Previous Issue
Volume 7, September

Table of Contents

Diseases, Volume 7, Issue 4 (December 2019)

  • Issues are regarded as officially published after their release is announced to the table of contents alert mailing list.
  • You may sign up for e-mail alerts to receive table of contents of newly released issues.
  • PDF is the official format for papers published in both, html and pdf forms. To view the papers in pdf format, click on the "PDF Full-text" link, and use the free Adobe Readerexternal link to open them.
Order results
Result details
Select all
Export citation of selected articles as:
Open AccessReview
Role of Gut Dysbiosis in Liver Diseases: What Have We Learned So Far?
Diseases 2019, 7(4), 58; https://doi.org/10.3390/diseases7040058 - 12 Nov 2019
Abstract
Accumulating evidence supports that gut dysbiosis may relate to various liver diseases. Alcoholics with high intestinal permeability had a decrease in the abundance of Ruminnococcus. Intestinal dysmotility, increased gastric pH, and altered immune responses in addition to environmental and genetic factors are [...] Read more.
Accumulating evidence supports that gut dysbiosis may relate to various liver diseases. Alcoholics with high intestinal permeability had a decrease in the abundance of Ruminnococcus. Intestinal dysmotility, increased gastric pH, and altered immune responses in addition to environmental and genetic factors are likely to cause alcohol-associated gut microbial changes. Alcohol-induced dysbiosis may be associated with gut barrier dysfunction, as microbiota and their products modulate barrier function by affecting epithelial pro-inflammatory responses and mucosal repair functions. High levels of plasma endotoxin are detected in alcoholics, in moderate fatty liver to advanced cirrhosis. Decreased abundance of Faecalibacterium prausnitzii, an anti-inflammatory commensal, stimulating IL-10 secretion and inhibiting IL-12 and interferon-γ expression. Proteobacteria, Enterobacteriaceae, and Escherichia were reported to be increased in NAFLD (nonalcoholic fatty liver disease) patients. Increased abundance of fecal Escherichia to elevated blood alcohol levels in these patients and gut microbiota enriched in alcohol-producing bacteria produce more alcohol (alcohol hypothesis). Some undetermined pathological sequences related to gut dysbiosis may facilitate energy-producing and proinflammatory conditions for the progression of NAFLD. A shortage of autochthonous non-pathogenic bacteria and an overgrowth of potentially pathogenic bacteria are common findings in cirrhotic patients. The ratio of the amounts of beneficial autochthonous taxa (Lachnospiraceae + Ruminococaceae + Veillonellaceae + Clostridiales Incertae Sedis XIV) to those of potentially pathogenic taxa (Enterobacteriaceae + Bacteroidaceae) was low in those with early death and organ failure. Cirrhotic patients with decreased microbial diversity before liver transplantation were more likely to develop post-transplant infections and cognitive impairment related to residual dysbiosis. Patients with PSC had marked reduction of bacterial diversity. Enterococcus and Lactobacillus were increased in PSC patients (without liver cirrhosis.) Treatment-naive PBC patients were associated with altered composition and function of gut microbiota, as well as a lower level of diversity. As serum anti-gp210 antibody has been considered as an index of disease progression, relatively lower species richness and lower abundance of Faecalibacterium spp. in gp210-positive patients are interesting. The dysbiosis-induced altered bacterial metabolites such as a hepatocarcinogenesis promotor DCA, together with a leaky gut and bacterial translocation. Gut protective Akkermansia and butyrate-producing genera were decreased, while genera producing-lipopolysaccharide were increased in early hepatocellular carcinoma (HCC) patients. Full article
Show Figures

Figure 1

Open AccessFeature PaperReview
Histone Deacetylases and Their Inhibitors in Cancer Epigenetics
Diseases 2019, 7(4), 57; https://doi.org/10.3390/diseases7040057 - 01 Nov 2019
Abstract
Histone deacetylases (HDAC) and histone deacetylase inhibitors (HDACi) have greatly impacted the war on cancer. Their role in epigenetics has significantly altered the development of anticancer drugs used to treat the most rare, persistent forms of cancer. During transcription, HDAC and HDACi are [...] Read more.
Histone deacetylases (HDAC) and histone deacetylase inhibitors (HDACi) have greatly impacted the war on cancer. Their role in epigenetics has significantly altered the development of anticancer drugs used to treat the most rare, persistent forms of cancer. During transcription, HDAC and HDACi are used to regulate the genetic mutations found in cancerous cells by removing and/or preventing the removal of the acetyl group on specific histones. This activity determines the relaxed or condensed conformation of the nucleosome, changing the accessibility zones for transcription factors. These modifications lead to other biological processes for the cell, including cell cycle progression, proliferation, and differentiation. Each HDAC and HDACi class or group has a distinctive mechanism of action that can be utilized to halt the progression of cancerous cell growth. While the use of HDAC- and HDACi-derived compounds are relatively new in treatment of cancers, they have a proven efficacy when the appropriately utilized. This following manuscript highlights the mechanisms of action utilized by HDAC and HDACi in various cancer, their role in epigenetics, current drug manufacturers, and the impact predicative modeling systems have on cancer therapeutic drug discovery. Full article
(This article belongs to the Special Issue Epigenetics and Disease)
Open AccessReview
HIV Capsid Inhibitors Beyond PF74
Diseases 2019, 7(4), 56; https://doi.org/10.3390/diseases7040056 - 30 Oct 2019
Abstract
Human immunodeficiency virus (HIV) capsid plays important roles at multiple stages of viral replication. At the initial stages, controlled uncoating (disassembly) of the capsid ensures efficient reverse transcription of the single-stranded RNA genome, into the double-stranded DNA. Whereas at later stages, a proper [...] Read more.
Human immunodeficiency virus (HIV) capsid plays important roles at multiple stages of viral replication. At the initial stages, controlled uncoating (disassembly) of the capsid ensures efficient reverse transcription of the single-stranded RNA genome, into the double-stranded DNA. Whereas at later stages, a proper assembly of capsid ensures the formation of a mature infectious virus particle. Hence, the inhibition of capsid assembly and/or disassembly has been recognized as a potential therapeutic strategy, and several capsid inhibitors have been reported. Of these, PF-3450074 (PF74) has been extensively studied. Recently reported GS-CA inhibitors (GS-CA1 and GS-6207), have shown a strong potential and appear to contain a PF74 scaffold. The location of resistance mutations and the results of structural studies further suggest that GS-CA compounds and PF74 share the same binding pocket, which is located between capsid monomers. Additionally, phenylalanine derivatives containing the PF74 scaffold show slightly enhanced capsid inhibiting activity. A comparison of capsid structures in complex with host factors and PF74, reveals the presence of common chemical entities at topologically equivalent positions. Here we present the status of capsid inhibitors that contain PF74 scaffolds and propose that the PF74 scaffold may be used to develop strong and safe capsid inhibitors. Full article
(This article belongs to the Section Infectious Disease)
Show Figures

Figure 1

Open AccessFeature PaperCase Report
Rapid Induction and Maintenance of Remission in Refractory Ulcerative Colitis with Ustekinumab
Diseases 2019, 7(4), 55; https://doi.org/10.3390/diseases7040055 - 28 Sep 2019
Viewed by 381
Abstract
Ulcerative colitis is a chronic debilitating disease characterized by relapsing in intestinal inflammation and ulcers with no available cure. This is a clinical case report of a 52-year-old female patient with 30 years history of left-sided chronic ulcerative colitis controlled with standard of [...] Read more.
Ulcerative colitis is a chronic debilitating disease characterized by relapsing in intestinal inflammation and ulcers with no available cure. This is a clinical case report of a 52-year-old female patient with 30 years history of left-sided chronic ulcerative colitis controlled with standard of care (mesalamine and azathioprine) which subsequently relapsed and developed into active refractory ulcerative colitis. The patient became unresponsive to her medications including different forms of mesalamines and did not respond favorably to any of the other current therapies. Numerous attempts to stabilize her condition with immunosuppressants, steroids, probiotics, antibiotics, mesalamines, and various biologic agents failed to improve her clinical symptoms, and the patient was being considered for colectomy. As the last resort, modified therapy was prescribed with ustekinumab, a non-selective, anti-IL12/23 p40 monoclonal antibody. This medication has not been yet approved for use in ulcerative colitis patients. In this clinical case we report the efficacy of ustekinumab to rapidly induce and maintain remission of the severe chronic ulcerative colitis in the patient. To the best of our knowledge, this is the first report of utilizing ustakinamub therapy for rapid induction in an active refractory ulcerative colitis patient resulting in complete remission for over one year. Full article
(This article belongs to the Special Issue Chronic Inflammatory and Infectious Diseases)
Show Figures

Figure 1

Open AccessCommunication
Pathology is Always Around Us: Apophenia in Pathology, a Remarkable Unreported Phenomenon
Diseases 2019, 7(4), 54; https://doi.org/10.3390/diseases7040054 - 25 Sep 2019
Viewed by 185
Abstract
People often wonder, “How do pathologists identify the patterns that lead to a diagnosis [...] Full article
(This article belongs to the Special Issue Diagnostic and Therapeutic Challenges in Oral Medicine)
Show Figures

Figure 1

Previous Issue
Back to TopTop