Management of a Patient with Oral Submucous Fibrosis Having Restricted Mouth Opening: A Case Report

 Objectives- Oral Submucous Fibrosis is a chronic inflammatory disease that results in progressive  juxtaepethelial Inflammatory reaction  followed by a fibroelastic change of lamina propia with epethial atrophy leading to stiffness of oral mucosa, causing trismus . This causes the difficulty in chewing, swallowing and speaking . Method- Sectional complete denture was an appropriate treatment to resolve the problem of Oral Submoucos  Fibrosis. The acylic  resins connectors in the form of sleeves and cross  pins reduced the overall costs and simplified the laboratory technique. Results-  The  rehabilitation of patient suffering from OSMF is a challenge to Prosthodontist. This  article  describes the prosthodontic management of such patient by using a sectional denture . Conclusions- This technique has  proven to be simple, inexpensive, and applicable to the selected Oral Submucous Fibrosis patient’s

Certain Unramified Metabelian Extensions Using Lemmermeyer Factorizations

We study solutions to the Brauer embedding problem with restricted ramification. Suppose $G$ and $A$ are a abelian groups, $E$ is a central extension of $G$ by $A$, and $f:\text{Gal}(\overline{\mathbf{Q}}/\mathbf{Q})\rightarrow G$ a continuous homomorphism. We determine conditions on the discriminant of $f$ that are equivalent to the existence of an unramified lift $\widetilde{f}:\text{Gal}(\overline{\mathbf{Q}}/\mathbf{Q})\rightarrow E$ of $f$. As a consequence of this result, we use conditions on the discriminant of $K$ for $K/\mathbf{Q}$ abelian to classify and count unramified nonabelian extensions $L/K$ normal over $\mathbf{Q}$ where the (nontrivial) commutator subgroup of $\text{Gal}(L/\mathbf{Q})$ is contained in its center. This generalizes a result due to Lemmermeyer, which states that a quadratic field $\mathbf{Q}(\sqrt{d})$ has an unramified extension normal over $\mathbf{Q}$ with Galois group $H_8$ the quaternion group if and only if the discriminant factors $d=d_1 d_2 d_3$ as a product of three coprime discriminants, at most one of which is negative, satisfying the following condition on Legendre symbols: $$\left(\frac{d_i d_j}{p_k}\right)=1$$ for $\{i,j,k\}=\{1,2,3\}$ and $p_i$ any prime dividing $d_i$

Molecular profiling of human prostate tissues: insights into gene expression patterns of prostate development during puberty

Testosterone production surges during puberty and orchestrates massive growth and reorganization of the prostate gland, and this glandular architecture is maintained thereafter throughout adulthood. Benign prostatic hyperplasia (BPH) and prostate adenocarcinoma (PCA) are common diseases in adulthood that do not develop in the absence of androgens. Our objective was to gain insight into gene expression changes of the prostate gland at puberty, a crucial juncture in prostate development that is androgen dependent. Understanding the role played by androgens in normal prostate development may provide greater insight into androgen involvement in prostatic diseases. Benign prostate tissues obtained from pubertal and adult age group cadaveric organ donors were harvested and profiled using 20,000 element cDNA microarrays. Statistical analysis of the microarray data identified 375 genes that were differentially expressed in pubertal prostates relative to adult prostates including genes such as Nkx3.1, TMEPAI, TGFBR3, FASN, ANKH, TGFBR2, FAAH, S100P, HoxB13, fibronectin, and TSC2 among others. Comparisons of pubertal and BPH expression profiles revealed a subset of genes that shared the expression pattern between the two groups. In addition, we observed that several genes from this list were previously demonstrated to be regulated by androgen and hence could also be potential in vivo targets of androgen action in the pubertal human prostate. Promoter searches revealed the presence of androgen response elements in a cohort of genes including tumor necrosis factor‐α induced adipose related protein, which was found to be induced by androgen. In summary, this is the first report that provides a comprehensive view of the molecular events that occur during puberty in the human prostate and provides a cohort of genes that could be potential in vivo targets of androgenic action during puberty.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154303/1/fsb2fj042415fje.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/154303/2/fsb2fj042415fje-sup-0001.pd

Metabolomic profiles delineate potential role for sarcosine in prostate cancer progression

Multiple, complex molecular events characterize cancer development and progression(1,2). Deciphering the molecular networks that distinguish organ- confined disease from metastatic disease may lead to the identification of critical biomarkers for cancer invasion and disease aggressiveness. Although gene and protein expression have been extensively profiled in human tumours, little is known about the global metabolomic alterations that characterize neoplastic progression. Using a combination of high- throughput liquid- and- gas- chromatography- based mass spectrometry, we profiled more than 1,126 metabolites across 262 clinical samples related to prostate cancer ( 42 tissues and 110 each of urine and plasma). These unbiased metabolomic profiles were able to distinguish benign prostate, clinically localized prostate cancer and metastatic disease. Sarcosine, an N- methyl derivative of the amino acid glycine, was identified as a differential metabolite that was highly increased during prostate cancer progression to metastasis and can be detected non- invasively in urine. Sarcosine levels were also increased in invasive prostate cancer cell lines relative to benign prostate epithelial cells. Knockdown of glycine- N- methyl transferase, the enzyme that generates sarcosine from glycine, attenuated prostate cancer invasion. Addition of exogenous sarcosine or knockdown of the enzyme that leads to sarcosine degradation, sarcosine dehydrogenase, induced an invasive phenotype in benign prostate epithelial cells. Androgen receptor and the ERG gene fusion product coordinately regulate components of the sarcosine pathway. Here, by profiling the metabolomic alterations of prostate cancer progression, we reveal sarcosine as a potentially important metabolic intermediary of cancer cell invasion and aggressivity.Early Detection Research Network ; National Institutes of Health ; MTTC ; Clinical Translational Science Award ; Fund for Discovery of the University of Michigan Comprehensive Cancer Center ; University of Michigan Cancer Biostatistics Training Grant ; Doris Duke Charitable FoundationWe thank J. Granger for help in manuscript preparation, J. Siddiqui and R. Varambally for help with the clinical database, and A. Vellaichamy and S. Pullela for technical assistance. We thank K. Pienta for access to metastatic prostate cancer samples from the University of Michigan Prostate SPORE rapid autopsy programme. This work is supported in part by the Early Detection Research Network (A.M.C., J.T.W.), National Institutes of Health (A.S., S.P., J.B., T.M.R., D.G., G.S.O. and A.M.C.) and an MTTC grant (G.S.O. and A.S.). A.M.C. is supported by a Clinical Translational Science Award from the Burroughs Welcome Foundation. A. S. is supported by a grant from the Fund for Discovery of the University of Michigan Comprehensive Cancer Center. L. M. P. is supported by the University of Michigan Cancer Biostatistics Training Grant. A. M. C and S. P. are supported by the Doris Duke Charitable Foundation.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62661/1/nature07762.pd

Prosthodontic rehabilitation of patient with ocular defect using an alternative technique

An ocular prosthesis is a simulation of of a perfectly normal healthy eye and surrounding tissues. The primary purpose of an ocular prosthesis is to maintain the volume of eye socket and create the illusion of a healthy eye and surrounding tissue. A custom ocular prosthesis is a good option when reconstruction by plastic surgery or the use of Osseo-integrated implants is not possible or not desired. Prosthetic rehabilitation of a patient with missing eye with custom made ocular prosthesis was described. Advantages include improved adaptation, increased mobility of prosthesis, improved facial contours and enhanced esthetics gained from the control of the iris and sclera. An accurate alignment of the artificial eye is one of the major prerequisites for esthetic success of the ocular prosthesis

Prosthetic Management of a patient with Occular Defect with Occular Prosthesis - A case report.

The eye is a vital organ not only in terms of vision but also being an important component of facial expression.Throughout history, human eye has been mentioned as the most precious of gifts . The rehabilitation of a patient who has suffered from an ocular loss , requires a prosthesis that will provide the optimum cosmetic and functional results. A 45 year-old male reported to the Department of Prosthodontics, Darshan dental college,Udaipur,Rajasthan, with a missing left eye. Treatment was initiated with psychological counselling and reassured treatment outcome regularly during treatment. Treatment of such cases includes implants and acrylic eye prosthesis. Although ocular implant eye prosthesis has superior outcome, due to economic factors it may not be advisable in all patients. So a custom-made ocular prosthesis is a good alternative. A case of a custom-made ocular acrylic prosthesis is presented here, which had acceptable fit, retention and esthetics.&nbsp

Human leukocyte antigen-G expression in differentiated human airway epithelial cells: lack of modulation by Th2-associated cytokines

<p>Abstract</p> <p>Background</p> <p>Human leukocyte antigen (HLA)-G is a nonclassical class I antigen with immunomodulatory roles including up-regulation of suppressor T regulatory lymphocytes. HLA-G was recently identified as an asthma susceptibility gene, and expression of a soluble isoform, HLA-G5, has been demonstrated in human airway epithelium. Increased presence of HLA-G5 has been demonstrated in bronchoalveolar lavage fluid recovered from patients with mild asthma; this suggests a role for this isoform in modulating airway inflammation though the mechanisms by which this occurs is unclear. Airway inflammation associated with Th2 cytokines such as IL-4 and IL-13 is a principal feature of asthma, but whether these cytokines elicit expression of HLA-G is not known.</p> <p>Methods</p> <p>We examined gene and protein expression of both soluble (G5) and membrane-bound (G1) HLA-G isoforms in primary differentiated human airway epithelial cells collected from normal lungs and grown in air-liquid interface culture. Cells were treated with up to 10 ng/ml of either IL-4, IL-5, or IL-13, or 100 ng/ml of the immunomodulatory cytokine IL-10, or 10,000 U/ml of the Th1-associated cytokine interferon-beta, for 24 hr, after which RNA was isolated for evaluation by quantitative PCR and protein was collected for Western blot analysis.</p> <p>Results</p> <p>HLA-G5 but not G1 was present in dAEC as demonstrated by quantitative PCR, western blot and confocal microscopy. Neither G5 nor G1 expression was increased by the Th2-associated cytokines IL-4, IL-5 or IL-13 over 24 hr, nor after treatment with IL-10, but was increased 4.5 ± 1.4 fold after treatment with 10,000 U/ml interferon-beta.</p> <p>Conclusions</p> <p>These data demonstrate the constitutive expression of a T lymphocyte regulatory molecule in differentiated human airway epithelial cells that is not modulated by Th2-associated cytokines.</p

Chemokine expression in the early response to injury in human airway epithelial cells

Basal airway epithelial cells (AEC) constitute stem/progenitor cells within the central airways and respond to mucosal injury in an ordered sequence of spreading, migration, proliferation, and differentiation to needed cell types. However, dynamic gene transcription in the early events after mucosal injury has not been studied in AEC. We examined gene expression using microarrays following mechanical injury (MI) in primary human AEC grown in submersion culture to generate basal cells and in the air-liquid interface to generate differentiated AEC (dAEC) that include goblet and ciliated cells. A select group of ~150 genes was in differential expression (DE) within 2–24 hr after MI, and enrichment analysis of these genes showed over-representation of functional categories related to inflammatory cytokines and chemokines. Network-based gene prioritization and network reconstruction using the PINTA heat kernel diffusion algorithm demonstrated highly connected networks that were richer in differentiated AEC compared to basal cells. Similar experiments done in basal AEC collected from asthmatic donor lungs demonstrated substantial changes in DE genes and functional categories related to inflammation compared to basal AEC from normal donors. In dAEC, similar but more modest differences were observed. We demonstrate that the AEC transcription signature after MI identifies genes and pathways that are important to the initiation and perpetuation of airway mucosal inflammation. Gene expression occurs quickly after injury and is more profound in differentiated AEC, and is altered in AEC from asthmatic airways. Our data suggest that the early response to injury is substantially different in asthmatic airways, particularly in basal airway epithelial cells

The metabolic footprint of the airway bacterial community in cystic fibrosis

Abstract Background Progressive, chronic bacterial infection of the airways is a leading cause of death in cystic fibrosis (CF). Culture-independent methods based on sequencing of the bacterial 16S rRNA gene describe a distinct microbial community that decreases in richness and diversity with disease progression. Understanding the functional characteristics of the microbial community may aid in identifying potential therapies and may assist in management, but current methods are cumbersome. Here, we demonstrate the use of an oxidative metabolic assay as a complement to sequencing methods to describe the microbiome in the airways of patients with CF. Methods Expectorated sputum was collected from 16 CF subjects and 8 control subjects. The Biolog Gen III Microplate was used in a community-level physiological profiling (CLPP)-based assay to examine oxidative metabolic activity. 16S rRNA V4 amplicon sequencing was used to characterize the taxonomy and diversity of the samples. Correlations were then identified among the oxidative activity and taxonomy data. In an additional paired analysis, sputum from seven CF subjects were collected at two separate clinic visits and compared for oxidative activity, taxonomy, and diversity. Results Significant differences in oxidative metabolic activity, microbial taxonomy, and diversity were found between the CF and control sputum samples. Oxidative activity correlated positively with total genera but not with other measures of diversity or taxonomy, demonstrating that the metabolic assay complements the structural aspects of the microbiome. As expected, Pseudomonas was significantly enriched in CF samples, while Streptococcus and Prevotella were similarly abundant in both CF and control samples. Paired analysis of CF samples at separate clinic visits revealed comparable oxidative activity that correlated with similar stability in taxonomy and diversity. Conclusions The CLPP assay used in this study complements existing sequencing methods to delineate the oxidative metabolic footprint of the CF airway bacterial community. This method may be useful to study the CF microbial community over time and with changes in disease state

Chemokine expression in the early response to injury in human airway epithelial cells

<div><p>Basal airway epithelial cells (AEC) constitute stem/progenitor cells within the central airways and respond to mucosal injury in an ordered sequence of spreading, migration, proliferation, and differentiation to needed cell types. However, dynamic gene transcription in the early events after mucosal injury has not been studied in AEC. We examined gene expression using microarrays following mechanical injury (MI) in primary human AEC grown in submersion culture to generate basal cells and in the air-liquid interface to generate differentiated AEC (dAEC) that include goblet and ciliated cells. A select group of ~150 genes was in differential expression (DE) within 2–24 hr after MI, and enrichment analysis of these genes showed over-representation of functional categories related to inflammatory cytokines and chemokines. Network-based gene prioritization and network reconstruction using the PINTA heat kernel diffusion algorithm demonstrated highly connected networks that were richer in differentiated AEC compared to basal cells. Similar experiments done in basal AEC collected from asthmatic donor lungs demonstrated substantial changes in DE genes and functional categories related to inflammation compared to basal AEC from normal donors. In dAEC, similar but more modest differences were observed. We demonstrate that the AEC transcription signature after MI identifies genes and pathways that are important to the initiation and perpetuation of airway mucosal inflammation. Gene expression occurs quickly after injury and is more profound in differentiated AEC, and is altered in AEC from asthmatic airways. Our data suggest that the early response to injury is substantially different in asthmatic airways, particularly in basal airway epithelial cells.</p></div