Aluminium (Al) is the most ubiquitous metal in the Earth’s crust. Even though its toxicity is well-documented, the role of Al in the pathogenesis of several neurological diseases remains debatable. To establish the basic framework for future studies, we review literature reports on Al toxicokinetics and its role in Alzheimer’s disease (AD), autism spectrum disorder (ASD), alcohol use disorder (AUD), multiple sclerosis (MS), Parkinson’s disease (PD), and dialysis encephalopathy (DE) from 1976 to 2022. Despite poor absorption via mucosa, the biggest amount of Al comes with food, drinking water, and inhalation. Vaccines introduce negligible amounts of Al, while the data on skin absorption (which might be linked with carcinogenesis) is limited and requires further investigation. In the above-mentioned diseases, the literature shows excessive Al accumulation in the central nervous system (AD, AUD, MS, PD, DE) and epidemiological links between greater Al exposition and their increased prevalence (AD, PD, DE). Moreover, the literature suggests that Al has the potential as a marker of disease (AD, PD) and beneficial results of Al chelator use (such as cognitive improvement in AD, AUD, MS, and DE cases).

The thyroid gland is an endocrine organ whose hormones enable the proper functioning of the organism. The normal function of this organ is influenced by internal and external factors. One of the external factors is trace elements. Trace elements in appropriate concentrations are necessary for the proper functioning of the thyroid. Fe, Cu, Mn, I, Zn, and Se are part of the enzymes involved in oxidative stress reduction, while Cd, Hg, and Pb can increase ROS production. Cu and Fe are necessary for the correct TPO synthesis. An imbalance in the concentration of trace elements such as Fe, Cu, Co, I, Mn, Zn, Ag, Cd, Hg, Pb, and Se in thyroid cells can lead to thyroid diseases such as Graves’ disease, Hashimoto’s thyroiditis, hypothyroidism, autoimmune thyroiditis, thyroid nodules, thyroid cancer, and postpartum thyroiditis. Lack of adequate Fe levels may lead to hypothyroidism and cancer development. The thyroid gland’s ability to absorb I is reversibly reduced by Co. Adequate levels of I are required for correct thyroid function; both deficiency and excess can predispose to the development of thyroid disorders. High concentrations of Mn may lead to hypothyroidism. Furthermore, Mn may cause cancer development and progression. Insufficient Zn supplementation causes hypothyroidism and thyroid nodule development. Cd affecting molecular mechanisms may also lead to thyroid disorders. Hg accumulating in the thyroid may interfere with hormone secretion and stimulate cancer cell proliferation. A higher risk of thyroid nodules, cancer, autoimmune thyroiditis, and hypothyroidism were linked to elevated Pb levels. Se deficiency disrupts thyroid cell function and may lead to several thyroid disorders. On the other hand, some of the trace elements may be useful in the treatment of thyroid diseases. Therefore, the effects of trace elements on the thyroid require further research.

Proper joint function has a significant impact on people’s quality of life. Joints are the point of connection between two or more bones and consist of at least three elements: joint surfaces, the joint capsule, and the joint cavity. Joint diseases are a serious social problem. Risk factors for the development of these diseases include overweight and obesity, gender, and intestinal microbiome disorders. Another factor that is considered to influence joint diseases is trace elements. Under normal conditions, elements such as iron (Fe), copper (Cu), cobalt (Co), iodine (I), manganese (Mn), zinc (Zn), silver (Ag), cadmium (Cd), mercury (Hg), lead (Pb), nickel (Ni) selenium (Se), boron (B), and silicon (Si) are part of enzymes involved in reactions that determine the proper functioning of cells, regulate redox metabolism, and determine the maturation of cells that build joint components. However, when the normal concentration of the above-mentioned elements is disturbed and toxic elements are present, dangerous joint diseases can develop. In this article, we focus on the role of trace elements in joint function. We describe the molecular mechanisms that explain their interaction with chondrocytes, osteocytes, osteoblasts, osteoclasts, and synoviocytes, as well as their proliferation, apoptosis, and extracellular matrix synthesis. We also focus on the role of these trace elements in the pathogenesis of joint diseases: rheumatoid arthritis (RA), osteoarthritis (OA), psoriatic arthritis (PsA), ankylosing spondylitis (AS), and systemic lupus erythematosus (SLE). We describe the roles of increased or decreased concentrations of individual elements in the pathogenesis and development of joint diseases and their impact on inflammation and disease progression, referring to molecular mechanisms. We also discuss their potential application in the treatment of joint diseases.

Hepatocellular carcinoma (HCC) is the most common primary liver cancer with an increasing worldwide mortality rate. Cholangiocarcinoma (CCA) is the second most common primary liver cancer. In both types of cancers, early detection is very important. Biomarkers are a relevant part of diagnosis, enabling non-invasive detection and control of cancer recurrence, as well as in the application of screening tests in high-risk groups. Furthermore, some of these biomarkers are useful in controlling therapy and treatment selection. Detection of some markers presents higher sensitivity and specificity in combination with other markers when compared with a single detection. Some gene aberrations are also prognostic markers in the two types of cancers. In the following review, we discuss the most common biomarkers and genetic markers currently being used in the diagnosis of hepatocellular carcinoma and cholangiocarcinoma.

Gastric cancer (GC) ranks third in terms of cancer-related deaths and is the fifth most commonly diagnosed type of cancer. Its risk factors include Helicobacter pylori infection, Epstein–Barr virus infection, the consumption of broiled and charbroiled animal meats, salt-preserved and smoke-enhanced foods, alcohol drinking, tobacco smoking, exposure to ionizing radiation, and positive family history. The limited effectiveness of conventional therapies and the widespread risk factors of GC encourage the search for new methods of treatment and prevention. In the quest for cheap and commonly available medications, numerous studies focus on herbal medicine, traditional brews, and spices. In this review, we outline the potential use of spices, including turmeric, ginger, garlic, black cumin, chili pepper, saffron, black pepper, rosemary, galangal, coriander, wasabi, cinnamon, oregano, cardamom, fenugreek, caraway, clove, dill, thyme, Piper sarmentosum, basil, as well as the compounds they contain, in the prevention and treatment of GC. We present the potential molecular mechanisms responsible for the effectivity of a given seasoning substance and their impact on GC cells. We discuss their potential effects on proliferation, apoptosis, and migration. For most of the spices discussed, we also outline the unavailability and side effects of their use.

Background: Free fatal falls (FFF) represent a distinct form of blunt force trauma (BFT) that is frequently encountered in forensic practice. Distinguishing FFF injuries from other forms of BFT, such as motor vehicle accidents (MVAs), can pose challenges. Despite its growing usage, the role of postmortem computed tomography (PMCT) in diagnosing FFF and its comparison with autopsy remains underexplored. Purpose: This review synthesizes fracture patterns in FFF, examining both extrinsic and intrinsic variables that influence skeletal injuries. It also compares PMCT and autopsy findings to establish a replicable database for forensic analysis. Methods: PubMed and Google Scholar were systematically searched by three independent reviewers. The inclusion criteria required studies to be published in English, report at least 10 cases, focus on fatal falls, and provide precise data on skeletal injuries. Studies lacking detailed descriptions, focusing on survivors, or involving non-free falls were excluded. Data extraction tables facilitated synthesis and analysis. Key Findings: FFF are characterized mainly by axial skeletal fractures, particularly of the chest, skull, and pelvis. A history of intoxication and psychiatric disorders often correlates with the manner of death. Fracture patterns vary by fall height, impact surface, and cause: accidental falls show greater chest and skull involvement, whereas suicidal falls present more pelvic and skull fractures. PMCT detects fractures more frequently than traditional autopsy. Conclusions: Distinct fracture patterns aid in differentiating suicidal from accidental FFF, shaped by extrinsic and intrinsic factors. Given its superior fracture detection capabilities, PMCT should be integrated into forensic protocols for FFF investigations.