blood syntenin-1 and ST SDC-1 transcriptome are linked to cyclic citrullinated peptide, erythrocyte sedimentation rate, ST thickness and bone erosion. Metabolic CD14+CD86+GLUT1+MΦs reprogrammed by syntenin-1 exhibit a wide range of proinflammatory interferon transcription factors, monokines and glycolytic factors, along with reduced oxidative intermediates that are downregulated by blockade of SDC-1, glucose uptake and/or mTOR signalling. Inversely, IL-5R and PDZ1 inhibition are ineffective on RA MΦs-reprogrammed by syntenin-1. In syntenin-1-induced arthritis, F4/80+iNOS+RAPTOR+MΦs represent glycolytic RA MΦs, by amplifying the inflammatory and glycolytic networks. Those networks are abrogated in SDC-1-/- animals, while joint prorepair monokines are unaffected and the oxidative metabolites are moderately replenished. In RA cells and/or preclinical model, syntenin-1-induced arthritogenicity is dependent on mTOR-activated MΦ remodelling and its ability to cross-regulate Th1 cells via IL-12 and IL-18 induction. Moreover, RA and joint myeloid cells exposed to Syntenin-1 are primed to transform into osteoclasts via SDC-1 ligation and RANK, CTSK and NFATc1 transcriptional upregulation. CONCLUSION: The syntenin-1/SDC-1 pathway plays a critical role in the inflammatory and metabolic landscape of RA through glycolytic MΦ and Th1 cell cross-regulation (graphical abstract).

Inhibition of IRAK4 dysregulates SARS-CoV-2 spike protein-induced macrophage inflammatory and glycolytic reprogramming.

Escalated innate immunity plays a critical role in SARS-CoV-2 pathology; however, the molecular mechanism is incompletely understood. Thus, we aim to characterize the molecular mechanism by which SARS-CoV-2 Spike protein advances human macrophage (MÏ´) inflammatory and glycolytic phenotypes and uncover novel therapeutic strategies. We found that human MÏ´s exposed to Spike protein activate IRAK4 phosphorylation. Blockade of IRAK4 in Spike protein-stimulated MÏ´s nullifies signaling of IRAK4, AKT, and baseline p38 without affecting ERK and NF-κB activation. Intriguingly, IRAK4 inhibitor (IRAK4i) rescues the SARS-CoV-2-induced cytotoxic effect in ACE2+HEK 293 cells. Moreover, the inflammatory reprogramming of MÏ´s by Spike protein was blunted by IRAK4i through IRF5 and IRF7, along with the reduction of monokines, IL-6, IL-8, TNFα, and CCL2. Notably, in Spike protein-stimulated MÏ´s, suppression of the inflammatory markers by IRAK4i was coupled with the rebalancing of oxidative phosphorylation over metabolic activity. This metabolic adaptation promoted by IRAK4i in Spike protein-activated MÏ´s was shown to be in part through constraining PFKBF3, HIF1α, cMYC, LDHA, lactate expression, and reversal of citrate and succinate buildup. IRAK4 knockdown could comparably impair Spike protein-enhanced inflammatory and metabolic imprints in human MÏ´s as those treated with ACE2, TLR2, and TLR7 siRNA. Extending these results, in murine models, where human SARS-CoV-2 Spike protein was not recognized by mouse ACE2, TLRs were responsible for the inflammatory and glycolytic responses instigated by Spike protein and were dysregulated by IRAK4i therapy. In conclusion, IRAK4i may be a promising strategy for severe COVID-19 patients by counter-regulating ACE2 and TLR-mediated MÏ´ hyperactivation. IRAK4i therapy counteracts MÏ´ inflammatory and glycolytic reprogramming triggered by Spike protein. This study illustrates that SARS-CoV-2 Spike protein activates IRAK4 signaling via ACE2 as well as TLR2 and TLR7 sensing in human MÏ´s. Remarkably, IRAK4i treatment can dysregulate both ACE-dependent and independent (via TLR sensing) SARS-CoV-2 Spike protein-activated inflammatory and metabolic imprints.

[Inspiration from the research advances in microcirculatory dysfunction to the treatment of burn shock and burn septic shock].

Microcirculatory dysfunction is an important pathophysiological change of shock. In the last decade, many researches on the mechanism of microcirculatory dysfunction have been involved in areas such as the glycocalyx damage of vascular endothelial cells, macrocirculation- microcirculation discoupling, vascular hyporeactivity, and microcirculation monitoring. Accordingly, this paper discussed how these research findings can be applied to burn patients, with the aim of alerting the clinicians to improving microcirculation, and maintaining hemodynamic coordination during the treatment of burn shock and burn septic shock. In addition, with the development of accurate and reliable microcirculation monitoring techniques, it is necessary to carry out multi-center clinical trials to reveal the clinical significance of target-oriented shock resuscitation protocol combining macrocirculatory and microcirculatory parameters.

[Controlling excessive fluid resuscitation in massive burn patients to prevent complications].

Excessive fluid resuscitation in massive burn patients is a common phenomenon in burn management, and the reasons are mostly related with administering resuscitation of crystalloid alone and pursuing a goal-directed resuscitation with targeting normal hemodynamic parameters in the first 24 h post burn. Tissue edema caused by excessive fluid resuscitation is a vital factor that induces complications including respiratory compromise, abdominal compartment syndrome, and so on. Therefore, in order to control excessive fluid resuscitation and prevent its subsequent complications in massive burn patients, it is necessary to determine the optimal resuscitation regime, set appropriate resuscitation endpoints, and implement precise management of fluid resuscitation.

Metabolic reprogramming of macrophages instigates CCL21-induced arthritis.

This study was designed to delineate the functional significance of CCL21 in metabolic reprogramming in experimental arthritis and differentiated rheumatoid arthritis (RA) macrophages (MΦs). To characterize the influence of CCL21 on immunometabolism, its mechanism of action was elucidated by dysregulating glucose uptake in preclinical arthritis and RA MΦs. In CCL21 arthritic joints, the glycolytic intermediates hypoxia-inducible factor 1α (HIF1α), cMYC and GLUT1 were overexpressed compared with oxidative regulators estrogen-related receptor γ and peroxisome proliferator-activated receptor gamma coactivator 1 (PGC1)-α. Interestingly, 2-deoxy-D-glucose (2-DG) therapy mitigated CCL21-induced arthritis by restraining the number of joint F4/80+ iNOS+ MΦs without impacting F4/80+ Arginase+ MΦs. Similar to the preclinical findings, blockade of glycolysis negated CCL21-polarized CD14+ CD86+ GLUT+ MΦ frequency; however, CD14+ CD206+ GLUT+ MΦs were not implicated in this process. In CCL21-induced arthritis and differentiated RA MΦs, the inflammatory imprint was uniquely intercepted by 2-DG via interleukin-6 (IL-6) downregulation. Despite the more expansive inflammatory response of CCL21 in the arthritic joints relative to the differentiated RA MΦs, 2-DG was ineffective in joint tumor necrosis factor-α, IL-1ß, CCL2 and CCL5 enrichment. By contrast, disruption of glycolysis markedly impaired CCL21-induced HIF1α and cMYC signaling in arthritic mice. Notably, in RA MΦs, glycolysis interception was directed toward dysregulating CCL21-enhanced HIF1α transcription. Nonetheless, in concurrence with the diminished IL-6 levels, CCL21 differentiation of CD14+ CD86+ GLUT1+ MΦs was reversed by glycolysis and HIIF1α inhibition. Moreover, in the CCL21 experimental arthritis or differentiated RA MΦs, the malfunctioning metabolic machinery was accompanied by impaired oxidative phosphorylation because of reduced PGC1α or peroxisome proliferator-activated receptor-γ expression. CCL21 reconfigures naïve myeloid cells into glycolytic RA CD14+ CD86+ GLUT+ IL-6high HIF1αhigh MΦs. Therefore, inhibiting the CCL21/CCR7 pathway may provide a promising therapeutic strategy.

[Observation on the clinical effect of self-designed modified rhomboid skin flap in facial wound repair].

Objective: To investigate the clinical effect of self-designed modified rhomboid flap in repairing rhomboid, round, and teardrop-shaped wounds on the face. Methods: A retrospective observational study was conducted. From August 2018 to April 2020, 30 patients with facial lesions admitted into Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine and the People's Hospital of Jianchuan County in Yunnan province met the inclusion criteria, including 16 males and 14 females, aged 23 to 88 years. The wound area ranged from 1.0 cm×1.0 cm to 7.0 cm×5.0 cm, with 10 cases of rhomboid wounds, 12 cases of round wounds, and 8 cases of teardrop-shaped wounds. The self-designed modified rhomboid flaps were applied to repair the wounds and after that, the patients were followed up for 1 to 18 months to record the survival of flaps, wound tension, scar formation and complications after surgery. Results: No necrosis or blackening was observed at the tip of the flaps after surgery. All the flaps survived and the wounds healed well with little tension, minimal scars, and no complications. Conclusions: The self-designed modified rhomboid flap is especially suitable for facial wounds with multiple important organs, multiple anatomical subunits, and areas with large changes in soft tissue tension, which can reduce not only the rotation of the flap, but also unnecessary excision of normal skin and soft tissue.

Electrophoresis and electric conduction in a salt-free suspension of charged particles.

The electrophoresis and electric conduction of a suspension of charged spherical particles in a salt-free solution are analyzed by using a unit cell model. The linearized Poisson-Boltzmann equation (valid for the cases of relatively low surface charge density or high volume fraction of the particles) and Laplace equation are solved for the equilibrium electric potential profile and its perturbation caused by the imposed electric field, respectively, in the fluid containing the counterions only around the particle, and the ionic continuity equation and modified Stokes equations are solved for the electrochemical potential energy and fluid flow fields, respectively. Explicit analytical formulas for the electrophoretic mobility of the particles and effective electric conductivity of the suspension are obtained, and the particle interaction effects on these transport properties are significant and interesting. The scaled zeta potential, electrophoretic mobility, and effective electric conductivity increase monotonically with an increase in the scaled surface charge density of the particles and in general decrease with an increase in the particle volume fraction, keeping each other parameter unchanged. Under the Debye-Hückel approximation, the dependence of the electrophoretic mobility normalized with the surface charge density on the ratio of the particle radius to the Debye screening length and particle volume fraction in a salt-free suspension is same as that in a salt-containing suspension, but the variation of the effective electric conductivity with the particle volume fraction in a salt-free suspension is found to be quite different from that in a suspension containing added electrolyte.

Transient electrophoresis in a suspension of charged particles with arbitrary electric double layers.

The startup of electrophoretic motion in a suspension of spherical colloidal particles, which may be charged with constant zeta potential or constant surface charge density, due to the sudden application of an electric field is analytically examined. The unsteady modified Stokes equation governing the fluid velocity field is solved with unit cell models. Explicit formulas for the transient electrophoretic velocity of the particle in a cell in the Laplace transforms are obtained as functions of relevant parameters. The transient electrophoretic mobility is a monotonic decreasing function of the particle-to-fluid density ratio and in general a decreasing function of the particle volume fraction, but it increases and decreases with a raise in the ratio of the particle radius to the Debye length for the particles with constant zeta potential and constant surface charge density, respectively. On the other hand, the relaxation time in the growth of the electrophoretic mobility increases substantially with an increase in the particle-to-fluid density ratio and with a decrease in the particle volume fraction but is not a sensitive function of the ratio of the particle radius to the Debye length. For specified values of the particle volume fraction and particle-to-fluid density ratio in a suspension, the relaxation times in the growth of the particle mobility in transient electrophoresis and transient sedimentation are equivalent.

Start-Up Electrophoresis of a Cylindrical Particle with Arbitrary Double Layer Thickness.

The start-up of electrophoretic motion of a charged circular cylindrical particle in an unbounded solution of arbitrary electrolytes is analytically investigated. The modified Stokes equation for the transient fluid flow field is solved by using the Laplace transform. Analytical formulas for the time-evolving electrophoretic velocities of the dielectric cylinder are determined for the transversely and axially imposed electric fields, and they can be superimposed linearly for an imposed electric field of arbitrary direction. The transient electrophoretic velocities normalized by their respective steady-state values increase monotonically with an increase in the ratio of the particle radius to the Debye screening length but decrease monotonically with an increase in the particle-to-fluid density ratio, keeping the other parameter unchanged. The normalized electrophoretic acceleration of the particle decreases monotonically with the elapsed time. In general, the electrophoretic velocity of the cylindrical particle is not collinear with the arbitrarily oriented imposed electric field. The effect of the relaxation time for the transient electrophoresis is much more important for a cylindrical particle than for a spherical particle.

Electrokinetic flow and electric conduction of salt-free solutions in a capillary.

The electrokinetic flow and accompanied electric conduction of a salt-free solution in the axial direction of a charged circular capillary are analyzed. No assumptions are made about the surface charge density (or surface potential) and electrokinetic radius of the capillary, which are interrelated. The Poisson-Boltzmann equation and modified Navier-Stokes equation are solved for the electrostatic potential distribution and fluid velocity profile, respectively. Closed-form formulas for the electroosmotic mobility and electric conductivity in the capillary are derived in terms of the surface charge density. The relative surface potential, electroosmotic mobility, and electric conductivity are monotonic increasing functions of the surface charge density and electrokinetic radius. However, the rises of the relative surface potential and electroosmotic mobility with an increase in the surface charge density are suppressed substantially when it is high due to the effect of counterion condensation. The analytical prediction that the electroosmotic mobility grows with increases in the surface charge density and electrokinetic radius agrees with the experimental results for salt-free solutions in circular microchannels in the literature.

Transient electrophoresis of a charged porous particle.

The starting electrophoretic motion of a porous, uniformly charged, spherical particle, which models a solvent-permeable and ion-penetrable polyelectrolyte coil or floc of nanoparticles, in an arbitrary electrolyte solution due to the sudden application of an electric field is studied for the first time. The unsteady Stokes/Brinkman equations with the electric force term governing the fluid velocity fields are solved by means of the Laplace transform. An analytical formula for the electrophoretic mobility of the porous sphere is obtained as a function of the dimensionless parameters κa , λa , ρp/ρ , and νt/a2 , where a is the radius of the particle, κ is the Debye screening parameter, λ is the reciprocal of the square root of the fluid permeability in the particle, ρp and ρ are the mass densities of the particle and fluid, respectively, ν is the kinematic viscosity of the fluid, and t is the time. The electrophoretic mobility normalized by its steady-state value increases monotonically with increases in νt/a2 and κa , but decreases monotonically with an increase in ρp/ρ , keeping the other parameters unchanged. In general, a porous particle with a high fluid permeability trails behind an identical porous particle with a lower permeability and a corresponding hard particle in the growth of the normalized electrophoretic mobility The normalized electrophoretic acceleration of the porous sphere decreases monotonically with an increase in the time and increases with an increase in λa from zero at λa=0 .

Macrophages are the primary effector cells in IL-7-induced arthritis.

Synovial macrophages are crucial in the development of joint inflammation and bone damage; however, the pathways that control macrophage remodeling in inflammatory M1 cells or bone-eroding osteoclasts are not fully understood. We determined that elevated IL-7R/CD127 expression is the hallmark of rheumatoid arthritis (RA) M1 macrophages and that these cells are highly responsive to interleukin-7 (IL-7)-driven osteoclastogenesis. We established that lipopolysaccharide (LPS), interferon-γ (IFNγ), and tumor necrosis factor-α (TNFα), the classic M1 macrophage mediators, enhance IL-7R expression in RA and murine macrophages. The local expression of IL-7 provokes arthritis, predominantly through escalating the number of F480+iNOS+ cells rather than CD3+ T cells. Ectopic LPS injection stabilizes IL-7-induced arthritis by increasing myeloid IL-7R expression, in part via IFNγ induction. Hence, in RAG-/- mice, IL-7-mediated arthritis is suppressed because of the reduction in myeloid IL-7R expression due to the lack of IFNγ. Moreover, the amelioration of IL-7-induced arthritis by anti-TNF therapy is due to a decrease in the number of cells in the unique F480+iNOS+IL-7R+CCL5+ subset, with no impact on the F480+Arginase+ cell or CD3+ T cell frequency. Consistent with the preclinical findings, the findings of a phase 4 study performed with RA patients following 6 months of anti-TNF therapy revealed that IL-7R expression was reduced without affecting the levels of IL-7. This study shifts the paradigm by discovering that IL-7-induced arthritis is dependent on F480+iNOS+IL-7R+CCL5+ cell function, which activates TH-1 cells to amplify myeloid IL-7R expression and disease severity.

CCL21/CCR7 signaling in macrophages promotes joint inflammation and Th17-mediated osteoclast formation in rheumatoid arthritis.

In rheumatoid arthritis (RA), synovial tissue abundantly expresses CCL21, a chemokine strongly associated with RA susceptibility. In this study, we aimed to characterize the functional significance of CCL21/CCR7 signaling in different phases of RA pathogenesis. We determined that CCR7 is a hallmark of RA M1 synovial fluid (SF) macrophages, and its expression in RA monocytes and in vitro differentiated macrophages is closely associated with disease activity score (DAS28). In early stages of RA, monocytes infiltrate the synovial tissue. However, blockade of SF CCL21 or CCR7 prevents RA SF-mediated monocyte migration. CCR7 expression in the newly migrated macrophages can be accentuated by LPS and IFNγ and suppressed by IL-4 treatment. We also uncovered that CCL21 stimulation increases the number of M1-polarized macrophages (CD14+CD86+), resulting in elevated transcription of IL-6 and IL-23. These CCL21-induced M1 cytokines differentiate naïve T cells to Th17 cells, without affecting Th1 cell polarization. In the erosive stages of disease, CCL21 potentiates RA osteoclastogenesis through M1-driven Th17 polarization. Disruption of this intricate crosstalk, by blocking IL-6, IL-23, or IL-17 function, impairs the osteoclastogenic capacity of CCL21. Consistent with our in vitro findings, we establish that arthritis mediated by CCL21 expands the joint inflammation to bone erosion by connecting the differentiation of M1 macrophages with Th17 cells. Disease progression is further exacerbated by CCL21-induced neovascularization. We conclude that CCL21 is an attractive novel target for RA therapy, as blockade of its function may abrogate erosive arthritis modulated by M1 macrophages and Th17 cell crosstalk.

Electrokinetic Flow of Salt-Free Solutions in a Fibrous Porous Medium.

The electrokinetic flow of a salt-free solution in the fibrous porous medium constituted by an array of parallel charged circular cylinders subject to a pressure gradient and an electric field imposed in the axial direction is analytically studied via the use of a unit cell model. The Poisson-Boltzmann equation and modified Navier-Stokes equation applicable to a unit cell accommodating the salt-free solution around an individual cylinder are solved to determine the electric potential profile and fluid velocity distribution. Results of the electroosmotic velocity and effective electric conductivity in the fiber matrix are obtained as functions of the surface charge density of the dielectric cylinders and the porosity of the fiber matrix. The effects of the porosity or interactions among the cylinders on the electric potential distribution, electroosmotic velocity, and effective electric conductivity are significant and interesting under practical conditions. The apparent zeta potential, electroosmotic velocity, and effective electric conductivity increase monotonically with an increase in the surface charge density of the cylinders. When the porosity of the fiber matrix and surface charge density of the cylinders are high, the increases of the apparent zeta potential and electroosmotic velocity with the surface charge density are substantially suppressed due to the counterion condensation effect. However, this effect becomes weak when the porosity is low.

Sedimentation Velocity and Potential in Dilute Suspensions of Charge-Regulating Porous Spheres.

The sedimentation of a charge-regulating porous sphere surrounded by an arbitrary electric double layer, which usually models a permeable polyelectrolyte coil or an aggregate of nanoparticles, is analyzed for the first time. The hydrodynamic frictional segments and ionogenic functional groups uniformly distribute in the porous sphere, and a regulation mechanism for the dissociation and association reactions occurring at these functional groups linearly relates the local electric potential to fixed charge density. The linearized electrokinetic equations governing the ionic concentration (or electrochemical potential energy), electric potential, and fluid velocity fields are solved for the case of a small basic fixed charge density by the regular perturbation method. Analytical formulae for the sedimentation velocity of a porous sphere and sedimentation potential of a dilute suspension of porous spheres are then obtained. The charge regulation tends to reduce the electrokinetic retardation to sedimentation velocity and the sedimentation potential (can be as much as 50 and 25%, respectively) compared to the case that the fixed charge density is a constant. Both the electrokinetic retardation to sedimentation velocity and the sedimentation potential vanish at the isoelectric point of the particles. The increase in the bulk concentration of the potential-determining ions crossing the isoelectric point changes signs of the fixed charges and thus causes a reversal in the direction of the sedimentation potential. The effects of charge regulation on the sedimentation of porous particles differ substantially from those of hard particles.

[Developing trend of wound dressing].

The ideal wound dressing should have the functions of keeping wound moist and warm, preventing and treating wound infection, promoting wound healing, and so on; However there is no such ideal wound dressing in clinic. Dressings are likely to capable application to different kinds of wounds with multi-functions in the future. For the purpose of good tissue compatibility and permanent wound cover, auto- or allo- skin living cells should be integrated with biological dressings as real artificial skin by employing tissue engineering technology. Clinical application of smart dressings can enable wound management more personalized, effective, optimized, and convenient.

[Further understanding of infection of carbapenems-resistant Klebsiella pneumoniae among burn patients and the related strategies for antimicrobial treatment].

The prevalence of carbapenems-resistant Klebsiella pneumoniae (CRKP ) in burn wards has become one of the most troublesome issues in current management of bacterial infections. It is necessary for us to reconsider the epidemiology, risk factors and clinical characteristics of CRKP infection as well as therapeutic options. Formulating the principles of antimicrobial therapy of CRKP infection and combined antibiotics therapy and implementing appropriate dosage regimens designed by pharmacokinetic and pharmacodynamic profiles will be of importance. Common antimicrobial agents for the treatment of CRKP infection include polymyxins, tigecycline, fosfomycin, and carbapenems. Infection control measures such as contact isolation, active screening, and environmental surface disinfection must be integrated with antimicrobial stewardship to effectively curb and prevent the spread of CRKP.