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Probiotic administration has become common practice in neonatal intensive care units (NICUs) to prevent necrotizing enterocolitis (NEC) and promote gut health in preterm infants. While probiotics are generally considered safe, rare cases of probiotic-related sepsis have been reported. We present a case of Lactobacillus rhamnosus sepsis in a preterm infant, highlighting the challenges involved in its diagnosis. The infant developed symptoms of sepsis on the 13th day of probiotic treatment. Laboratory analyses, including MALDI-TOF, BioFire BCID2 panel, and whole-genome sequencing (WGS), helped confirm the diagnosis and the presence of Lactobacillus rhamnosus. In this case, accurately identifying the Lactobacillus rhamnosus strain proved challenging, as initial analyses using the Vitek 2 system yielded incorrect identifications. This highlights the limitations of automated systems in distinguishing closely related species, reinforcing the need for advanced molecular techniques to achieve precise strain identification and confirm a probiotic-related infection. Given these diagnostic complexities, it is crucial for clinicians to maintain a high index of suspicion for probiotic-related infections in cases of unexplained sepsis, as this awareness can prompt further diagnostic investigations to ensure accurate pathogen identification. The infant responded to ampicillin therapy, showing clinical improvement within 10 days and was discharged in good health at 67 days of life. This case underscores the importance of advanced molecular diagnostic methods to confirm probiotic-related infections and highlights the need for caution in administering probiotics to vulnerable populations, such as preterm infants. Clinicians must maintain a high index of suspicion for probiotic-associated sepsis in unexplained cases of infection and tailor antibiotic therapy based on susceptibility profiles. These findings emphasize the need for rigorous monitoring, appropriate probiotic strain selection, and optimized safety protocols in NICUs to mitigate potential risks. [ABSTRACT FROM AUTHOR]

Simple Summary: In cancer research, the EMT is recognized as a hallmark of cancer metastasis, and a leading cause of cancer-related deaths. During the EMT, epithelial cells lose their cell–cell adhesion properties and acquire mesenchymal traits, enabling them to evade the surrounding tissues and migrate to distant sites. Several transcriptional factors are involved in the activation of the EMT. Our study focuses on how EMT transcriptional factors (e.g., SNAIL, TWIST, and ZEB) drive the EMT mechanism in both hematological malignancies and solid tumors. Understanding the role of EMT-TFs in cancer could lead to the development of targeted therapies to inhibit metastases. Background: The epithelial mesenchymal transition (EMT) is a biological process in which epithelial cells lose their polarity and adhesion characteristics, and adopt a mesenchymal phenotype. While the EMT naturally occurs during tissue fibrosis, wound healing, and embryonic development, it can be exploited by cancer cells and is strongly associated with cancer stem cell formation, tissue invasiveness, apoptosis, and therapy resistance. Transcription factors (TFs) such as SNAIL, ZEB, and TWIST play a pivotal role in driving the EMT. This systematic review aims to assess the impact of EMT-TFs on hematological malignancy and solid tumors. Methods: English-language literature published between 2010 and 2024 was systematically reviewed, utilizing databases such as PubMed and Google Scholar. Results: A total of 3250 studies were extracted. Of these, 92 publications meeting the inclusion criteria were analyzed to elucidate the role of EMT-TFs in cancer. The results demonstrated that the EMT-TFs play a critical role in both hematological and solid tumor development and progression. They promote invasive, migratory, and metastatic properties in these tumors, and contribute to therapeutic challenges by enhancing chemoresistance. A strong correlation between EMT-TFs and poor overall survival has been identified. Conclusions: Our research concluded that EMT-TFs may serve as important predictive and prognostic factors, as well as potential therapeutic targets to mitigate cancer progression. [ABSTRACT FROM AUTHOR]

Simple Summary: This study looks at the risk of developing breast cancer in survivors of Hodgkin lymphoma (HL), especially those who received chest radiation as part of their treatment. HL survivors are at a higher risk of breast cancer, and this risk increases over time. The research shows that radiation therapy used to treat HL can cause long-term damage to breast tissue, leading to an increased chance of developing cancer later on. The study also found that early screening and continuous monitoring are important for detecting cancer early in these survivors. Overall, it highlights the need for special care and surveillance for people who survived Hodgkin lymphoma, especially if they had been subjected to chest radiation. Hodgkin lymphoma (HL) treatment has dramatically improved, with high survival rates in early stages. However, long-term survivors face an increased risk of secondary cancers, particularly breast cancer (BC), which emerge as a leading cause of mortality decades after therapy. Background/Objectives: This study explores the risk of BC and the toxic effects of radiation therapy (RT) in long-term HL survivors compared to age-matched high-risk women, including BRCA1 and BRCA2 mutation carriers. A prospective study was conducted on 62 women who had undergone chemotherapy and involved-field RT for HL, with MRI used to assess breast tissue changes. This study's primary endpoint was to analyze BC incidence in HL survivors, while secondary objectives focused on the analysis of background parenchymal enhancement (BPE) in irradiated areas. Results: The findings revealed a 5% incidence of BC in HL survivors, with 50% showing moderate or marked BPE, similar to that observed in high-risk BC controls. No significant differences in BPE distribution were found between the two groups. Conclusions: The study highlights the long-term risk of BC in HL survivors and suggests that advanced RT techniques and targeted therapies may help reduce the incidence of secondary tumors. Future research should focus on understanding the genetic and biological mechanisms behind treatment-induced cancers [ABSTRACT FROM AUTHOR]

Autism spectrum disorder (ASD) is a neurological disease and lifelong condition. The treatment gap in ASD has led to growing interest in alternative therapies, particularly in phytocannabinoids, which are naturally present in Cannabis sativa. Studies indicate that treatment with cannabidiol (CBD)-rich cannabis may possess the potential to improve fundamental ASD symptoms as well as comorbid symptoms. This systematic review aims to assess the safety and efficacy of CBD-rich cannabis in alleviating the symptoms of ASD in both children and adults, addressing the treatment gap and growing interest in CBD as an alternative treatment. A comprehensive literature search was conducted in February 2024 using the PUBMED and Scopus databases while following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The search focused on studies from 2020 onward involving human populations diagnosed with ASD and treated with CBD. Four studies met the inclusion criteria and were analyzed. The review included 353 participants with ASD from studies conducted in Israel, Turkey, and Brazil. The studies varied in design, sample size, dose, and treatment duration. Dosages of CBD were often combined with trace amounts of THC. Improvements were noted in behavioral symptoms, social responsiveness, and communication, but cognitive benefits were less consistent. Adverse effects ranged in severity. Mild effects such as somnolence and decreased appetite were common, while more concerning effects, including increased aggression, led to some cases of treatment discontinuation. CBD-rich cannabis shows promise in improving behavioral symptoms associated with ASD. However, variations in study designs, dosages, and outcome measures highlight the need for standardized assessment tools and further research to understand pharmacological interactions and optimize treatment protocols. Despite the mild adverse effects observed, larger, well-controlled trials are necessary to establish comprehensive safety and efficacy profiles. [ABSTRACT FROM AUTHOR]

Background: The mouth and the oropharyngeal system are home to numerous bacterial species that constitute the so-called oral microbiome and play an important role for the integrity of the oral cavity, influencing the overall health of the body, as demonstrated by several studies. The aim of this study was to evaluate the bacterial modulation potential of a toothpaste (bioredoxin) containing curcumin and melatonin. Both substances have anti-inflammatory properties, as documented in several scientific reports. Methods: The in vivo study we present was a single-center, double-blind trial and was conducted in parallel groups. We enlisted 20 volunteers who were randomly assigned to four distinct groups using blinded four different toothpaste preparations: a standard toothpaste indicated as placebo, a toothpaste with curcumin, a toothpaste with melatonin, and a toothpaste with melatonin and curcumin. Results: The samples from the gingival tasks were taken at time 0 and after 8 weeks of toothpaste treatment. By evaluating the DNA content of the most significant periodontal bacteria related to the total bacteria count using quantitative PCR assays, including the saprophyte component of the microbiome, we demonstrated that the Curcumin and Melatonin treatment has a statistically relevant effect on decreasing the level of periodontal pathogenic bacteria DNA. The toothpaste with the addition of curcumin and melatonin showed a modulation between t0 and t1 of the Campylobacter rectus (14,568 vs. 3532.8) and Peptostreptococcus micro (1320.8 vs. 319) bacteria. In addition, a modulation of pathogenic bacteria and saprophytic bacteria was shown. The synergistic action of the two additives would therefore appear to lead to promising results. Conclusions: Despite the fact that additional studies may be necessary in evaluating the effect of the Curcumin/melatonin combination in modulating a proposed therapeutic effect on infections of the oropharyngeal apparatus, in this report, we show for the first time that a combination of curcumin and melatonin supplemented using an oral cosmetic vehicle has the capacity to decrease the level of periodontal pathogenic bacteria, possibly ameliorating health and the physiological conditions in the buccal scenario. [ABSTRACT FROM AUTHOR]

Myocardial Infraction and a therothrombotic ishemic stroke are considered to be caused by the rupture of vulnerable atherosclerotic plaques, which are complex disorders that result from multifaceted interactions between an individual's genetic makeup and environmental factors.

A study was conducted to determine another mechanism by which the BLC6 gene, which encodes a zinc-finger transcription factor, may be altered other than chromosomal rearrangements in its 5' noncoding region. Frequent somatic mutations in 5' noncoding sequences in diffuse large-cell lymphoma and follicular lymphoma were performed. The results showed that multiple mutations alter BCL6 expression.

Myocardial Infraction and a therothrombotic ishemic stroke are considered to be caused by the rupture of vulnerable atherosclerotic plaques, which are complex disorders that result from multifaceted interactions between an individual's genetic makeup and environmental factors.

Faccio, Lucia, Ang Chen, Carlo Fusco, Stefano Martinotti, Joseph V. Bonventre, and Antonis S. Zervos. Mxi2, a splice variant of p38 stress-activated kinase, is a distal nephron protein regulated with kidney ischemia. Am J Physiol Cell Physiol 278: C781-C790, 2000.--Mxi2 is one of three known alternative spliced forms of the stress-activated mitogen-activated protein kinase p38 (CSBP). Mxi2 was originally identified as a Max-interacting protein and is the smallest member of the family of stress-activated kinases isolated to date. Mxi2 lacks most of the XI domain found in p38 and instead has a distinct COOH-terminal sequence of 17 amino acids. Here we present the genomic structure of the Mxi2/p38 locus on human chromosome 6q21.2/21.3 and establish the origin of the three spliced forms of p38. Using Mxi2-specific antibodies in mouse organs, we found the Mxi2 protein to be present exclusively in the kidney. Mxi2 is present predominantly in the distal tubule of the nephron and the level of the protein decreased during kidney ischemia-reperfusion. Stress signals or other known activators of the p38 pathway including MAP kinase-kinase 3 and MAP kinase-kinase 6 did not induce the kinase activity of Mxi2 using ATF-2 as a substrate. With the use of hybrid proteins encoding different portions of Mxi2 and p38 polypeptides, the different properties of Mxi2 can be assigned to its unique COOH terminus. Mxi2 kinase; stress signaling; p38 kinase; distal tubule; Mxi2/p38 genomic locus