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    Review Article Open Access
    The Origin of BPH and Prostate Cancer in Different Prostate Zones and the Impact on the Incidence of Prostate Cancer: A Systematic Review and Update of the Literature for Urologists and Clinicians
    Jake Sellers, Sarah Neal Secrest Horne, Werner T.W. de Riese
    Exploratory Research and Hypothesis in Medicine, Published online March 30, 2023. doi:10.14218/ERHM.2022.00120
    Abstract
    Numerous clinical studies over recent years have reported an inverse relationship between benign prostatic hyperplasia (BPH) size and the incidence of prostate cancer (PCa), leading [...] Read more.
    Numerous clinical studies over recent years have reported an inverse relationship between benign prostatic hyperplasia (BPH) size and the incidence of prostate cancer (PCa), leading to the clinical hypothesis that the expanding BPH zone damages the glandular tissue where PCa predominately develops. This systematic review aims to establish a historical basis and reference on the zonal origin of BPH and prostate cancer (PCa) within the prostate. Using the PRISMA guidelines, an in-depth review was conducted of studies published in the PubMed database between January 1978 and November 2022. Due to clinical heterogeneity in type of study designs, meta-analysis was not possible, and a narrative review approach was adopted. Thirty-eight studies met the inclusion criteria, all of which showed that BPH predominantly develops within the transition zone (TZ) and that PCa predominantly develops in the peripheral zone (PZ) of the prostate respectively. This report provides a systemic overview of the historical evolution on the concept of zonal origin for BPH and PCa. The listed studies support the current clinical understanding that BPH mainly originates in the TZ and that the majority of PCa originates in the PZ of the prostate. To our knowledge, this is the first systemic review on the zonal origin of BPH and PCa and is an important step in the context of evidence-based medicine. This review should encourage other clinicians and investigators to further study the dynamic interactions between the different prostate zones, in particular between the TZ and the PZ, and whether BPH size may be protective against development of PCa. Full article
    Review Article Open Access
    Evolution of Non-alcoholic Fatty Liver Disease to Liver Cancer: Insights from Genome-wide Association Studies
    Sathish Kumar Mungamuri, Yogendra Kumar Gupta, Padaki Nagaraja Rao, Bagepally Ravishankar
    Gene Expression, Published online March 28, 2023. doi:10.14218/GE.2022.00014
    Abstract
    Non-alcoholic fatty liver disease (NAFLD) is the most prevalent liver disease, affecting a quarter of the world’s population. The spectrum of NAFLD ranges from simple steatosis, non-alcoholic [...] Read more.
    Non-alcoholic fatty liver disease (NAFLD) is the most prevalent liver disease, affecting a quarter of the world’s population. The spectrum of NAFLD ranges from simple steatosis, non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and ultimately to hepatocellular carcinoma (HCC). Multiple factors are involved in the pathogenesis and progression of NAFLD, wherein genetic, epigenetic, environmental, gut-microbiome, and dietary factors play a substantial role. Robust genome-wide association studies (GWAS) have recently identified several genetic alterations contributing to NAFLD progression to liver cancer. This review describes the most critical genetic variations identified in various genes that modulate NAFLD pathogenesis. As expected, NAFLD shows gene variations that regulate or influence hepatocyte lipid metabolism. In addition to polymorphisms in genes that regulate insulin signaling, fibrosis, inflammation, and oxidative stress, cytokine/chemokine-expressing genes also participate in NAFLD pathogenesis. GWAS helped us distinguish genetic polymorphisms that modulate steatosis, fibrosis, or both in NAFLD patients. Identifying genetic factors predisposing an individual to NAFLD helps stratify people at high risk and aids in imparting preventive strategies early in life. Such studies should also help in adopting prevention strategies and targeted treatment regimes. Full article
    Original Article Open Access
    Metabolic Effects of Coconut Oil on Fatty Liver and Oxidative Stress Induced by a High-fat Diet in Rats
    Laura Perreira Barreto, Raissa Yolanda de Oliveira Silva, Bianca Bellizzi de Almeida, Paula Payão Ovídio, Alceu Afonso Jordao
    Gene Expression, Published online March 28, 2023. doi:10.14218/GE.2022.00006
    Abstract
    This study aimed to evaluate the effect of coconut oil (CO) on steatosis and oxidative stress in rats fed a high-fat diet. Three groups of male Wistar rats were used: the control group [...] Read more.
    This study aimed to evaluate the effect of coconut oil (CO) on steatosis and oxidative stress in rats fed a high-fat diet. Three groups of male Wistar rats were used: the control group (CG, n = 10) received a standard diet for 50 days, the hyperlipidic group (HL, n = 10) received a high-fat diet with 50% lard for 50 days, and the hyperlipidic-CO group (HL+CO, n = 10) received a high-fat diet with 50% lard for 30 days followed by 25% lard and 25% CO for 20 days. Then, the animals were euthanized, and their blood, liver, and adipose tissue were collected for biochemical analyses. The groups that received a high-fat diet had pronounced liver steatosis. Compared to the CG and HL groups, the HL+CO group had less weight gain, but liver fat and triglycerides were increased, with a significant reduction in liver cholesterol. Glutathione increased significantly and vitamin E decreased in the livers of the experimental groups compared to the control. Lipid peroxidation in the serum and liver was less in the HL+CO group compared to that in the HL group, but it was higher than that in the control group. CO caused significant accumulation of hepatic fat, triglycerides, and fat content, despite decreasing the hepatic cholesterol levels. There was a better hepatic antioxidant response in the CO group, especially compared with the HL group. CO was not able to prevent or improve liver fat levels, but the HL+CO group had a better antioxidant profile. Additional clinical studies are necessary to verify the efficacy and safety of different CO doses on both hepatic and lipid metabolism. Full article
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    Review Article Open Access
    Targeting the Wnt Signaling Pathway in Liver Fibrosis for Drug Options: An Update
    Kristina Duspara, Kristina Bojanic, Josipa Ivanusic Pejic, Lucija Kuna, Tea Omanovic Kolaric, Vjera Nincevic, Robert Smolic, Aleksandar Vcev, Marija Glasnovic, Ines Bilic Curcic, Martina Smolic
    Journal of Clinical and Translational Hepatology, Published online September 13, 2021. doi:10.14218/JCTH.2021.00065
    Abstract
    Liver fibrosis is a life-threatening disease, with challenging morbidity and mortality for healthcare systems worldwide. It imparts an enormous economic burden to societies, making [...] Read more.
    Liver fibrosis is a life-threatening disease, with challenging morbidity and mortality for healthcare systems worldwide. It imparts an enormous economic burden to societies, making continuous research and informational updates about its pathogenesis and treatment crucial. This review′s focus is on the current knowledge about the Wnt signaling pathway, serving as an important pathway in liver fibrosis development and activation of hepatic stellate cells (HSCs). Two types of Wnt pathways are distinguished, namely the ß-catenin-dependent canonical and non-canonical Ca2+ or planar cell polarity (PCP)-dependent pathway. The dynamic balance of physiologically healthy liver and hepatocytes is disturbed by repeated liver injuries. Activation of the ß-catenin Wnt pathway prevents the regeneration of hepatocytes by the replacement of extracellular matrix (ECM), leading to the appearance of scar tissue and the formation of regenerated nodular hepatocytes, lacking the original function of healthy hepatocytes. Therefore, liver function is reduced due to the severely advanced disease. Selective inhibition of ß-catenin inhibits inflammatory processes (since chemokines and pro-inflammatory cytokines are produced during Wnt activation), reduces growth of activated HSCs and reduces collagen synthesis and angiogenesis, thereby reducing the progression of liver fibrosis in vivo. While the canonical Wnt pathway is usually inactive in a physiologically healthy liver, it shows activity during cell regeneration or renewal and in certain pathophysiological conditions, such as liver diseases and cancer. Targeted blocking of some of the basic components of the Wnt pathway is a therapeutic approach. These include the frizzled transmembrane receptor (Fz) receptors using the secreted frizzled-related protein family (sFRP), Fz-coreceptors low-density LRP 5/6 through dickkopf-related protein 1 (DKK1) or niclosamide, glycogen kinase-3 beta (GSK-3β) using SB-216763, cyclic-AMP response element-binding protein (CBP) using PRI-724 and ICG-001, the lymphoid enhancer binding factor (LEF)/T cell-specific transcription factor (TCF) system as well as Wnt inhibitory factor 1 (WIF1) and miR-17-5p using pinostilbene hydrate (PSH). Significant progress has been made in inhibiting Wnt and thus stopping the progression of liver fibrosis by diminishing key components for its action. Comprehending the role of the Wnt signaling pathway in liver fibrosis may lead to discovery of novel targets in liver fibrosis therapeutic strategies’ development. Full article
    Original Article Open Access
    Prognostic Nomogram for Patients with Hepatitis E Virus-related Acute Liver Failure: A Multicenter Study in China
    Jian Wu, Cuifen Shi, Xinyu Sheng, Yanping Xu, Jinrong Zhang, Xinguo Zhao, Jiong Yu, Xinhui Shi, Gongqi Li, Hongcui Cao, Lanjuan Li
    Journal of Clinical and Translational Hepatology, Published online May 6, 2021. doi:10.14218/JCTH.2020.00117
    Abstract
    Timely and effective assessment scoring systems for predicting the mortality of patients with hepatitis E virus-related acute liver failure (HEV-ALF) are urgently needed. The present [...] Read more.
    Timely and effective assessment scoring systems for predicting the mortality of patients with hepatitis E virus-related acute liver failure (HEV-ALF) are urgently needed. The present study aimed to establish an effective nomogram for predicting the mortality of HEV-ALF patients. The nomogram was based on a cross-sectional set of 404 HEV-ALF patients who were identified and enrolled from a cohort of 650 patients with liver failure. To compare the performance with that of the model for end-stage liver disease (MELD) scoring and CLIF-Consortium-acute-on-chronic liver failure score (CLIF-C-ACLFs) models, we assessed the predictive accuracy of the nomogram using the concordance index (C-index), and its discriminative ability using time-dependent receiver operating characteristics (td-ROC) analysis, respectively. Multivariate logistic regression analysis of the development set carried out to predict mortality revealed that γ-glutamyl transpeptidase, albumin, total bilirubin, urea nitrogen, creatinine, international normalized ratio, and neutrophil-to-lymphocyte ratio were independent factors, all of which were incorporated into the new nomogram to predict the mortality of HEV-ALF patients. The area under the curve of this nomogram for mortality prediction was 0.671 (95% confidence interval: 0.602–0.740), which was higher than that of the MELD and CLIF-C-ACLFs models. Moreover, the td-ROC and decision curves analysis showed that both discriminative ability and threshold probabilities of the nomogram were superior to those of the MELD and CLIF-C-ACLFs models. A similar trend was observed in the validation set. The novel nomogram is an accurate and efficient mortality prediction method for HEV-ALF patients. Full article
    Original Article Open Access
    Underlying Causes of Death among Adults in the United States, 2013–2017
    Xin Hu, Yong Lin, Gangjian Qin, Lanjing Zhang
    Exploratory Research and Hypothesis in Medicine, Published online December 1, 2020. doi:10.14218/ERHM.2020.00065
    Abstract
    Overall mortality among U.S. adults has been stable in past years; however, racial disparity influenced 10 leading causes of death or age-specific mortality in Blacks or African Americans. [...] Read more.
    Overall mortality among U.S. adults has been stable in past years; however, racial disparity influenced 10 leading causes of death or age-specific mortality in Blacks or African Americans. Unfortunately, the trends in sex- and race-adjusted age-standardized cause-specific mortality are poorly understood. We here aimed to identify the underlying causes of death (UCD) with sex- and race-adjusted, and age-standardized mortality that has changed in recent years. We extracted the data of UCD from the Multiple Cause of Death database of the Centers for Disease Control and Prevention (CDC). Multivariable log-linear regression models were used to estimate trends in sex- and race-adjusted, and age-standardized mortality of UCD during 2013–2017. A total of 31,029,133 deaths were identified. Among the list of 113 UCDs compiled by the CDC, there were 29 UCDs exhibiting an upward trend, 33 UCDs exhibiting a downward trend and 56 UCDs with no significant trends. The 2 UCDs with the largest annual percent change were both nutrition related (annual percent change [APC] = 17.73, 95% CI [15.13–20.33] for malnutrition, and APC = 17.49, 95% CI [14.94–20.04] for Nutritional deficiencies), followed by accidental poisoning and exposure to noxious substances. The 4 UCDs with the largest decreasing APC were viral hepatitis (APC = −11.71), chronic and unspecified bronchitis (APC = −8.26), emphysema (APC = −7.11) and human immunodeficiency virus disease (APC = −7.10). This study thus reports UCDs with changing mortality in recent years after sex- and race-adjustments and age-standardizations. More effort and resources should focus on understanding, preventing and controling the mortality linked to these UCDs. Continuous monitoring of mortality trends is recommended. Full article
Special Features

Call for Papers for Special Issue 'Frontier research on the toxicity and efficacy of Chinese medicine'

Journal: Future Integrative Medicine
Special Issue: Frontier research on the toxicity and efficacy of Chinese medicine
Submission deadline: June 30, 2023
Publication date: An article will be published online as soon as it is accepted

Call for Papers for Special Issue ‘New Translational Challenges in Primary Biliary Cholangitis’

Journal: Journal Clinical and Translational Hepatology
Special Issue: New Translational Challenges in Primary Biliary Cholangitis
Submission deadline: June 30, 2023
Publication date: An article will be published online as soon as it is accepted

Call for Papers for Special Issue ‘A Spotlight on Progress and Pitfalls in NAFLD/MAFLD Studies, 2022’

Journal: Journal of Clinical and Translational Hepatology
Special Issue: A Spotlight on Progress and Pitfalls in NAFLD/MAFLD Studies, 2022
Submission deadline: March 30, 2023
Publication date: An article will be published online as soon as it is accepted

Call for Papers for Special Issue 'Comparative study of traditional medicine in the world'

Journal: Future Integrative Medicine
Special Issue: Comparative study of traditional medicine in the world
Submission deadline: June 30, 2023
Publication date: An article will be published online as soon as it is accepted

Call for Papers for Special Issue 'Therapeutic effects of herbal medicines on neurological impairment and related mental disorders based on the evidence of clinical and basic studies'

Journal: Future Integrative Medicine
Special Issue: Therapeutic effects of herbal medicines on neurological impairment and related mental disorders based on the evidence of clinical and basic studies
Submission deadline: June 30, 2023
Publication date: An article will be published online as soon as it is accepted

Call for Papers for Special Issue ‘Immunoregulatory Mechanisms of Herbal Medicines in Cancer and Infectious Diseases’

Journal: Future Integrative Medicine
Special Issue: Immunoregulatory Mechanisms of Herbal Medicines in Cancer and Infectious Diseases
Submission deadline: June 30, 2023
Publication date: An article will be published online as soon as it is accepted