Role of solution concentration in formation kinetics of bromide perovskite thin films during spin-coating monitored by optical in situ metrology.

Optoelectronic devices based on metal halide perovskites continue to show a improved performance, and solution-based coating techniques pave the way for large-area applications. However, not all parameters influencing the thin film formation process of metal halide perovskites are identified and entirely rationalised over their full compositional range, thus hampering optimised thin film fabrication. Furthermore, while the perovskite deposition via spin-coating and annealing is an easily accessible technique, more profound insights into the chemical formation process are still lacking. Varying the precursor solution concentration is commonly used to vary the resulting thin film thickness. This study shows that varying the precursor solution concentration also affects the thin film morphology and optoelectronic quality. Hence, we herein investigate the influence of the precursor solution concentration on the formation process of a pure bromide-based triple cation perovskite (Cs0.05MA0.10FA0.85PbBr3) by fiber-based optical in situ measurement. During the spin-coating process, in situ UV-vis and PL measurements reveal formation kinetics are strongly dependent on the concentration. Furthermore, we identify delayed nucleation and retarded growth kinetics for more concentrated precursor solutions. In addition, we quantify the shifting chemical equilibrium of colloidal pre-coordination in the precursor solution depending on concentration. Namely, colloids are pre-organised to a higher degree and higher-coordination lead-bromide complexes tend to form in more concentrated precursor solutions. Thus, the modified solution chemistry rationalises retarded perovskite formation kinetics and highlights the precursor concentration as an influential and optimisable parameter for solution-based thin film deposition.

Soft tissue augmentation of ridge defects in the maxillary anterior area using two different methods: a randomized controlled clinical trial.

OBJECTIVES: To test whether or not vascularized interpositional periosteal-connective tissue grafts are as successful as free subepithelial connective tissue grafts in augmenting volume defects in the anterior maxilla. MATERIAL AND METHODS: Twenty subjects with Seibert class 1 ridge defects in the anterior maxilla were randomly, equally assigned to augmentation by vascularized interpositional periosteal-connective tissue graft (test) or free subepithelial connective tissue graft (control). Clinical periodontal parameters at teeth adjacent to the gap were recorded, and conventional impressions were taken prior to surgery (baseline = t(0)) and 1 (t(1)), 3 (t(3)) and 6 (t(6)) months after surgery. The casts were optically scanned, digitized and analyzed for ridge contour changes in the augmented area. Data were subjected to nonparametric statistics. RESULTS: The contour changes in labial distance between baseline and follow-up for the control group were (median, range) 1 mm, 0.37-1.45 (t(0)-t(1)); 1.18 mm, 0.39-1.40 (t(0)-t(3)); and 0.63 mm, 0.28-1.22 (t(0)-t(6)) and for test group 1.21 mm, 0.74-2.47 (t(0)-t(1)); 1.26 mm, 0.50-1.71 (t(0)-t(3)); and 1.18 mm, 0.16-1.75 (t(0)-t(6)). Significantly less shrinkage of the graft was observed in the test group after 6 months (P = 0.03). Clinical periodontal parameters at the neighboring teeth were stable over the follow-up period and did not differ between groups. CONCLUSIONS: Augmentation of single tooth gaps with moderate ridge defects in the anterior maxilla was successfully performed using both techniques. However, after 6 months, sites treated by the pediculated graft were superior in maintaining the initially augmented volume and showed less shrinkage of the graft. This could be attributed to better perfusion of the pediculated graft.

Multifocal eosinophilic granuloma with sequential periodontitis-like lesions.

Eosinophilic granuloma (EG) is the localized and mildest form of the triad commonly known as Langerhans cell histiocytosis. This report describes a case manifesting itself as a periodontal problem with the localized osseous lesions in jawbones which was first diagnosed as early-onset periodontitis. Later on, the diagnosis of EG was established, relying on histopathological and immunohistochemical evaluations. Immunohistochemical findings confirm that a minor component of cell aggregates is phenotypically related to Langerhans cells among the sheet-like accumulations of histiocytes and eosinophils. The aetiology of the disease remains largely unknown. Although surgical curettage of lesions is usually effective in treatment of EG of bone, corticosteroids might be used as an adjunctive. This multifocal case of EG stresses the importance of clinical follow-up examinations, since the sequential lesions appear with irregular intervals, and this may cause diagnostic problems as well as a delay in starting the treatment regimen.

Immunohistochemical characterization of lymphocyte subsets in chronic adult periodontitis.

It is well known that interactions between microbial dental plaque and the host immune system play a major role in the etiopathogenesis of periodontal disease. The aim of the present study was to analyze the phenotypic properties of gingival T lymphocytes and subsets in patients with chronic inflammatory adult periodontitis (AP) showing various degrees of inflammation and to relate the results to the immunopathogenesis of AP. Gingival biopsies were obtained from patients aged between 26 and 52 yr who were grouped according to gingival index scores (GI) of 1, 2, and 3. Using immunohistochemical techniques, T cells (CD2+), T-helper cells (CD4+) and T-suppressor cells (CD8+) were identified in three well-defined areas of the biopsy samples. Moreover, peripheral blood was collected from the same patients, and relative counts of B cells (CD19+), HLA-DR+ cells and IL-2R+ cells as well as CD3+, CD4+, CD8+ cells were determined using three color flow cytometry. While the blood results were found to be within the normal ranges, the relative counts of CD4+ cells showed statistically significant decreases as the GI score increased. Similarly, the CD4+/CD8+ ratio also decreased. Moreover, gingival T lymphocyte and subset counts appeared to be related to the severity of gingival inflammation. Particularly, CD4+ cells showed a significant increase with the GI score. Furthermore, the CD4+/CD8+ ratio beneath the pocket epithelium was apparently correlated with increasing GI score (p < 0.05). The cytotoxic effect of CD8+ cells seems to be more prominent at the local level while the suppressor effect is more active systematically. This means that the price of systemic protection appears to be local destruction.

Ho:CaF(2) solid-state saturable-absorber Q switch for the 2-µm Tm,Cr:Y(3)Al(5)O(12) laser.

The holmium-doped calcium fluoride (Ho:CaF(2)) crystal was shown to be an effective solid-state saturable-absorber Q-switch for a flash-lamp-pumped Tm,Cr:Y(3)Al(5)O(12) laser at 2.017 µm. With a 1-cm-thick Ho(0.5%),Er(5%):CaP(2) saturable absorber and a 6.3% output coupler, a single Q-switched laser pulse of 51 mJ in energy and 60 ns in duration was obtained at a flash-lamp input energy of 85 J. With a 14.6% output coupler, a typical Q-switched laser pulse of 84 mJ and 82 ns was observed.

Metabolism and tumorigenicity of 7-, 8-, 9-, and 10-fluorobenzo(a)pyrenes.

The skin tumor-initiating activities of 7-, 8-, 9-, and 10-fluorobenzo(a)pyrenes have been compared to that of benzo(a)pyrene in female Sencar mice after 16 weeks of promotion with 12-O-tetradecanoylphorbol-13-acetate. Single initiating doses of 200 or 400 nmol of each hydrocarbon were tested, and the mice were treated twice weekly with 3.2 nmol of the promoter. Under these conditions, benzo(a)pyrene caused an average of 2.9 and 5.7 papillomas/mouse, respectively, whereas none of the four fluorinated hydrocarbons had significant tumor-initiating activity. Examination of the hepatic metabolism of 7- and 8-fluorobenzo(a)pyrene revealed that a 7,8-dihydrodiol was not detected as a metabolite; thus, the bay-region diol-epoxide pathway known to be responsible for the tumorigenic activity of benzo(a)pyrene is blocked. Although 7,8-dihydrodiols are formed from 9- and 10-fluorobenzo(a)pyrene, these dihydrodiols with fluorine substituted on the 9,10-double bond may not be converted to diol-epoxides by the cytochrome P-450 system, or such fluorinated 7,8-diol-9,10-epoxides may not be tumorigenic.