Membrane Formation Research Articles

Formation of hydrophobic membranes by surface spray assisted NIPS: Effects of solvent/non-solvent and spraying conditions

Membrane distillation has long been a potential desalination technology. Recently, spray-assisted non-solvent induced phase inversion (SANIPS) was proposed as a facile and effective method to prepare microporous hydrophobic membranes for membrane distillation. However, the membrane formation process is not fully disclosed. In this paper, SANIPS is employed to fabricate hydrophobic PVDF membranes. The influencing factors on membrane structure and performance are investigated. Membrane structure is greatly affected by the choice of solvent and non-solvent spray. The interactions between different non-solvent sprays (water and ethanol) and solvents (TEP, NMP and DMF) and the effects of operating conditions on membrane formation are explored. Thermodynamic and kinetic analyses of the membrane formation process suggest that the membrane formation process is dominated by the kinetic factors with water being the spray while thermodynamic factors play the major role with ethanol being the spray. A hydrophobic membrane with water contact angle of 135.93 ± 4.38° and LEP of 2.5 ± 0.4 bar was successfully prepared by using ethanol as the non-solvent spray, which demonstrates a stable desalination performance (initial flux of 19.88 ± 1.39 kg·m−2·h−1 and salt rejection higher than 99.97 %) in vacuum membrane distillation. This study may provide pertinent insights into the rational control of membrane structure and performance of hydrophobic PVDF membranes.

Phakic intraocular lens exchange due to severe uveitis/inflammation: case report

Introduction: Phakic intraocular lenses (IOLs) provide excellent visual and refractive outcomes with a high safety profile. This report illustrates a case of a rare episode of severe anterior segment inflammation after iris-claw foldable lens implantation, which required surgical reintervention. Patient and Clinical Findings: A 22-year-old woman was submitted to Artiflex implantation for the correction of myopia. Three months postoperatively, a severe anterior segment inflammation developed with pigment deposition, pupillary membrane formation, and decreased visual acuity in the left eye. Diagnosis, Intervention, and Outcomes: Given the nonresponse to medical treatment (topical and systemic corticosteroid for 3 months), surgical explantation of the IOL with peeling of a pigmentary membrane over the crystalline lens was performed. During a 24-month follow-up period, the patient was monitored to exclude the development of cataract or glaucoma. Afterward, an implantable collamer lens was implanted with an uneventful intraoperative and postoperative period. During the long-term follow-up, no further pigment dispersion, uveitis, or cataract was described. Conclusions: Persistent anterior uveitis with pigmentary membrane formation after iris-claw lens implantation is a rare complication. IOL explantation needs to be considered to prevent further sequelae after severe uveitis when the situation is unresponsive to medical treatment.

Waste cigarette filters-based polymer blends membrane for filtration of high loaded natural organic matter river water

Waste cigarette filter (WCF) is one of the most common wastes found in the environment. Cigarette filters contain up to 96% cellulose acetate (CA), which can be used as a material for membrane fabrication. However, the CA-based membrane from WCF posed a weak mechanical property (brittle). Therefore, the objective of this work is to improve mechanical property of CA-based membrane from WCF by preparing blend membranes with polyvinylidene fluoride (PVDF) polymer and evaluate their performance for filtration of real river water containing high natural organic matter (NOM) concentrations. The variations of WCF and PVDF used were 100:0, 75:25, 50:50, 25:75, and 0:100. The membranes were then characterized to determine the morphology, pore size and pore size distribution, hydrophilicity, mechanical properties, and filtration performance of the membrane using clean water and river water. The SEM test results showed the presence of spherulites on the surface of the blend membrane, indicating that crystallization occurred during membrane formation. The spherulites resulted in smaller pore size, narrower pore size distribution, higher hydrophilicity, and mechanical properties. Meanwhile, the filtration test results showed that blend membranes produced higher permeability compared to pristine WCF, PVDF, and commercial-based CA membranes, where the result of river water permeability was in the range of 875–1062.5 L/m2.h.bar. The membrane fouling formation was aligned well with the result of permeability and is dominated by irreversible fouling formation from the dynamic cake layer built on the membrane surface, with NOM rejections of 26.6–33.8%, suggesting the need for further developments.

Red fluorescent AIE bioprobes with a large Stokes shift for droplet-specific imaging and fatty liver diagnosis

Lipid droplets (LDs) as spherical dynamic subcellular organelles, play an important role in various cellular functions such as protein degradation, lipid metabolism, energy storage, signal transduction, and membrane formation. Abnormal function of LDs will lead to a series of diseases and hence monitoring the status of LDs is particularly important. In this study, we synthesized a water-insoluble red fluorescent emitting small molecule fluorescent probe (TPE-TCF), which exhibited aggregation-induced emission (AIE) properties and enabled highly selective real-time imaging of LDs (Pearson’s R value was 0.90). More interestingly, this probe was able to track the dynamic processes of LDs in living cells, including lipophagy, and monitor fatty liver disease in mice. Therefore, TPE-TCF with red fluorescence emission, good biocompatibility, large Stokes shift, AIE properties, LDs imaging, and fatty liver recognition capabilities can be practically used in more LDs-related diseases.

MENISCUS MICROPYON: An Ophthalmoscopic Sign Possibly Associated With Epiretinal Proliferation After Retinal Surgery With Gas Tamponade.

To describe an ophthalmoscopic sign, termed a meniscus micropyon, and its possible association with proliferative vitreoretinopathy/epiretinal membrane (ERM) formation after retinal surgery with gas tamponade. Patients with intravitreal gas were examined postoperatively by one of six vitreoretinal surgeons from four institutions. A micropyon was defined as a white-yellow, solid-appearing consolidation along the meniscus (i.e., the fluid-gas interface). A micropyon was visualized and photographed in 49 patients who received intravitreal gas. Preoperatively, retinal breaks were present in all 49 eyes and rhegmatogenous retinal detachment in 45 (92%). Postoperatively, 39 eyes (80%) developed epiretinal proliferation: 16 eyes (33%) developed recurrent rhegmatogenous retinal detachment from proliferative vitreoretinopathy, 6 eyes (12%) re-detached without frank proliferative vitreoretinopathy, 9 eyes (18%) developed postoperative ERM/worsening, and 8 eyes (16%) had postoperative ERM but no preoperative optical coherence tomography to determine if the postoperative ERM was new or worsening. The single-operation anatomical success in eyes with a micropyon was 51%, which was lower than that of a contemporaneous rhegmatogenous retinal detachment control group (91%) in which no micropyon was detected. In two patients, micropyons were biopsied during pars plana vitrectomy and examined histopathologically; they consist predominantly of white blood cells. The meniscus micropyon is an ophthalmoscopic sign that can occur after retinal surgery with gas tamponade. Features that distinguish a micropyon from postvitrectomy fibrin/fibrinoid syndrome include delayed appearance, hyperautofluorescence, absence of translucent strands or sheets in the anterior chamber or vitreous cavity, and the histopathologic identification of white blood cells. A clinically detectable micropyon may be a biomarker of proliferative vitreoretinopathy/ERM formation.

HIV-1 assembly - when virology meets biophysics.

Cells naturally produce vesicles that bud from different lipid membranes using dedicated molecular machineries. Enveloped RNA viruses, including human immunodeficiency virus type 1 (HIV-1), also generate particles that bud from host cell membranes by hijacking cellular factors and signaling pathways similar to those involved in the budding of extracellular vesicles. HIV-1 buds from the host cell plasma membrane mainly via the self-assembly of Gag, a structural protein. Gag is a polyprotein that forms assembly complexes containing viral genomic RNA (gRNA), host cell lipids and proteins. HIV-1 Gag binds and segregates host cell plasma membrane lipids while self-assembling simultaneously on the gRNA and the plasma membrane. This self-assembly causes membrane bending and formation of a new viral particle with the help of host cell proteins, likely including cortical actin-associated factors. However, it is unclear whether the energy of Gag self-assembly is sufficient to generate new HIV-1 particles. In this Review, we discuss these processes in the light of the past and recent virology literature, incorporating lessons from studies on the quantitative biophysics of viral self-assembly, and explore how Gag might reorganize the plasma membrane and divert host cell membrane curving proteins and cortical actin-related factors to achieve particle assembly and budding.

ORAL CURCUMIN TO REDUCE RISK OF PROLIFERATIVE VITREORETINOPATHY FOLLOWING RHEGMATOGENOUS RETINAL DETACHMENT REPAIR.

To evaluate outcomes of patients who underwent rhegmatogenous retinal detachment repair and were started on oral curcumin for proliferative vitreoretinopathy (PVR) prevention. Retrospective, observational case series of eyes of patients undergoing high-risk rhegmatogenous retinal detachment repair that was started on curcumin postoperatively. Recommended dosage was 500 mg twice daily for 30 days followed by 500 mg daily for 60 days. The primary outcome was recurrent PVR-related rhegmatogenous retinal detachment within 6 months and a single-surgery retinal reattachment rate. Secondary outcomes included epiretinal membrane formation, visual acuity, and curcumin safety profile. Thirty-two eyes of 31 patients met the study inclusion criteria. Postoperatively, 2 eyes developed a PVR-related detachment (6.3%), and 2 eyes redetached due to new breaks without PVR (6.3%). Overall, single-surgery retinal reattachment rate was 87.5%. Single-surgery retinal reattachment rate without silicone oil was 92.6% (25/27). Of the 12 cases with Grade C PVR-related retinal detachment, the single-surgery retinal reattachment rate was 91.7%. Postoperatively, 7 eyes developed an epiretinal membrane (21.9%), of which 3 underwent epiretinal membrane removal (9.4%). No patient had gastrointestinal upset or anemia. This proof-of-concept clinical study suggests that oral curcumin is well tolerated and warrants further investigation for its potential to reduce the risk of PVR after rhegmatogenous retinal detachment repair in eyes at higher risk of PVR.

Human salivary histatin 1 regulating IP3R1/GRP75/VDAC1 mediated mitochondrial-associated endoplasmic reticulum membranes (MAMs) inhibits cell senescence for diabetic wound repair

RationaleDifficulty in skin wound healing is a concern for diabetic patients across the world. Impaired mitochondrial dysfunction and aging-related vascular dysfunction in human umbilical vein endothelial cells (HUVECs) caused by oxidative stress are major impediments to diabetic wound healing. However, research on skin repair at the mechanistic level by improving mitochondrial function and inhibiting oxidative stress-induced HUVEC senescence remains lacking. Methods and resultsHuman saliva effectively inhibits the natural aging of HUVECs through immunodepletion experiments. Histatin 1 (Hst1), a short peptide comprising 38 amino acids, is the primary component of human saliva that prevents HUVEC aging. Based on in vitro findings, Hst1 decreased staining for senescence-associated β-galactosidase activity and expression of mediators of senescence signaling, including p53, p21, and p16. Mechanistically, HUVEC senescence is associated with Hst1-modulated nuclear factor Nrf2 signaling as Hst1 induces ERK-mediated Nrf2 nuclear translocation through NADPH oxidase-dependent ROS regulation, reinforced Nrf2 antioxidant response, and suppressed oxidative stress. RNA sequencing identified that the mitochondrial-related gene set was enriched in the Hst1 group. Coimmunoprecipitation indicated that Hst1 delayed hydrogen peroxide-induced HUVEC senescence by inhibiting mitochondria-associated endoplasmic reticulum (ER) membrane formation mediated by inositol 1,4,5-trisphosphate receptor 1-glucose-regulated protein 75-voltage-dependent anion channel 1 (VDAC1) complex interactions. Furthermore, in aging HUVECs, Hst1 treatment or VDAC1 silencing with small interfering RNA hindered calcium (Ca2+) transfer from the ER to the mitochondria, thereby ameliorating mitochondrial Ca2+ overload and restoring mitochondrial function. In an in vivo mouse model of diabetes mellitus skin defects, Hst1 facilitated wound healing by stimulating the new blood vessel formation and impeding the expression of senescent biomarkers. ConclusionsThis study proposes a theoretical solution that Hst1 can restore mitochondrial function by inhibiting oxidative stress or cellular senescence, thereby promoting angiogenesis and diabetic wound repair.

Mitigation of lipopolysaccharide-induced intestinal injury in rats by Chimonanthus nitens Oliv. essential oil via suppression of mitochondrial fusion protein mitofusin 2 (MFN2)-mediated mitochondrial-associated endoplasmic reticulum membranes (MAMs) formation

Ethnopharmacological relevanceChimonanthus nitens Oliv. is a traditional Chinese medicine with anti-inflammatory and antioxidant properties that has commonly been used for colds, fevers, and other diseases. However, its role and specific mechanism in sepsis-associated intestinal injury have not been reported. Aim of the studyC. nitens Oliv. essential oil (CEO), an organic active compound extracted from the traditional Chinese medicine C. nitens Oliv. exhibits notable anti-inflammatory and antioxidant properties. Nevertheless, the therapeutic potential of CEO for septic intestinal injury remains undocumented. This study thus aims to elucidate the anti-inflammatory and antioxidant effects of CEO in the context of acute intestinal injury and to investigate its mechanisms of action in septic rats. Materials and methodsCell and animal models were established using LPS to investigate the impact of CEO on LPS-induced intestinal pathological injury and the secretion of inflammatory factor IL-1β. The effects of CEO on the expression of NLRP3, caspase-1, and MFN2, p-p65 protein were also examined, as well as its influence on oxidative stress injury and mitochondrial-associated endoplasmic reticulum membrane (MAM) formation. Generation of an MFN2 knockout IEC-6 cell line allowed comprehensive investigation of the protective mechanism of CEO. ResultsIn rat models, CEO reduced IL-1β secretion, inhibited caspase-1, ZO-1 expression and NF-κB p65 phosphorylation, while also decreasing malondialdehyde levels and enhancing superoxide dismutase activity in intestinal tissues. Cellular experiments demonstrated its ability to decrease IL-1β secretion; NLRP3, caspase-1, and MFN2 expression; NF-κB p65 phosphorylation; reactive oxygen species (ROS) production, and mitochondrial dysfunction. MFN2 knockdown enhanced these effects synergistically with CEO, indicating potential therapeutic synergy. Further, MFN2 knockdown significantly mitigated LPS-induced NLRP3 and caspase-1 expression, IL-1β secretion, ROS production, NF-κB p65 phosphorylation and MMP reduction in IEC-6 cells, while inhibiting MAM formation and NLRP3 localization on MAMs. Importantly, MFN2 downregulation and CEO synergistically reduced LPS-induced IL-1β secretion and ROS production while inhibiting MAM formation in IEC-6 cells, thus inhibiting NLRP3 inflammasome activation. ConclusionCEO mitigates inflammation and oxidative stress by inhibiting MAM formation and is thus a promising intervention for septic intestinal injury.

Sensitive Profiling of Mouse Liver Membrane Proteome Dysregulation Following a High-Fat and Alcohol Diet Treatment.

Alcohol consumption and high-fat (HF) diets often coincide in Western society, resulting in synergistic negative effects on liver function. Although studies have analyzed the global protein expression in the context of alcoholic liver disease (ALD) and metabolic dysfunction-associated steatotic liver disease (MASLD), none has offered specific insights on liver dysregulation at the membrane proteome level. Membrane-specific profiling of metabolic and compensatory phenomena is usually overshadowed in conventional proteomic workflows. In this study, we use the Peptidisc method to isolate and compare the membrane protein (MP) content of the liver with its unique biological functions. From mice fed with an HF diet and ethanol in drinking water, we annotate over 1500 liver proteins with half predicted to have at least one transmembrane segment. Among them, we identify 106 integral MPs that are dysregulated compared to the untreated sample. Gene Ontology analysis reveals several dysregulated membrane-associated processes like lipid metabolism, cell adhesion, xenobiotic processing, and mitochondrial membrane formation. Pathways related to cholesterol and bile acid transport are also mutually affected, suggesting an adaptive mechanism to counter the upcoming steatosis of the liver model. Taken together, our Peptidisc-based profiling of the diet-dysregulated liver provides specific insights and hypotheses into the role of the transmembrane proteome in disease development, and flags desirable MPs for therapeutic and diagnostic targeting.

Di-(2-ethylhexyl) phthalate induces prepubertal testicular injury through MAM-related mitochondrial calcium overload in Leydig and Sertoli cell apoptosis

As one of the most prevalent environmental endocrine disruptors, di-(2-ethylhexyl) phthalate (DEHP) is known for its significant developmental toxicity to the male reproductive system in humans and mice. Prepubertal exposure to DEHP has been shown to cause testicular damage, but the underlying mechanisms require further investigation. To investigate this effect, prepubertal mice were exposed to 100, 250 or 500 mg/kg body weight (bw) of DEHP for 14 days, which resulted in impaired histological structure and increased apoptosis of the testes. RNA sequencing (RNA-seq) of testicular tissue suggested that DEHP led to injury in Leydig and Sertoli cells. To further elucidate these mechanisms, we conducted experiments using immature mouse Leydig (TM3) and Sertoli (TM4) cells, and exposed them to 200 μM mono-(2-ethylhexyl) phthalate (MEHP), the primary metabolite of DEHP, for 24 h. We found that MEHP exposure induced oxidative stress injury and promoted cell apoptosis, and that cotreatment with N-acetylcysteine partially reversed these injuries. Given the close association between oxidative stress and mitochondrial calcium levels, we demonstrated that MEHP exposure disrupted mitochondria and increased mitochondrial calcium levels. In addition, MEHP exposure facilitated the formation of mitochondria-associated endoplasmic reticulum membranes (MAMs), upregulated protein expression and enhanced the interactions of the IP3R3-Grp75-VDAC1 complex. Furthermore, inhibition of calcium transfer in the IP3R3-Grp75-VDAC1-MCU axis relieved MEHP-induced mitochondrial injury, oxidative stress and apoptosis in TM3 and TM4 cells. This study highlights the importance of MAM-mediated mitochondrial calcium overload and the subsequent apoptosis of Leydig and Sertoli cells as pivotal factors contributing to testicular injury induced by prepubertal exposure to DEHP.

Homogeneous CaAlg/PES hybrid ultrafiltration membranes prepared with in situ ionic crosslinking and phase inversion method

Calcium alginate hydrogel/polyethersulfone (CaAlg/PES) hybrid membranes were synthesized via combining in situ ion crosslinking with phase conversion method. Once the Sodium alginate (NaAlg) uniformly dispersed in the casting solution contacted with Ca2+ dissolved in coagulation bath solution in the phase conversion membrane formation process, nanoscale CaAlg hydrogel was in situ formed through ion exchange and evenly dispersed in the membrane matrix. FT-IR and XPS were adopted to confirm the formation of CaAlg hydrogel distributed in PES membrane matrix. SEM, AFM, BET analysis and contact Angle analyzer were all used to characterize the surface changes of morphology, roughness and hydrophilicity in detail. Specific separation performance was also evaluated and compared by cross-flow ultrafiltration tests. Comprehensive analysis of the measured properties of all obtained membranes, when the content of NaAlg was 1.5 wt%, the CaAlg/PES hydrogel membrane M32 had the most excellent performance. The pure water flux increased from 1967 to 2193 L/m2hMPa, rejection rate of BSA was up to 99.87 %, and RFR value was almost 76.83 % after 4 cycles BSA filtration. XPS characterization of the membrane after filtration for 72 hours showed that the retention rate of Ca (2 P) reached 95 %, which further proved the stability of the membrane operation.

OVO positively regulates essential maternal pathways by binding near the transcriptional start sites in the Drosophila female germline.

Differentiation of female germline stem cells into a mature oocyte includes the expression of RNAs and proteins that drive early embryonic development in Drosophila. We have little insight into what activates the expression of these maternal factors. One candidate is the zinc-finger protein OVO. OVO is required for female germline viability and has been shown to positively regulate its own expression, as well as a downstream target, ovarian tumor, by binding to the transcriptional start site (TSS). To find additional OVO targets in the female germline and further elucidate OVO's role in oocyte development, we performed ChIP-seq to determine genome-wide OVO occupancy, as well as RNA-seq comparing hypomorphic and wild type rescue ovo alleles. OVO preferentially binds in close proximity to target TSSs genome-wide, is associated with open chromatin, transcriptionally active histone marks, and OVO-dependent expression. Motif enrichment analysis on OVO ChIP peaks identified a 5'-TAACNGT-3' OVO DNA binding motif spatially enriched near TSSs. However, the OVO DNA binding motif does not exhibit precise motif spacing relative to the TSS characteristic of RNA polymerase II complex binding core promoter elements. Integrated genomics analysis showed that 525 genes that are bound and increase in expression downstream of OVO are known to be essential maternally expressed genes. These include genes involved in anterior/posterior/germ plasm specification (bcd, exu, swa, osk, nos, aub, pgc, gcl), egg activation (png, plu, gnu, wisp, C(3)g, mtrm), translational regulation (cup, orb, bru1, me31B), and vitelline membrane formation (fs(1)N, fs(1)M3, clos). This suggests that OVO is a master transcriptional regulator of oocyte development and is responsible for the expression of structural components of the egg as well as maternally provided RNAs that are required for early embryonic development.

OVO positively regulates essential maternal pathways by binding near the transcriptional start sites in the Drosophila female germline

Differentiation of female germline stem cells into a mature oocyte includes the expression of RNAs and proteins that drive early embryonic development in Drosophila. We have little insight into what activates the expression of these maternal factors. One candidate is the zinc-finger protein OVO. OVO is required for female germline viability and has been shown to positively regulate its own expression, as well as a downstream target, ovarian tumor, by binding to the transcriptional start site (TSS). To find additional OVO targets in the female germline and further elucidate OVO’s role in oocyte development, we performed ChIP-seq to determine genome-wide OVO occupancy, as well as RNA-seq comparing hypomorphic and wild type rescue ovo alleles. OVO preferentially binds in close proximity to target TSSs genome-wide, is associated with open chromatin, transcriptionally active histone marks, and OVO-dependent expression. Motif enrichment analysis on OVO ChIP peaks identified a 5’-TAACNGT-3’ OVO DNA binding motif spatially enriched near TSSs. However, the OVO DNA binding motif does not exhibit precise motif spacing relative to the TSS characteristic of RNA polymerase II complex binding core promoter elements. Integrated genomics analysis showed that 525 genes that are bound and increase in expression downstream of OVO are known to be essential maternally expressed genes. These include genes involved in anterior/posterior/germ plasm specification (bcd, exu, swa, osk, nos, aub, pgc, gcl), egg activation (png, plu, gnu, wisp, C(3)g, mtrm), translational regulation (cup, orb, bru1, me31B), and vitelline membrane formation (fs(1)N, fs(1)M3, clos). This suggests that OVO is a master transcriptional regulator of oocyte development and is responsible for the expression of structural components of the egg as well as maternally provided RNAs that are required for early embryonic development.

Ohta–Kawasaki energy for amphiphiles: Asymptotics and phase-field simulations

We study the minimizers of a degenerate case of the Ohta–Kawasaki energy, defined as the sum of the perimeter and a Coulombic nonlocal term. We start by investigating radially symmetric candidates which give us insights into the asymptotic behaviors of energy minimizers in the large mass limit. In order to numerically study the problems that are analytically challenging, we propose a phase-field reformulation which is shown to Gamma-converge to the original sharp interface model. Our phase-field simulations and asymptotic results suggest that the energy minimizers exhibit behaviors similar to the self-assembly of amphiphiles, including the formation of lipid bilayer membranes.

Free Energy Analysis of Peptide-Induced Pore Formation in Lipid Membranes by Bridging Atomistic and Coarse-Grained Simulations.

Antimicrobial peptides (AMPs) are attractive materials for combating the antimicrobial resistance crisis because they can kill target microbes by directly disrupting cell membranes. Although thousands of AMPs have been discovered, their molecular mechanisms of action are still poorly understood. One broad mechanism for membrane disruption is the formation of membrane-spanning hydrophilic pores which can be stabilized by AMPs. In this study, we use molecular dynamics simulations to investigate the thermodynamics of pore formation in model single-component lipid membranes in the presence of one of three AMPs: aurein 1.2, melittin and magainin 2. To overcome the general challenge of modeling long time scale membrane-related behaviors, including AMP binding, clustering, and pore formation, we develop a generalizable methodology for sampling AMP-induced pore formation. This approach involves the long equilibration of peptides around a pore created with a nucleation collective variable by performing coarse-grained simulations, then backmapping equilibrated AMP-membrane configurations to all-atom resolution. We then perform all-atom simulations to resolve free energy profiles for pore formation while accurately modeling the interplay of lipid-peptide-solvent interactions that dictate pore formation free energies. Using this approach, we quantify free energy barriers for pore formation without direct biases on peptides or whole lipids, allowing us to investigate mechanisms of pore formation for these 3 AMPs that are a consequence of unbiased peptide diffusion and clustering. Further analysis of simulation trajectories then relates variations in pore lining by AMPs, AMP-induced lipid disruptions, and salt bridges between AMPs to the observed pore formation free energies and corresponding mechanisms. This methodology and mechanistic analysis have the potential to generalize beyond the AMPs in this study to improve our understanding of pore formation by AMPs and related antimicrobial materials.

Quaternary phase-field simulation of the effect of additives on the structure of polyvinylidene fluoride microporous membranes

This study builds upon the existing phase-field model of the non-solvent-induced phase separation (NIPS) method, simulating factors that influence membrane formation in a ternary system. A polyvinylidene fluoride (PVDF) membrane system is utilized, and a fourth substance, an additive, is introduced based on the original mathematical model of the ternary system. The interaction parameters of the additives within the system are calculated using the Krevelen method. The simulation is configured to set the values of additive mobility and loss coefficients of the concentration gradient, thereby simulating the effect of additives in the quaternary system on the evolution of the micropore membrane structure. Finally, simulated images of different concentrations of additives with various types are compared with experimental results of microporous structure and porosity formation. This comparison serves to validate the model.

How coat proteins shape autophagy in plant cells.

Autophagy is a membrane trafficking pathway through which eukaryotic cells target their own cytoplasmic constituents for degradation in the lytic compartment. Proper biogenesis of autophagic organelles requires a conserved set of autophagy-related (ATG) proteins and their interacting factors, such as signalling phospholipid phosphatidylinositol 3-phosphate (PI3P) and coat complex II (COPII). The COPII machinery, which was originally identified as a membrane coat involved in the formation of vesicles budding from the endoplasmic reticulum, contributes to the initiation of autophagic membrane formation in yeast, metazoan, and plant cells; however, the exact mechanisms remain elusive. Recent studies using the plant model species Arabidopsis thaliana have revealed that plant-specific PI3P effectors are involved in autophagy. The PI3P effector FYVE2 interacts with the conserved PI3P effector ATG18 and with COPII components, indicating an additional role for the COPII machinery in the later stages of autophagosome biogenesis. In this Update, we examined recent research on plant autophagosome biogenesis and proposed working models on the functions of the COPII machinery in autophagy, including its potential roles in stabilizing membrane curvature and sealing the phagophore.

Vitreoschisis-induced vitreous cortex remnants in proliferative vitreoretinopathy: A comprehensive review from basic research to clinical practice.

Proliferative vitreoretinopathy (PVR) significantly impacts the prognosis of rhegmatogenous retinal detachment (RRD), one of the most critical and increasing causes of vision loss in the Western world. Despite advancements in surgical instruments and techniques, the failure rate due to PVR remains substantial, necessitating additional surgeries and often leading to unsatisfactory visual outcomes. This comprehensive review explores the role of vitreoschisis-induced vitreous cortex remnants (VCR) as a critical, previously under-recognised factor contributing to PVR. Vitreoschisis, a phenomenon where the inner lamellae of the posterior vitreous cortex detach while the outermost layers remain attached to the retina, creates VCR that may contain hyalocytes and serve as scaffolds for fibrocellular proliferation. These remnants are difficult to visualise without triamcinolone acetonide (TA) staining, leading to their frequent lack of recognition in clinical practice. Moreover, removing VCR can be challenging and time-consuming, often requiring meticulous surgical techniques to avoid retinal damage and ensure complete elimination. This review consolidates insights from basic research and clinical practice, emphasising the importance of complete vitreous removal and effective VCR detection and removal to mitigate PVR risks. It highlights the histopathological and clinical evidence supporting the hypothesis that VCR, containing hyalocytes, play a pivotal role in preretinal membrane formation. The review also discusses epidemiological data, surgical management strategies and potential future directions, including improved visualisation techniques and the development of new surgical tools and methods. This review aims to improve surgical outcomes and reduce the frequency and burden of RRD-related complications by addressing VCR as a critical factor in PVR.

The mechanics of the retina: Müller glia role on retinal extracellular matrix and modelling.

The retina is a highly heterogeneous tissue, both cell-wise but also regarding its extracellular matrix (ECM). The stiffness of the ECM is pivotal in retinal development and maturation and has also been associated with the onset and/or progression of numerous retinal pathologies, such as glaucoma, proliferative vitreoretinopathy (PVR), age-related macular degeneration (AMD), epiretinal membrane (ERM) formation or uveitis. Nonetheless, much remains unknown about the biomechanical milieu of the retina, and specifically the role that Müller glia play as principal mechanosensors and major producers of ECM constituents. So far, new approaches need to be developed to further the knowledge in the field of retinal mechanobiology for ECM-target applications to arise. In this review, we focus on the involvement of Müller glia in shaping and altering the retinal ECM under both physiological and pathological conditions and look into various biomaterial options to more accurately replicate the impact of matrix stiffness in vitro.