Dexterous magnetic manipulation of conductive non-magnetic objects.

Dexterous magnetic manipulation of ferromagnetic objects is well established, with three to six degrees of freedom possible depending on object geometry1. There are objects for which non-contact dexterous manipulation is desirable that do not contain an appreciable amount of ferromagnetic material but do contain electrically conductive material. Time-varying magnetic fields generate eddy currents in conductive materials2-4, with resulting forces and torques due to the interaction of the eddy currents with the magnetic field. This phenomenon has previously been used to induce drag to reduce the motion of objects as they pass through a static field5-8, or to apply force on an object in a single direction using a dynamic field9-11, but has not been used to perform the type of dexterous manipulation of conductive objects that has been demonstrated with ferromagnetic objects. Here we show that manipulation, with six degrees of freedom, of conductive objects is possible by using multiple rotating magnetic dipole fields. Using dimensional analysis12, combined with multiphysics numerical simulations and experimental verification, we characterize the forces and torques generated on a conductive sphere in a rotating magnetic dipole field. With the resulting model, we perform dexterous manipulation in simulations and physical experiments.

Assessing the impact of rurality on oesophagogastric cancer survival in the North-East of Scotland- a prospective population cohort study.

INTRODUCTION: Despite advances in oncology therapies and surgical techniques, survival from oesophagogastric cancer remains low. Poorer cancer outcomes and survival for rural dwellers is documented worldwide and has been an area of focus in Scotland since 2007 when changes to suspected cancer national referral guidelines and governmental mandates on delivering remote and rural healthcare occurred. Whether these changes in clinical practice has impacted upon upper gastrointestinal cancer remains unclear. METHODS: A prospective, single-centre observation study was performed. Data from the regional oesophagogastric cancer MDT between 2013 and 2019 were included. The Scottish Index of Multiple Deprivation 2020 tool provided a rurality code (1 or 2) based on patient postcode at time of referral. Survival outcomes for urban and rural patients were compared across demographic factors, disease factors and stage at presentation. RESULTS: A total of 1038 patients were included in this study. There was no significant difference between rural and urban groups in terms of sex of patient, age at diagnosis, cancer location, or tumour stage. Furthermore, no difference was identified between those commenced on a radical therapy with other treatment plans. Despite this, rurality predicted for an improved outcome on survival analysis (p = 0.012) and this was independent of other factors on multivariable analysis (HR = 0.78, 95%CI 0.66-0.98; p = 0.032). DISCUSSION: The difference in survival demonstrated here between urban and rural groups is not easily explained but may represent improvements to rural access to healthcare delivered as a result of Scottish Government reports.

Length-Dependent Evolution of Type II Heterojunctions in Bottom-Up-Synthesized Graphene Nanoribbons.

The ability to tune the band-edge energies of bottom-up graphene nanoribbons (GNRs) via edge dopants creates new opportunities for designing tailor-made GNR heterojunctions and related nanoscale electronic devices. Here we report the local electronic characterization of type II GNR heterojunctions composed of two different nitrogen edge-doping configurations (carbazole and phenanthridine) that separately exhibit electron-donating and electron-withdrawing behavior. Atomically resolved structural characterization of phenanthridine/carbazole GNR heterojunctions was performed using bond-resolved scanning tunneling microscopy and noncontact atomic force microscopy. Scanning tunneling spectroscopy and first-principles calculations reveal that carbazole and phenanthridine dopant configurations induce opposite upward and downward orbital energy shifts owing to their different electron affinities. The magnitude of the energy offsets observed in carbazole/phenanthridine heterojunctions is dependent on the length of the GNR segments comprising each heterojunction with longer segments leading to larger heterojunction energy offsets. Using a new on-site energy analysis based on Wannier functions, we find that the origin of this behavior is a charge transfer process that reshapes the electrostatic potential profile over a long distance within the GNR heterojunction.

Urinalysis and culture results of free-catch urine samples in dogs: a randomised controlled trial.

OBJECTIVES: To evaluate the prevalence of bacterial presence in free-catch urine samples preceded by either a standardised prepped ("clean-catch") protocol versus unprepped (non-cleaned) voiding. MATERIALS AND METHODS: The study was a single-centre prospective single-blinded randomised controlled trial. Urine samples were obtained from 100 client-owned dogs presenting for routine evaluation. Dogs were randomly assigned to either the prepped group (preputial or peri-vulvar area cleaned with sterile saline before collection) or the unprepped group (no preliminary cleansing) stratified by sex. Urinalysis and urine culture (blood and MacConkey agar) were performed on all samples. Significant bacterial presence on urine culture was defined as >104 colony forming units (CFU)/mL. RESULTS: There were no statistically significant associations between prepped versus unprepped collection method or sex with a urinalysis positive for bacteriuria. However, on culture, significant bacterial growth was almost five times more likely to be associated with males relative to females (odds ratio 4.59, 95% confidence interval 1.61 to 13.10). The probability of finding a positive culture was not statistically associated with prep method (odds ratio 1.43, 95% confidence interval 0.50 to 4.08). CLINICAL SIGNIFICANCE: For the majority of dogs without clinical signs of urinary tract infection, free-catch urine collection does not result in significant bacteriuria found on analysis or culture. The presence of bacteria found in free-catch samples may be secondary to sample contamination or subclinical bacteriuria. Sample contamination or subclinical bacteriuria may be more prevalent in male dogs.

Stress in client-owned dogs related to clinical exam location: a randomised crossover trial.

OBJECTIVES: To quantify the effects of wellness examinations conducted in the common treatment area on fear, anxiety and stress indicators in client-owned dogs. MATERIALS AND METHODS: The study was a prospective, non-blinded, randomised, two-period two-treatment crossover trial. Client-owned healthy adult dogs presenting for wellness or dental evaluations at a single veterinary teaching hospital received three consecutive rapid assessment exams; a baseline exam (owner present), followed by two identical physical exams differing in location and presented in random order (isolated exam room with owner present versus common treatment area, owner absent). Primary endpoints were a cumulative fear, anxiety and stress score for five standardised behaviours and heart rate (bpm) measured for each exam. RESULTS: Forty-four dogs were enrolled. Modal fear, anxiety and stress score at baseline was 1 of 5, indicating none to mild stress. Both fear, anxiety and stress and heart rates measured in the common treatment area were clinically elevated relative to assessments conducted in the exam room. Relative to baseline, animals examined in the common treatment area showed increased fear, anxiety and stress (+2.6 units, se 0.5; P<0.0001) and heart rate (20 bpm, 95% confidence interval 13, 28; P<0.0001. Twenty-eight dogs (64%) exhibited fear, anxiety and stress scores ≥3 of 5 (moderate to severe stress) in the common treatment area, compared to 19 (43%) during exam room assessments. CLINICAL SIGNIFICANCE: Stress assessments in this study may have been biased by inability to blind assessors to location. However, stress metrics showed clinically significant, consistent and directionally symmetrical increases when dogs were examined in the common treatment area. When physical exam locations are highly stimulating, dogs may experience increased stress and anxiety, with detrimental effects on clinical assessments and behavioural welfare. Whenever possible, physical exams and procedures should take place in low-stress environments with the owner present.

Effects of soluble immune complexes on Fc receptor- and C3b receptor-mediated phagocytosis by macrophages.

The effects of ingestion of soluble immune complexes upon macrophage phagocytic function was studied. Ingestion of immune complexes severely impaired the macrophage's ability to ingest IgG-coated particles but did not alter its ability to interact with particles by means other than its Fc receptors. Treatment of macrophages that had ingested immune complexes with supernates containing the previously described lymphokine that augments macrophage complement receptor function failed to enhance the cells' interaction with either IgG-coated erythrocytes or zymosan particles but markedly enhanced their ability to phagocytize via their complement receptors. The possible significance of these findings in immunologically mediated inflammation is discussed.

Characterization of the macrophage receptro for complement and demonstration of its functional independence from the receptor for the Fc portion of immunoglobulin G.

The complement receptor of the macrophage membrane recognizes particle-bound C3b but does not recognize particle-bound C3d. C3-b-coated sheep erythrocytes were bound to macrophages via their C3b receptors, and the preparations were then incubated with either latex particles or opsonized pneumococci (test particles). Macrophages ingested the test particles, but erythrocytes were not ingested; they remained bound to C3b receptors of the macrophage plasma membrane. Thus, a signal initiating ingestion via one type of receptor is not transmitted to all receptors which have the potential to mediate phagocytosis.

Studies of the macrophage complement receptor. Alteration of receptor function upon macrophage activation.

We have examined the roles of Fc receptors and complement receptors in mediating the interaction of sensitized sheep erythrocytes (E) with activated and with nonactivated mouse peritoneal macrophages. Both activated and nonactivated macrophages ingest IgG-coated erythrocytes [E(IgG)]; activated cells intest 1.5-2 times as man E(IgG) as do nonactivated macrophages. Thus, there is a quantitative difference in Fc receptor-mediated ingestion between activated and nonactivated macrophages. There is, however, a qualitative difference in function of complement receptors of activated and nonactivated macrophages. Nonactivated macrophages avidly bind complement-coated E [E(IgM)Ia1, but do not ingest them to a significant degree. Activated macrophages, on the other hand, bind and ingest E(IgM)C. The possibility of Fc receptor participation in mediating ingestion of E(IgM)C by activated macrophages was eliminated by blocking Fc receptors with an antimacrophage IgG fraction. Activated macrophages treated with antimacrophage IgG did not ingest E(igG) but did ingest both E(IgM)C AND E(IgM)C. Nonactivated macrophages treated with antimacrophage IgG did not interact at all with E(IgG). These cells bound, but did not ingest, E(IgM)C and E(IgM)C. Complement receptor-mediated ingestion is a marker for macrophage activation and may be physiologically important in the elimination of complement-coated particles.

Segmental response of the macrophage plasma membrane to a phagocytic stimulus.

A method of attaching mouse RBCs to mouse macrophages is described. Both cell types were coated with rabbit anti-mouse macrophage F(ab')(2), and cross-linkage of cells was effected with sheep F(ab')(2) directed against rabbit F(ab')(2). 98% of macrophages attached an average of 11 RBCs each. Attachment occurred at 37 degrees C and was stable for at least 4 h. Less than 0.1% of macrophages ingested RBCs under these conditions. Latex particles and opsonized pneumococci were ingested as avidly by RBC-coated macrophages as by native macrophages. Ingestion of these particles did not prompt ingestion of attached RBCs. When anti-RBC IgG was added, however, over 90% of macrophages ingested an average of six RBCs each. Thus, ingestion of one particle does not trigger generalized phagocytosis of all particles attached to the cell's plasma membrane, and the phagocytic stimulus is confined to the segment of the cell's plasma membrane immediately adjacent to the particle being ingested.

Augmentation of macrophage complement receptor function in vitro. III. C3b receptors that promote phagocytosis migrate within the plane of the macrophage plasma membrane.

We have previously reported that treatment with a unique lymphokine enables resident mouse peritoneal macrophages to phagocytize via their complement receptors and we have presented evidence that the lymphokine act by enabling complement receptor engagement by C3b ligands to generate a phagocytic signal, thereby linking the cell surface binding event with the intracellular phagocytic machinery. In the present experiments, we used immobilized immune complexes to study the topography of C3b receptors of resident mouse peritoneal macrophages treated with the lymphokine. Our results indicate that lymphokine treatment enables the macrophages' C3b receptors to migrate within the plane of the cells' plasma membrane and that manipulations of macrophages that abrogate one response to the lymphokine, complement receptor mobility, also abrogate the other response, complement receptor-mediated phagocytosis. These findings strongly suggest that lateral mobility of a ligand-bound receptor within the macrophage plasma membrane is an essential component of the phagocytic signal. Moreover, our results indicate that the difference in complement receptor function among various populations of macrophages is not due to the expression of different types of complement receptors by the different macrophage populations but rather to a difference in the relationship of the C3b receptor with other plasma membrane or intracellular components.

Augmentation of macrophage complement receptor function in vitro. I. Characterization of the cellular interactions required for the generation of a T-lymphocyte product that enhances macrophage complement receptor function.

The function of complement receptors of mouse peritoneal macrophages was converted in vitro from mediating only attachment of macrophage complement receptor function was achieved by treating freshly explanted macrophages with supernates from cultures containing T lymphocytes and appropriately triggered macrophages. Fc receptor-mediated phagocyctosis by macrophages was required for the production of active supernates, for neither ingestion via the cells' complement receptors nor ingestion via nonimmunologic means was a sufficient stimulus for the macrophages' participation in the generation of supernatant activity. Fc receptor-triggered macrophages interacted by a contact dependent, but histocompatibility independent, mechanism with T lymphocytes, thereby signalling the lymphocytes to elaborate the active product. The possible significance of enhanced macrophage complement receptor function in inflammation, host defense against microbial pathogens, immune complex disease, and neoplasia is discussed.

In vivo activation of macrophage C3 receptors for phagocytosis.

We assessed the effects of exposure to immune complexes in vivo on macrophages' Fc receptor function and C3 receptor function. Peritoneal macrophages from mice injected intraperitoneally with immune complexes were markedly impaired in their ability to phagocytize via their Fc receptors but had acquired the ability to phagocytize via their C3 receptors. In vivo activation of macrophages' C3 receptors for phagocytosis required T lymphocytes, because macrophages from athymic mice could not be activated by injection of immune complexes. The requirement for both T lymphocytes and immune complexes for activation of macrophages' C3 receptors in vivo is identical to the requirements for activation of macrophages' C3 receptors in vitro, suggesting that the mechanisms we have identified for activation of these receptors in vitro are the same mechanisms by which the receptors are activated for phagocytosis in vivo. The susceptibility of macrophages' Fc receptors to blockade by immune complexes and the activation of their C3 receptors for phagocytosis in a milieu containing immune complexes suggest that it may be macrophages' C3 receptors, not their Fc receptors, that are primarily responsible for promoting phagocytosis of opsonized microorganisms in immune hosts.

Augmentation of macrophage complement receptor function in vitro. IV. The lymphokine that activates macrophage C3 receptors for phagocytosis binds to a fucose-bearing glycoprotein on the macrophage plasma membrane.

Macrophage receptors for the third component of complement (C3) are normally immobilized and unable to diffuse within the cell's plasma membrane and, even though they promote avid particle binding, are unable to promote phagocytosis of C3-coated particles. We have previously identified a lymphokine that activates macrophage C3 receptors for phagocytosis and have found that it acts by freeing the receptors so that they can diffuse within the macrophage plasma membrane. It seemed likely to us that the initial lymphokine-macrophage interaction would occur at the macrophage surface, perhaps via a specific lymphokine receptor. Since the binding of many ligands to cells is mediated by cell surface glycoproteins, we examined the protein and sugar requirements for murine peritoneal macrophages to respond to the lymphokine. Macrophages treated with the neutral protease Dispase lost the ability to respond to the lymphokine, and inclusion of L-fucose in the incubation medium containing lymphokine and macrophages inhibited markedly the macrophages' response to the lymphokine, suggesting that the lymphokine exerts its effects by first binding to fucose residues on a glycoprotein receptor on the macrophage surface. Further evidence for the essential role of macrophage surface fucose was obtained by demonstrating that pretreatment of macrophages with either fucosidase or gorse lectin, a fucose-binding lectin, strikingly disabled the cells from responding to the lymphokine. All treatments that prevented lymphokine activation of macrophage C3 receptors for phagocytosis also prevented lymphokine-induced C3 receptor mobility. These results strongly suggest that the lymphokine binds to a fucose-bearing macrophage surface glycoprotein, perhaps a specific lymphokine receptor. They also strengthen our hypothesis that, for a receptor to be able to promote phagocytosis, it must be able to diffuse within the macrophage plasma membrane.

Studies on the mechanism of phagocytosis. II. The interaction of macrophages with anti-immunoglobulin IgG-coated bone marrow-derived lymphocytes.

We have examined the effect of the distribution of anti-immunoglobulin IgG molecules on the surface of bone marrow-derived lymphocytes upon the interaction of these cells with macrophages. Lymphocytes which were diffusely coated with antibodies to surface immunoglogulin were ingested by macrophages. Lymphocytes which had the same number of anti-immunoglobulin IgG molecules redistributed to one pole of the surface bound to the macrophages' Fc receptors but were not ingested. These results confirm our previous hypothesis that ingestion of an immunologically coated particle requires the sequential, circumferential binding of specific receptors on the plasma membrane of a phagocytic cell to immunologic ligands distributed over the entire particle surface. Macrophages which had bound capped lymphocytes by the macrophages' Fc receptors removed the immune complex caps from the lymphocyte surface without destroying the lymphocytes. These lymphocytes remained attached to the macrophage surface. The finding that macrophages can phagocytize immune complexes from the surface of a cell without destroying the cell to which these complexes are attached may be important in understanding the effects of antigens and antibodies on cells participating in a humoral immune response, in identifying the mechanisms by which chronic viral infections are established, and in defining the roles of blocking antibodies in tumor immunity.

Studies on the mechanism of phagocytosis. I. Requirements for circumferential attachment of particle-bound ligands to specific receptors on the macrophage plasma membrane.

These experiments were designed to evaluate the role of macrophage plasma membrane receptors for the third component of complement (C) and for the Fc portion of IgG in the ingestion phase of phagocytosis. Sheep erythrocyte (E) were coated with anti-E IgG [E(IgG)]; these E(IgG) were then attached to cultivated monolayers of mouse peritoneal macrophages under conditions which reversibly inhibit ingestion of E(IgG). The E(IgG)-macrophage complexes were further incubated under similar conditions with an antimacrophage IgG fraction which blocks Fc receptor-mediated ingestion but has no effect upon ingestion mediated by other phagocytic receptors. When these cultures were subsequently incubated under conditions optimal for particle ingestion, phagocytosis of the IgG-coated erythrocytes did not occur; the erythrocytes remained bound to the Fc receptors of the macrophage plasma membrane. To determine whether ligands must cover the entire surface of an attached particle to permit ingestion of that particle, C-coated E [E(IgM)C] were bound to the C receptors of thioglycollate-induced (activated) macrophages at 4 degrees C. E(IgM)C-macrophage complexes were then trypsinized at 4 degrees C, a procedure which resulted in cleavage of erythrocyte-bound C3b molecules to a form of C3 not recognized by the macrophage receptors for C3b. Under the conditions used, trypsin did not affect the attachment of E(IgM)C to the macrophage surface or the macrophage receptors for C3b. When these trypsin treated E(IgM)C-macrophage complexes were incubated at 37 degrees C, the bound E(IgM)C were not ingested; the erythrocytes remained attached to the macrophage plasma membrane via the macrophage's C receptors. These results indicate that attachment of a particle to specific receptors on the macrophage plasma membrane is not sufficient to trigger ingestion of that particle. Rather, ingestion requires the sequential, circumferential interaction of particle-bound ligands with specific plasma membrane receptors not involved in the initial attachment process.

Atypical disease after Bordetella pertussis respiratory infection of mice with targeted disruptions of interferon-gamma receptor or immunoglobulin mu chain genes.

Using a murine respiratory challenge model we have previously demonstrated a role for Th1 cells in natural immunity against Bordetella pertussis, but could not rule out a role for antibody. Here we have demonstrated that B. pertussis respiratory infection of mice with targeted disruptions of the genes for the IFN-gamma receptor resulted in an atypical disseminated disease which was lethal in a proportion of animals, and was characterized by pyogranulomatous inflammation and postnecrotic scarring in the livers, mesenteric lymph nodes and kidneys. Viable virulent bacteria were detected in the blood and livers of diseased animals. An examination of the course of infection in the lung of IFN-gamma receptor-deficient, IL-4-deficient and wild-type mice demonstrated that lack of functional IFN-gamma or IL-4, cytokines that are considered to play major roles in regulating the development of Th1 and Th2 cells, respectively, did not affect the kinetics of bacterial elimination from the lung. In contrast, B cell-deficient mice developed a persistent infection and failed to clear the bacteria after aerosol inoculation. These findings demonstrate an absolute requirement for B cells or their products in the resolution of a primary infection with B. pertussis, but also define a critical role for IFN-gamma in containing bacteria to the mucosal site of infection.

Lipolytic surface remnants of triglyceride-rich lipoproteins are cytotoxic to macrophages but not in the presence of high density lipoprotein. A possible mechanism of atherogenesis?

Hypertriglyceridemic (HTG) serum, lipolyzed in vitro by purified bovine milk lipoprotein lipase, was found to be cytotoxic to cultured macrophages. Surviving macrophages contained numerous lipid inclusions similar to those found in foam cells. Individual lipoprotein fractions isolated from the lipolyzed HTG serum, including HDL, were also cytotoxic. Lipolysis of isolated lipoprotein fractions (either HTG or normal) allowed localization of cytotoxicity to postlipolysis remnant VLDL and chylomicron particles. The presence of a critical concentration of HDL in either the lipolysis mixture or the culture dishes inhibited the cytotoxicity. Below this critical concentration HDL itself became cytotoxic, producing lipid inclusions in surviving macrophages. The lipid fraction of the cytotoxic remnants contained the cytotoxic factor(s); neither FFA nor lysolecithin alone could account for this cytotoxicity. Postprandial lipemic sera from subjects with a brisk chylomicron response, when lipolyzed in vitro, were cytotoxic to cultured macrophages; neither fasted sera from these subjects, nor postprandial sera from normolipidemic subjects with a normal chylomicron response, were cytotoxic. Postheparin (in vivo lipolyzed) serum and its isolated lipoprotein fractions obtained 30 min after heparin injection in subjects with HTG were shown to be cytotoxic to macrophages; by 60 min most of the cytotoxicity had disappeared. The postprandial and postheparin observations support an in vivo significance for remnant-associated cytotoxicity. We hypothesize that cytotoxic remnants of lipolyzed VLDL and chylomicrons may be one of the major atherogenic lipoproteins. Further, we suggest that inhibition of the cytotoxicity of these remnants may be one important way that HDL prevents atherosclerosis.

The role of adhesion junctions in the biomechanical behaviour and osteogenic differentiation of 3D mesenchymal stem cell spheroids.

Osteogenesis of mesenchymal stem cells (MSC) can be regulated by the mechanical environment. MSCs grown in 3D spheroids (mesenspheres) have preserved multi-lineage potential, improved differentiation efficiency, and exhibit enhanced osteogenic gene expression and matrix composition in comparison to MSCs grown in 2D culture. Within 3D mesenspheres, mechanical cues are primarily in the form of cell-cell contraction, mediated by adhesion junctions, and as such adhesion junctions are likely to play an important role in the osteogenic differentiation of mesenspheres. However the precise role of N- and OB-cadherin on the biomechanical behaviour of mesenspheres remains unknown. Here we have mechanically tested mesenspheres cultured in suspension using parallel plate compression to assess the influence of N-cadherin and OB-cadherin adhesion junctions on the viscoelastic properties of the mesenspheres during osteogenesis. Our results demonstrate that N-cadherin and OB-cadherin have different effects on mesensphere viscoelastic behaviour and osteogenesis. When OB-cadherin was silenced, the viscosity, initial and long term Young's moduli and actin stress fibre formation of the mesenspheres increased in comparison to N-cadherin silenced mesenspheres and mesenspheres treated with a scrambled siRNA (Scram) at day 2. Additionally, the increased viscoelastic material properties correlate with evidence of calcification at an earlier time point (day 7) of OB-cadherin silenced mesenspheres but not Scram. Interestingly, both N-cadherin and OB-cadherin silenced mesenspheres had higher BSP2 expression than Scram at day 14. Taken together, these results indicate that N-cadherin and OB-cadherin both influence mesensphere biomechanics and osteogenesis, but play different roles.

Control of bovine tuberculosis in a farmed red deer herd in England.

This report describes how Mycobacterium bovis infection was controlled and eventually eradicated in a farmed red deer herd in the north of England, following sustained tuberculin skin testing supplemented with serological (antibody) tests over a period of approximately two years. By taking advantage of the anamnestic antibody response produced by the skin test to detect skin test-negative, antibody-positive infected individuals, a total of 35 additional animals were identified, including 2 with gross visible lesions typical of bovine tuberculosis (BTB). Without detection and removal, these animals would have posed a continued risk of BTB persistence within the herd and potentially contributed to the spread of infection from deer into wildlife and surrounding cattle farms in an area of low BTB incidence. This case supports the use of ancillary diagnostic serological tests to speed up the resolution of incidents of BTB caused by M bovis in captive deer herds.

Preventing Thin Film Dewetting via Graphene Capping.

A monolayer 2D capping layer with high Young's modulus is shown to be able to effectively suppress the dewetting of underlying thin films of small organic semiconductor molecule, polymer, and polycrystalline metal, respectively. To verify the universality of this capping layer approach, the dewetting experiments are performed for single-layer graphene transferred onto polystyrene (PS), semiconducting thienoazacoronene (EH-TAC), gold, and also MoS2 on PS. Thermodynamic modeling indicates that the exceptionally high Young's modulus and surface conformity of 2D capping layers such as graphene and MoS2 substantially suppress surface fluctuations and thus dewetting. As long as the uncovered area is smaller than the fluctuation wavelength of the thin film in a dewetting process via spinodal decomposition, the dewetting should be suppressed. The 2D monolayer-capping approach opens up exciting new possibilities to enhance the thermal stability and expands the processing parameters for thin film materials without significantly altering their physical properties.