Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0043352 (xerostomia)
4,250 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy and tolerability of moclobemide and sertraline were compared in a 13 week trial on 55 depressive patients. Patients were diagnosed according to DSM-III-R criteria using SCID (Structured Clinical Interview for DSM-III-R). The study group was composed of 48 patients with major depression and 7 with minor depression. Patients were randomized in two drug groups and raters were blind to the drugs patients used. HDRS and CGI were used to assess the change in depressive symptoms. Twenty seven patients received moclobemide and 28 patients received sertraline. The dose of moclobemide used was 300-600 mg/day and that of sertraline was 50-200 mg/day. At the end of 13 weeks mean drop in HDRS for the overall group was 14.78 and the response rate calculated as percentage of patients showing a 50% drop in HDRS score was 77.8. The response rate was 76.5% for moclobemide and 78.5% for sertraline. The difference was not significant. The side effects were assessed by using UKU Side Effects Rating Scale. The most three observed side effects were dry mouth, headache and insomnia.
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PMID:Moclobemide and sertraline in the treatment of depressive disorders: a comparative study. 852 56

Saliva contains a wide variety of secretory proteins, including alpha-amylase, lysozyme, peroxidase, immunoglobulins, and mucins. Hyposecretion of saliva and consequent dry mouth will lead to severe dental caries, periodontal disease, and mucosal infections, resulting in degrade of quality of life. Polyposia development is one of sign usually seen in dry mouth patients. However, little is reported in dry mouth-model animal regarding the entire process of polyposia development. We investigated the behavior of polyposia in E2F1-deficient non-obese diabetic/severe combined immunodeficiency disease (NOD/SCID) mice, as a dry mouth-model. E2F1-deficient NOD/SCID mice secreted small amount of saliva under the stimulation with a cholinergic agonist, pilocarpine, compared with control mice. The frequency of water intake by E2F-1-deficient NOD/SCID mice was more than that by control mice. These results suggest that E2F-1-deficient NOD/SCID mice show a behavior similar to polyposia and are very useful experimental model of dry mouth patients.
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PMID:E2F1-deficient NOD/SCID mice are an experimental model for dry mouth. 2022 95

Non-obese diabetic (NOD) mice have been used as a model for dry mouth. NOD mice lacking the gene encoding E2f1, a transcription factor, develop hyposalivation more rapidly progressively than control NOD mice. However, the model mice are associated with an underlying disease such as diabetes. We have now established E2f1-deficient NOD/severe combined immunodeficiency disease (NOD/SCID.E2f1(-/-)) mice to avoid the development of diabetes (Matsui-Inohara et al., Exp Biol Med (Maywood) 234(12):1525-1536, 2009). In this study, we investigated the pathophysiological features of dry mouth using NOD/SCID.E2f1(-/-) mice. In NOD/SCID.E2f1(-/-) mice, the volume of secreted saliva stimulated with pilocarpine is about one third that of control NOD/SCID mice. In behavioral analysis, NOD/SCID.E2f1(-/-) mice drank plenty of water when they ate dry food, and the frequency and time of water intake were almost double compared with control NOD/SCID mice. Histological analysis of submandibular glands with hematoxylin-eosin stain revealed that NOD/SCID.E2f1(-/-) mice have more ducts than NOD/SCID mice. In western blot analysis, the expression of aquaporin 5 (AQP5), a marker of acinar cells, in parotid and in submandibular glands of NOD/SCID.E2f1(-/-) mice was lower than in NOD/SCID mice. Immunohistochemical analysis of parotid and submandibular acini revealed that the localization of AQP5 in NOD/SCID.E2f1(-/-) mice differs from that in NOD/SCID mice; AQP5 was leaky and diffusively localized from the apical membrane to the cytosol in NOD/SCID.E2f1(-/-) mice. The ubiquitination of AQP5 was detected in submandibular glands of NOD/SCID.E2f1(-/-) mice. These findings suggest that the change of acinar/duct structure and the down-regulation of AQP5 in the salivary gland cause the pathogenesis of hyposalivation in NOD/SCID.E2f1(-/-) mice.
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PMID:E2f1-deficient NOD/SCID mice have dry mouth due to a change of acinar/duct structure and the down-regulation of AQP5 in the salivary gland. 2317 81

Atrophy or hypofunction of the salivary gland because of aging or disease causes hyposalivation and has an effect on the quality of life of patients, for example not only dry mouth but deterioration in mastication/deglutition disorder and the status of oral hygiene. Currently conducted therapies for atrophy or hypofunction of the salivary gland in clinical practice are only symptomatic treatments with drugs and artificial saliva, and therefore it is preferable to establish a radical therapy. At this time, as a fundamental investigation, by co-culturing mouse early ES (mEES-6) cells with human salivary gland-derived fibroblasts (hSG-fibro), differentiation of mEES-6 cells to salivary gland cells has been attempted. Also, the possibility of cell engraftment was examined. After identifying the cells which were co-cultured with GFP-transfected mEES-6 cells and hSG-fibro, the cells were transplanted into the submandibular gland of SCID mice, and the degree of differentiation into tissues was examined. The possibility of tissue functional reconstitution from co-cultured cells in a three-dimensional culture system was examined. Our results confirmed that the co-cultured cells expressed salivary gland-related markers and had an ability to generate neo-tissues by transplantation in vivo. Moreover, the cells could reconstitute gland structures in a three-dimensional culture system. By co-culture with hSG-fibro, mEES-6 cells were successfully differentiated into salivary gland cells which were transplantable and have tissue neogenetic ability.
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PMID:Functional transplantation of salivary gland cells differentiated from mouse early ES cells in vitro. 2368 39

Atrophy or hypofunction of the salivary gland because of aging or disease leads to hyposalivation that affects patient quality of life by causing dry mouth, deterioration of mastication/deglutition, and poor oral hygiene status. Current therapy for atrophy or hypofunction of the salivary gland in clinical practice focuses on symptom relief using drugs and artificial saliva; therefore, there is still a need to develop new therapies. To investigate potential novel therapeutic targets, we induced the differentiation of salivary gland cells by co-culturing human adipose-derived stem cells isolated from buccal fat pads (hBFP-ASCs) with human salivary-gland-derived fibroblasts (hSG-fibros). We examined their potential for transplantation and tissue neogenesis. Following the culture of hBFP-ASCs and hSG-fibros, differentiated cells were transplanted into the submandibular glands of SCID mice, and their degree of differentiation in tissues was determined. We also examined their potential for functional tissue reconstitution using a three-dimensional (3D) culture system. Co-cultured cells expressed salivary-glandrelated markers and generated new tissues following transplantation in vivo. Moreover, cell reconstituted glandular structures in the 3D culture system. In conclusion, coculture of hSG-fibros with hBFP-ASCs led to successful differentiation into salivary gland cells that could be transplanted to generate new tissues.
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PMID:Induction and differentiation of adipose-derived stem cells from human buccal fat pads into salivary gland cells. 2684 56