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Background: The alveolar process is a tooth-dependent structure, and hence, removal of teeth results in the alteration of alveolar process. To alter bone remodeling after dental extraction, various techniques have been put forward for ridge preservation. Aim: The aim of this study is to evaluate and compare the changes of hard and soft tissues in postextraction socket after the application of bone graft material. Materials and Methods: Healthy patients of sample size of 40 were selected who underwent the extraction of anterior tooth irrespective of the arch, from premolar of one side to another, with the exception of incisors in mandible. Twenty patients were randomly selected as the control group and other 20 as the experimental group using an allograft bone material, i.e., beta-tricalcium phosphate to fill the socket. Cone-beam computed tomography (CBCT) was done as baseline preoperative and postoperative at 14 weeks after the extraction. CBCTs data help in recording linear and volumetric measurements which was performed by calibrated examiners to record all the measurements. After measurements, digital planning of dental implants was performed. Results: Forty participants were selected, in which 20 patients each were as the experimental and control groups. No significant difference was found at basal line at any of the cases. At follow-up of 14 weeks, statistical significance was seen in buccal and lingual plate height in the experimental group, and no significant difference was seen in the control group.(P = 0.023). Conclusions: This study clearly points out that an alveolar ridge preservation technique provides therapeutic benefit by limiting bone resorption in comparison to extraction alone.

We present the design of a compact 5-mode division (de)multiplexer based on silicon-on-insulator waveguides for on-chip optical interconnects. The configuration consists of two coupled sections where each section comprises of two collocated asymmetric directional couplers to couple light from two input waveguides carrying independent signals into two TE modes (TE1, TE2 or TE3, TE4) of an interconnect trunk waveguide. For coupling into the TE0 mode of the trunk waveguide, an adiabatic taper is used to connect a fifth input waveguide. The proposed design with collocated directional couplers offers an advantage of a small footprint compared to sequential designs. The total coupling length of the device for multiplexing TE1 to TE4 modes is only 38.89 $\mu $ m. In addition, the device exhibits low insertion loss ~0.24 dB and crosstalk better than −33 dB at the design wavelength of 1550 nm.

Sexual and gender minority (SGM) individuals include, but are not limited to, those who identify as lesbian, gay, bisexual, transgender, and queer (LGBTQ). LGBTQ individuals are considered a marginalized and at-risk population, facing significant health care inequities when compared with heterosexual and cisgendered (ie, "gender-conforming") populations. They are more likely than heterosexual and cisgendered individuals to experience discrimination, bias, and dissatisfaction with the medical system. This article provides a broad overview of systemic inequalities confronting SGM patients.

We propose the design of a nonvolatile, low-loss optical phase shifter based on optical phase change material (O-PCM). The optical phase change material Ge2Sb2Se4Te1 (GSST), which exhibits low loss at telecommunication wavelength $1.55~\mu \text{m}$ as compared to other commonly used O-PCMs, is used in this work as the active material. Instead of direct interaction of the waveguide mode with the O-PCM, the design utilizes coupling between the primary SiN strip waveguide and a waveguide formed by O-PCM, in its amorphous state. The phase matching in the amorphous state inhibits the interaction of the waveguide mode with GSST in its highly lossy crystalline state resulting in low loss operation. Due to a high differential refractive index between the two states of GSST, the design requires a very small length of the phase shifter to accumulate the desired phase difference. The overall response of the Mach-Zehnder Interferometer (MZI) configuration using the designed phase shifter shows that the design can be used to obtain optical switching with a very small insertion loss and crosstalk over the entire C-band.

A compact seven-channel hybrid mode- and polarization-division multiplexer based on a silicon-on-insulator (SOI) waveguide platform is proposed for on-chip optical interconnects. Three independent signals are coupled into the T E 0 , T M 0 , and T E 1 mode of a three moded waveguide using a taper, a polarization beam splitter, and an asymmetric directional coupler in the first coupler section. In the adiabatically connected second and third sections, two collocated asymmetric directional couplers are used to couple two TE modes ( T E 2 , T E 3 ) and two TM modes ( T M 1 , T M 2 ) to reduce the footprint of the device. A coupling length of ∼ 44.29 µ m is achieved with low insertion loss < 0.09 d B and crosstalk better than − 30 d B at the designed wavelength of 1.55 µm.

In this paper, we propose the use of a coaxial fiber as a suitable first order dispersive medium to achieve pulse repetition rate multiplication by use of the temporal Talbot effect. A design optimization of the coaxial fiber is discussed to achieve first order dispersion over a desired bandwidth. Pulse repetition rate multiplication is demonstrated by simulating the propagation of a Gaussian pulse train through the coaxial fiber using analytical expressions. The results are compared with those obtained in an ideal first order dispersive medium and by use of the conventional single mode fiber.

The paper reports on the design of a silicon photonic TM-pass polarizer intended for photonic integrated circuits with a high component density. The device, whose design is compliant with the technological constraints imposed by a typical state-of-the-art silicon photonic process, exhibits a record IL of 0.05 dB @ 1.55 μm, a high ER of 38 dB @ 1.55 µm, and a broadband operation with IL 30 dB over 200 nm covering the S, C, and L bands.

We present the design of an asymmetric slot waveguide to facilitate selective TM mode coupling from a strip waveguide as basic building block of a TM-pass polarizer with record IL of 0.05 dB @ 1.55 μm.

Transgender individuals may transition to their identified gender through social, hormonal, and procedural methods by using a multidisciplinary team of health care providers, including dermatologists. In this review, we discuss the medical and aesthetic dermatologic needs related to the transitioning of transgender patients and provide therapeutic and procedural recommendations. In addition to routine cutaneous conditions, dermatologists may need to treat hormonal therapy–related complications. Acumen for genital dermatology and familiarity with gender reassignment surgery is important for the dermatologist caring for a transgender patient. From a structural standpoint, transgender beauty poses a unique aesthetic task. We identify key differences in the facial structure and physique of males versus those of females. Dermatologists may have a tremendous impact on the lives of transgender individuals who seek to realize their gender identity.

Design of electro-optic ON-OFF switches based on well-known phase change material Ge2Sb2Te5(GST) is presented. The electro-optic switch is achieved by implementing by co-directional coupling between a 220 nm thick silicon nanowire and a silicon waveguide topped with ITO-GST-ITO layers at the 1.55μm wavelength. By introducing the electric field via the ITO electrodes, the GST layer can be changed between the amorphous and crystalline states. As the modal loss in the crystalline state is much higher than the amorphous state, through a rigorous modal analysis of the coupled silicon nanowire and GST waveguide by using the finite element method, the optimal ITO spacing is obtained at 75nm which is less sensitive to device parameter variations and thus offering better tolerances. The GST thickness is also optimized for the phase matching point at 25 nm in order to efficiently transfer power from silicon nanowire to GST waveguide to attain the OFF state. Once the device is phase matched in crystalline state, the power in the amorphous state will pass with very little interaction with the GST waveguide resulting in an ON state. The Eigenmode Expansion Method of Fimmprop is used as a junction analysis approach to calculate the optical power coupling efficiencies to the output silicon nanowire. The extinction ratio of the electro-optic switch and insertion loss in ON state at phase matching can be obtained as a function of the device length. A compact 1.75 μm long device shows a high extinction ratio of 22 dB with an insertion loss of only 0.56 dB.

An interferometric refractive index sensor based on use of a fiber segment between two concatenated LPGs as the sensing probe is proposed. A sensitivity of 670 nm/RIU can be obtained in the refractive index range of 1.33 to 135.

Ingredients found in the nail cosmetic industry, including but not limited to methacrylate and acrylate monomers, formaldehyde, and toluene sulfonamide-formaldehyde resin, can incite allergic contact dermatitis. An eczematous outbreak presents on areas surrounding the nail plate and may spread through contact transfer of the allergen, commonly to the face and neck. Even components that were originally deemed nonsensitizing, such as the ubiquitous cyanoacrylate adhesive family, have been found to be allergenic. They do not, however, cross-react with methacrylates and acrylates. Alternative options for individuals with allergic contact dermatitis reactions to these ingredients can be avoidance of these procedures or use of products that are "3, 4, 5 free" in which the common allergens dibutyl phthalate, toluene, and formaldehyde are absent. In cases where strengthening of the nail is the sole purpose, nail wraps or preformed nails can be applied for non-cyanoacrylate-sensitive individuals.

Background: Atopic dermatitis (AD) is classified as extrinsic and intrinsic, representing approximately 80% and 20% of patients with the disease, respectively. Although sharing a similar clinical phenotype, only extrinsic AD is characterized by high serum IgE levels. Because most patients with AD exhibit high IgE levels, an ‘‘allergic’’/IgE-mediated disease pathogenesis was hypothesized. However, current models associate AD with T-cell activation, particularly TH2/TH22 polarization, and epidermal barrier defects. Objective: We sought to define whether both variants share a common pathogenesis. Methods: We stratified 51 patients with severe AD into extrinsic AD (n 5 42) and intrinsic AD (n 5 9) groups (with similar mean disease activity/SCORAD scores) and analyzed the molecular and cellular skin pathology of lesional and nonlesional intrinsic AD and extrinsic AD by using gene expression (real-time PCR) and immunohistochemistry. Results: A significant correlation between IgE levels and SCORAD scores (r 5 0.76, P

Current atopic dermatitis (AD) models link epidermal abnormalities in lesional skin to cytokine activation. However, there is evolving evidence of systemic immune activation and detectable abnormalities in nonlesional skin. Because some of the best single correlations with severity (Scoring of AD, or SCORAD) are detected not only in lesional but also nonlesional skin and blood, more complex biomarker models of AD are needed. We thus performed extensive biomarker measures in these compartments using univariate and multivariate approaches to correlate disease biomarkers with SCORAD and with a combined hyperplasia score [thickness and keratin 16 (K16) mRNA] at baseline and after cyclosporine A treatment in 25 moderate to severe AD patients. Increases in serum cytokines and chemokines (IL-13, IL-22, CCL17) were found in AD versus healthy individuals and were reduced with treatment. SCORAD correlated with immune (IL-13, IL-22) and epidermal (thickness, K16) measures in lesional and, even more strongly, in nonlesional AD. Serum cytokines also had higher correlations with nonlesional markers at baseline and with treatment. Multivariate U statistics improved baseline and treatment-response SCORAD correlations. Nonlesional models showed the strongest correlations, with further improvement upon integration of serum markers. Even better correlations were obtained between biomarkers and the hyperplasia score. Larger cohorts are needed to confirm these preliminary data.

This paper reports on the design optimization of compact optical ON-OFF switches based on a GST-clad silicon rib waveguide and compares it to a GST-clad silicon nanowire at the telecommunication wavelength 1.55 µm. Effective index and modal loss of the quasi-TE modes are calculated by a full-vectorial H-field finite element method. It shows that the electro-refraction effect-based switch may not be viable because of the higher modal loss in the GST crystalline state. On the other hand, the larger modal loss difference between GST amorphous and crystalline states would be more suitable for an electro-absorption type switch design. The effect of silicon slab thickness, silicon core width, and GST layer thickness for both the waveguides are presented. As the presence of the GST layer modifies the mode field profiles, so the incurring coupling loss at the butt-coupled junctions between the input/output silicon waveguide and Si-GST waveguide are also calculated by using the least squares boundary residual method. These results show that the GST-clad silicon rib waveguide with a 500-nm-wide silicon core, 60-90 nm thick silicon slab, and 15-25 nm thick GST layer is the optimal self-sustained switch design. In this case, a very compact, 2-5 µm long device is expected to show an extinction ratio of more than 20 dB with the total insertion loss of only 0.36 dB.

Background Atopic dermatitis (AD) is the most common inflammatory disease. The prevalence of allergic contact dermatitis to allergens (eg, fragrance) is higher in patients with AD, despite a trend toward weaker clinical allergic contact dermatitis reactions. The role of the AD skin phenotype in modulating allergic sensitization to common sensitizers has not been evaluated. Objective We sought to investigate whether patients with AD have altered tissue immune responses on allergen challenge. Methods Gene expression and immunohistochemistry studies were performed on biopsy specimens from 10 patients with AD and 14 patients without AD patch tested with common contact allergens (nickel, fragrance, and rubber). Results Although 1085 differentially expressed genes (DEGs) were commonly modulated in patch-tested skin from patients with AD and patients without AD versus control skin, 1185 DEGs were uniquely altered in skin from patients without AD, and only 246 DEGs were altered in skin from patients with AD. Although many inflammatory products (ie, matrix metalloproteinase 12/matrix metalloproteinase 1/S100A9) were upregulated in both groups, higher-magnitude changes and upregulation of interferon responses were evident only in the non-AD group. Stratification by allergen showed decreased expression of immune, T H 1-subset, and T H 2-subset genes in nickel-related AD responses, with increased T H 17/IL-23 skewing. Rubber/fragrance showed similar trends of lesser magnitude. Negative regulators showed higher expression in patients with AD. Conclusions Through contact sensitization, our study offers new insights into AD. Allergic immune reactions were globally attenuated and differentially polarized in patients with AD, with significant decreases in levels of T H 1 products, some increases in levels of T H 17 products, and inconsistent upregulation in levels of T H 2 products. The overall hyporesponsiveness in skin from patients with background AD might be explained by baseline immune abnormalities, such as increased T H 2, T H 17, and negative regulator levels compared with those seen in non-AD skin.

Background Allergic contact dermatitis (ACD) is the most common occupational disease. Although murine contact hypersensitivity provides a framework for understanding ACD, it carries important differences from its human counterpart. Unlike the contact hypersensitivity model, which is induced by potent sensitizers (ie, dinitrofluorobenzene), human ACD is induced by weak-to-moderate sensitizers (ie, nickel), which cannot induce reactions in mice. Distinct hapten-specific immune-polarizing responses to potent inducers were suggested in mice, with unclear relevance to human ACD. Objective We explored the possibility of distinct T-cell polarization responses in skin to common clinically relevant ACD allergens. Methods Gene-expression and cellular studies were performed on common allergens (ie, nickel, fragrance, and rubber) compared with petrolatum-occluded skin, using RT-PCR, gene arrays, and immunohistochemistry. Results Despite similar clinical reactions in all allergen groups, distinct immune polarizations characterized different allergens. Although the common ACD transcriptome consisted of 149 differentially expressed genes across all allergens versus petrolatum, a much larger gene set was uniquely altered by individual allergens. Nickel demonstrated the highest immune activation, with potent inductions of innate immunity, T H 1/T H 17 and a T H 22 component. Fragrance, and to a lesser extent rubber, demonstrated a strong T H 2 bias, some T H 22 polarization, and smaller T H 1/T H 17 contributions. Conclusions Our study offers new insights into the pathogenesis of ACD, expanding the understanding of T-cell activation and associated cytokines in allergen-reactive tissues. It is the first study that defines the common transcriptome of clinically relevant sensitizers in human skin and identifies unique pathways preferentially activated by different allergens, suggesting that ACD cannot be considered a single entity.

Nikhil Dhingra, BSa,b,c, Mayte Suarez-Farinas, PhDa,c, Judilyn Fuentes-Duculan, MDa, Julia K. Gittler, BAa,d, Avner Shemer, MDe, Assaf Raz, PhDf, Vincent A. Fischetti, PhDf, James G. Krueger, MD, PhDa, and Emma Guttman-Yassky, MD, PhDa,g Emma Guttman-Yassky: eguttman@rockefeller.edu aThe Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY bColumbia University College of Physicians & Surgeons, New York, NY cThe Center for Clinical and Translational Science, The Rockefeller University, New York, NY dAlbert Einstein College of Medicine, Bronx, NY eThe Department of Dermatology, Tel-Hashomer, Tel Aviv, Israel fThe Laboratory of Bacterial Pathogenesis and Immunology, The Rockefeller University, New York, NY gThe Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY

Atopic dermatitis (AD) is a common inflammatory skin disease regulated by genetic and environmental factors. Both skin barrier defects and aberrant immune responses are believed to drive cutaneous inflammation in AD. Existing therapies rely largely on allergen avoidance, emollients and topical and systemic immune-suppressants, some with significant toxicity and transient efficacy; no specific targeted therapies are in clinical use today. As our specific understanding of the immune and molecular pathways that cause different subsets of AD increases, a variety of experimental agents, particularly biologic agents that target pathogenic molecules bring the promise of safe and effective therapeutics for long-term use.This paper discusses the molecular pathways characterizing AD, the contributions of barrier and immune abnormalities to its pathogenesis, and development of new treatments that target key molecules in these pathways. In this review, we will discuss a variety of biologic therapies that are in development or in clinical trials for AD, perhaps revolutionizing treatment of this disease.Biologic agents in moderate to severe AD offer promise for controlling a disease that currently lacks good and safe therapeutics posing a large unmet need. Unfortunately, existing treatments for AD aim to decrease cutaneous inflammation, but are not specific for the pathways driving this disease. An increasing understanding of the immune mechanisms underlying AD brings the promise of narrow targeted therapies as has occurred for psoriasis, another inflammatory skin disease, for which specific biologic agents have been demonstrated to both control the disease and prevent occurrence of new skin lesions. Although no biologic is yet approved for AD, these are exciting times for active therapeutic development in AD that might lead to revolutionary therapeutics for this disease.

Petrolatum is a common moisturizer often used in the prevention of skin infections after ambulatory surgeries and as a maintenance therapy of atopic dermatitis (AD). However, the molecular responses induced by petrolatum in the skin have never been assessed.We sought to define the cutaneous molecular and structural effects induced by petrolatum.Thirty-six healthy subjects and 13 patients with moderate AD (mean SCORAD score, 39) were studied by using RT-PCR, gene arrays, immunohistochemistry, and immunofluorescence performed on control skin, petrolatum-occluded skin, and skin occluded with a Finn chamber only.Significant upregulations of antimicrobial peptides (S100A8/fold change [FCH], 13.04; S100A9/FCH, 11.28; CCL20/FCH, 8.36; PI3 [elafin]/FCH, 15.40; lipocalin 2/FCH, 6.94, human β-defensin 2 [DEFB4A]/FCH, 4.96; P.001 for all) and innate immune genes (IL6, IL8, and IL1B; P.01) were observed in petrolatum-occluded skin compared with expression in both control and occluded-only skin. Application of petrolatum also induced expression of key barrier differentiation markers (filaggrin and loricrin), increased stratum corneum thickness, and significantly reduced T-cell infiltrates in the setting of "normal-appearing" or nonlesional AD skin, which is known to harbor barrier and immune defects.Petrolatum robustly modulates antimicrobials and epidermal differentiation barrier measures. These data shed light on the beneficial molecular responses of petrolatum in barrier-defective states, such as AD and postoperative wound care.

Atopic dermatitis (AD) is generally regarded as a type 2 helper T (Th2)-mediated inflammatory skin disease. Although the number of IL-17A-producing cells is increased in the peripheral blood and in acute skin lesion of AD patients, the role of IL-17A in the pathogenesis of AD remains unclear. To clarify this issue, we used murine AD models in an IL-17A-deficient condition. In a repeated hapten application-induced AD model, skin inflammation, IL-4 production in the draining lymph nodes (LNs), and hapten-specific IgG1 and IgE induction were suppressed in IL-17A-deficient mice. Vγ4(+) γδ T cells in the skin-draining LNs and Vγ5(-) dermal γδ T cells in the skin were the major sources of IL-17A. Consistently, in flaky-tail (Flg(ft/ft) ma/ma) mice, spontaneous development of AD-like dermatitis and IgE induction were attenuated by IL-17A deficiency. Moreover, Th2 differentiation from naive T cells was promoted in vitro by the addition of IL-17A. Taken together, our results suggest that IL-17A mediates Th2-type immune responses and that IL-17A signal may be a therapeutic target of AD.

Atopic dermatitis (AD) is a common inflammatory skin disease characterized by wet, oozing, erythematous, pruritic lesions in the acute stage and xerotic, lichenified plaques in the chronic stage. It frequently coexists with asthma and allergic rhinitis, sharing some mechanistic features with these diseases as part of the "atopic march." Controversy exists as to whether immune abnormalities, epidermal barrier defects, or both are the primary factors responsible for disease pathogenesis. In AD patients, there is often a coexisting irritant contact dermatitis (ICD) or allergic contact dermatitis (ACD) that is sometimes clinically difficult to distinguish from AD. ACD shares molecular mechanisms with AD, including increased cellular infiltrates and cytokine activation (Gittler et al., 2013). In this issue, Newell et al. (2013) used an experimental contact sensitization model with dinitrochlorobenzene (DNCB) to gain insight into the unique immune phenotype of AD patients.

BackgroundSevere atopic dermatitis (AD) has a high unmet need for effective and safe therapeutics. In early-phase trials, dupilumab, a fully human mAb targeting IL-4 receptor α, markedly improved disease activity, but the effect of IL-4/IL-13 blockade on AD at the molecular level has not been characterized.ObjectivesWe sought to evaluate dupilumab modulation of the AD molecular signature.MethodsWe performed transcriptomic analyses of pretreatment and posttreatment skin biopsy specimens from patients with moderate-to-severe AD treated weekly with 150 or 300 mg of dupilumab or placebo.ResultsExacerbation of the AD transcriptome was observed in placebo-treated patients. Dupilumab improved the AD signature in a dose-dependent manner. Expression of genes upregulated in AD lesions decreased in patients treated with dupilumab by 26% (95% CI, 21% to 32%) and 65% (95% CI, 60% to 71%) for treatment with 150 and 300 mg, respectively. Genes downregulated in AD lesions increased by 21% (95% CI, 16% to 27%) and 32% (95% CI, 26% to 37%) with dupilumab (150 and 300 mg, respectively). The molecular changes paralleled improvements in clinical scores. A dupilumab treatment signature of 821 probes (>2-fold change, P < .05) significantly modulated in the 300-mg dupilumab group at week 4 compared with baseline was identified in this sample set. Significant (P < .05) decreases in mRNA expression of genes related to hyperplasia (K16 and MKI67), T cells, and dendritic cells (CD1b and CD1c) and potent inhibition of TH2-associated chemokines (CCL17, CCL18, CCL22, and CCL26) were noted without significant modulation of TH1-associated genes (IFNG).ConclusionsThis is the first report showing rapid improvement of the AD molecular signature with targeted anti–IL-4 receptor α therapy. These data suggest that IL-4 and IL-13 drive a complex, TH2-centered inflammatory axis in patients with AD.