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Heparan sulfate (HS) is a major component of cell surface glycocalyx with extensive negative charges and plays a protective role by preventing toxins, including small molecule drugs and anticancer cationic lytic peptides (ACLPs), from cells. However, this effect may compromise the treatment efficiency of anticancer drugs. To overcome the impedance of cancer cell glycocalyx, an HS-targeting ACLP PTP-7z was designed by fusion of an ACLP and a Zn2+-binding HS-targeting peptide. Upon Zn2+ion binding, PTP-7z could self-assemble into uniform nanoparticles and show improved serum stability and reduced hemolysis, which enable it to self-deliver to tumor sites. The peptide PTP-7z showed a pH- and Zn2+ion-dependent HS-binding ability, which triggers the HS-induced in situself-assembling on the cancer cell surface in the acidic tumor microenvironment (TME). The self-assembled PTP-7z can overcome the impedance of cell glycocalyx by either disrupting cell membranes or translocating into cells through endocytosis and inducing cell apoptosis. Moreover, PTP-7z can also inhibit cancer cell migration. These results proved that HS-responsive in situself-assembling is a practical strategy to overcome the cancer cell glycocalyx barrier for ACLPs and could be extended to the design of other peptide drugs to promote their in vivoapplication.

Orlistat, an FDA-approved fatty acid inhibitor for obesity treatment, demonstrates certain low and greatly varied anticancer abilities. In a previous study, we revealed a synergistic effect between orlistat and dopamine in cancer treatment. Here, orlistat-dopamine conjugates (ODCs) with defined chemical structures were synthesized. The ODC by design underwent polymerization and self-assembly in the presence of oxygen to form nano-sized particles (Nano-ODCs) spontaneously. The resulted Nano-ODCs of partial crystalline structures demonstrated good water dispersion to form stable Nano-ODC suspensions. Because of the bioadhesive property of the catechol moieties, once administered, Nano-ODCs were quickly accumulated on cell surfaces and efficiently uptaken by cancer cells. In the cytoplasm, Nano-ODC experienced biphasic dissolution followed by spontaneous hydrolysis to release intact orlistat and dopamine. Besides elevated levels of intracellular reactive oxygen species (ROS), the co-localized dopamine also induced mitochondrial dysfunctions through monoamine oxidases (MAOs)-catalyzed dopamine oxidation. The strong synergistic effects between orlistat and dopamine determined a good cytotoxicity activity and a unique cell lysis mechanism, explaining the distinguished activity of Nano-ODC to drug-sensitive and -resistant cancer cells. This new technology-enabled orlistat repurposing will contribute to overcoming drug resistance and the improvement of cancer chemotherapy.

We hypothesized that oleic acid (OA) in the absence of a thiazolidinedione (i.e., a synthetic peroxisome proliferator-activated receptorγ [PPARγ] agonist) would increase adipogenic gene expression in bovine muscle satellite cells (BSC). The BSC were cultured in differentiation medium containing 10 µM ciglitazone (CI), 100 µM OA, or 100 µM OA plus 10 µM CI (CI-OA). Control (CON) BSC were cultured only in differentiation media (containing 2% horse serum). The presence of myogenin, desmin, and paired box 7 proteins was confirmed in the BSC by immunofluorescence staining, demonstrating that we had isolated myogenic cells. The OA BSC had lesser paired box 3 (Pax3) and myogenic differentiation 1 expression but greater Pax7 and mygogenin (MYOG) expression (P < 0.05), than the CON BSC. The CI BSC had greater Pax3, Pax7, and MYOG expression than CON BSC (P < 0.05), suggesting that CI would promote BSC myogenesis under pro-myogenic conditions (i.e., when cultured with horse serum). However, both the OA and CI treatments upregulated the expression of PPARγ, CCAAT/enhancer-binding protein alpha (C/EBPα) and C/EBPß, sterol regulatory element-binding protein 1, lipoprotein lipase, and glycerol-3-phosphate acyltransferase 3 gene expression, as well as media adiponectin concentration (P < 0.05). The CI, OA, and CI-OA treatments also increased triacylglycerol and lipid droplet accumulation, in spite of upregulation (relative to CON BSC) of adenosine monophosphate-activated protein kinase alpha-1, perilipin 2 (PLIN2), and PLIN3 in BSC and downregulation of G protein-coupled protein receptor 43, acyl-CoA synthetase long chain family member 3, and stearoyl-CoA desaturase (P < 0.05). These results indicate that OA in the absence of a synthetic PPARγ agonist can effectively increase adipogenic gene expression in BSC.

Orlistat, an FDA-approved antiobesity drug, has recently been shown to have anticancer effects. However, orlistat is extremely hydrophobic with low absorption. Therefore, new approaches are needed to effectively deliver orlistat for cancer therapy. Herein, we developed a fast and simple method to use polydopamine-coated hollow capsule (PHC) as a drug nanocarrier for enhancing the therapeutic effects of orlistat. Orlistat-loaded PHC had an average size of 200 nm, which was characterized by using dynamic light scattering and scanning electron microscope. Furthermore, the polydopamine layer provided an excellent control of orlistat release because it was extremely sensitive to pH values. The cellular uptake and cytotoxicity experiments were performed to show that orlistat packaged in PHC could be endocytosed into cells and then significantly improved the cytotoxic activity against cancer cell lines in a short time compared with free orlistat. Moreover, dynamic study of cell membrane lysis was performed by staining with the LIVE/DEAD kit to demonstrate the cancer-killing mechanism. The size of the cell surface area has also been proven to be a key parameter which affected drug efficacy. Taken all together, these results present that orlistat-loaded PHC is a very promising formula for cancer treatments.

Cytolytic peptides (CPs) have long been employed as broad-spectrum antibiotic agents to overcome multidrug resistance. However, the development of novel peptide drugs is still limited by the elusive molecular understanding of the membrane-lysis mechanism and modeling of CPs, especially of the short helical species. In this study, a known anticancer CP named PTP-7b (FLGALFKALSHLL) in disrupting membranes via self-assembling approach was studied by combining experiments and time-extended coarse-grained dynamic simulations. Effective membrane disintegration was induced by aggregation of the membrane-bound peptide individuals, rather than the preassembled peptide clusters. The disturbance level of lipid bilayers depended on the peptide concentrations, which was responsible for the long time-costing of PTP-7b in killing cells. On the basis of lines of simulations and energy-landscape calculations, the dynamics of membrane deformation evolving toward preliminary leakage resulted from the aggregated PTP-7b was demonstrated, which was subjected to the spatiotemporal cooperation of the membrane-inserted and the periplasmic peptides. The molecular mechanism incorporated the 11th histidine interaction coupled with the peptide amphiphilicity in accelerating phospholipid migration outward. This study revealed elaborate modeling and dynamics information about the short helical CPs in membrane lysis, which would be helpful to understand the underlying mechanisms and rational design of CPs for drug application.

ABSTRACTTwo new species in Lepiotasect. Ovisporaeare described from tropical China. Lepiota angusticystidiatahas a pileus with brownish yellow squamules covering a trichodermial palisade, ellipsoidal basidiospores, and narrowly clavate cheilocystidia; L. brunneosquamulosahas a tomentose, squamulose pileus with brownish yellow to yellowish brown concentric zones covering a trichodermial palisade, rarely with short elements, ellipsoidal or subcylindrical basidiospores with straight adaxial side, and no cheilocystidia. Phylogenetic relationships among species of sect. Ovisporaewere inferred based on DNA sequences of the internal transcribed spacer region (ITS1-5.8S-ITS2 = ITS), the 5′ end of the 28S gene (D1-D2-D3 variable domains), and partial sequences of the intergenic spacer (IGS1) of the nuc rDNA and the mitochondrial small ribosomal RNA gene (mtSSU), supporting the delineation of these new species.

The solubility of drug molecules is closely related to its bioactivity as it affects the dissolution rate and bioavailability, especially in the case of BCS IV drugs like camptothecin (CPT), a potential broad-spectrum anticancer agent. In this study, we construct a novel boric acid (BA)-coated CPT nanocomposite by means of a simple heat-treatment approach, which combines nanoscale size range and amorphous solid state together to improve the overall dissolution rate of CPT. This new CPT formulation showed a rod-like structure with nanoscale size and amorphous solid nature. These BA-coated CPT nanocomposites exhibited a dramatically improved dissolution rate, water dispersion property, and long-term chemical and physical stability. More importantly, the specific reactivity of BA groups to diols in the cell glycocalyx facilitated a rapid cross-membrane translocation of the drug nanocomposite, leading to efficient intracellular drug delivery. When tested on A549 cells and SKBR3 cells, this formulation demonstrated a much higher anticancer activity in comparison with free CPT, naked amorphous CPT nanoparticles, and control CPT nanocrystals. This formulation has great potential for clinical application; it is easy to scale up and be applied on other hydrophobic drugs.

Sortase A catalyzed ligation of ultra-short peptides leads to inter/intra-molecular transpeptidation to form either linear or cyclic oligomers dependent upon the peptide length. Cyclic peptides were the main products for peptides with more than 15aa. However, for ultra-short (<15aa) peptides, cyclic oligomers became predominant in prolonged reactions. Peptides with 1–3 aminoglycines were equally active but peptide oligomers from peptide containing more than one aminoglycine were prone to hydrolysis.

Camptothecin (CPT) is a potent chemotherapeutic agent that shows a broad spectrum of anticancer activities. However, it is clinically inactive because of poor aqueous solubility, rapid aqueous hydrolysis, and unexpected side effects. Three strategies have extensively been adopted to improve its dissolution rate including reduction of drug particle size to a nanoscale, use of an amorphous state, and the formation of inclusion compounds. In our study, we combined these three strategies together by constructing CPT nanoparticles by creating an inclusion complex with β-cyclodextrin (BCD). This new CPT formulation showed a rod-like structure of nanoscaled size and with semiamorphous or amorphous CPT. These BCD–CPT nanoparticles showed improved dissolution rate, stability, dispersion, and cellular uptake. When tested on cancer cells, BCD–CPT nanoparticles showed a much higher anticancer activity (IC50=14–28 μmol/l) in comparison with free CPT (IC50>500 μmol/l) and CPT nanocrystals (IC50>200 μmol/l). In addition, BCD–CPT nanoparticles can be physically mixed with CPT nanocrystals, leading to CPT formulations with tailored drug-release profiles to achieve customized therapeutics and flexible treatments in clinics.

Lepiotasect. Stenosporae(J.E. Lange) Kühner contains species with spurred or truncate basidiospores and pileus covering composed of adnate, ascending or erect long and slender elements. Seven species from southwestern, northeastern and southern China in this section have been identified, described and illustrated. Lepiota mandarinaand L. subcastaneaare described as new. Lepiota mandarinais characterized by densely orange red to brownish red squamules on pileus and stipe, subtriangular basidiospores with truncate bottom, narrowly clavate cheilocystidia and pileus covering a trichodermial palisade. Lepiota subcastaneahas a pileus with yellow-brown to dark brown squamules, non-dextrinoid subtriangular basidiospores with a distinct sac-like spur, narrowly clavate or narrowly utriform cheilocystidia, and pileus covering a trichodermial palisade with short clavate elements. It is hypothesized that this section evolved from sect. Ovisporaesubsect. Helveolinae.It also is speculated that subtriangular and spurred basidiospores have evolved from ellipsoidal basidiospores and that a trichodermial pileus covering composing long, erect elements and basal short, clavate elements might have evolved from a cutis or a trichoderm lacking such an under layer of short elements.

Nuestro objetivo es investigar si la obesidad, la hipertensión y la diabetes mellitus (DM) aumentan la tasa de complicaciones tras nefrectomía empleando métodos de clasificación estandarizados.

F-actin networks are involved in cell mechanical processes ranging from motility to endocytosis. The mesoscale architecture of assemblies of individual F-actin polymers that gives rise to micrometer-scale rheological properties is poorly understood, despite numerous in vivo and vitro studies. In vitro networks have been shown to organize into spatial patterns when spatially confined, including dense spherical shells inside spherical emulsion droplets. Here we develop a simplified model of an isotropic, compressible, viscoelastic material continually assembling and disassembling. We demonstrate that spherical shells emerge naturally when the strain relaxation rate (corresponding to internal network reorganization) is slower than the disassembly rate (corresponding to F-actin depolymerization). These patterns are consistent with recent experiments, including a collapse of shells to a central high-density focus of F-actin when either assembly or disassembly is reduced with drugs. Our results demonstrate how complex spatio-temporal patterns can emerge without spatially distributed force generation, polar alignment of F-actin polymers, or spatially nonuniform regulation of F-actin by upstream biochemical networks.

Cell surface receptors have been extensively studied because they initiate and regulate signal transduction cascades leading to a variety of functional cellular outcomes. An important class of immune receptors (e.g., T-cell antigen receptors) whose ligands are anchored to the surfaces of other cells remain poorly understood. The mechanism by which ligand binding initiates receptor phosphorylation, a process termed “receptor triggering”, remains controversial. Recently, direct measurements of the (two-dimensional) receptor-ligand complex lifetimes at cell-cell interface were found to be smaller than (three-dimensional) lifetimes in solution but the underlying mechanism is unknown. At the cell-cell interface, the receptor-ligand complex spans a short intermembrane distance (15 nm) compared to long surface molecules (LSMs) whose ectodomains span >40 nm and these LSMs include phosphatases (e.g., CD45) that dephosphorylate the receptor. It has been proposed that size-based segregation of LSMs from a receptor-ligand complex is a mechanism of receptor triggering but it is unclear whether the mechanochemistry supports such small-scale segregation. Here we present a nanometer-scale mathematical model that couples membrane elasticity with the compressional stiffness and lateral mobility of LSMs. We find robust supradiffusive segregation of LSMs from a single receptor-ligand complex. The model predicts that LSM redistribution will result in a time-dependent tension on the complex leading to a decreased two-dimensional lifetime. Interestingly, the model predicts a nonlinear relationship between the three- and two-dimensional lifetimes, which can enhance the ability of receptors to discriminate between similar ligands.

Aseptic loosening of the femoral component is one cause of failure in total knee replacement (TKR). Inadequate bone stock in the distal femur after TKR, due to the stress shielding, was often found in revision of the femoral component. The pegs in the femoral component are used as an aid to the correct placement of the component but they also help to transfer the load to the diaphyseal part of the bone and improve stability. This paper investigates the influence of femoral component peg design on stress distribution and bone remodelling in the distal femur after TKR. Eight different peg designs were investigated and reported in this paper. The bone remodelling parameters in the distal femur are presented, compared and analysed. Results show that a slender peg is advantageous in TKR.

Microtubules anchored to the two-dimensional cortex of plant cells collide through plus-end polymerization. Collisions can result in rapid depolymerization, directional plus-end entrainment, or crossover. These interactions are believed to give rise to cellwide self-organization of plant cortical microtubules arrays, which is required for proper cell wall growth. Although the cell-wide self-organization has been well studied, less emphasis has been placed on explaining the interactions mechanistically from the molecular scale. Here we present a model for microtubule-cortex anchoring and collision-based interactions between microtubules, based on a competition between cross-linker bonding, microtubule bending, and microtubule polymerization. Our model predicts a higher probability of entrainment at smaller collision angles and at longer unanchored lengths of plus-ends. This model addresses observed differences between collision resolutions in various cell types, including Arabidopsiscells and Tobacco cells.

Plant cortical microtubules self-organize into parallel yet dispersed arrays transverse to the elongation axis of elongating plant cells. Computational modeling yields several novel predictions and shows that plus-end entrainment can give rise to order.

Microtubules confined to the two-dimensional cortex of elongating plant cells must form a parallel yet dispersed array transverse to the elongation axis for proper cell wall expansion. Some of these microtubules exhibit free minus-ends, leading to migration at the cortex by hybrid treadmilling. Collisions between microtubules can result in plus-end entrainment ("zippering") or rapid depolymerization. Here, we present a computational model of cortical microtubule organization. We find that plus-end entrainment leads to self-organization of microtubules into parallel arrays, whereas catastrophe-inducing collisions do not. Catastrophe-inducing boundaries (e.g., upper and lower cross-walls) can tune the orientation of an ordered array to a direction transverse to elongation. We also find that changes in dynamic instability parameters, such as in mor1-1 mutants, can impede self-organization, in agreement with experimental data. Increased entrainment, as seen in clasp-1 mutants, conserves self-organization, but delays its onset and fails to demonstrate increased ordering. We find that branched nucleation at acute angles off existing microtubules results in distinctive sparse arrays and infer either that microtubule-independent or coparallel nucleation must dominate. Our simulations lead to several testable predictions, including the effects of reduced microtubule severing in katanin mutants.

Importance of the field:Fluoropyrimidines, in particular 5-fluorouracil (5-FU), have been the mainstay of treatment for several solid tumors, including colorectal, breast and head and neck cancers, for > 40 years.Areas covered in this review:This article reviews the pharmacology and efficacy of capecitabine with a special emphasis on its safety.What the reader will gain:The reader will gain better insight into the safety of capecitabine in special populations such as patients with advanced age, renal and kidney disease. We also explore different dosing and schedules of capecitabine administration.Take home message:Capecitabine is an oral prodrug of 5-FU and was developed to fulfill the need for a more convenient therapy and provide an improved safety/efficacy profile. It has shown promising results alone or in combination with other chemotherapeutic agents in colorectal, breast, pancreaticobiliary, gastric, renal cell and head and neck cancers. The most commonly reported toxic effects of capecitabine are diarrhea, nausea, vomiting, stomatitis and hand–foot syndrome. Capecitabine has a well-established safety profile and can be given safely to patients with advanced age, hepatic and renal dysfunctions.

Maternal obesity coupled with Western-style high-energy diets represents a special problem that can result in poor fetal development, leading to harmful, persistent effects on offspring, including predisposition to obesity and type 2 diabetes. Mechanisms linking maternal obesity to the increased incidence of obesity and other metabolic diseases in offspring remain poorly defined. Because skeletal muscle is the principal site for glucose and fatty acid utilization and composes 40%–50% of total body mass, changes in the properties of offspring skeletal muscle and its mass resulting from maternal obesity may be responsible for the increase in type 2 diabetes and obesity. Fetal stage is crucial for skeletal muscle development because there is no net increase in the muscle fiber number after birth. Fetal skeletal muscle development involves myogenesis, adipogenesis, and fibrogenesis, which are all derived from mesenchymal stem cells (MSCs). Shifting commitment of MSCs from myogenesis to adipogenesis and fibrogenesis will result in increased intramuscular fat and connective tissue, as well as reduced numbers of muscle fiber and/or diameter, all of which have lasting negative effects on offspring muscle function and properties. Maternal obesity leads to low-grade inflammation, which changes the commitment of MSCs in fetal muscle through several possible mechanisms: 1) inflammation downregulates wingless and int (WNT) signaling, which attenuates myogenesis; 2) inflammation inhibits AMP-activated protein kinase, which promotes adipogenesis; and 3) inflammation may induce epigenetic modification through polycomb group proteins. More studies are needed to further explore the underlying mechanisms associated with maternal obesity, inflammation, and the commitment of MSCs.

Reports on chemical immobilization of proteins and enzymes first appeared in the 1960s. Since then, immobilized proteins and enzymes have been widely used in the processing of variety of products and increasingly used in the field of medicine. Here, we present a review of recent developments in immobilized enzyme use in medicine. Generally speaking, the use of immobilized enzyme in medicine can be divided into two major categories: biosensors and bioreactors. A brief overview of the evolution of the biosensor and bioreactor technology, of currently existing applications of immobilized enzymes, of problems that researchers encountered, and of possible future developments will be presented. © 2000 Wiley‐Liss, Inc. and the American Pharmaceutical Association J Pharm Sci 89: 979–990, 2000

Reports on chemical immobilization of proteins and enzymes first appeared in the 1960s. Since then, immobilized proteins and enzymes have been widely used in the processing of variety of products and increasingly used in the field of medicine. Here, we present a review of recent developments in immobilized enzyme use in medicine. Generally speaking, the use of immobilized enzyme in medicine can be divided into two major categories: biosensors and bioreactors. A brief overview of the evolution of the biosensor and bioreactor technology, of currently existing applications of immobilized enzymes, of problems that researchers encountered, and of possible future developments will be presented. © 2000 Wiley-Liss, Inc. and the American Pharmaceutical Association J Pharm Sci 89: 979–990, 2000

Treatment and pretreatment of hepatocytes with 2% dimethyl sulfoxide (DMSO) inhibited lipopolysaccharide and cytokine mixture (LPS/CM)-mediated NO synthesis in hepatocytes without any obvious effects on cell viability. DMSO at concentrations of 0.5–4% stimulated DNA replication and increased albumin secretion in LPS/CM-treated hepatocytes. Genisein, a inhibitor of protein tyrosine kinase (PTK), inhibited LPS/CM-mediated NO synthesis in hepatocytes. These results suggest that PTK is critical for hepatocyte NO synthesis, and DMSO-inhibited NO synthesis may be associated with prevention of LPS/CM-induced PTK activation in hepatocytes.

Induction of nitric oxide synthase by bacterial endotoxinin vivocan be mimicked by treating cultured hepatocytes with a combination of lipopolysaccharide and cytokines (LPS/cytokines), but the role of LPS/cytokine-induced nitric oxide in hepatocyte glucose metabolism is ambiguous. In this study, intermediary metabolite effects on LPS/cytokine-induced hepatocyte nitric oxide synthesis were examined. Pyruvate, lactate, oxaloacetate, and fumarate all showed some inhibitory effects on hepatocyte nitric oxide synthesis. However, these metabolic intermediates could not improve the mitochondrial respiration of LPS/cytokine-treated hepatocytes. Phosphoenolpyruvate carboxykinase activity (or flux) relating factors, glucocorticoids and cAMP, also blocked LPS/cytokine-induced nitric oxide synthesis. Insulin was much less potent than cAMP and glucocorticoids, and phorbol ester did not show any effect on hepatocyte nitric oxide synthesis. These results suggest that LPS/cytokine-induced nitric oxide synthesis is related, at least partly, to phosphoenolpyruvate carboxykinase activity (or flux) in hepatocytes.

Hepatocellular mitogen (HGF and EGF) inhibited lipopolysaccharide and cytokine mixture (referred as LPS/CM)-induced NO synthesis and cellular injury in hepatocytes. Mitogenic inhibitors such as hydroxyurea and Wortmannin could not reverse EGF or HGF-inhibited NO production, whereas both of them showed some inhibitory effect on hepatocyte NO synthesis. Although activation of protein kinase C (PKC) by phorbol 12-myristate 13-acetate (PMA) had no effect on hepatocyte NO synthesis, deletion of PKC activity by long-term treatment of hepatocytes with PMA abolished LPS/CM-induced NO production. In addition, pretreatment of hepatocytes with HGF and EGF also blocked LPS/CM-induced NO synthesis in the hepatocyte. These results suggest that proliferating signal is not directly involved in mitogen-inhibited NO synthesis in the hepatocyte, and LPS/CM-mediated NO synthesis is associated with the metabolic/redox state of hepatocytes.

Nitric oxide (NO) from artificial NO donors induces cell death through complete inhibition of mitochondrial respiration of hepatocytes. Treatment of hepatocytes with lipopolysaccharide (LPS) and cytokine mixture (interferon γ and tumor necrosis factor α) not only results in NO production but also causes cellular respiration suppression and cell death in hepatocytes. NG-monomethyl-L-arginine, a specific inhibitor of nitric oxide synthase, inhibits hepatocyte NO synthesis but cannot prevent hepatocytes from LPS and cytokine mixture-induced cellular injuries. Similarly, some metabolic intermediates capable of inhibiting hepatocyte NO synthesis cannot block LPS and cytokine mixture-mediated cellular injuries in hepatocytes. These results imply that lipopolysaccharide and cytokine mixture-induced cellular injuries and NO syntheses are parallel events, NO is not involved in LPS and cytokine mixture-induced cell damage.

A binuclear aluminiumiii chelate with rigid and flexible mixed ligands has been synthesized and structurally characterized, which exhibits polymer-like molecular packing and solution-processiblity, as well as high photoluminescence quantum yield for organic light-emitting diodes OLEDs; with this new compound as the emissive and host layer, the multi-layer OLEDs prepared vialow-cost spin-coating showed encouraging performance.

Microbial contamination on cotton textiles (CT) negatively affects people's health as well as the textile itself during use and storage. Using antimicrobial CT in a body‐safe manner is currently still a challenge because it is difficult to balance killing microbes and protecting skin flora. Herein, a borneol‐decorated CT (BDCT) through coupling of borneol 4‐formylbenzoate molecules onto the amino‐modified CT is reported. This BDCT shows strong and broad‐spectrum microbially antiadhesive activities against gram‐positive bacteria (Staphylococcus aureusand S. epidermidis), gram‐negative bacteria (Escherichia coliand Pseudomonas aeruginosa), and fungi (Aspergillus niger, Mucor racemosus, and Candida albicans). Because of its unique stereochemical microbial antiadhesion mechanism, BDCT is harmless to skin flora. In addition, BDCT exhibits prominent durability of microbially antiadhesive capability by bearing 50 times of accelerated laundering. Therefore, this stereochemical BDCT strategy shows great potential for applications in the new generation of textiles, food packaging, and medical protection. Borneol‐decorated cotton textile (BDCT) with strong microbially antiadhesive properties and laundering stabilityis presented. It achieves broad‐spectrum inhibition of microbial adhesion through employing the unique stereochemical strategy. BDCT is thus meeting the frontier of functional CT, which advances antimicrobial CT to protect us from potentially harmful microorganisms and do no harm to skin flora.

To be, or not to be, that is the microbe's question when they meet a borneol modified surface. In this case, a borneol‐decorated cotton textile (BDCT) is presented in article number 1900232by Xing Wang and co‐workers. The unique stereochemical strategy will lead to new opportunities for managing and controlling microbes.