Wireless capsule endoscopy is currently considered the gold standard in the investigation of the small bowel. It is both practical for physicians and easily accepted by patients. Prior to its development, two types of imaging investigations of the small bowel were available: radiologic and endoscopic. The first category is less invasive and comfortable for patients; it presents the ensemble of the small bowel, but it may imply radiation exposure. Images are constructed based on signals emitted by various equipment and require special interpretation. Endoscopic techniques provide real‑time colored images acquired by miniature cameras from inside the small bowel, require interpretation only from a medical point of view, may allow the possibility to perform biopsies, but the investigation only covers a part of the small bowel and are more difficult to accept by patients. Wireless capsule endoscopy is the current solution that overcomes a part of the previous drawbacks: it covers the entire small bowel, it provides real‑time images acquired by cameras, it is painless for patients, and it represents an abundant source of information for physicians. Yet, it lacks motion control and the possibility to perform biopsies or administer drugs. However, significant effort has been oriented in these directions by technical and medical teams, and more advanced capsules will surely be available in the following years.

Developmental defects of enamel (DDEs) are deviations from the normal appearance in terms of the quantity and quality of tooth enamel. They may be genetic or acquired. The most important DDEs are hypomineralization and hypoplasia. The aim of this study was to produce “in vivo” DDE in Wistar rats by administering amoxicillin to pregnant females and to highlight these lesions after sacrifice of the pups by macroscopic and microscopic examination and optical coherence tomography (OCT). Amoxicillin (100 mg/kg) was administered to two pregnant Wistar female rats for the production of DDEs. When the pups were 2 months old, they were sacrificed, and their jaws were harvested together with their teeth. The jaws were examined macroscopically, microscopically, and by OCT. Following the macroscopic and microscopic examination, it was established that four pups had a total of 42 DDE lesions. At the OCT examination, the hypomineralization was characterized by an intense, inhomogeneous OCT signal, and the hypoplasia was characterized by the absence of the signal. Administration of amoxicillin to pregnant females of Wistar rats resulted in DDEs in their offspring. The OCT examination confirmed the presence of these lesions in the teeth of rat pups.

Obstructive sleep apnea (OSA) and metabolic dysfunction-associated steatotic liver disease (MASLD) frequently coexist and share a common cardiometabolic substrate through a shared cardiometabolic substrate. This narrative review critically appraises the epidemiological, experimental, and interventional evidence proposed to link chronic intermittent hypoxia (CIH) and sleep fragmentation to hepatic steatosis, steatohepatitis, and fibrosis. We summarize the candidate mechanisms, including mitochondrial oxidative stress, hypoxia-inducible factor 1-alpha signaling, sympathetically driven lipolysis, and Kupffer and stellate cell activation and then examine the limits of the evidence supporting them: hypoxia-induced hypophagia and the scarcity of pair-fed controls in rodent models, species differences in the physiological response to hypoxia, publication bias, common-cause confounding by age and systemic inflammation, and the rarity of progressive liver disease in lean patients with anatomically driven OSA. We further review non-invasive diagnostic tools, polysomnographic hypoxemia indices, transient elastography, METS-IR, FIB-4, and emerging biomarkers, such as omentin-1 and follistatin-like 1, that enable bidirectional screening between sleep and hepatology clinics. Finally, we discuss therapeutic strategies, including continuous positive airway pressure, structured weight loss, and incretin-based pharmacotherapy (GLP-1 and dual GIP/GLP-1 receptor agonists), highlighting recent phase 3 evidence for tirzepatide in OSA and semaglutide in metabolic dysfunction-associated steatohepatitis. Current evidence supports CIH as a context-dependent amplifier of liver injury in patients with pre-existing metabolic dysfunction rather than as an established independent cause of MASH. This interpretation still justifies integrated screening and treatment pathways, while identifying the study designs needed to test causality directly.

Wastewater from the food industry is characterized by major changes in quality indicators, and their discharge into the natural water cycle causes contamination of the receiving basin. The most important categories of wastewater from sugar beet processing technology (in terms of quantity and quality) are represented by: wastewater resulting from the transport and washing of raw materials; wastewater resulting from the diffusion and pressing process; condensation water. Wastewater from the diffusion and pressing process is characterized by a high nutrient content. The discharge of these wastewaters into a receiving river can cause its rapid siltation, followed by rapid oxygen consumption. Due to the high temperatures specific to this category of wastewater, the discharge area in particular is likely to be completely devoid of oxygen. This process can also be accompanied by anaerobic fermentations (generating a specific unpleasant smell), as well as the development of biocenoses specific to dirty water. A first step in the treatment of wastewater from sugar beet processing technology consists of its decantation (in order to remove suspended matter). with or without coagulation. The process is carried out using decanters which can be: horizontal, vertical, radial or multi-stage. As a rule, vertical or radial decanters are used, which require a smaller installation space.

Obstructive sleep apnea (OSA) is strongly associated with hypertension, yet the apnea–hypopnea index (AHI), while it defines the presence and frequency of respiratory events, predicts cardiovascular risk less reliably in the individual patient than metrics that incorporate the depth and duration of hypoxic exposure. Patients with comparable AHI values can differ substantially in nocturnal hypoxemia, sympathetic activation, ambulatory blood pressure behavior, and target-organ damage, exposing a persistent gap between respiratory classification and cardiovascular prognosis. This review synthesizes current evidence on the mechanisms linking OSA to hypertension, intermittent hypoxia, chemoreflex-mediated sympathetic overactivity, renin–angiotensin–aldosterone system activation, hypoxia-associated insulin resistance and examines emerging metrics, including hypoxic burden, oxygen desaturation index, and ambulatory blood pressure monitoring, that capture cardiovascular risk more accurately than AHI alone. We describe six cardiovascular phenotypes of hypertension in OSA: resistant, nocturnal, non-dipping/reverse-dipping, masked, and morning-surge hypertension, alongside hypertension-mediated target-organ damage, each with distinct mechanisms, prognosis, and treatment response. Because intermittent hypoxia and sympathetic activation are also implicated in insulin resistance and MASLD, this shared metabolic pathway is integrated throughout rather than treated as an incidental comorbidity. Building on this evidence, we propose a phenotype-oriented clinical framework spanning cardiovascular screening, multidomain phenotyping, risk stratification, and personalized therapy intended to complement, not replace, AHI-based diagnosis and current hypertension guidelines. This framework is presented as a conceptual, expert-derived proposal intended to structure clinical reasoning, and it has not been derived from or validated in an independent cohort. We conclude with future directions, including digital biomarkers, multimodal imaging, and artificial intelligence-assisted phenotyping, as pathways toward precision cardiovascular medicine in hypertensive patients with OSA.