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Background: Polycystic ovary syndrome (PCOS) affects approximately 4% to 12% of females of reproductive age. Previous studies have shown an association between systemic and periodontal diseases. This study aimed to compare the prevalence of periodontal disease in women with PCOS and healthy women., Methods: A total of 196 women aged 17 to 45 years were included in this study. Oral hygiene index-simplified (OHI-S), gingival index (GI), community periodontal index (CPI), and loss of attachment (LA) were assessed. Individuals who smoked, were pregnant, had any systemic disease (such as type 1 or type 2 diabetes mellitus, cardiovascular disease, malignancy, osteoporosis, and thyroid dysfunction), had a history of systemic antibiotic use in the past three months, or received any periodontal intervention in the past 6 months of screening were excluded. Student t-test was used to analyze the data. A p-value of <0.05 was considered statistically significant., Results: Despite similar OHI-S scores (p=0.972) in the two groups, women with PCOS had significantly higher GI, CPI, and LA scores than healthy women (p<0.001)., Conclusion: Periodontal disease was more prevalent in women with PCOS than in healthy women. This finding may be due to the synergistic effects of PCOS and periodontitis on proinflammatory cytokines. PCOS may have an effect on periodontal disease, and vice versa. Hence, education on periodontal health and early detection and intervention for periodontal diseases is of paramount importance in patients with PCOS.

Paediatric facial fractures are relatively rare. The inherent elasticity of the bones with more of the cartilage than that of the mineralised bone accounts for this. The principles involved in the management of facial fractures are the same irrespective of the age of the patient; however, in children, the techniques used are necessarily modified by certain anatomical, physiological, psychological and feeding factors related to childhood and the parents. In an attempt to keep the treatment and fixation technique simple, the case, presented here, describes the management of a mandibular parasymphyseal fracture in a 16-month-old child with the use of a prefabricated adaptable surgical splint., Competing Interests: None

Aim: The present study was carried out to know the expression level of survivin, an inhibitor of apoptosis protein with an objective to determine its prognostic importance in cutaneous and subcutaneous tissue tumors of dogs., Materials and Methods: Forty cases of canine cutaneous and subcutaneous tissue tumors on histopathological examination revealed various round cell, epithelial, and mesenchymal cell tumors. Survivin gene expression was detected in all tumors tested by TaqMan real-time polymerase chain reaction assay by comparative cycle threshold method., Results: The mean survivin gene expression value of benign tumors was 0.94±0.63 folds and that of malignant tumors was 18.87±5.30 folds. Postsurgical follow up of 30 malignant tumor cases revealed death in 8, recurrence in 7, and neoplastic free alive status in 15 dogs with mean survivin fold difference values of 48.49±12.39, 14.63±6.37, and 5.034±2.27, respectively. The mean survivin gene expression value was significantly higher in malignant (30 cases, 18.87±5.30) compared to benign tumors (10 cases, 0.94±0.63), and it varied between various postsurgical follow-up groups (p<0.05). Survival analysis, using survivin gene expression median cutoff value of 3.74 in 30 malignant tumors, was performed to predict probable survival period in malignant cutaneous and subcutaneous tumors of dogs., Conclusions: Results of the present study indicated that the expression of survivin in canine cutaneous and subcutaneous tumors has prognostic value, and survivin expression greater than median cutoff value of 3.74 has a poor prognosis.

Background: Blocking vascular endothelial growth factor (VEGF) mediated tumor angiogenesis by phytochemicals has emerged as an attractive strategy for cancer prevention and therapy., Methods: We investigated the anti-angiogenic effects of ellagic acid in a hamster model of oral oncogenesis by examining the transcript and protein expression of hypoxia-inducible factor-1alpha (HIF-1α), VEGF, VEGFR2, and the members of the PI3K/Akt and MAPK signaling cascades. Molecular docking studies and cell culture experiments with the endothelial cell line ECV304 were performed to delineate the mechanism by which ellagic acid regulates VEGF signaling., Results: We found that ellagic acid significantly inhibits HIF-1α-induced VEGF/VEGFR2 signalling in the hamster buccal pouch by abrogating PI3K/Akt and MAPK signaling via downregulation of PI3K, PDK-1, p-Akt(ser473), mTOR, p-ERK, and p-JNK. Ellagic acid was also found to reduce the expression of histone deacetylases that could inhibit neovascularization. Analysis of the mechanism revealed that ellagic acid inhibits hypoxia-induced angiogenesis via suppression of HDAC-6 in ECV304 cells. Furthermore, knockdown of endogenous HDAC6 via small interfering RNA abrogated hypoxia-induced expression of HIF-1α and VEGF and blocked Akt activation. Molecular docking studies confirmed interaction of ellagic acid with upstream kinases that regulate angiogenic signaling., Conclusions: Taken together, these findings demonstrate that the anti-angiogenic activity of ellagic acid may be mediated by abrogation of hypoxia driven PI3K/Akt/mTOR, MAPK and VEGF/VEGFR2 signaling pathways involving suppression of HDAC6 and HIF-1α responses., General Significance: Ellagic acid offers promise as a lead compound for anticancer therapeutics by virtue of its ability to inhibit key oncogenic signaling cascades and HDACs.

Background: The oncogenic transcription factors NF-κB and β-catenin, constitutively activated by upstream serine/threonine kinases control several cellular processes implicated in malignant transformation including apoptosis evasion. The aim of this study was to investigate the chemopreventive effects of astaxanthin, an antioxidant carotenoid, in the hamster buccal pouch (HBP) carcinogenesis model based on its ability to modulate NF-κB and Wnt signaling pathways and induce apoptosis., Methods: We determined the effect of dietary supplementation of astaxanthin on the oncogenic signaling pathways - NF-κB and Wnt/β-catenin, their upstream activator kinases - Erk/MAPK and PI-3K/Akt, and the downstream event - apoptosis evasion by real-time quantitative RT-PCR, western blot, and immunohistochemical analyses., Results: We found that astaxanthin inhibits NF-κB and Wnt signaling by downregulating the key regulatory enzymes IKKβ and GSK-3β. Analysis of gene expression and docking interactions revealed that inhibition of these pathways may be mediated via inactivation of the upstream signaling kinases Erk/Akt by astaxanthin. Astaxanthin also induced caspase-mediated mitochondrial apoptosis by downregulating the expression of antiapoptotic Bcl-2, p-Bad, and survivin and upregulating proapoptotic Bax and Bad, accompanied by efflux of Smac/Diablo and cytochrome-c into the cytosol, and induced cleavage of poly (ADP-ribose) polymerase (PARP)., Conclusions: The results provide compelling evidence that astaxanthin exerts chemopreventive effects by concurrently inhibiting phosphorylation of transcription factors and signaling kinases and inducing intrinsic apoptosis., General Significance: Astaxanthin targets key molecules in oncogenic signaling pathways and induces apoptosis and is a promising candidate agent for cancer prevention and therapy., (Copyright © 2013 Elsevier B.V. All rights reserved.)

In the title compound, C(4)H(10)NO(+)·C(4)H(5)O(6) (-)·H(2)O, the morpholine ring adopts a chair conformation. In the crystal, the tartrate anions are linked via O-H⋯O hydrogen bonds, forming chains propagating along [101]. These chains are linked via N-H⋯O and O-H⋯O hydrogen bonds, involving the morpholinium cation and the water molecule, forming a three-dimensional network.