Acute pancreatitis (AP) is a common inflammatory state characterized by a clinical course that can lead to serious local and extrapancreatic organ malfunction and failure. Interleukins (ILs) are biologically active glycoproteins primarily produced by macrophages and lymphocytes. According to the literature, there are many ILs. However, this article represents a summary of the role of ILs in AP, such as IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-7, IL-8, IL-9, IL-10, IL-11, IL-12, IL-13, IL-14, IL-15, IL-16, IL-17, IL-18, IL-19, and IL-20. The ways to modulate IL activity to reduce inflammation and improve outcomes in individuals with this condition are under investigation. Drugs that target specific ILs might be developed to mitigate the effects of AP.

The existing literature highlights the presence of numerous coagulation factors and markers. Elevated levels of coagulation factors are associated with both existing and newly diagnosed cases of atrial fibrillation (AF). However, this article summarizes the role of coagulation in the pathogenesis of AF, which includes fibrinogen and fibrin, prothrombin, thrombomodulin, soluble urokinase plasminogen activator receptor, von Willebrand factor, P-selectin, D-dimer, plasminogen activator inhibitor-1, and platelet activation. Coagulation irregularities play a significant role in the pathogenesis of AF.

Nanoparticles are defined as structures of size ranges from 1-100 nm in diameter in at least one direction. Metallic nanoparticles are considered the most potent agents in the modern world because they are used in every field of life, including the biotechnology, medical, textile, and food industries. Owing to their increased application, humans are constantly exposed to these nanoparticles. Their physiochemical characteristics, as their large surface to volume ratio might enhance their toxicity, increased surface area of NPs exhibit increased biological activity i.e reactive oxygen species generation when compared to large particles of the same mass. Consequently, their biosafety is a matter of major concern. The liver is the primary organ for detoxification and the major organ exposed to nanoparticles. After penetrating the body, nanoparticles enter the bloodstream and are internalized by hepatocytes. After penetration, they cause genotoxicity, oxidative stress and histopathology in hepatic tissues.

Recently, innovative developments have been made in the rapidly developing field of nanotechnology. However, toxicity due to long-term exposure to various types of metal-based nanoparticles, especially metal and metal oxide nanoparticles, is gradually increasing. The kidney is prone to toxin-induced impairment because it is one of the main organs for eliminating multiple potentially dangerous substances, including nanoparticles (NPs), from mammals. However, the mechanisms underlying cytotoxicity triggered by various NPs have not yet been reported. This review summarizes the various mechanisms involved in metal-based nanoparticle-induced nephrotoxicity, focusing on Reactive Oxygen Species (ROS) production, which leads to oxidative stress and apoptosis. The mechanisms by which metal-based NPs cause serious side effects in the renal system and the specific toxicity of different types of metal NPs are also summarized.

GEMIN5 is a multifunctional RNA-binding protein required for the assembly of survival motor neurons. Several bi-allelic truncating and missense variants in this gene are reported to cause a neurodevelopmental disorder characterized by cerebellar atrophy, intellectual disability (ID), and motor dysfunction. Whole exome sequencing of a Pakistani consanguineous family with three brothers affected by ID, cerebral atrophy, mobility, and speech impairment revealed a novel homozygous 3bp-deletion NM_015465.5:c.3162_3164del that leads to the loss of NM_015465.5 (NP_056280.2):p. (Asp1054_Ala1055delinsGlu) amino acid in one of the α-helixes of the tetratricopeptide repeats of GEMIN5. In silico 3D representations of the GEMIN5 dimerization domain show that this variant likely affects the orientation of the downstream sidechains out of the helix axis, which would affect the packing with neighboring helices. The phenotype of all affected siblings overlaps well with previously reported patients, suggesting that NM_015465.5: c.3162_3164del (NP_056280.2):p. (Asp1054_Ala1055delinsGlu) is a novel GEMIN5 pathogenic variant. Overall, our data expands the molecular and clinical phenotype of the recently described neurodevelopmental disorder with cerebellar atrophy and motor dysfunction (NEDCAM) syndrome.