Optic nerve neuropathies – causative factors, methods of diagnostics, current and future possibilities of treatment

Introduction:  Optic neuropathies are a broad group of diseases in which the dominant disturbance is damage to the optic nerve, often irreversible. Underlying causes of neuropathy are both genetic and environmental. Despite limited treatment options, much research is currently being done on substances that could improve optic nerve function and alleviate the clinical consequences of optic nerve damage. Purpose: This article describes current findings in both the optic nerve neuropathy pathophysiology and diagnosis of the disorder, as well as treatment options and future perspectives. State of knowledge: The pathogenetic cause of neuropathy is mainly demyelination within the neural sheath, often caused by inflammation. It is characterized by progressive loss of vision. The most common genetic cause of optic neuropathy is mitochondrially inherited Leber hereditary optic neuropathy (LHON) and is characterized by mostly sudden and painless loss of visual acuity. Toxic neuropathies are a group of diseases caused by heavy metals, pharmaceuticals, methanol and carbon monoxide. Nutritional neuropathy is mainly related to vitamin B1, B9 and B12 deficiency, and is a rare example of neuropathy that can be curable at the early stage of the disease. Another group of neuropathies is caused by ischemia and can be divided according to the place of the optic nerve affected – AION (anterior ischemic optic neuropathy) and PION (posterior ischemic optic neuropathy). Conclusions: The therapeutic options in the treatment of optic neuropathy strictly depend on the causative factor. Nutritional deficiencies are treated with appropriate supplementation, so it is vital to truly determine the missing vitamins and elements

WHO global research priorities for antimicrobial resistance in human health

The WHO research agenda for antimicrobial resistance (AMR) in human health has identified 40 research priorities to be addressed by the year 2030. These priorities focus on bacterial and fungal pathogens of crucial importance in addressing AMR, including drug-resistant pathogens causing tuberculosis. These research priorities encompass the entire people-centred journey, covering prevention, diagnosis, and treatment of antimicrobial-resistant infections, in addition to addressing the overarching knowledge gaps in AMR epidemiology, burden and drivers, policies and regulations, and awareness and education. The research priorities were identified through a multistage process, starting with a comprehensive scoping review of knowledge gaps, with expert inputs gathered through a survey and open call. The priority setting involved a rigorous modified Child Health and Nutrition Research Initiative approach, ensuring global representation and applicability of the findings. The ultimate goal of this research agenda is to encourage research and investment in the generation of evidence to better understand AMR dynamics and facilitate policy translation for reducing the burden and consequences of AMR.info:eu-repo/semantics/publishedVersio

Immunological Aspects of the Tumor Microenvironment and Epithelial-Mesenchymal Transition in Gastric Carcinogenesis

Infection with Helicobacter pylori, a Gram-negative, microaerophilic pathogen often results in gastric cancer in a subset of affected individuals. This explains why H. pylori is the only bacterium classified as a class I carcinogen by the World Health Organization. Several studies have pinpointed mechanisms by which H. pylori alters signaling pathways in the host cell to cause diseases. In this article, the authors have reviewed 234 studies conducted over a span of 18 years (2002–2020). The studies investigated the various mechanisms associated with gastric cancer induction. For the past 1.5 years, researchers have discovered new mechanisms contributing to gastric cancer linked to H. pylori etiology. Alongside alteration of the host signaling pathways using oncogenic CagA pathways, H. pylori induce DNA damage in the host and alter the methylation of DNA as a means of perturbing downstream signaling. Also, with H. pylori, several pathways in the host cell are activated, resulting in epithelial-to-mesenchymal transition (EMT), together with the induction of cell proliferation and survival. Studies have shown that H. pylori enhances gastric carcinogenesis via a multifactorial approach. What is intriguing is that most of the targeted mechanisms and pathways appear common with various forms of cancer

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Helicobacter pylori (H. pylori) is one of the most common human pathogens, affecting half of the world’s population. Approximately 20% of the infected patients develop gastric ulcers or neoplastic changes in the gastric stroma. An infection also leads to the progression of epithelial–mesenchymal transition within gastric tissue, increasing the probability of gastric cancer development. This paper aims to review the role of H. pylori and its virulence factors in epithelial–mesenchymal transition associated with malignant transformation within the gastric stroma. The reviewed factors included: CagA (cytotoxin-associated gene A) along with induction of cancer stem-cell properties and interaction with YAP (Yes-associated protein pathway), tumor necrosis factor α-inducing protein, Lpp20 lipoprotein, Afadin protein, penicillin-binding protein 1A, microRNA-29a-3p, programmed cell death protein 4, lysosomal-associated protein transmembrane 4β, cancer-associated fibroblasts, heparin-binding epidermal growth factor (HB-EGF), matrix metalloproteinase-7 (MMP-7), and cancer stem cells (CSCs). The review summarizes the most recent findings, providing insight into potential molecular targets and new treatment strategies for gastric cancer

Toxic and Nutritional Optic Neuropathies—An Updated Mini-Review

Optic neuropathies constitute a group of conditions with various etiologies and might be caused by different factors; we can distinguish the genetic and acquired causes of optic neuropathies. Even though the symptoms are not highly specific, this condition is primarily characterized by unilateral or bilateral vision loss with worsening color detection. The loss may be acute or gradual depending on the causation. In this article, we included a specification of toxic optic neuropathy (TON) mainly triggered by alcohol abuse and also the usage of other substances, including drugs or methanol, as well as intoxication by metals, organic solvents, or carbon dioxide. Nutritional deficiencies, vitamin absorption disorder, and anemia, which usually appear during excessive alcohol intake, and their effect on the etiology of the optic neuropathy have been likewise discussed