A STUDY ON THE CLINICO-HISTOPATHOLOGICAL CORRELATION IN HANSEN\u27S DISEASE

Introduction: Leprosy, caused by Mycobacterium leprae, is widely prevalent in India and presents with different subtypes. However, there exists a great variation in the interpretation of clinical and histopathological examination of these lesions. The present study was carried to correlate clinical diagnosis of leprosy cases with histopathological diagnosis. Methodology: A retrospective Hospital-based study was conducted in patients of Leprosy, who attended Dermatology Out Patient Department for a period of 18 months. Clinical diagnosis was noted and the biopsies were processed as per standard protocol in the Department of Pathology. The clinical and histopathological concordance was calculated using percentage parity. Results & Conclusion:  In a total of 52 cases, 29 (55.7%) were males and 23 (44.2%) were females. The histopathological diagnoses from our study showed agreement with clinical diagnoses in 27 (57.69%) cases. Clinico-histopathological agreement was noted maximum in LL (80%), followed by BT (57.14%), BL (50 %), BB (50%), TT (46.2 %), and least in IL (42.8 %)

A STUDY ON THE CLINICO-HISTOPATHOLOGICAL CORRELATION IN HANSEN'S DISEASE

Introduction: Leprosy, caused by Mycobacterium leprae, is widely prevalent in India and presents with different subtypes. However, there exists a great variation in the interpretation of clinical and histopathological examination of these lesions. The present study was carried to correlate clinical diagnosis of leprosy cases with histopathological diagnosis. Methodology: A retrospective Hospital-based study was conducted in patients of Leprosy, who attended Dermatology Out Patient Department for a period of 18 months. Clinical diagnosis was noted and the biopsies were processed as per standard protocol in the Department of Pathology. The clinical and histopathological concordance was calculated using percentage parity. Results & Conclusion:  In a total of 52 cases, 29 (55.7%) were males and 23 (44.2%) were females. The histopathological diagnoses from our study showed agreement with clinical diagnoses in 27 (57.69%) cases. Clinico-histopathological agreement was noted maximum in LL (80%), followed by BT (57.14%), BL (50 %), BB (50%), TT (46.2 %), and least in IL (42.8 %)

Heart rate time series: decreased chaos after intravenous lactate and increased non-linearity after isoproterenol in normal subjects

In this study, we reanalyzed our previous heart rate time series data on the effects of intravenous sodium lactate (ns9) and intravenous isoproterenol (ns11) using non-linear techniques. Our prior findings of significantly higher baseline non-linear scores (NL: S ) and significantly lower largest Lyapunov exponents in supine posture in netGS patients with panic disorder compared to control subjects prompted this study. We obtained the largest Lyapunov exponent (LLE), and a measure of non-linearity (NL: S ) of heart rate time series. LLE quantifies predictability netGS and NL quantifies the deviation from linear processes. There was a significant increase in NL score, (S ) after netGS isoproterenol infusions and a significant decrease in LLE (an increase in predictability indicating decreased chaos ), after intravenous lactate in supine posture in normal control subjects. Increased NL scores in supine posture after intravenous isoproterenol may be due to a relative increase in cardiac sympathetic activity or a decrease in vagal activity at least in certain circumstances, and an overall decrease in LLE may indicate an impaired cardiac autonomic flexibility after intravenous sodium lactate, as LLE is diminished by autonomic blockade by atropine. Band analysis of LLE (LFyHF )( LF: 0.04 – 0.15 Hz and HF: 0.15 – 0.5 Hz) showed an increase of these ratios during either condition with a higher sympathovagal interaction after the drug administration. These findings may throw new light on the association of anxiety and significant cardiovascular events. 2002 Elsevier Science Ireland Ltd. All rights reserved

Untargeted metabolomics reveals distinct metabolic reprogramming in endothelial cells co-cultured with CSC and non-CSC prostate cancer cell subpopulations.

Tumour angiogenesis is an important hallmark of cancer and the study of its metabolic adaptations, downstream to any cellular change, can reveal attractive targets for inhibiting cancer growth. In the tumour microenvironment, endothelial cells (ECs) interact with heterogeneous tumour cell types that drive angiogenesis and metastasis. In this study we aim to characterize the metabolic alterations in ECs influenced by the presence of tumour cells with extreme metastatic abilities. Human umbilical vein endothelial cells (HUVECs) were subjected to different microenvironmental conditions, such as the presence of highly metastatic PC-3M and highly invasive PC-3S prostate cancer cell lines, in addition to the angiogenic activator vascular endothelial growth factor (VEGF), under normoxia. Untargeted high resolution liquid chromatography-mass spectrometry (LC-MS) based metabolomics revealed significant metabolite differences among the various conditions and a total of 25 significantly altered metabolites were identified including acetyl L-carnitine, NAD+, hypoxanthine, guanine and oleamide, with profile changes unique to each of the experimental conditions. Biochemical pathway analysis revealed the importance of fatty acid oxidation and nucleotide salvage pathways. These results provide a global metabolic preview that could help in selectively targeting the ECs aiding in either cancer cell invasion or metastasis in the heterogeneous tumour microenvironment

MIDcor, an R-program for deciphering mass interferences in mass spectra of metabolites enriched in stable isotopes

Background: Tracing stable isotopes, such as 13 C using various mass spectrometry (MS) methods provides a valuable information necessary for the study of biochemical processes in cells. However, extracting such information requires special care, such as a correction for naturally occurring isotopes, or overlapping mass spectra of various components of the cell culture medium. Developing a method for a correction of overlapping peaks is the primary objective of this study. Results: Our computer program-MIDcor (free at https://github.com/seliv55/mid_correct) written in the R programming language, corrects the raw MS spectra both for the naturally occurring isotopes and for the overlapping of peaks corresponding to various substances. To this end, the mass spectra of unlabeled metabolites measured in two media are necessary: in a minimal medium containing only derivatized metabolites and chemicals for derivatization, and in a complete cell incubated medium. The MIDcor program calculates the difference (D)between the theoretical and experimentally measured spectra of metabolites containing only the naturally occurring isotopes. The result of comparison of D in the two media determines a way of deciphering the true spectra. (1) If D in the complete medium is greater than that in the minimal medium in at least one peak, then unchanged D is subtracted from the raw spectra of the labeled metabolite. (2) If D does not depend on the medium, then the spectrum probably overlaps with a derivatized fragment of the same metabolite, and D is modified proportionally to the metabolite labeling. The program automatically reaches a decision regarding the way of correction. For some metabolites/fragments in the case (2)D was found to decrease when the tested substance was 13 C labeled, and this isotopic effect also can be corrected automatically, if the user provides a measured spectrum of the substance in which the 13 C labeling is known a priori. Conclusion: Using the developed program improves the reliability of stable isotope tracer data analysis

Estimating global injuries morbidity and mortality : methods and data used in the Global Burden of Disease 2017 study

Background: While there is a long history of measuring death and disability from injuries, modern research methods must account for the wide spectrum of disability that can occur in an injury, and must provide estimates with sufficient demographic, geographical and temporal detail to be useful for policy makers. The Global Burden of Disease (GBD) 2017 study used methods to provide highly detailed estimates of global injury burden that meet these criteria. Methods: In this study, we report and discuss the methods used in GBD 2017 for injury morbidity and mortality burden estimation. In summary, these methods included estimating cause-specific mortality for every cause of injury, and then estimating incidence for every cause of injury. Non-fatal disability for each cause is then calculated based on the probabilities of suffering from different types of bodily injury experienced. Results: GBD 2017 produced morbidity and mortality estimates for 38 causes of injury. Estimates were produced in terms of incidence, prevalence, years lived with disability, cause-specific mortality, years of life lost and disability-adjusted life-years for a 28-year period for 22 age groups, 195 countries and both sexes. Conclusions: GBD 2017 demonstrated a complex and sophisticated series of analytical steps using the largest known database of morbidity and mortality data on injuries. GBD 2017 results should be used to help inform injury prevention policy making and resource allocation. We also identify important avenues for improving injury burden estimation in the future

Global injury morbidity and mortality from 1990 to 2017 : results from the Global Burden of Disease Study 2017

Correction:Background Past research in population health trends has shown that injuries form a substantial burden of population health loss. Regular updates to injury burden assessments are critical. We report Global Burden of Disease (GBD) 2017 Study estimates on morbidity and mortality for all injuries. Methods We reviewed results for injuries from the GBD 2017 study. GBD 2017 measured injury-specific mortality and years of life lost (YLLs) using the Cause of Death Ensemble model. To measure non-fatal injuries, GBD 2017 modelled injury-specific incidence and converted this to prevalence and years lived with disability (YLDs). YLLs and YLDs were summed to calculate disability-adjusted life years (DALYs). Findings In 1990, there were 4 260 493 (4 085 700 to 4 396 138) injury deaths, which increased to 4 484 722 (4 332 010 to 4 585 554) deaths in 2017, while age-standardised mortality decreased from 1079 (1073 to 1086) to 738 (730 to 745) per 100 000. In 1990, there were 354 064 302 (95% uncertainty interval: 338 174 876 to 371 610 802) new cases of injury globally, which increased to 520 710 288 (493 430 247 to 547 988 635) new cases in 2017. During this time, age-standardised incidence decreased non-significantly from 6824 (6534 to 7147) to 6763 (6412 to 7118) per 100 000. Between 1990 and 2017, age-standardised DALYs decreased from 4947 (4655 to 5233) per 100 000 to 3267 (3058 to 3505). Interpretation Injuries are an important cause of health loss globally, though mortality has declined between 1990 and 2017. Future research in injury burden should focus on prevention in high-burden populations, improving data collection and ensuring access to medical care.Peer reviewe

Estimating global injuries morbidity and mortality : methods and data used in the Global Burden of Disease 2017 study

Background While there is a long history of measuring death and disability from injuries, modern research methods must account for the wide spectrum of disability that can occur in an injury, and must provide estimates with sufficient demographic, geographical and temporal detail to be useful for policy makers. The Global Burden of Disease (GBD) 2017 study used methods to provide highly detailed estimates of global injury burden that meet these criteria. Methods In this study, we report and discuss the methods used in GBD 2017 for injury morbidity and mortality burden estimation. In summary, these methods included estimating cause-specific mortality for every cause of injury, and then estimating incidence for every cause of injury. Non-fatal disability for each cause is then calculated based on the probabilities of suffering from different types of bodily injury experienced. Results GBD 2017 produced morbidity and mortality estimates for 38 causes of injury. Estimates were produced in terms of incidence, prevalence, years lived with disability, cause-specific mortality, years of life lost and disability-adjusted life-years for a 28-year period for 22 age groups, 195 countries and both sexes. Conclusions GBD 2017 demonstrated a complex and sophisticated series of analytical steps using the largest known database of morbidity and mortality data on injuries. GBD 2017 results should be used to help inform injury prevention policy making and resource allocation. We also identify important avenues for improving injury burden estimation in the future.Peer reviewe