A series of mono- and heteronuclear platinum(II) and zinc(II) complexes with 4,4′,4″-tri-tert-butyl-2,2′:6′,2″-terpyridine ligand were synthesized and characterized. The DNA and protein binding properties of [ZnCl₂(terpy^tBu)] (C1), [{cis-PtCl(NH₃)₂(μ-pyrazine)ZnCl(terpy^tBu)}](ClO₄)₂ (C2), [{trans-PtCl(NH₃)₂(μ-pyrazine)ZnCl(terpy^tBu)}](ClO₄)₂ (C3), [{cis-PtCl(NH₃)₂(μ-4,4′-bipyridyl)ZnCl(terpy^tBu)}](CIO₄)₂ (C4) and [{trans-PtCl(NH₃)₂(μ-4,4′-bipyridyl)ZnCl(terpy^tBu)}](CIO₄)₂ (C5) (where terpy^tBu = 4,4′,4″-tri-tert-butyl-2,2′:6′,2″-terpyridine), were investigated by electronic absorption, fluorescence spectroscopic, and molecular docking methods. Complexes featuring transplatin exhibited lower K_b and K_sv constant values compared to cisplatin analogs. The lowest K_sv value belonged to complex C1, while C4 exhibited the highest. Molecular docking studies reveal that the binding of complex C1 to DNA is due to van der Waals forces, while that of C2–C5 is due to conventional hydrogen bonds and van der Waals forces. The tested complexes exhibited variable cytotoxicity toward mouse colorectal carcinoma (CT26), human colorectal carcinoma (HCT116 and SW480), and non-cancerous mouse mesenchymal stem cells (mMSC). Particularly, the mononuclear C1 complex showed pronounced selectivity toward cancer cells over non-cancerous mMSC. The C1 complex notably induced apoptosis in CT26 cells, effectively arrested the cell cycle in the G0/G1 phase, and selectively down-regulated Cyclin D.

Esophageal motility disorders are common conditions that impede the normal movement of food and liquids from the esophagus to the stomach, frequently manifesting as dysphagia, chest pain, and regurgitation. These disorders arise from a variety of etiological factors and can greatly diminish patients’ quality of life. If left untreated, esophageal motility disorders may lead to severe complications, including malnutrition, weight loss, and aspiration pneumonia. This chapter offers an in-depth examination of the etiology and pathogenesis of both primary and secondary EMDs. It thoroughly investigates the clinical manifestations and diagnostic methods, highlighting the critical role of differential diagnosis in the accurate identification of these conditions. Additionally, the chapter reviews current treatment options, including pharmacological interventions, endoscopic procedures, and surgical techniques, and discusses the potential of novel therapies and future research directions. Through a detailed analysis of these aspects, the chapter aims to provide a comprehensive understanding of esophageal motility disorders and to guide effective clinical management and innovative therapeutic approaches.

The coronavirus disease of 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2), includes a clinical spectrum of diseases from mild to severe progressive pneumonia, which has affected and still affects the human population worldwide. Most commonly, it is presented by respiratory symptoms, but studies have shown that about 50% of patients with SARS-CoV-2 infection have at least one gastrointestinal symptom (GI), predominantly nausea, diarrhea, vomiting, or loss of appetite. In addition, abnormal liver functional tests are commonly present in the SARS-CoV-2 virus. The aim of our study was to examine the GI and hepatic manifestations of COVID-19 in patients hospitalized due to COVID-19 pneumonia in “COVID hospital Batajnica”, University Clinical Center of Serbia in Belgrade. The study included 498 consecutive patients, and the data was obtained from the patient’s electronic medical history. GI symptoms included nausea, vomiting, diarrhea, and anorexia. Collected laboratory values included baseline and peak values of blood count, inflammatory parameters, liver function tests, renal function tests, and cardiac enzyme tests. The results have shown that GI symptoms occurred in 26% of cases at diagnosis, which indicates the great susceptibility of the GI system to SARS-CoV-2. There was a high risk of liver injury in patients with COVID-19 pneumonia (>60%). The level of AST is more often increased compared to ALT, which is different from other virus-induced liver lesions and may be a useful indicator of SARS-CoV-2 infection. Further research should focus on the causes of liver damage in SARS-CoV-2 virus and the impact on treatment and outcome of COVID-19 disease.

Chemerin, encoded by the RARRES2 gene, is an adipokine with potent immunometabolic functions mediated through CMKLR1, GPR1, and CCRL2. Its regulation is tissue- and context-dependent, conferring dual protective and pathogenic roles. In the upper GI tract, chemerin facilitates immune tolerance in Barrett’s adenocarcinoma and promotes invasion in esophageal and gastric cancers. In pancreatic disease, it acts as a biomarker of acute and chronic injury, while modulating β-cell function and carcinogenesis. In the liver, chemerin contributes to NAFLD/NASH pathogenesis with both anti-inflammatory and pro-steatotic actions, predicts prognosis in cirrhosis, and demonstrates tumor-suppressive potential in hepatocellular carcinoma. In IBD, chemerin exacerbates colitis via impaired macrophage polarization, yet protects epithelial antimicrobial defense, underscoring its context-specific biology. Collectively, these findings position chemerin as a versatile regulator bridging metabolic dysfunction, inflammation, and gastrointestinal malignancy, and as a potential candidate for biomarker development and therapeutic intervention.