RESUMEN
A metastatic condition involving signet ring cells rich in mucin is the Krukenberg tumor, which affects the ovaries. Usually, the metastatic disease does not include both ovaries and usually originates from the stomach side, while it can also occur less frequently from other locations. Krukenberg tumors are uncommon in younger age groups and usually occur after the age of 40. We report a case of a 34-year-old female patient with a primary form of past medical history. The patient was treated with multiple rounds of chemotherapy.
RESUMEN
One of the hallmarks of rheumatoid arthritis (RA) is inflammation of the synovial membrane, and oxidative stress is a mediator of tissue damage. RA is characterized by persistent joint inflammation, which leads to pain, edema, and finally joint destruction. Numerous biochemical markers can cause RA because of their impact on systemic and local inflammation. Numerous biomarkers have been investigated for their potential application in the diagnosis and prognosis of RA. In this review article, we evaluate the role of RA factor or rheumatoid factor (RF), uric acid, C-reactive protein (CRP), and adenosine deaminases (ADAs) as biomarkers in patients with and without arthritis. Studies that analyze and compare the levels of uric acid, ADAs, CRP, and RF in patients with and without arthritis. Although recent research has shown higher levels of uric acid, ADA, CRP, and RA in patients with RF compared to healthy controls, these findings may indicate a role for these markers in reflecting inflammation and disease activity. In the metabolism of purines, the enzyme ADA is involved. The liver produces CRP, which is then released into the bloodstream. In inflammatory situations, there is a rise in CRP levels. This biomarker is frequently used for systemic inflammatory assessment in RA. The pathophysiology and severity of RA have both been connected to uric acid, which has historically been linked to gout. One particular biomarker for RA is RF. When compared to a healthy control group of individuals with arthritis, this review provides valuable insights into the diagnostic and prognostic use of uric acid, CRP, ADAs, and RF.
RESUMEN
Sudden infant death is a complex event characterized by biochemical features that are difficult to understand in general settings. Herein, we present a case report of a three-month-old infant who succumbed to sudden infant death syndrome (SIDS), focusing on the biochemical abnormalities identified through post-mortem analysis. The infant, previously healthy and meeting developmental milestones, was found lifeless in the crib during sleep. An autopsy revealed no anatomical abnormalities or signs of external trauma, consistent with SIDS diagnosis. Biochemical analysis of SIDS continued after post-mortem samples revealed dysregulation in neurotransmitter pathways, particularly serotonin, within the brain stem. These findings suggest a potential disruption in serotonin signaling, which may contribute to the vulnerability of infants to sudden death during sleep. Furthermore, metabolic profiling revealed deficiencies in enzymes involved in mitochondrial energy metabolism, particularly those related to fatty acid oxidation. These metabolic disturbances may compromise cellular function and contribute to the pathogenesis of SIDS. Environmental factors were also explored, with analysis revealing elevated levels of nicotine metabolites in post-mortem samples, suggesting maternal smoking exposure during pregnancy. Nicotine and its derivatives have known effects on neurotransmitter systems, potentially exacerbating underlying biochemical vulnerabilities in susceptible infants. This case report underscores the complex interplay of biochemical factors in the pathogenesis of SIDS and highlights the importance of multidisciplinary approaches in unraveling its mysteries. Further research is warranted to elucidate the precise mechanisms underlying these biochemical abnormalities and to develop targeted interventions aimed at reducing the incidence of SIDS and safeguarding infant health.
RESUMEN
Healthcare workers continue to struggle with skin wound management. Despite the fact that there have been many methods created throughout the decades for skin regeneration, contemporary developments in regenerative medicine provide highly reliable methods for creating synthetic skin replacements, such as electrospinning, 3D bioprinting, or spraying, among all others. Specifically, skin sprays have been a cutting-edge method that is currently undergoing clinical testing and has lots of promise for providing cells and hydrogels to cure both acute and chronic wounds. Deposition of cells and scaffolding materials in successive layers over the burnt regions characterises 3D bioprinting for burn injury repair. Depending on the desired outcome, bioprinting of skin may be performed in vivo or in vitro. However, the location of the printing and the time required for the tissue to mature separates these two methods. Bioprinted skin for use in burn repair faces technical and regulatory hurdles before it may be used in clinical settings. Skin sprays provide various benefits to traditional wound care methods, inclusive of ease of administration, the ability to treat broad wound regions, and a consistent dispersion of the sprayed substance. The most recent developments in this technology are reviewed in this article, along with a thorough explanation of investigational and presently marketed acellular and cellular skin spray solutions that are utilized to treat a range of illnesses and administer various experimental materials. Additionally, we describe regulatory processes for their capitalization and cover key clinical studies for various skin illnesses and associated treatment circumstances because skin spray products are susceptible to several classifications. Finally, we provide an argument and offer potential future developments in the biotechnology of skin sprays for improved clinical dermatological applications.