Determination of sex from the width and the area of human sternum & manubrium in Gujarat population

Background: Determination of sex from the skeletal remains is of immense importance in the field of forensic medicine, physical anthropometry and anthropology. Various previous studies have demonstrated sternum as an important tool for the determination of sex. Aims: Aim of the present study was to establish normal range of values for the width and the area of sternum in the studied population and evaluate the sexual dimorphism in the sternum. Material & Methods: The present study was conducted at M.P. Shah Govt. Medical College, Jamnagar on Computed tomography scans of a total of 83 adult Gujarati individuals (57 males, 26 females). The sternal width and the sternal area were measured and analysed. Results: The width of the sternum at 1st and 3rd sternebrae and sternal area were found to be larger in male and the difference was statistically significant. The sternal area was found to be the most accurate for determination of sex among all studied parameters, which accurately identified 59.63% of sterna as male and 30.77% as female by the method of identification point. Conclusion: The sternal area is the most reliable criteria for the determination of the sex of a sternum. The widths of the sternum were found to be non-accurate for the determination of sex of a sternum. The sternum of the female is on average narrower and smaller than the male sternum

Adaptation and Mal-Adaptation to Ambient Hypoxia; Andean, Ethiopian and Himalayan Patterns

The study of the biology of evolution has been confined to laboratories and model organisms. However, controlled laboratory conditions are unlikely to model variations in environments that influence selection in wild populations. Thus, the study of “fitness” for survival and the genetics that influence this are best carried out in the field and in matching environments

RIP4 inhibits STAT3 signaling to sustain lung adenocarcinoma differentiation.

Loss of epithelial differentiation and extracellular matrix (ECM) remodeling are known to facilitate cancer progression and are associated with poor prognosis in patients with lung cancer. We have identified Receptor-interacting serine/threonine protein kinase 4 (RIP4) as a regulator of tumor differentiation in lung adenocarcinoma (AC). Bioinformatics analyses of human lung AC samples showed that poorly differentiated tumors express low levels of RIP4, whereas high levels are associated with better overall survival. In vitro, lung tumor cells expressing reduced RIP4 levels showed enhanced activation of STAT3 signaling and had a greater ability to invade through collagen. In contrast, overexpression of RIP4 inhibited STAT3 activation, which abrogated interleukin-6-dependent induction of lysyl oxidase, a collagen cross-linking enzyme. In an autochthonous mouse model of lung AC initiated by Kras(G12D) expression with loss of p53, Rip4 knockdown tumors progressed to a poorly differentiated state marked by an increase in Hmga2, reduced Ttf1, and enrichment of genes regulating extracellular remodeling and Jak-Stat signaling. Tail vein injections of cells overexpressing Rip4 showed a reduced potential to invade and form tumors, which was restored by co-expression of Stat3. Altogether, our work has identified that loss of RIP4 enhances STAT3 signaling in lung cancer cells, promoting the expression of ECM remodeling genes and cancer dedifferentiation

Frequency drift in MR spectroscopy at 3T

Purpose: Heating of gradient coils and passive shim components is a common cause of instability in the B-0 field, especially when gradient intensive sequences are used. The aim of the study was to set a benchmark for typical drift encountered during MR spectroscopy (MRS) to assess the need for real-time field-frequency locking on MRI scanners by comparing field drift data from a large number of sites.Method: A standardized protocol was developed for 80 participating sites using 99 3T MR scanners from 3 major vendors. Phantom water signals were acquired before and after an EPI sequence. The protocol consisted of: minimal preparatory imaging; a short pre-fMRI PRESS; a ten-minute fMRI acquisition; and a long post-fMRI PRESS acquisition. Both pre- and post-fMRI PRESS were non-water suppressed. Real-time frequency stabilization/adjustment was switched off when appropriate. Sixty scanners repeated the protocol for a second dataset. In addition, a three-hour post-fMRI MRS acquisition was performed at one site to observe change of gradient temperature and drift rate. Spectral analysis was performed using MATLAB. Frequency drift in pre-fMRI PRESS data were compared with the first 5:20 minutes and the full 30:00 minutes of data after fMRI. Median (interquartile range) drifts were measured and showed in violin plot. Paired t-tests were performed to compare frequency drift pre- and post-fMRI. A simulated in vivo spectrum was generated using FID-A to visualize the effect of the observed frequency drifts. The simulated spectrum was convolved with the frequency trace for the most extreme cases. Impacts of frequency drifts on NAA and GABA were also simulated as a function of linear drift. Data from the repeated protocol were compared with the corresponding first dataset using Pearson's and intraclass correlation coefficients (ICC).Results: Of the data collected from 99 scanners, 4 were excluded due to various reasons. Thus, data from 95 scanners were ultimately analyzed. For the first 5:20 min (64 transients), median (interquartile range) drift was 0.44 (1.29) Hz before fMRI and 0.83 (1.29) Hz after. This increased to 3.15 (4.02) Hz for the full 30 min (360 transients) run. Average drift rates were 0.29 Hz/min before fMRI and 0.43 Hz/min after. Paired t-tests indicated that drift increased after fMRI, as expected (p &lt; 0.05). Simulated spectra convolved with the frequency drift showed that the intensity of the NAA singlet was reduced by up to 26%, 44 % and 18% for GE, Philips and Siemens scanners after fMRI, respectively. ICCs indicated good agreement between datasets acquired on separate days. The single site long acquisition showed drift rate was reduced to 0.03 Hz/min approximately three hours after fMRI.Discussion: This study analyzed frequency drift data from 95 3T MRI scanners. Median levels of drift were relatively low (5-min average under 1 Hz), but the most extreme cases suffered from higher levels of drift. The extent of drift varied across scanners which both linear and nonlinear drifts were observed.</p

An Incidental Finding of the Thyroidea Ima Artery:-A Case Report Study

We are here reporting a case of an incidental finding of the thyroidea ima artery emerging from the brachiocephalic trunk with a typical inferior thyroid vessels on both sides emerging from the thyrocervical trunk. The thyroidea ima artery entered the thyroid gland near to anterior surface of right lobe of thyroid gland. It arose from the brachiocephalic artery proximal to its bifurcation

Radical Anion Complexes of Tris(1,3-diphenyltriazenido)aluminum More About This Article Radical Anion Complexes of Tis( 1,3-diphenyltiazenido)aluminum

Abstract: Electrochemical studies of Al(dpt)3 (Hdpt = 1,3-diphenyltriazene) by cyclic voltammetry in THF solution reveal three successive pseudo reversible one-electron reduction waves (E112 = -1.50, -1.84, and -2.16 V). The chemical reduction of Al(dpt)3 by sodium metal in THF allows for the isolation of the radical anion complexes [Na(THF)x]n[Al(dpt)3], n = 1 ( l ) , 1 (2), and 3 (3). Characterization by EPR, NMR, UV-visible, and X-ray photoelectron (XP) spectroscopy, in addition to the X-ray structural determination of [PPN] [Al(dpt)3] (4), supports the formation of the f i s t homologous series of ligand-centered aluminum(II1) radical anion complexes. Analogous electrochemical reduction series are observed for the p-methyl-and p-methoxy-substituted triazenides. The dependence of the complex reduction potentials is discussed with respect to the UV-visible spectra of the unreduced complex and the ligand&apos;s Hammett substituent constant (a). In contrast, irreversible electrochemical reduction (-1.5 to -2.2 V) occurs for the pentafluoro-and p-fluoro-, p-chloro-, and p-bromo-substituted triazenido complexes. Irreversible reduction also occurs for the alkyl and aryloxide compounds Al(R)z(dpt) (R = &apos;Bu, &apos;Bu), Al(&apos;Bu)(dpt)z, Al(BHT)z-(dpt), and Al(BHT)(dpt)z (BHT-H = 2,6-di-tert-butyl-4-methylphenol). Ab initio molecular orbital calculations have been carried out on the model compounds Al(HNNNH)3 and [Al(HNNNH)3I3-. The identity of the frontier molecular orbitals and calculated structures are considered in relation to experimental data

Mature neutrophils suppress T cell immunity in ovarian cancer microenvironment

Epithelial ovarian cancer (EOC) often presents with metastases and ascites. Granulocytic myeloid-derived suppressor cells are an immature population that impairs antitumor immunity. Since suppressive granulocytes in the ascites of patients with newly diagnosed EOC were morphologically mature, we hypothesized that PMN were rendered suppressive in the tumor microenvironment (TME). Circulating PMN from patients were not suppressive but acquired a suppressor phenotype (defined as ≥1 log10 reduction of anti-CD3/CD28-stimulated T cell proliferation) after ascites supernatant exposure. Ascites supernatants (20 of 31 supernatants) recapitulated the suppressor phenotype in PMN from healthy donors. T cell proliferation was restored with ascites removal and restimulation. PMN suppressors also inhibited T cell activation and cytokine production. PMN suppressors completely suppressed proliferation in naive, central memory, and effector memory T cells and in engineered tumor antigen-specific cytotoxic T lymphocytes, while antigen-specific cell lysis was unaffected. Inhibition of complement C3 activation and PMN effector functions, including CR3 signaling, protein synthesis, and vesicular trafficking, abrogated the PMN suppressor phenotype. Moreover, malignant effusions from patients with various metastatic cancers also induced the C3-dependent PMN suppressor phenotype. These results point to PMN impairing T cell expansion and activation in the TME and the potential for complement inhibition to abrogate this barrier to antitumor immunity