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Introduction: Fibro-osseous lesion is a broad term for a diverse group of jaw and craniofacial disorders that are often painless, but grow progressively, if uncontrolled. They are characterized by the replacement of normal bone by fibrous connective tissue matrix displaying varying degrees of mineralization in the form of woven bone or cementum-like structures. Methods: Retrospective survey of the records of all patients seen between 2000 and 2013 at the department of Oral and Maxillofacial Surgery Clinic, Ahmadu Bello University Teaching Hospital, Zaria, Nigeria was undertaken. Results: A total of 104 patients were seen over the period of study. Of these, males comprised 40 and females comprised 64 giving a male to female ratio of 1:1.6. The age ranged from 4 years to 66 years and mean was 25.8 (13.21) years. There was no gender difference in terms of age (t = 1.78; p = 0.078). Fibrous dysplasia was the most common lesion and accounted for 60 (57.7%) of the cases and this was followed by ossifying fibroma (n = 39; 37.5%). Conclusion: Due to late presentation, the size of the lesion, the outcome is usually not good aesthetically, especially for maxillary lesions. [ABSTRACT FROM AUTHOR]

Bi 12 O 17 Cl 2 is a potential photocatalyst in practical applications due to its excellent photostability, visible light activity, and competitive bandgap energy. However, the fast recombination of photogenerated charge carriers makes it impractical for pollution mitigation. Recently, aggregated porphyrins have emerged as photosensitizers in light-dependent applications such as photocatalysis. Although Bi 12 O 17 Cl 2 and porphyrin can function as separate photocatalysts, their photocatalytic properties in terms of visible light adsorption, charge separation and transport, can be improved when they are combined to form heterostructure. In this study, rod-shaped aggregated 5,10,15, 20-Tetrakis (4-carboxyphenyl) porphyrin was synthesized by CTAB-assisted, self-assembly strategy and Bi 12 O 17 Cl 2 by a facile microwave method. The porphyrin and Bi 12 O 17 Cl 2 were combined to generate a series of x%Porphyrin@Bi 12 O 17 Cl 2 having 0.02% wt., 0.1% wt., 0.4% wt., 1% wt. and 10% wt. as compositions of porphyrin. The materials' photocatalytic degradation efficiency was tested on Rhodamine B dye as a representative pollutant. The best and worst performances were reported for 1%Porphyrin@Bi 12 O 17 Cl 2 and 10%Porphyrin@Bi 12 O 17 Cl 2 , respectively, which are 3.1 and 0.5 times increases in efficiency compared to pure Bi 12 O 17 Cl 2 . From the radical trapping experiment, electrons and superoxide were the dominant reactive species in the degradation process. The enhanced photocatalytic capability of the materials was attributed to the photosensitizing property of porphyrin and the heterojunction formation, which promotes the separation of photogenerated charge carriers. A plausible step-scheme (S-scheme) was proposed for the photocatalytic degradation mechanism. The S-scheme provided the high redox potential of the photogenerated charge carriers. The findings herein offer a new option for improving the photocatalytic performance of Bi 12 O 17 Cl 2 for environmental applications through the photosensitization strategy., (© 2023. The Author(s).)

Purpose: Digoxin, a major medication for heart disease, was recently reported to have immunosuppressive capacity. Here, we determined the immunosuppressive capacity of digoxin on the development of experimental autoimmune uveitis (EAU) and on related immune responses., Methods: The B10.A mice were immunized with interphotoreceptor retinoid-binding protein (IRBP) and were treated daily with digoxin or vehicle control. On postimmunization day 14, the mouse eyes were examined histologically, while spleen cells were tested for cytokine production in response to IRBP and purified protein derivative. The immunosuppressive activity of digoxin was also tested in vitro, by its capacity to inhibit development of Th1 or Th17 cells. To investigate the degenerative effect of digoxin on the retina, naïve (FVB/N × B10.BR)F1 mice were similarly treated with digoxin and tested histologically and by ERG., Results: Treatment with digoxin inhibited the development of EAU, as well as the cellular response to IRBP. Unexpectedly, treatment with digoxin suppressed the production of interferon-γ to a larger extent than the production of interleukin 17. Importantly, digoxin treatment induced severe retinal degeneration, determined by histologic analysis with thinning across all layers of the retina. Digoxin treatment also induced dose-dependent vision loss monitored by ERG on naïve mice without induction of EAU., Conclusions: Treatment of mice with digoxin inhibited the development of EAU and cellular immune response to IRBP. However, the treatment induced severe damage to the retina. Thus, the use of digoxin in humans should be avoided due to its toxicity to the retina.

Background: Mutations in LRRK2 are related to certain forms of Parkinson's disease and, possibly, to the pathogenesis of Crohn's disease. In both these diseases inflammatory processes participate in the pathogenic process. LRRK2 is expressed in lymphoid cells and, interestingly, Lrrk2 (-/-) mice were reported to develop more severe experimental colitis than their wild type (WT) controls. Here, we examined the possible involvement of LRRK2 in the pathogenesis of experimental autoimmune uveitis (EAU), an animal model for human uveitis, by testing Lrrk2 (-/-) mice for their capacity to develop this experimental eye disease and related immune responses., Methods: Lrrk2 (-/-) mice and their WT controls (C57Bl/6) were immunized with interphotoreceptor retinoid-binding protein (IRBP) and compared for their development of EAU, delayed type hypersensitivity (DTH) by skin tests, production of cytokines in culture, and expression of interferon (IFN)-γ, interleukin (IL)-17 and FoxP3 by spleen cells, using flow cytometry. Peritoneal macrophages were examined for their production of cytokines/chemokines in culture following stimulation with LPS or the oligodeoxynucleotide CpG. The Lrrk2 (-/-) and WT mice were also compared for their response to bovine serum albumin (BSA)., Results: The Lrrk2 (-/-) mice developed lower levels of EAU, DTH responses and cytokine production by lymphocytes than did their WT controls. Intracellular expression of IFN-γ and IL-17, by spleen cells, and secretion of cytokines/chemokines by activated peritoneal macrophages of Lrrk2 (-/-) mice trended toward diminished levels, although variabilities were noted. The expression levels of FoxP3 by Lrrk2 (-/-) spleen cells, however, were similar to those seen in WT controls. Consistent with their low response to IRBP, Lrrk2 (-/-) mice responded to BSA less vigorously than their WT controls., Conclusions: Lrrk2 deficiency in mice diminished the development of EAU and the related adaptive immune responses to IRBP as compared to the WT controls.

Purpose: Ligands for aryl hydrocarbon receptor (AHR), such as dioxins, are highly toxic. One such ligand, TCDD, was found to exert potent immunosuppressive capacities in mice developing pathogenic autoimmune processes, including EAU, but its toxicity makes it unusable for humans. A recently identified endogenous AHR ligand, ITE, is also immunosuppressive, but is nontoxic and could therefore be useful for therapy in humans. Here, we tested ITE for its capacity to inhibit EAU and related immune responses., Methods: EAU was induced in B10.A mice by immunization with interphotoreceptor retinoid-binding protein (IRBP; 40 μg) in CFA. Treatment with ITE was by daily intraperitoneal injection of 0.2 mg. Disease severity was assessed by both fundoscopy and histological examination. Draining lymph node cells were tested for proliferation by thymidine uptake and for cytokine production and release by ELISA. In addition, the intracellular expression of cytokines and Foxp3 was determined by flow cytometry. Serum antibodies were measured by ELISA., Results: Treatment with ITE efficiently inhibited the development of EAU in mice, as well as the cellular immune responses against IRBP and PPD. ITE treatment inhibited the expansion of both Th1 and Th17 subpopulations, as well as their release of the signature cytokines, IFN-gamma and IL-17. The treatment moderately increased, however, the proportion of Foxp3 expressing T-regulatory cells. Antibody production was not affected by the treatment., Conclusions: ITE, an endogenous AHR ligand, efficiently inhibits EAU development and related cellular immune responses. Being nontoxic, ITE may be considered for treatment of pathogenic immunity in humans.

Fetal alcohol spectrum disorder (FASD) occurs when pregnant mothers consume alcohol, causing embryonic ethanol exposure and characteristic birth defects that include craniofacial, neural and cardiac defects. Gastrulation is a particularly sensitive developmental stage for teratogen exposure, and zebrafish is an outstanding model to study gastrulation and FASD. Epiboly (spreading blastomere cells over the yolk cell), prechordal plate migration and convergence/extension cell movements are sensitive to early ethanol exposure. Here, experiments are presented that characterize mechanisms of ethanol toxicity on epiboly and gastrulation. Epiboly mechanisms include blastomere radial intercalation cell movements and yolk cell microtubule cytoskeleton pulling the embryo to the vegetal pole. Both of these processes were disrupted by ethanol exposure. Ethanol effects on cell migration also indicated that cell adhesion was affected, which was confirmed by cell aggregation assays. E-cadherin cell adhesion molecule expression was not affected by ethanol exposure, but E-cadherin distribution, which controls epiboly and gastrulation, was changed. E-cadherin was redistributed into cytoplasmic aggregates in blastomeres and dramatically redistributed in the extraembryonic yolk cell. Gene expression microarray analysis was used to identify potential causative factors for early development defects, and expression of the cell adhesion molecule protocadherin-18a (pcdh18a), which controls epiboly, was significantly reduced in ethanol exposed embryos. Injecting pcdh18a synthetic mRNA in ethanol treated embryos partially rescued epiboly cell movements, including enveloping layer cell shape changes. Together, data show that epiboly and gastrulation defects induced by ethanol are multifactorial, and include yolk cell (extraembryonic tissue) microtubule cytoskeleton disruption and blastomere adhesion defects, in part caused by reduced pcdh18a expression.