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Background: Perforated peptic ulcer (PPU) is one of the common complications of peptic ulcers. Open repair (OR) is the traditional surgical treatment for this condition, but with advances in laparoscopic and minimally invasive surgery, laparoscopic repair (LR) has gained popularity. Many studies have compared the effectiveness of OR vs. LR for PPU. However, the superiority of one method over the other remains a topic of debate. We conducted this review to investigate the advantages and disadvantages of LR over OR. Methods: PubMed, Scopus, Google Scholar, and Web of Science were searched from 2000 to 2022 for systematic reviews and meta‐analyses comparing OR and LR for PPU. Previous studies included seven postoperative outcomes, including mortality, reoperation, postoperative ileus, intra‐abdominal abscess, leakage, pneumonia, and wound infection. Two researchers independently extracted data and assessed the quality of the eligible studies using the AMSTAR 2 tool. Results: Five systematic reviews and meta‐analyses were included, involving 36 studies. The pooled estimate showed that the risks for mortality, postoperative ileus, and wound infection were significantly lower with LR. In comparison, the risks for reoperation and leakage were less with OR. Based on the pooled estimate, no significant relationship was noted between the surgical method and intraabdominal abscess or postoperative pneumonia. Conclusion: Evidence suggests that in stable patients with PPU, LR is better than OR in terms of mortality. However, more high‐quality evidence is needed to determine which is more appropriate for different circumstances (e.g., unstable or high‐risk patients). [ABSTRACT FROM AUTHOR]

Simple Summary: Xeroderma pigmentosum (XP) is a very rare recessive disease caused by the incapacity to resolve ultraviolet-induced DNA lesions through Nucleotide Excision Repair (NER). Some XP patients suffer from aggressive skin carcinoma and melanoma at a very early age (<8). Our previous results show that primary XP fibroblasts isolated from healthy, non-photo-exposed skin negatively impact the extracellular matrix and the activation of the innate immune system. Here, we show for the first time that XP group C primary fibroblasts also play a major role in cancer cell invasion ex vivo and in vivo through the overexpression of Hepatocyte Growth Factor/Scatter Factor (HGF/SF) in the absence of genotoxic attacks. Using inhibitors of the activation of the HGF/SF pathway counteracted the effects of XP fibroblasts on the growth of cancer cells, suggesting new perspectives in the care of XP patients. Xeroderma pigmentosum (XP) is a very rare recessive disease caused by the incapacity to resolve ultraviolet-induced DNA lesions through Nucleotide Excision Repair (NER). Most XP patients suffer from aggressive skin carcinoma and melanoma at a very early age (<8). Our previous results showed that primary XP fibroblasts isolated from healthy (non-photo-exposed) skin negatively impact the extracellular matrix and fail to activate the innate immune system. Here, we show for the first time that XP-C fibroblasts also play a major role in cancer cell invasion ex vivo and in vivo through the overexpression of Hepatocyte Growth Factor/Scatter Factor (HGF/SF) in the absence of genotoxic attacks. The use of inhibitors of the activation of the HGF/SF pathway counteracted the effects of XP fibroblasts on the growth of cancer cells, suggesting new perspectives in the care of XP patients. [ABSTRACT FROM AUTHOR]

Background & Objective: Mast cells play a role in the immune responses to fatty liver disease. The present study aimed to investigate the diagnostic value of hepatic mast cell concentration (MCC) in NAFLD and NASH severity and fibrosis grade. Methods: The present cross-sectional unremarkable hepatic histology, NAFLD, or NASH cases were enrolled. Demographic variables, BMI, hepatic stiffness assessed using fibroscan, portal inflammation, hepatic disease grade assessed using the NAFLD Activity Score (NAS), and hepatic fibrosis severity assessed using the NASH fibrosis stage, hepatic necrosis severity, and hepatic steatosis severity of the patients were collected. The hepatic specimens underwent immunohistochemical (IHC) staining. Results: Of a total of 92 patients with a mean age of 38.7±13.3 years, 56 (60.9%) were males. There were significant relationships between the NAS score of the patients and hepatic steatosis. Moreover, the NASH fibrosis stage had significant relationships with the variables of hepatic necrosis, steatosis, and stiffness. There were significant positive correlations between the mast cell concentration (MCC) in all zones of the hepatic tissue (zone 1, zone 2, zone 3, portal area, and total) and the variables of age, BMI, and hepatic necrosis, steatosis, and stiffness. The patients with a higher NASH fibrosis stage showed a significantly higher MCC in all zones of the hepatic tissue. Conclusion: Hepatic mast cell number may have a significant impact on the grade and fibrosis in NAFLD. However, it is recommended to perform further studies with larger sample sizes on patients with various etiologies for hepatic injury to confirm the present study results. [ABSTRACT FROM AUTHOR]

Primary cutaneous lymphomas (PCLs) are a heterogeneous group of lymphoproliferative disorders caused by the accumulation of neoplastic T or B lymphocytes in the skin. Sézary syndrome (SS) is an aggressive and rare form of cutaneous T cell lymphoma (CTCL) characterized by an erythroderma and the presence of atypical cerebriform T cells named Sézary cells in skin and blood. Most of the available treatments for SS are not curative, which means there is an urgent need for the development of novel efficient therapies. Recently, targeting cancer metabolism has emerged as a promising strategy for cancer therapy. This is due to the accumulating evidence that metabolic reprogramming highly contributes to tumor progression. Genes play a pivotal role in regulating metabolic processes, and alterations in these genes can disrupt the delicate balance of metabolic pathways, potentially contributing to cancer development. In this review, we discuss the importance of targeting energy metabolism in tumors and the currently available data on the metabolism of Sézary cells, paving the way for potential new therapeutic approaches aiming to improve clinical outcomes for patients suffering from SS. [ABSTRACT FROM AUTHOR]

Background: UV skin exposure is an important matter of public health, as the worldwide rising prevalence of skin cancers indicates. However, a wide majority of commercially available sunscreens are responsible for ocean ecosystem damages such as coral reef degradation and phytoplankton mortality. Aims: To answer the urge for new eco‐friendly UV filters, we studied the use of lecithin‐based multilamellar liposomes (MLLs) of controlled size and elasticity as a bio‐sourced and biodegradable alternative to classic sunscreens. These parameters control allows different skin layers targeting. Methods: The performance of two different MLLs compositions and a commercially available SPF50+ water‐resistant liposomal sunscreen was compared on skin explants. SC‐MLLs target the stratum corneum and Epi‐MLLs the whole epidermis. Preparations were applied prior to skin irradiation. Their efficiencies were evaluated histologically (hematoxylin and eosin staining plus cyclobutane pyrimidine dimer [CPD] immunostaining) and by skin barrier quality assessment (trans‐epithelial electrical resistance). Adhesiveness to the skin was also investigated. Results: Altogether, ex vivo results indicate MLLs offer a solar protection as effective as a SPF50+ water‐resistant liposomal sunscreen but with a better skin adhesiveness and an improved skin barrier function. Conclusion: Lecithin‐based MLLs of controlled physicochemical parameters can be used as a new eco‐friendly and water‐resistant agent for solar protection. The stratum corneum targeted action of SC‐MLLs appears to be more interesting, as SC‐MLLs exhibit an overall better performance than Epi‐MLLs at a lower cost. The skin barrier improvement showcased could be of interest to people suffering from dry skin or skin barrier impairment related disease. [ABSTRACT FROM AUTHOR]

Introduction Lung cancer is the leading cause of cancer death worldwide. Causative gene alterations have been identified in various signaling pathways including the MAPK, PI3K, oxidative stress response, RNA splicing, [...], Metabolic reprogramming is a common hallmark of cancer, but a large variability in tumor bioenergetics exists between patients. Using high-resolution respirometry on fresh biopsies of human lung adenocarcinoma, we identified 2 subgroups reflected in the histologically normal, paired, cancer-adjacent tissue: high ([OX.sup.+]) mitochondrial respiration and low ([OX.sup.-]) mitochondrial respiration. The [OX.sup.+] tumors poorly incorporated [[sup.18]F]fluorodeoxy-glucose and showed increased expression of the mitochondrial trifunctional fatty acid oxidation enzyme (MTP; HADHA) compared with the paired adjacent tissue. Genetic inhibition of MTP altered [OX.sup.+] tumor growth in vivo. Trimetazidine, an approved drug inhibitor of MTP used in cardiology, also reduced tumor growth and induced disruption of the physical interaction between the MTP and respiratory chain complex I, leading to a cellular redox and energy crisis. MTP expression in tumors was assessed using histology scoring methods and varied in negative correlation with [[sup.18]F]fluorodeoxy-glucose incorporation. These findings provide proof-of-concept data for preclinical, precision, bioenergetic medicine in oxidative lung carcinomas.