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Task allocation is a characteristic feature of social insects. This phenomenon is self-organized by workers in a colony without central instructions. Workers perform the necessary tasks while communicating and determining their colony's local situations or outside environments. They can also allocate the workload of the task to finish quickly. To explain the self-organized phenomenon, we develop a theoretical model that includes the local interaction mechanism among the workers. We extend the fixed response threshold model by introducing the interaction network among workers. The new model is called the interaction network response threshold model. This model analyzes the effects of the interaction network structure on the workload allocation mechanism using the Gini coefficient. We find that the network structure affects the information diffusion process, and the network features affect workload allocation. Our results indicate that communication among the workers in a colony is an essential system for workload allocation. [ABSTRACT FROM AUTHOR]

The present study attempts to elucidate the role of TRPV1 cation channel receptor on primary repair in an incision-wounded mouse cornea in vivo. Previous study revealed that blocking TRPV1 suppressed myofibroblast formation and expression of transforming growth factor β1 (TGFβ1) in cultured keratocytes or ocular fibroblasts. Male C57BL/6 (wild-type; WT) mice and male C57BL/6 Trpv1-null (KO) mice incurred a full-thickness incision injury (1.8 mm in length, limbus to limbus) in the central cornea of one eye with a surgical blade under general and topical anesthesia. The injury was not sutured. On days 0, 5, and 10, the eyes were enucleated, processed for histology, immunohistochemistry, and real-time RT-PCR gene expression analysis to evaluate the effects of the loss of TRPV1 on primary healing. Electron microscopy observation was also performed to know the effect of the loss of TRPV1 on ultrastructure of keratocytes. The results showed that the loss of Trpv1 gene delayed closure of corneal stromal incision with hindered myofibroblast transdifferentiation along with declines in the expression of collagen Ia1 and TGFβ1. Inflammatory cell infiltration was not affected by the loss of TRPV1. Ultrastructurally endoplasmic reticulum of TRPV1-null keratocytes was more extensively dilated as compared with WT keratocytes, suggesting an impairment of protein secretion by TRPV1-gene knockout. These results indicate that injury-related TRPV1 signal is involved in healing of stromal incision injury in a mouse cornea by selectively stimulating TGFβ-induced granulation tissue formation. [ABSTRACT FROM AUTHOR]

Abstract Background. We examined the effects of interferon-γ (IFN-γ) on protein production of extracellular matrix (ECM) components in cultured human subconjunctival fibroblasts or those stimulated by exogenous transforming growth factor β1 (TGFβ1). IFN-γ reportedly up-regulates Smad7, an inhibitory mediator of TGFβ-Smad signaling, and blocks TGFβ effects. Methods. Proliferation and migration as well as the ultrastructure of these cells were examined in the presence and absence of IFN-γ. Cell migration was examined using an in vitro wound healing model in monolayer fibroblast cultures. Results. The results showed that IFN-γ reduced ECM production in normal subconjunctival fibroblasts, as well as in those treated with TGFβ1, below the control levels. IFN-γ had no effect on cell proliferation and fibroblast ultrastructure. On the other hand, IFN-γ delayed defect closure in monolayer cell sheets in a dose-dependent manner. Immunohistochemistry also revealed that the addition of IFN-γ attenuated the translocation of Smads2/4 into the nuclei of TGFβ1-treated subconjunctival fibroblasts. Conclusion. These findings suggest that IFN-γ may be clinically effective in attenuating excessive ECM accumulation in conjunctiva after ocular surgery and in the presence of inflammatory ocular surface disorder. IFN-γ modulates the Smads2/4 pathway of TGFβ1 signal transduction toward the up-regulation of ECM components. [ABSTRACT FROM AUTHOR]

Purpose: To examine immunohistochemically whether extracellular matrix (ECM) of the filtering bleb and of cultured human subconjunctival fibroblasts contains latent TGFβ binding protein-1 (LTBP-1) and TGFβ. Methods: An enucleated human eye that had undergone trabeculectomy and cultured human subconjunctival fibroblasts were processed for light microscopic immunohistochemistry. Antibodies against LTBP-1, collagen types, fibrillin-1 and TGFβs were used. TGFβ1 was located by detecting β1-latency associated peptide (LAP). Results: LTBP-1, β1-LAP and fibrillin-1 were all located in the subepithelial ECM as well as in the basal epithelial cells of the conjunctiva over the filtering bleb. TGFβ2 and β3 were immunolocated to epithelium and/or fibroblasts/keratocytes. ECM deposited in confluent fibroblast cultures was positive for β1-LAP, LTBP-1 and fibrillin-1, whereas sparse cells were negative. Conclusions: LTBP-1, β1-LAP and fibrillin-1 are co-localized to the ECM of the filtering bleb and of cultured conjunctival fibroblasts. Both conjunctival epithelium and fibroblasts are considered to be the source of TGFβ in healing bleb. ECM secreted by in vivo and in vitro subconjunctival fibroblasts may works as a scavenger or repository of TGFβ. [ABSTRACT FROM AUTHOR]

Background: We examined the immunolocalization of proto-oncogene products, including c-Fos and c-Jun, in the rat cornea during epithelial and stromal wound healing after simple epithelial ablation, penetrating injury or alkali burn. · Methods: Eighty-four male Wistar rats were divided into three groups and subjected to treatments as follows: (a) ablation of central corneal epithelium leaving basement membrane intact, (b) alkali burn in the central cornea with 1 N NaOH and (c) penetrating injury at the central cornea. The affected eyes were then enucleated after various intervals of healing. The frozen sections were immunohistochemically stained with the antibodies against proto-oncogene products. · Results: c-Fos- and c-Jun-immunoreactive cells were detected in the epithelium around the epithelial defect from 60 to 120 min after these treatments. The distribution of these cells were varied in these three types of injury. The immunoreactivities for these proteins were also detected in keratocytes after epithelial ablation. In the corneas with alkali burn, the immunoreactivities were detected in the keratocytes in the whole corneal stroma, and these immunoreactions were stronger than those observed in simple epithelial ablation. In the corneas with penetrating injury, such immunoreaction was seen only in keratocytes around the wound. · Conclusion: These findings indicate that activator protein 1-mediated transcriptional activation for epithelial migration is initiated in the early phase after each injury, and that stromal keratocytes are also transcriptionally activated not only by alkali burn or penetrating injury but also by simple epithelial ablation in which basement membrane was not affected. [ABSTRACT FROM AUTHOR]

· Purpose: We used immunohistochemistry to characterize cellular and proteinaceous deposits on the surfaces of explanted posterior chamber intraocular lenses (PC-IOLs). · Methods: A total of 30 PC-IOLs were immunostained for the α- or β-subunits of prolyl 4-hydroxylase, which is involved in collagen biosynthesis; cellular fibronectin; αB crystalline; and CD68, a macrophage marker, to characterize the cellular deposits that adhere to the IOL surfaces and to evaluate the distribution of cells involved in the deposition of extracellular matrix on IOLs. · Results: Cellular or proteinaceous deposits were observed on all 30 PC-IOLs. Cells that showed positive staining for αB crystallin were classified as lens epithelial cells; CD68-positive cells were considered to be of macrophagic origin. Positivity for cellular fibronectin, including the macrophages and related cells, appeared to be responsible for the accumulation of fibronectin on the surfaces of PC-IOLs. Prolyl 4-hydroxylase-positive cells were involved in the deposition of collagen on PC-IOLs. · Conclusion: Immunohistochemical study revealed that macrophages, foreign-body giant cells, and lens epithelial cells adhered to explanted PC-IOLs. Such adherent cells are responsible for the deposition of extracellular matrix on the surfaces of PC-IOLs and may regulate the assembly of the extracellular matrix, influencing the biocompatibility of PC-IOLs. [ABSTRACT FROM AUTHOR]

• Background: The excessive accumulation of extracellular matrix (ECM) with the repopulation of fibroblasts may lead to an unsuccessful outcome of glaucoma filtering surgery. We examined the immunolocalization of ECM components and prolyl 4-hydroxylase, an enzyme involved in collagen biosynthesis, in cultured Tenon's capsule fibroblasts (TCFs) of humans to evaluate the production of ECM in the cells. • Methods: We used light microscopy to evaluate the immunolocalization of prolyl 4-hydroxylase and ECM components, collagen types I, III, and IV, cellular fibronectin, and laminin in TCFs. Ultrastructural localization of the enzyme was also evaluated by electron microscopy. • Results: Immunoreactivity with monoclonal antibodies against the α and β subunits of the enzyme or with the polyclonal antibody against it was detected in the cytoplasm of the cells in a fine granular pattern, indicating its localization in the indoplasmic reticulum (ER). Immunoreactivity for the enzyme was detected in the cisternae of the ER on electron microscopy. Types I and III collagen reactivities were also observed in the cytoplasm in a fine granular pattern. T reactivity was present diffusely on the cell surface. The distribution of laminin reactivity in the cytoplasm resembled that of types I and III collagen. Cellular fibronectin reactivity was observed in the ECM in a reticular pattern. • Conclusion: Prolyl 4-hydroxylase was located in the cisternae of the ER. TCFs produced a variety of ECM components in vitro. The results provide insight into the fibrotic process during scar formation at the site of a bleb following filtering surgery. [ABSTRACT FROM AUTHOR]

• Background: Minoxidil is an inhibitor of lysyl hydroxylase, an enzyme involved in collagen production, and decreases collagen production in vitro. We investigated the in vitro effects of minoxidil on behavior such as proliferation and migration of rabbit subconjunctival fibroblasts (SCFs). The ultrastructural effect of the drug on SCFs was also examined. • Methods: Proliferation of SCFs and closure of the defect produced in monolayer cultures in the presence or absence of minoxidil was studied. The ultrastructure of SCFs treated with minoxidil was also examined. • Results: Minoxidil inhibited SCF proliferation and the closure of the defect produced in monolayer cell sheets. Ultrastructural observations revealed extensive areas of irregularly dilated endoplasmic reticulum in cells treated with minoxidil, indicating the accumulation of protein, probably underhydroxylated collagen precursors, in the cisternae of endoplasmic reticulum. • Conclusions: The results indicated that minoxidil attenuated cellular activities of SCFs such as proliferation and migration in vitro. The exact mechanism of the inhibitory effects of minoxidil on these cellular activities is unknown. The findings suggest that the drug might help to prevent bleb scarring after glaucoma filtering surgery. [ABSTRACT FROM AUTHOR]

⊎ Background: The spreading of epithelium is critical in the healing of corneal wounds. Such epithelial spreading requires the continuous production of protein and glycoprotein. To determine whether collagen production is required for the spreading of corneal epithelium, we studied the effects of inhibitors for collagen production on spreading of corneal epithelium in vitro. ⊎ Methods: We examined the effect of two proline analogs, l-azetidine 2-carboxylic acid and cis-hydroxyproline, a prolyl hydroxylase inhibitor, ethyl-3,4-dihydroxybenzoate, and a lysyl hydroxylase inhibitor, minoxidil, on the spreading of epithelium of organ-cultured rabbit cornea. ⊎ Results: Both analogs and inhibitors inhibited epithelial spreading in a dose-dependent manner. ⊎ Conclusion: These observations indicate that collagen production may be involved in the spreading of corneal epithelium. [ABSTRACT FROM AUTHOR]

• Purpose: To investigate the effect of fibrostatin C, a prolyl 4-hydroxylase (PH) inhibitor produced by Streptomyces catenutae subsp. griseospora, on type I collagen secretion by human Tenon's capsule fibroblasts (TCFs) in vitro, as an indication of the potential therapeutic efficacy of this compound in antifibrotic therapy after glaucoma filtering surgery. • Methods: The concentrations of type II procollagen COOH-terminal peptide (PIP) in culture medium or cell lysate were determined by immunoassays. For comparison with its effect on PIP secretion, we determined the effects of the agent on the secretion of other peptides, including laminin, vitronectin receptor, and a metalloproteinase inhibitor. The expression of collagens I and 111, fibronectin, and PH by TCFs was examined by immunohistochemistry, and cellular ultrastructure was evaluated by transmission electron microscopy. • Results: Fibrostatin C (50 μM) significantly reduced the concentration of PIP in culture medium and increased its concentration in the cell lysate in a dose-dependent manner, but it had no effect on the secretion of other peptides. Cell viability and proliferation were not affected by fibrostatin C. Fibrostatin C also increased the number of cytoplasmic granules immunoreactive with antibodies to collagen I or III, but had no effect on fibronectin or PH immunoreactivity. Ultrastructurally, cisternae of the endoplasmic reticulum were dilated in fibrostatin C-treated TCFs, consistent with the retention of underhydroxylated collagen precursors in this organelle. • Conclusions: Fibrostatin C inhibits the secretion of type I collagen by cultured TCFs. This agent may thus prove therapeutically beneficial for inhibiting the excess fibrosis in the wound of filtering surgery. [ABSTRACT FROM AUTHOR]