Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Spreading”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 559 records · Page 31Linked to original sources
PubMed2001

The role of phosphoinositide 3-kinase in spreading osteoclasts induced by colony-stimulating factor-1.

BACKGROUND: Colony-stimulating factor-1 (CSF-1), a growth and survival factor for osteoclasts, stimulates these cells to spread and migrate towards a gradient of CSF-1. This may support the translocation of osteoclasts to new sites on the bone surface to be resorbed. Phosphoinositide 3-kinase (PI 3-K) is a lipid kinase participating in various signal transduction pathways. OBJECTIVE: To investigate the role of PI 3-K in the CSF-1-induced spreading of osteoclasts. METHODS: In isolated rat osteoclasts treated with or without CSF-1, the distribution of PI 3-K and proteins phosphorylated on tyrosine were investigated using immunofluorescence. In murine osteoclast-like cells grown from bone marrow cells co-cultured with osteoblasts, the activation of the PI 3-K by CSF-1 was determined both in vivo and in vitro. In vivo, the enzyme product in the cell was determined after extraction and separation with thin layer chromatography; in vitro, PI 3-K activity was measured in the pellet immunoprecipitated from the cell lysate. RESULTS: Inhibition of PI 3-K blocked the CSF-1-induced spreading of osteoclasts. In spreading osteoclasts, a portion of PI 3-K was translocated to the periphery where proteins phosphorylated on tyrosine appeared simultaneously. In osteoclast-like cells, CSF-1 stimulated PI 3-K activity. This activity could be immunoprecipitated with antibody against phophotyrosine residues. CONCLUSION: PI 3-K participates in the CSF-1-induced spreading of osteoclasts. The activated PI 3-K may induce the reorganization of the cytoskeleton resulting in spreading and migration.

Androstadienes↗
PubMed2006

A nephritogenic peptide induces intermolecular epitope spreading on collagen IV in experimental autoimmune glomerulonephritis.

This group previously identified a peptide p13 of alpha3(IV)NC1 domain of type IV collagen that induces experimental autoimmune glomerulonephritis (EAG) in rats with generation of antibodies to sites on alpha3(IV)NC1 external to the peptide as a result of intramolecular epitope spreading. It was hypothesized that intermolecular epitope spreading to other collagen IV chains also was induced. Rats were immunized with nephritogenic peptide that was derived from the amino terminal part of rat alpha3(IV)NC1 domain, and serum and kidney eluate were examined for antibodies to both native and recombinant NC1 domains of collagen IV. Peptide induced EAG with proteinuria and decreased renal function and glomerular basement membrane IgG deposits. Sera from these rats were examined by ELISA, which revealed reactivity not only to immunizing peptide but also to human and rat alpha3(IV)NC1 and to human alpha4(IV)NC1 domains. Kidney eluate that was depleted of alpha3(IV)NC1 antibodies still reacted to alpha4(IV)NC1, and alpha3(IV)NC1 column-bound antibody reacted with alpha3(IV)NC1. There was minimal reactivity to other collagen chains. Eluate that was adsorbed to NC1 hexamer from rat glomerular basement membrane lost all reactivity to glomerular constituents, and the eluted antibodies reacted to alpha3(IV)NC1 and alpha4(IV)NC1 domains. These studies show that a T cell epitope of alpha3(IV)NC1 induces EAG, intramolecular epitope spreading along alpha3(IV)NC1, and intermolecular epitope spreading to alpha4(IV)NC1 domain with minimal or no reactivity to other collagen chains or glomerular constituents. This is the first demonstration in EAG of intermolecular epitope spreading and identification of the spread epitopes.

Animals↗
PubMed1998

Risk factors for the spread of antibiotic-resistant bacteria.

The emergence of antibiotic resistance is primarily due to excessive and often unnecessary use of antibiotics in humans and animals. Risk factors for the spread of resistant bacteria in hospitals and the community can be summarised as over-crowding, lapses in hygiene or poor infection control practices. Increasing antibiotic resistance in bacteria has been exacerbated by the slow pace in developing newer antibiotics. Methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant enterococci (VRE) and multiresistant Gram-negative bacteria are spread primarily by direct or indirect person-to-person contact. Independent risk factors for MRSA include the use of broad spectrum antibiotics, the presence of decubitus ulcers and prosthetic devices while those for VRE include prolonged hospitalisation and treatment with glycopeptides or broad spectrum antibiotics. For the spread of resistant Gram-negative bacteria risk factors include urinary catheterisation, excessive use of antibiotics and contamination of humidifiers and nebulisers. The spread of penicillin-resistant pneumococci (PRP) and drug-resistant and multidrug-resistant tuberculosis (MDRTb) is due to airborne transmission. Risk factors for the spread of PRP include overcrowding, tracheostomies and excessive use of penicillins for viral respiratory infections; for MDRTb they include poor compliance, convergence of immunosuppressed patients, delayed diagnosis or treatment, and poor or inadequate ventilation and isolation facilities. Recent developments in the genomic mapping of many bacteria and advances in combinatorial chemistry promise to usher in a new era of antibiotic development. While this may result in our regaining some of the ground lost to resistant bacteria, there will still be a continuing need to minimise the spread of antibiotic resistance through the rational use of antibiotic agents and stringent infection control practice.

Animals↗
PubMedDate not supplied

[Evaluation of local and regional spread of malignant tumors of the tongue and floor of the mouth].

Malignant tumors of the oral cavity grow rapidly, frequently and early metastazing to the surrounding regional lymph nodes. The aim of this study was to evaluate the correlation between clinically confirmed local and regional spread and intraoperatively and histopathologically verified local spread. A series of 74 patients with carcinoma of the tongue and floor of the mouth were analyzed. All the patients were surgically treated during the period 1991-1995. Clinical evidence of local spread (cT) was in high accord with intraoperatively and histopathologically evidenced spread (pT) amounting to 83.8%. The degree of correlation decreased with the increase of T stage. Clinically observed regional spread (cN) and intraoperatively and histopathologically confirmed regional spread (pN) was lower, amounting to 56.8% in comparison to the corresponding T categories.

Carcinoma, Squamous Cell↗
PubMed2005

Peroral cholangioscopy for non-invasive papillary cholangiocarcinoma with extensive superficial ductal spread.

Papillary carcinoma arising from the extrahepatic bile duct often shows superficial ductal spread. We report herein the case of a patient with extensive superficial spread of non-invasive papillary cholangiocarcinoma, which was depicted with peroral cholangioscopy. A 65-year-old woman presented with the sudden-onset of severe epigastric pain. Ultrasonography revealed acute acalculous cholecystitis. Endoscopic retrograde cholangiography found small protruding lesions around the confluence of the cystic duct, suggestive of a cholangiocarcinoma. As the contour of the middle and upper bile ducts it was slightly irregular on the cholangiogram, the presence of superficial ductal spread was suspected. Peroral cholangioscopy revealed small papillary lesions around the confluence of the cystic duct and fine granular mucosal lesions in the middle and upper bile ducts and the right hepatic duct, suggesting a superficially spreading tumor. A right hepatectomy with bile duct resection was performed and no residual tumor was found. Histological examination revealed a non-invasive papillary carcinoma arising from the cystic duct with extensive superficial spread. Our experience of this case and a review of the literature suggest that a fine granular or fine papillary appearance of the ductal mucosae on cholangioscopy indicates superficial spread of papillary cholangiocarcinoma, for which peroral cholangioscopy is an efficient diagnostic option.

Aged↗
PubMed2005

Complementary factors contributing to the rapid spread of HIV-I in sub-Saharan Africa: a review.

OBJECTIVE: To examine and establish complementary factors that contribute to the alarmingly high prevalence of HIV-1 in sub-Saharan Africa (SSA) in order to create awareness and suggest possible measures to avert the spread of the pandemic. DATA SOURCES: Review of literature via Medline, the Internet, articles in refereed journals, and un-refereed features from the East Africa media houses and personal communications. DATA SELECTION: Most published data from 1981 to September 2004 found to have revealed an impact on the spread of HIV-1 in SSA were included in the review. Therefore, all selected articles were read and critically evaluated. Where possible the number of citations articles which had been received were sought to established the degree of impact. DATA EXTRACTION: Abstracts of all articles identified were accessed, read and analysed to determined possible relevance to the spread of HIV-1. When relevance was established from the abstract the entire paper was read and important points were included in the review. DATA SYNTHESIS: A matrix was drawn to include all subtitles (e.g. polygamy, circumcision, poverty, etc). Below each subtitle all published works were included and prioritised. Published works that were found to have impact were included in the review. Finally a percent composite picture of all factors was drawn in an attempt to prioritise the factors, not withstanding the fact that most factors are interrelated and complementary. CONCLUSIONS: There are many reasons why the spread of HIV-1 in SSA has not been declining over the years. Main risk factors for HIV-1 infection and AIDS disease in SSA were found to include poverty, famine, low status of women in society, corruption, naive risk taking perception, resistance to sexual behaviour change, high prevalence of sexually transmitted infections (STI), internal conflicts and refugee status, antiquated beliefs, lack of recreational facilities, ignorance of individual's HIV status, child and adult prostitution, uncertainty of safety of blood intended for transfusion, widow inheritance, circumcision, illiteracy and female genital cutting and polygamy. It is suggested that control programmes both local and donor-driven seeking to mitigate the spread of HIV-1 in SSA should take into account the apparent multiplicity of sub-Saharan African cultures and beliefs, some of which augment the spread of HIV-1.

Africa South of the Sahara↗
PubMed1999

Ethanol feeding selectively impairs the spreading of rat perivenous hepatocytes on extracellular matrix substrates.

BACKGROUND: Hepatocytes require attachment and subsequent spreading on an extracellular matrix for their proper growth, function and survival. Our previous studies have shown that ethanol feeding selectively impairs perivenule hepatocyte attachment to various extracellular matrices. This study was undertaken to determine whether zonal differences in hepatocyte spreading in response to ethanol feeding occurs and to ascertain the influence of ethanol consumption on the zonal expression of the beta1 subunit of integrins, which are the major surface receptors responsible for matrix binding and subsequent interactions. METHODS: Hepatocytes from the perivenous and periportal regions of the liver were isolated by digitonin/collagenase perfusion from rats that were pair-fed for 2 to 3 weeks with a liquid diet containing either ethanol or isocaloric carbohydrate. The ability of perivenous and periportal hepatocytes to spread on plates coated with either type IV collagen, laminin, fibronectin or polylysine was determined. In addition, the isolated cells were used for the analysis of total cellular and surface beta1 integrin expression. RESULTS: With all of the matrix substrates tested, the spreading of perivenous hepatocytes isolated from the ethanol-fed animals was markedly impaired, while the spreading of periportal hepatocytes was essentially unaffected by ethanol feeding. Both the total cellular as well as the surface expression of the beta1 integrin subunit in perivenous cells from the ethanol-fed rats were significantly higher than from the perivenous control cells, whereas the total and surface expression of the beta1 integrin in periportal cells isolated from ethanol-fed and control rats were not significantly different. CONCLUSIONS: The results indicated that in addition to impairing hepatocyte attachment, ethanol feeding also impairs another critical step of the adhesion process, that of hepatocyte spreading on extracellular matrix substrates. This defect occurred preferentially in perivenous cells and not periportal cells and was associated with an increase in beta1 integrin expression, suggesting that a compensatory mechanism occurs as an attempt by the perivenous cells to overcome impaired cell-matrix interactions caused by ethanol. Overall, these alterations in extracellular matrix-hepatocyte interactions could lead to alterations of hepatocyte structure and function and potentially play a role in alcoholic liver injury.

Animals↗
PubMed2000

[Spreading of porcine kidney epithelial cells under normal conditions and under the effect of inhibitors of energy metabolism. II. Behavior of cellular organelles].

In the present work the behavior of mitochondria and lysosomes during cell spreading has been investigated in normal conditions and under ATP-synthesis inhibitors: sodium aside and N,N-dicyclohexylcarbodiimide (DCCD). In the control culture, microtubules run along the stable edge and perpendicular to the leading edge in most of spreading cells. As a whole, microtubules form a dense network in these cells. However, the radial cells contain bundles of microtubules, radiating from the perinuclear area or form circular arrays around the nucleus. The microtubule network is more dense under inhibitory treatment, than in control conditions. In the control culture the spherical cells display numerous small mitochondria (staining with Rhodamine 123). In the process of cell spreading some elongated mitochondria appear, most of them being localized in the perinuclear area. The mitochondria of cells with radial microtubule organization are directed towards the cell periphery, while in cells with circular bundles of microtubules the mitochondria are localized chaotically. Under DCCD treatment the mitochondria retain the staining for 2-3 h. In the spreading cells, round mitochondria may be distributed all over the cytoplasm. In the presence of sodium aside the mitochondria are not stained. However, by means of phase contrast microscopy some disoriented thread-shaped structures are observed, obviously corresponding to mitochondria. In the control conditions, lysosomes (stained with Acridine orange) in spreading cells are dispersed chaotically, all over the cytoplasm, or are localized in the perinuclear area. In the presence of sodium aside lysosomes are observed only in the perinuclear area. Under DCCD treatment lysosomes do not accumulate the dye. Thus, the cytoskeleton modification and changes in the properties of membrane organelles, induced by ATP-synthesis inhibitors, do not prevent attachment, spreading or cell polarization.

Adenosine Triphosphate↗
PubMedDate not supplied

Biliary cystadenocarcinoma with superficial spread to the extrahepatic bile duct.

We report a case of biliary cystadenocarcinoma of the liver with superficial spread to the extrahepatic bile duct. Preoperative endoscopic retrograde cholangiography revealed communication between a 4.5-cm cyst in segment 4 of the liver and the bile duct. From the findings obtained by peroral cholangioscopy and intraoperative cholangioscopy, the granular mucosa in the bile duct was diagnosed as superficially spreading cancer. The right posterior segmental bile duct and the right anterior segmental bile duct were resected at the point where the spread of cancer was no longer traceable and left lobectomy plus caudate lobectomy was carried out. This achieved radical resection, leaving the resected margin of the bile duct free from cancer. Histopathologically, well-differentiated papillary adenocarcinoma was found on the inner surface of the cyst, and the cancer had superficially spread from the cyst to the extrahepatic bile duct via the 2.5-mm diameter communication between the cyst and bile duct. The cancer was limited only to the mucosal layer all over the lesion. When performing radical surgery for biliary cystadenocarcinoma, it is recommended that cholangioscopy be performed to examine whether the cancer has superficial spread to the extrahepatic bile duct or not. Bile duct resection should be carried out, depending on the extent of the superficial spread, so that the resected margin of the bile duct is free from cancer.

Adult↗
PubMedDate not supplied

Methods of spread of velogenic viscerotropic Newcastle disease virus in the southern Californian epidemic of 1971-1973.

Data collected during the velogenic viscerotropic Newcastle disease (VVND) epidemic that occurred in southern California from 1971 to 1973 were analyzed to determine the methods of spread of the disease. Spread between chicken flocks was extensive and due mainly to the movement of live birds and mechanical transport of virus by man, especially by vaccination and poultry service crews. Spread to exotic birds was from contact with infected imported stock. Spread to other species was most probably through contact with infected chickens. Infection persisted in commercial chicken flocks because of intensive vaccination programs, heavy traffic and contact between layer operations, and the maintenance of multi-age flocks. These foci of infection probably led to spread of the disease to areas from which VVND had been eradicated several months before. There was no evidence of significant wind-borne spread of virus between flocks.

Air Microbiology↗
PubMed1999

Biochemical changes and gene expression following traumatic brain injury: Role of spreading depression.

The effects of spreading depression-like DC depolarizations on biochemical changes and gene expression were examined following trau-matic neocortical lesions, as induced by transcranial cold injury. The surrounding of traumatic cold lesions was characterized by increased glu-cose and lactate contents, without major disturbances of protein synthesis or energy state. A transient pH decrease by 0.4 units was noticed 1 h post-injury, which shifted towards alkaline values by 3 h. These changes were similar in animals with spontaneous spreading depression-like DC shifts (n = 14) and those without spreading depressions (n = 7), but there was a marked difference in the gene response. In injured animals without SD, only a short-lasting response of c-fos, junB, c-jun and MKP-1 mRNAs as well as c-Fos protein was bilaterally found in the piri-form cortex, and - with ipsilateral dominance - the dentate gyrus and hippocampal CA3/4 fields at 1 h after lesioning. In injure d animals with spreading depressions, on the contrary, a strong elevation was seen in layers II-IV and VI of the injury-remote ipsilateral cerebral cortex, which persisted over as long as 6 h. The expression of c-fos, junB and MKP-1 mRNAs was closely related to the time interval between the last spreading depression and the end of the experiments. Levels were highest shortly after transient DC shifts, and decreased thereafter mono-exponentially with half-lives of 48, 75 and 58 min for c-fos, junB and MKP-1 mRNAs, respectively. Thus, spreading depression is a prominent factor influencing the trauma-related gene response, but - in contrast to focal ischemia - it does not aggravate the metabolic dysfunction.

Journal Article↗
PubMed1992

Phospholipase activation during monocyte adherence and spreading.

Phospholipase activation is an important element in cellular signal transduction. In our study we investigated the role and regulation of phospholipase activation during human monocyte adherence and spreading. In human monocytes, phospholipase inhibition (with bromophenacyl bromide (BPB) or manoalide) impaired cell adherence and spreading. In contrast, neither cyclooxygenase/lipoxygenase inhibition nor platelet activating factor receptor blockade affected these responses. The impaired adherence and spreading induced by phospholipase inhibition with BPB could be partially reversed by the addition of nM levels of arachidonate (20:4(n - 6)). Dihomogammalinolenic acid (20:3(n - 6)) could substitute for arachidonate, but other polyunsaturated fatty acids were ineffective in this regard. The phospholipase inhibitor, BPB was selective in its effects on cellular phospholipase activities. BPB inhibited adherence/spreading-related and PMA-stimulated phospholipase activities, but not Ca2+ ionophore-stimulated phospholipase activity. To further probe for the role of Ca2+ in monocyte adherence and spreading, monocytes were loaded with MAPTAM (bis-(2-amino-5-methylphenoxy)-ethane-N,N,N',N', tetraacetic acid tetraacetoxymethyl ester), an EGTA analog. In contrast to phospholipase inhibition, intracellular Ca2+ chelation with MAPTAM did not affect monocyte adherence but did inhibit monocyte spreading. MAPTAM partially inhibited adherence/spreading-stimulated phospholipase activity, but did not inhibit PMA-stimulated phospholipase activity. These data suggest that human monocyte adherence and spreading may sequentially activate Ca(2+)-independent and then Ca(2+)-dependent phospholipases to release arachidonate. The activation of phospholipase and the release of arachidonate appear to be integral parts of the adhesion process.

Acetophenones↗
PubMed1991

Effects of warm air-drying and spreading on resin bonding.

The purpose of this study was to compare the effect on resin-to-enamel bonding produced by warm air from a hair dryer, and to correlate changes in resin bond strength with resin tag structure. Herculite-XR resin composite and Bondlite bonding resin were used. The three technique variables were the type of air used for drying, air dryer distance, and drying and spreading time. Control samples were dried and the bonding resin spread with a dental air syringe, whereas warm air from a hair dryer was used on the experimental samples. The bond strength (MPa) was determined in shear at a crosshead speed of 1 mm/min. Following bond strength evaluation, the teeth were immersed in 10% HCl for enamel dissolution and the resin tag structure was examined with the SEM. ANOVA analyses of shear bond strengths were performed. Warm air-drying and spreading for 15 seconds at 6 cm and 5 seconds at 6 cm respectively, produced statistically greater shear bond strengths (x = 20.4 +/- 4.4 MPa, P less than 0.05). The other drying time/distance combinations, including the control (x = 14.4 +/- 3.3 MPa), were not statistically different. Differences in resin tag structure were qualitatively evident under the SEM, with sharp tags produced by the warm air-drying and spreading techniques, compared to the blunt tags created by syringe air-drying and spreading. Warm air-drying and spreading significantly improved the bond strength. No apparent correlation exists between bond strength and tag length.

Air↗
PubMed1990

Spreading of cultured corneal epithelial cells on fibronectin and other extracellular matrices.

Previous investigations demonstrated that fibronectin is an essential adhesive glycoprotein for the corneal epithelial cells. Fibronectin mediates attachment and spreading of the corneal epithelial cells. However, it seems to be important to know the changes in cellular receptor activity in order to understand the interactions of corneal epithelial cells and underlying extracellular matrix. In this investigation, we studied the effects of various culture times and conditions on the receptor activity of rabbit corneal epithelial cells for fibronectin. The cultured cells were placed on tissue culture plates that were coated with various concentrations of four extracellular matrices: fibronectin, laminin and collagen types I and IV. Freshly isolated corneal epithelial cells without culture did not spread on fibronectin and laminin; they spread only on collagen types I and IV. When the epithelial cells were cultured for 12 h or more, they spread on fibronectin. However, the spreading of the cells on collagen types I and IV was the same regardless of the culture period (up to 20 h). Only a small number of epithelial cells spread on laminin at the highest concentration examined after culture for 12 h or more. Thus, the corneal epithelial cells responded differently to fibronectin, collagen types I and IV, and laminin. Perhaps the receptor for fibronectin appears when epithelial cells are cultured, but the receptor(s) for collagen types I and IV are always present on the cell surface of corneal epithelial cells.

Animals↗
PubMed1990

pH regulation in spread cells and round cells.

The aim of this work was to characterize the changes in pH regulation that lead to increased intracellular pH (pHi) in well-spread cells on tissue culture plastic relative to cells on a nonadhesive surface. Bicarbonate was not required for maintenance of a control steady state pHi or of the difference in pHi between round and spread cells. In the absence of bicarbonate, lowering the sodium content of the medium led to decreased pHi and elimination of the difference between round and spread cells. In the presence or absence of bicarbonate, adding ethylisopropyl amiloride lowered pHi and eliminated the difference between round and spread cells. Measurements of recovery from acute acidification in the absence of bicarbonate confirmed that Na+/H+ exchange was enhanced in spread cells. However, recovery from both acidification and alkalinization in the presence of bicarbonate showed that bicarbonate-dependent recovery in both directions, most likely due to sodium-dependent and -independent HCO3-/Cl- exchangers, was also stimulated in spread cells. We conclude that Na+/H+ exchange has a primary role in determining steady state pHi in 3T3 cells in serum and is responsible for the lower pHi in round cells. Bicarbonate-dependent pH regulatory mechanisms are also inhibited in round cells.

Amiloride↗
PubMedDate not supplied

Microtubule assembly in Friend erythroleukemia cells spread on fibronectin- and lectin-coated substrates.

A comparison was carried out between parental Friend Erythroleukemia cells (FLC, 745 A clone) and highly fibronectin (FN)-sensitive clones of FLC for their ability to adhere, spread and organize microtubular (MT) apparatus, when seeded on FN- or lectin-coated plastic substrates. While FN was able to induce the spreading only in the FN-sensitive FLC clones (further referred to as FF clones) and not in the parental 745 A cells, the lectins Concanavalin A (ConA) and Leukoagglutinin (LeuA) promoted the spreading of both 745 A and FF cells, with no differences between the two cell lines. Wheat germ agglutinin (WGA), instead, is almost ineffective in triggering cell spreading in both cell clones. The spreading of FLC, either 745 A or FF, on any of the ligands tested, is always accompanied by a massive reorganization of the MT apparatus of the cell. Possible mechanisms involved in the selective spreading effect, exerted by FN, are discussed.

Agglutinins↗
PubMedDate not supplied

In vitro inhibition of macrophage spreading by antigens and lymphokines: correlation with the footpad test and kinetics of inhibition.

As inhibition of spreading of mouse peritoneal macrophages is the basis for an in vitro test of cellular immunity, this test was used to investigate the correlation between in vitro and in vivo results and the kinetics of inhibition of spreading. BALB/c and NIH strain mice were immunized with human or bovine serum albumin or bovine gamma globulin. They displayed a positive footpad test when challenged with the specific antigen (21 days later). Peritoneal cells (PC) of mice with a strong footpad reaction were used for the spreading inhibition test. Intensity of spreading inhibition correlated well (r = -0.93) with that of the footpad reaction. Spreading inhibition had a cyclic pattern. A similar pattern was observed after incubation of PC with preformed lymphokines. The cyclic pattern was probably caused by a repeated action of lymphokines on spread macrophages, resulting in reversible and re-inducible inhibition.

Animals↗
PubMed1970

Stability of fatty acid monolayers and the relationship between equilibrium spreading pressure, phase transformations, and polymorphic crystal forms.

Force-area isotherms were obtained for hexadecanoic, octadecanoic, eicosanoic, and docosanoic acid monolayers at different compression rates. Equilibrium spreading pressures were determined both by monolayer collapse and by spreading from the bulk phase. Monolayers formed metastable phases at all pressures above their equilibrium spreading pressures and at all surface areas smaller than the surface areas at their equilibrium spreading pressures. These metastable phases collapsed to stable phases at the equilibrium spreading pressures of the fatty acids. Collapse phenomena and compression experiments at very slow compression rates suggested that a previously unrecognized phase transformation occurred at the equilibrium spreading pressure. The surface area at this phase transformation corresponded to the cross-sectional area of the C-form of the fatty acid crystal. Fatty acid monolayers at the phase transformations previously described by other workers had surface areas which were closely related to molecular areas in their A and B polymorphic crystal forms. These correlations indicated that molecular structure in saturated fatty acid monolayers was similar to molecular structure in fatty acid crystals.

Chemical Phenomena↗