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Micro-osteoperforations is one of the non-invasive surgical techniques used in attempt to accelerate OTM. Conflicting reports on its effectiveness has been reported in the literature.
The objectives of this trial were to investigate the effect of micro-osteoperforations on the rate of space closure and on molar anchorage loss during mini-implant supported maxillary anterior en-masse retraction.
A single center, parallel arm, randomized controlled trial was conducted.
Sixty, male and female subjects (age range 16-25 years) having Class I bimaxillary protrusion or Class II div 1 malocclusion, who required fixed mechanotherapy with either upper 1st premolar or all four 1st premolar extractions were allocated into two groups using 11 allocation ratio. The allocation was done by block randomization method with a block size of 6. In the experimental group, 5 MOPs per side were performed only once just before the en-masse anterior retraction. Mini-screws were placed in order to obtain maximum anchorage. Impr18140).
The trial was registered at www.ctri.nic.in with CTRI No- CTRI/2019/03/018140).
Out of all non-communicable diseases, cancer is the leading cause of death in the 21st century. Oral cancer ranks in top ten cancers in the world and oncogenic viruses contribute to its development and are a major preventable risk factor for it.
In the present study we intend to find the incidence of HPV and EBV by PCR in 108 sporadic oral cancer patients and study the clinico-pathological variables in agreement to their presence or absence.
We found that the incidence of EBV in oral cancer is much higher (30/108; 27.8%) than HPV 16 (14/108; 13%) and, a complete absence of HPV 18 (0/108) was reported by real time PCR. Co-infection by EBV and HPV was reported in 5.6% cases (6/108). However, on comparing this data with the corresponding clinico-pathological cofactors (age, gender, grade of tumour, tumour size, nodal status, metastasis, DOI, TIL, ENE) it was found that there was no statistical significance between the two.
Hence, we conclude that these oncogenic viruses are independent cofactors to oral cancer development and none of the clinico-morphologic variable is associated with the viral etiology.
Hence, we conclude that these oncogenic viruses are independent cofactors to oral cancer development and none of the clinico-morphologic variable is associated with the viral etiology.
Osteosarcoma is a primary cause of cancer-associated death in children and adolescents worldwide. Long non-coding RNAs SNHG16 (lncRNA SNHG16) and integrin subunit-a 6 (ITGA6) are recently reported to be involved in the tumorigenesis of osteosarcoma by multiple mechanisms. However, the correlation between SNHG16 and ITGA6 in osteosarcoma remains undetermined.
Expression of miR-488, SNHG16 and ITGA6, as well as epithelial-mesenchymal transition (EMT) associated markers in osteosarcoma tissues and cell lines were examined by qRT-PCR or Western blotting. Effects of miR-488, SNHG16 and ITGA6 on cell migration, invasion were evaluated by wound-healing assay and transwell assay. Bioinformatics analysis and dual-luciferase reported assays were applied to assess the interaction among miR-488, SNHG16 and ITGA6. RNA immunoprecipitation (RIP) was also used to verify SNHG16 and miR-488 interaction. learn more Finally, animal study was used to detect the effect of SNHG16 on osteosarcoma
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SNHG16 and ITGA6 were significantly increased while miR-488 was decreased in osteosarcoma. ITGA6 was screened as a target gene of miR-488, and SNHG16 was sponged by miR-488 in osteosarcoma cells. MiR-488 overexpression and SNHG16 knockdown suppressed migration, invasion and EMT of osteosarcoma cells. Moreover, rescue assays proved that the influences of SNHG16 on osteosarcoma cells migration, invasion and EMT were dependent on miR-488 and ITGA6. In addition, the promotive effects of SNHG16 on osteosarcoma tumor growth and metastasis were further supported by xenograft tumor growth assay.
SNHG16 promoted migration, invasion and EMT of osteosarcoma by sponging miR-488 to release ITGA6.
SNHG16 promoted migration, invasion and EMT of osteosarcoma by sponging miR-488 to release ITGA6.
Most risk assessment models for type 2 diabetes (T2DM) have been developed in Caucasians and Asians; little is known about their performance in other ethnic groups.
We aimed to identify existing models for the risk of prevalent or undiagnosed T2DM and externally validate them in a multi-ethnic population currently living in the Netherlands.
A literature search to identify risk assessment models for prevalent or undiagnosed T2DM was performed in PubMed until December 2017. We validated these models in 4,547 Dutch, 3,035 South Asian Surinamese, 4,119 African Surinamese, 2,326 Ghanaian, 3,598 Turkish, and 3,894 Moroccan origin participants from the HELIUS (Healthy LIfe in an Urban Setting) cohort study performed in Amsterdam. Model performance was assessed in terms of discrimination (C-statistic) and calibration (Hosmer-Lemeshow test). We identified 25 studies containing 29 models for prevalent or undiagnosed T2DM. C-statistics varied between 0.77-0.92 in Dutch, 0.66-0.83 in South Asian Surinamese, 0.70-0.nded to be used in.
The association between HIV status and hypertension is not well described within sub-Saharan Africa. We examined prevalence and risk factors for hypertension among HIV positive and negative individuals living in a rural district of Uganda.
We conducted a cross-sectional analysis in two concurrent cohorts of 600 HIV negative and 721 HIV seropositive individuals aged ≥35 years.
Of the 721 HIV positive participants, 59.8% were women and the median age was 44.3 years, while for HIV negative individuals, 55% were women and the median age was 47.8 years. Over 90% of HIV positive individuals were on antiretroviral treatment. The prevalence of hypertension (≥140/≥90 mmHg) was 33.5% in HIV negative individuals and 23.9% in HIV positive individuals. Age (adjusted OR = 1.05, 95% CI 1.03 to 1.06) and BMI (adjusted OR = 1.08, 95% CI 1.05 to 1.12) were associated with higher odds of hypertension. Having HIV was associated with lower odds of hypertension (adjusted OR = 0.66, 95% CI 0.50 to 0.88), lower systolic blood pressure (-5.
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