Endometrial hyperplasia (EH) comprises a spectrum of changes in the endometrium ranging from a slightly disordered pattern that exaggerates the alterations seen in the late proliferative phase of the menstrual cycle to irregular, hyperchromatic lesions that are similar to endometrioid adenocarcinoma. Generally, EH is caused by continuous exposure of estrogen unopposed by progesterone, polycystic ovary syndrome, tamoxifen, or hormone replacement therapy. Since it can progress, or often occur coincidentally with endometrial carcinoma, EH is of clinical importance, and the reversion of hyperplasia to normal endometrium represents the key conservative treatment for prevention of the development of adenocarcinoma. Presently, cyclic progestin or hysterectomy constitutes the major treatment option for EH without or with atypia, respectively. However, clinical trials of hormonal therapies and definitive standard treatments remain to be established for the management of EH. Moreover, therapeutic options for EH patients who wish to preserve fertility are challenging and require nonsurgical management. Therefore, future studies should focus on evaluation of new treatment strategies and novel compounds that could simultaneously target pathways involved in the pathogenesis of estradiol-induced EH. Novel therapeutic agents precisely targeting the inhibition of estrogen receptor, growth factor receptors, and signal transduction pathways are likely to constitute an optimal approach for treatment of EH.
BackgroundHuman genetic diversity observed in Indian subcontinent is second only to that of Africa. This implies an early settlement and demographic growth soon after the first 'Out-of-Africa' dispersal of anatomically modern humans in Late Pleistocene. In contrast to this perspective, linguistic diversity in India has been thought to derive from more recent population movements and episodes of contact. With the exception of Dravidian, which origin and relatedness to other language phyla is obscure, all the language families in India can be linked to language families spoken in different regions of Eurasia. Mitochondrial DNA and Y chromosome evidence has supported largely local evolution of the genetic lineages of the majority of Dravidian and Indo-European speaking populations, but there is no consensus yet on the question of whether the Munda (Austro-Asiatic) speaking populations originated in India or derive from a relatively recent migration from further East.ResultsHere, we report the analysis of 35 novel complete mtDNA sequences from India which refine the structure of Indian-specific varieties of haplogroup R. Detailed analysis of haplogroup R7, coupled with a survey of ~12,000 mtDNAs from caste and tribal groups over the entire Indian subcontinent, reveals that one of its more recently derived branches (R7a1), is particularly frequent among Munda-speaking tribal groups. This branch is nested within diverse R7 lineages found among Dravidian and Indo-European speakers of India. We have inferred from this that a subset of Munda-speaking groups have acquired R7 relatively recently. Furthermore, we find that the distribution of R7a1 within the Munda-speakers is largely restricted to one of the sub-branches (Kherwari) of northern Munda languages. This evidence does not support the hypothesis that the Austro-Asiatic speakers are the primary source of the R7 variation. Statistical analyses suggest a significant correlation between genetic variation and geography, rather than between genes and languages.ConclusionOur high-resolution phylogeographic study, involving diverse linguistic groups in India, suggests that the high frequency of mtDNA haplogroup R7 among Munda speaking populations of India can be explained best by gene flow from linguistically different populations of Indian subcontinent. The conclusion is based on the observation that among Indo-Europeans, and particularly in Dravidians, the haplogroup is, despite its lower frequency, phylogenetically more divergent, while among the Munda speakers only one sub-clade of R7, i.e. R7a1, can be observed. It is noteworthy that though R7 is autochthonous to India, and arises from the root of hg R, its distribution and phylogeography in India is not uniform. This suggests the more ancient establishment of an autochthonous matrilineal genetic structure, and that isolation in the Pleistocene, lineage loss through drift, and endogamy of prehistoric and historic groups have greatly inhibited genetic homogenization and geographical uniformity.
Progression of rheumatoid arthritis (RA) and osteoarthritis (OA) is associated with inflammation and oxidative stress. Previous studies have shown that there was no difference between RA and OA patients regarding the percentages of the different lymphocytes subsets reflecting the abnormalities in T cells and its subsets that may contribute to the pathogenesis of OA as in RA. Therefore, the present study was aimed to analyze that whether disease activity of OA is able to affect a few serological and biochemical parameters in the same way as RA does or differently. The study was done on 36 asymptomatic controls (25 women), 28 patients with OA (20 women), 36 patients with RA (22 women). Patients with OA were screened according to radiological and clinical finding of Kellgren and Lawrence grade and ACR criteria and assessed by VAS and WOMAC score. Patients with RA were selected who were fulfilling 4/5 symptoms of ACR criteria, and their DAS28-CRP, VAS score, and RF positivity were evaluated. Participants of the groups were matched for sex, age, weight, and height (body mass index). The BMI of all three groups was also found to be the same (P > 0.05). The mean level of LDL, cholesterol, MDA, CRP, and triglyceride was significantly (P < 0.05 or P < 0.01) higher in both OA and RA as compared to control. The mean level of total lipid, cholesterol, MDA, CRP, and triglyceride was found to be significantly (P < 0.05 or P < 0.01) higher in RA as compared to OA. The pre-treatment CRP level of both groups of patients showed significant and direct relation with total lipid (r = 0.27, P < 0.05) and cholesterol (r = 0.66, P < 0.01). Inverse relation was observed between uric acid and creatinine (r = -0.26, P < 0.05) and cholesterol and HDL (r = -0.34, P < 0.01). Our study shows the similar trend in lipid profile and other parameters studied in both patients with OA and patients with RA with more pronounced changes in RA.
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