Miracle-dz/UniFAR-FTUs huggingface dataset:
Study Of Serum Lipid Profile In Pre-Eclampsia And Eclampsia

The present study was designed to evaluate the association of lipid profile in pre- eclampsia and eclampsia. This case-control study was carried out in the department of biochemistry, M.A.G. Osmani Medical College, Sylhet, during July 2005 to June 2006. Total 100 study subjects were evaluated, 40 normotensive pregnant women (mean age 24.90 ± 4.04) as normal and 60 already diagnosed preeclamptic & eclamptic women (mean age 24.17 ± 4.90) as study group. Age range was 15-45 years, gestational age 24 weeks to term were included. Patients with pre-existing hypertension were excluded. Serum lipid profile (total lipids, cholesterol, triglycerides, HDL-cholesterol and LDLcholesterol) of hundred women with Pre-eclampsia and Eclampsia (n=60), normotensive women (n=40) were monitored. The preeclampsia was associated with a significant rise in triglyceride (225.6 ± 28.93 vs 165.6 ± 17.22) and fall in HDL cholesterol concentration (42.4 ± 9.29 vs 55.7 ± 7.11), while eclamptic women showed significant fall in HDL cholesterol (41.8 ± 8.79 vs 55.7 ± 7.11) and rise in LDL cholesterol (133.4 ± 11.75 vs 115.2 ± 10.72) as compared to normal pregnant women. Lipid metabolism plays a key role in the pathophysiology of Pre-eclampsia and Eclampsia. Increased triglycerides levels along with decreased HDL-cholesterol levels and delayed triglycerides clearance and high blood pressure are associated with development of preeclampsia and eclampsia. This association may be significant in understanding the pathologic processes of preeclampsia and may help in developing strategies for prevention or early diagnosis of the disorder. Key Words: Preeclampsia; High Density Lipoproteins; Triglycerides; Low Density Lipoprotein. DOI: 10.3329/fmcj.v5i2. 6823 Faridpur Med. Coll. J. 2010;5(2):56-59
Drug‐induced liver injury associated with stevens‐Johnson syndrome/toxic epidermal necrolysis: Patient characteristics, causes, and outcome in 36 cases

The liver and skin are the organs most commonly involved in serious adverse drug reactions. Rarely a drug reaction can affect both organs concurrently. The association of drug‐induced liver injury (DILI) and Stevens‐Johnson syndrome (SJS) or toxic epidermal necrosis (TEN) is even rarer and not well studied. We describe our experience of DILI occurring in association with SJS/TEN including the etiologic agents, clinical and biochemical characteristics, and outcome. We identified patients who developed DILI in association with SJS/TEN from a registry of DILI patients from a single center. Causality assessment for DILI and SJS/TEN was carried out with the Roussel Uclaf Causality Assessment Method and the Algorithm for Drug Causality for Epidermal Necrolysis, respectively. Among 748 consecutive patients with DILI from 1997 to March 2015, 36 (4.8%) had associated features of SJS/TEN. The mean age was 32 years (females 19). Children and patients with human immunodeficiency virus constituted 25% (n = 9) and 22% (n = 8), respectively. Only a small number of “high‐risk” drugs such as antiepileptic agents, sulfonamides, and antiretroviral drugs accounted for the majority of cases. Overall mortality was 36% (n = 13), which rose to 45.5% in the presence of jaundice. Mortality was less in children 11% (n = 1) and human immunodeficiency virus patients 12.5% (n = 1). Conclusions: DILI associated with SJS/TEN is rare and associated with a high death rate, particularly in those with jaundice; however, children and human immunodeficiency virus–infected individuals have a favorable outcome; a small group of drugs contributed to a disproportionate number of cases, and causality with Roussel Uclaf Causality Assessment Method and the Algorithm for Drug Causality for Epidermal Necrolysis was highly probable or probable in all cases. (Hepatology 2016;63:993–999)
Diagnosis of Acute Appendicitis During Pregnancy: A Systematic Review

Objective: To perform a systematic review to evaluate the diagnostic performance of computed tomography (CT) and magnetic resonance imaging (MRI) for the diagnosis of appendicitis in pregnancy. Data Sources: A systematic literature search of MEDLINE from 1966 through August 2008, MEDION database, OVID MEDLINE from 1950 through August 2008, and bibliographies of review articles and eligible studies. Methods of Study Selection: Three articles related to the use of CT and 5 to the use of MRI for the diagnosis of acute appendicitis during pregnancy were identified. All of the identified studies were retrospective. Findings were compared to surgical pathology and/or clinical follow-up. Results were pooled using the Mantel–Haenszel fixed-effects model and the DerSimonian–Laird random-effects model. Tabulation, Integration, and Results: The pooled estimates of sensitivity and specificity, positive and negative likelihood ratios for the performance of CT in patients with prior normal/inconclusive ultrasonography result were 85.7% (95% CI: 63.7%–97%) and 97.4% (95% CI: 86.2%–99.9%), 10.1 (95% CI: 3.4–30.1), and 0.21 (95% CI: 0.05–0.88), respectively. The pooled estimates of sensitivity and specificity, positive and negative likelihood ratios for performance of MRI in patients with prior normal/inconclusive ultrasonography result were 80% (95% CI: 44%–98%) and 99% (95% CI: 94%–100%), 22.7 (95% CI: 6.0–87.5), and 0.29 (95% CI: 0.13–0.68), respectively. Conclusion: This review is limited by the small number and retrospective nature of the available studies. With these limitations in mind, CT and MRI seem to be highly sensitive and specific for the diagnosis of appendicitis in pregnancy and their use should be considered when the results of ultrasonography are normal or inconclusive and appendicitis is suspected. Target Audience: Obstetricians & Gynecologists, Family Physicians Learning Objectives: After completion of this article, the reader should be able to recall the obstacles to correct diagnosis of appendicitis in pregnancy, compare the advantages and disadvantages of magnetic resonance imaging and computed tomography in the evaluation of the gravid patient with suspected appendicitis, and state the risks to a pregnant patient and her fetus with appendicitis in pregnancy.
Integrin αvβ6 critically regulates hepatic progenitor cell function and promotes ductular reaction, fibrosis, and tumorigenesis

Integrin αvβ6 is rapidly up‐regulated on cells of epithelial lineage during tissue injury, where one of its primary functions is activation of latent transforming growth factor beta 1 (TGFβ1). In human liver cirrhosis, αvβ6 is overexpressed by cells comprising the ductular reaction, and its inhibition suppresses experimental biliary fibrosis in rodents. Here, we show that αvβ6 is expressed on the actively proliferating subset of hepatic progenitor cells and is required for their progenitor function in vivo and in vitro through integrin αvβ6‐dependent TGFβ1 activation. Freshly isolated αvβ6+ liver cells demonstrate clonogenic potential and differentiate into cholangiocytes and functional hepatocytes in vitro, whereas colony formation by epithelial cell adhesion molecule‐positive progenitor cells is blocked by αvβ6‐neutralizing antibody and in integrin beta 6‐deficient cells. Inhibition of progenitors by anti‐αvβ6 antibody is recapitulated by TGFβ1 neutralization and rescued by addition of bioactive TGFβ1. Genetic disruption or selective targeting of αvβ6 with 3G9 antibody potently inhibits progenitor cell responses in mouse models of chronic biliary injury and protects from liver fibrosis and tumorigenesis, two conditions clinically associated with exacerbated ductular reaction. Conclusion: These results suggest that αvβ6 is a promising target for chronic fibrotic liver diseases and associated cancers. (Hepatology 2016;63:217–232)
Inhibition of hedgehog signaling ameliorates hepatic inflammation in mice with nonalcoholic fatty liver disease

Hedgehog (Hh) signaling plays a critical role in liver development, regeneration, injury repair, and carcinogenesis. Activation of Hh signaling has been observed in patients with nonalcoholic fatty liver diseases (NAFLD); however, the pathobiological function and regulatory mechanism of hepatic Hh signaling in the pathogenesis of NAFLD remain to be further defined. This study was designed to examine the effect and mechanism of hepatic Hh signaling in high‐fat diet‐induced NAFLD by using pharmacological Smoothened (Smo) inhibitors (GDC‐0449 and LED225) and liver‐specific Smo knockout mice. Administration of Smo inhibitors to high‐fat diet‐fed wild‐type mice significantly reduced the numbers of activated macrophages and decreased the expression of proinflammatory cytokines (tumor necrosis factor‐α, interleukin‐1β, monocyte chemoattractant protein 1, and interleukin‐6) as assessed by F4/80 immunohistochemistry and quantitative reverse‐transcription polymerase chain reaction, respectively. The Smo inhibitors were noted to have variable effects on hepatic fat accumulation. Liver‐specific deletion of Smo also reduced macrophage activation and inhibited proinflammatory cytokine expression, while it did not significantly alter fat accumulation in the liver. Mechanistically, we found that activation of glioma‐associated oncogene 1 by Hh signaling in primary hepatocytes increased the production of osteopontin, which subsequently enhanced the macrophage‐mediated proinflammatory response through paracrine signaling. Conclusion: Hepatocyte Hh signaling can promote liver inflammation through osteopontin‐mediated macrophage activation; this mechanism importantly contributes to the progression of NAFLD. (Hepatology 2016;63:1155–1169)
Evoked Potential Primer: Visual, Auditory, and Somatosensory Evoked Potentials in Clinical Diagnosis

This small volume is dedicated "to the concept of efficient, accurate and functional educational processes" and attempts to replace the-traditional approach of "memorising long lists and pieces of information" about individual nerves by a discussion of cranial nerve anatomy and function on a systems basis. The introduction provides an elementary overview of basic neurological terms (such as axon, afferent and efferent) and a brief summary of the anatomy and function of each cranial nerve. The remainder of the volume is divided into short tersely written chapters on motor innervation, sensory innervation, visceral sensory innervation, motor nuclei, sensory nuclei, etc. and is supplemented by abundant simple line drawings, tables and aspects. While the systems approach advocated in this book may be of value as an introduction to the cranial nerves for undergraduates in all branches ofmedicine, the presentation of the text appears to offer no great advantage over the traditional approach and appears merely an alternative way of compiling unending lists. The low price of the book would naturally attract medical undergraduates, but the oversimplified and sometimes confusing line drawings are of limited value to clinicians requiring a detailed working knowledge of cranial nerve anatomy.
Role of human papillomaviruses in esophageal squamous cell carcinoma

Esophageal cancer (EC) is responsible for almost half a million deaths worldwide annually and has a multifactorial etiology, which may account for its geographical variation in incidence. In the last 30 years the potential of human papillomaviruses (HPV) as oncogenes or co‐factors in the tumorigenic process of esophageal squamous cell carcinoma (ESCC) has been widely studied. While the etiology of HPV in cervical and certain other anogenital and aerodigestive cancers has been established, results regarding its role in EC have been largely inconclusive. A causal association can be evaluated only with a case‐control study, where normal controls are compared to ESCC cases for the presence of HPV. We reviewed all studies investigating ESCC tissue for HPV DNA and identified 139 that met our inclusion criteria, of which only 22 were case‐control studies. Our results support previous findings of higher levels of HPV detection in high‐risk ESCC regions than in areas of low risk. In addition, we confirm that the role of HPV in ESCC remains unclear, despite an accumulation of studies on the subject. The variations in investigative technique, study design and sample types tested may account for the lack of consistency in results. There is a need for a meta‐analysis of all case‐control studies to date, and for large, well‐designed case‐control studies with adequate power to investigate the association. The potential benefits of prophylactic HPV vaccines could be evaluated if HPV is identified as an etiological factor in EC, highlighting the need for further research in this area.
Melatonin attenuates MPTP-induced neurotoxicity via preventing CDK5-mediated autophagy and SNCA/α-synuclein aggregation

Autophagy is involved in the pathogenesis of neurodegenerative diseases including Parkinson disease (PD). However, little is known about the regulation of autophagy in neurodegenerative process. In this study, we characterized aberrant activation of autophagy induced by neurotoxin 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) and demonstrated that melatonin has a protective effect on neurotoxicity. We found an excessive activation of autophagy in monkey brain tissues and C6 cells, induced by MPTP, which is mediated by CDK5 (cyclin-dependent kinase 5). MPTP treatment significantly reduced total dendritic length and dendritic complexity of cultured primary cortical neurons and melatonin could reverse this effect. Decreased TH (tyrosine hydroxylase)-positive cells and dendrites of dopaminergic neurons in the substantia nigra pars compacta (SNc) were observed in MPTP-treated monkeys and mice. Along with decreased TH protein level, we observed an upregulation of CDK5 and enhanced autophagic activity in the striatum of mice with MPTP injection. These changes could be salvaged by melatonin treatment or knockdown of CDK5. Importantly, melatonin or knockdown of CDK5 reduced MPTP-induced SNCA/α-synuclein aggregation in mice, which is widely thought to trigger the pathogenesis of PD. Finally, melatonin or knockdown of CDK5 counteracted the PD phenotype in mice induced by MPTP. Our findings uncover a potent role of CDK5-mediated autophagy in the pathogenesis of PD, and suggest that control of autophagic pathways may provide an important clue for exploring potential target for novel therapeutics of PD.
Assessing Cephalopelvic Disproportion: Back to the Basics

Dystocia, or abnormally slow progress in labor, can result from cephalopelvic disproportion (CPD), malposition of the fetal head as it enters the birth canal, or ineffective uterine propulsive forces. Cephalopelvic disproportion occurs when there is mismatch between the size of the fetal head and size of the maternal pelvis, resulting in “failure to progress” in labor for mechanical reasons. Untreated, the consequence is obstructed labor that can endanger the lives of both mother and fetus. Despite the use of imaging technology in an attempt to predict CPD, there is poor correlation between radiologic pelvimetry and the clinical outcome of labor. Clinical pelvimetry still has a place in obstetrics for predicting or confirming CPD, but without appropriate training and repeated practice of this clinical skill, it is in danger of becoming a lost art. For this review, a computerized search of the terms cephalopelvic disproportion, dystocia, pelvimetry, obstructed labor, and malposition was done using MEDLINE, PUBMED, SCOPUS, and CINAHL, and historical articles, texts, articles from indexed journals, and references cited in published works were also reviewed. Target Audience: Obstetricians & Gynecologists, Family Physicians Learning Objectives: After completion of this article, the reader will be able to interpret how cephalopelvic disproportion is diagnosed. Distinguish the 4 basic pelvic shapes. Evaluate pelvic measurements that best indicate adequacy or inadequacy of the pelvis.
Cryptococcal Osteomyelitis Complicating Intestinal Lymphangiectasia: A Case Report and Review of the Literature

Abstract We report the first documented case of cryptococcal skeletal infection associated with intestinal lymphangiectasia (IL). This poorly recognized form of protein-losing enteropathy results in a loss of lymph with leakage of immunoglobulins and/or lymphocytes into the gut. This leads to the depletion of primarily naive CD4+ T cells, leaving the patient with impaired T-cell function. An esophagogastroduodenoscopy and small-bowel biopsy are often needed for diagnosis. Multiple case reports have documented the onset of cryptococcal infection in human immunodeficiency virus-negative patients with idiopathic T-cell deficiency. We assert that IL may be responsible for a considerable number of cases of invasive cryptococcal disease in patients with CD4+ T-cell lymphopenia in whom no other source of immunodeficiency has been identified. We also discuss skeletal involvement in disseminated cryptococcal infection and review the cases of cryptococcal disease and IL in the English language literature.
Anthropometric correlates of bench press performance following resistance training

Fifty‐four moderately trained men were evaluated following resistance training to determine the contribution of structural dimensions to maximal bench press lifting capacity. Muscle circumferences were taken around the flexed upper arm and the relaxed chest. Skeletal dimensions included the length of the upper and lower arm, the drop distance of the bar during the bench press lift, and the width between the hands on the lifting bar. Skinfolds were used to estimate body composition. Multiple regression analysis selected upper arm muscle plus bone cross‐sectional area, age, upper arm length, and lean body mass as the best predictors of bench press performance (r = 0.79, standard error of estimate = 13.8 kg). Prediction of Schwartz rating bench press (r = 0.59) and bench press/ kg (r = 0.56) from anthropometric dimensions were less successful but used similar variables. Body mass, either in the form of total body mass or lean body mass, appeared to be the major factor influencing bench press performance. In .
Prospective validation of ab initio liver transplantation in hepatocellular carcinoma upon detection of risk factors for recurrence after resection

A decade ago we proposed to enlist for transplantation those patients with resected hepatocellular carcinoma in whom pathology registered pejorative histological markers (microvascular invasion and/or satellites; ab initio indication) and not wait for the appearance of recurrence. This study evaluates the outcome of this approach. From 1995 to 2012, 164 patients with hepatocellular carcinoma underwent resection. Eighty‐five patients were potential candidates for liver transplantation and were considered for it upon detection of pejorative histological markers. Patients without these markers were followed, and salvage liver transplantation was considered upon development of tumor recurrence/liver function impairment. Thirty‐seven patients were at high risk and 48 at low risk of recurrence at pathology. Twenty‐three out of 37 high‐risk patients recurred during follow‐up, but in nine of them the tumor burden extent contraindicated liver transplantation. Seventeen were finally transplanted: 10 of them presented recurrence at imaging/explant. After a median posttransplant follow‐up of 50.9 months, hepatocellular carcinoma had recurred in two patients and five patients had died, the 5‐year survival being 82.4%. Twenty‐six of the 48 low‐risk patients developed recurrence, and 11 of them were transplanted. After a median posttransplant follow‐up of 59 months, two patients developed recurrence and five died, their 5‐year survival being 81.8%. Conclusion: Enlistment of patients at high risk of HCC recurrence after resection but before recurrence development seems a valid strategy and is associated with excellent long‐term outcome; as early (<6 months) recurrence reflects an aggressive tumor behavior leading to tumor extent exceeding transplant criteria, we propose to wait at least 6 months before enlistment; however, once included on the waiting list, priority strategies should be implemented in order to reach effective transplantation prior to the appearance of recurrence. (Hepatology 2016;63:839–849)
Screening for thyroid dysfunction during pregnancy

Introduction: Thyroid disorders are among the common endocrine disorders in pregnant women. It is now well established that not only overt but subclinical thyroid dysfunction can also have adverse effects on fetal and maternal outcome. Maternal hypothyroidism during pregnancy raises serious concern about long-lasting psycho-neurologic consequences for the progeny, due to the risk of insuf-ficient placental transfer of maternal thyroid hormones to the developing fetus during the first half of gestation. To validate the need of antenatal screening for maternal thyroid dysfunction this study was undertaken to know the prevalence of thyroid dysfunction among pregnant women in Central India. Materials and Methods: In this ongoing study so far 73 patients in the first trimester of pregnancy have been recruited from Matru Seva Sangh Hospital. Detailed history and examination were done. Serum thyroid-stimulating hormone (TSH) estimation was done by the immunoradiometric assay method. Results: Out of 73 patients, 30 (41%) had TSH less than 2 mIU/ml, 35 out of 73 (47.95%) had TSH between 2 mIU/ml and 4 mIU/ml. The TSH value of more than or equal to 4 mIU/ml was seen in 8/73 (10.96%). Two patients also had gestational diabetes. TSH levels were more than 2 in both. Conclusions: Prevalence of hypothyroidism is more than 10%. As per recommendations all patients with TSH levels more than 2 should be evaluated for free T4 and thyroid antibody estimation. Screening for thyroid dysfunction should be done early in pregnancy. Looking at the high percentage of abnormal TSH in pregnancies, universal screening should be considered.
The presence of LC3B puncta and HMGB1 expression in malignant cells correlate with the immune infiltrate in breast cancer

ABSTRACT Several cell-intrinsic alterations have poor prognostic features in human breast cancer, as exemplified by the absence of MAP1LC3B/LC3B (microtubule-associated protein 1 light chain 3 β)-positive puncta in the cytoplasm (which indicates reduced autophagic flux) or the loss of nuclear HMGB1 expression by malignant cells. It is well established that breast cancer is under strong immunosurveillance, as reflected by the fact that scarce infiltration of the malignant lesion by CD8+ cytotoxic T lymphocytes or comparatively dense infiltration by immunosuppressive cell types (such as FOXP3+ regulatory T cells or CD68+ tumor-associated macrophages), resulting in low CD8+:FOXP3+ or CD8+:CD68+ ratios, has a negative prognostic impact. Here, we reveal the surprising finding that cell-intrinsic features may influence the composition of the immune infiltrate in human breast cancer. Thus, the absence of LC3B puncta is correlated with intratumoral (but not peritumoral) infiltration by fewer CD8+ cells and more FOXP3+ or CD68+ cells, resulting in a major drop in the CD8+:FOXP3+ or CD8+:CD68+ ratios. Moreover, absence of HMGB1 expression in nuclei correlated with a general drop in all immune effectors, in particular FOXP3+ and CD68+ cells, both within the tumor and close to it. Combined analysis of LC3B puncta and HMGB1 expression allowed for improved stratification of patients with respect to the characteristics of their immune infiltrate as well as overall and metastasis-free survival. It can be speculated that blocked autophagy in, or HMGB1 loss from, cancer cells may favor tumor progression due to their negative impact on anticancer immunosurveillance.