Colorectal cancer (CRC), like all other cancers, results from genetic and epigenetic alterations of the genome. The mechanisms leading to epigenetic alterations include DNA methylation, histone modifications, and small non-coding RNAs. As shown in many studies, some histone modifications such as acetylation, methylation, and phosphorylation are reported to be altered in CRC. Since these epigenetic alterations are reversible, they can be targeted as a strategy for CRC treatment. Numerous studies demonstrate the effects of molecules (both natural and synthetic) as inhibitors of enzymes responsible for histone acetylation, methylation, and phosphorylation in CRC cell lines. Some of these molecules have reached clinical trial stages. Vorinostat and belinostat, as histone deacetylase inhibitors; pinometostat and ribavirin, as histone methyltransferase inhibitors; and staurosporine and barasertib, which target histone phosphorylation, are among the promising epigenetic modifiers targeting histone alterations. Some of these modifiers can be used alone or in combination with other anticancer drugs or radiotherapy to increase efficacy. This review aims to identify molecules that target enzymes responsible for altering acetylation, methylation, and phosphorylation of histones in CRC.

Potential celiac disease (PCD) is defined as elevated celiac serology with a preserved small intestinal mucosa. This study aimed to identify baseline characteristics and the outcomes of children with PCD consuming a gluten-containing diet.

This was a retrospective cohort study of pediatric PCD patients diagnosed between 12/2018 and 10/2024. Baseline data included demographics, anthropometrics, clinical symptoms and signs, celiac serology, and biopsy results. Follow-up data included repeat serology and biopsy results when performed.

PCD was diagnosed in 75/517 (14.5%) children undergoing upper endoscopy for suspected celiac disease (CeD). Baseline anti-transglutaminase IgA (TTG) was above 10× the upper limit of normal (ULN) in 18 (24%), between 3–10× ULN in 52 (69.3%), and <3× ULN in five (6.6%). Anti-endomysial antibody was positive in 57 (76%). Among 48 children (64%) with at least one year of follow-up, TTG normalized in 26 (54.1%), decreased to <3× ULN in 13 (27.1%), was between 3–10× ULN in six (12.5%), and was above 10× ULN in three (6.3%). Nine children had a repeat endoscopy, and six (66.7%) were diagnosed with CeD, while three remained PCD. Among the 11 children with TTG >10× ULN and at least one year of follow-up, TTG normalized in three, declined in five, and increased or remained above 10× ULN in three.

PCD is common and may be found in children with TTG above 10× ULN; approximately half will normalize TTG. The omission of biopsies may result in an erroneous diagnosis of CeD.

Guaiac fecal occult blood test (gFOBT) is often used to evaluate evidence of food protein-induced allergic proctocolitis (FPIAP) in children in primary care and gastroenterology settings; however, it has not been validated for this diagnosis, and little is known about the positivity rates in early infancy. In this study, we used samples from healthy asymptomatic infants aged two weeks to two months to evaluate the gFOBT positivity rate compared to those diagnosed with FPIAP.

This was a nested case-control study. Frozen stool samples from infants aged two days to five months enrolled in the Gastrointestinal Microbiome and Allergic Proctocolitis study were evaluated using gFOBT (n = 123). The results were interpreted by three blinded staff members, including a trained clinical research coordinator, a pediatric gastroenterologist, and an experienced medical assistant. Additionally, the samples were analyzed using a quantitative fecal immunochemical test (FIT) for hemoglobin to compare with gFOBT results.

Eight percent of samples from the 100 healthy asymptomatic infants were gFOBT positive (11% when including positive and equivocal results). Seventy-four percent of samples from infants diagnosed with FPIAP were gFOBT positive. The interrater reliability of gFOBT interpretation was 81%. Of the healthy samples that yielded a positive gFOBT result, 50% also yielded a positive FIT result. Of the 23 FPIAP samples that yielded a positive gFOBT result, 29% yielded a positive FIT result.

Healthy asymptomatic infants in early infancy were gFOBT positive up to 11% of the time. Caution should be used when interpreting gFOBT results in young infants in a diagnostic setting.

Temporal lobe epilepsy (TLE) is the most common focal epilepsy, with many patients developing drug-resistant epilepsy. Surgical interventions, including stereoelectroencephalography (SEEG)-guided temporal lobe resection (TLR) and SEEG-guided responsive neurostimulation (RNS), are key treatment options. This systematic review compares the efficacy and safety of these interventions in drug-resistant TLE.

A systematic review was conducted following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) 2020 guidelines. A comprehensive search of multiple databases was performed (January 23–February 14, 2025). Eligible studies included adult patients with drug-resistant TLE undergoing SEEG-guided TLR or RNS (where SEEG was used pre-implant for localization). Primary outcomes assessed included seizure freedom, seizure reduction, adverse events, and quality of life (QoL) improvements. Quality assessments were performed using appropriate tools for randomized and observational studies.

Fifteen studies met the inclusion criteria, with sample sizes ranging from 10 to 440 participants. SEEG-guided TLR achieved an average seizure freedom rate of 58.5% (range: 32–85%) and a mean seizure reduction of 75% (range: 60–90%). SEEG-guided RNS resulted in an average seizure freedom rate of 12.85% and seizure reduction of 63.2%, with variability across studies. QoL improvements were reported in 80–82% of patients. Adverse events were infrequent but varied between interventions.

This review highlights the effectiveness of SEEG-guided TLR and RNS in managing drug-resistant TLE. While both interventions reduce seizure burden and improve QoL, seizure freedom rates are higher with resection. However, gaps remain in understanding long-term cognitive outcomes and demographic influences on treatment response. Future research should address these factors to refine patient selection and optimize epilepsy care.

COVID-19 has resulted in significant long-term sequelae in convalescent patients, impacting overall quality of life. Traditional Chinese medicine (TCM) has shown promise in managing post-COVID-19 symptoms through syndrome differentiation. This study aimed to evaluate the efficacy and safety of TCM in COVID-19 convalescent patients in a real-world setting.

This prospective, real-world study will be conducted at Guangdong Provincial Hospital of Traditional Chinese Medicine. A total of 528 COVID-19 convalescent patients will be recruited and divided into two groups: a control group receiving routine Western medical treatment and an intervention group receiving additional TCM treatment based on syndrome differentiation. Patients will be assessed for three major TCM syndromes: Lung-Spleen Qi Deficiency, Qi-Yin Deficiency, and Cold Phlegm Obstructing the Lung, with corresponding TCM prescriptions administered accordingly. The primary outcome measure will be the improvement in clinical symptom scores based on a TCM symptom scoring system. Secondary outcomes will include changes in laboratory tests, imaging studies, heart function classification, and quality of life scores. Safety will be assessed through liver and kidney function tests and adverse event monitoring.

The study is expected to demonstrate that TCM treatment, based on syndrome differentiation, can significantly improve clinical symptoms and overall health in COVID-19 convalescent patients compared to routine Western medical treatment. These findings will provide evidence for integrating TCM into post-acute COVID-19 care.

This study will contribute to the evidence supporting TCM as an effective treatment for post-COVID-19 syndrome, enhancing patient outcomes and informing comprehensive recovery strategies.

Lactate exerts regulatory effects on both cellular homeostasis and disease progression, far beyond being a mere metabolic waste product. As lactate accumulates, the level of lactylation increases significantly. Lactylation, a novel type of post-translational modification, bridges metabolic reprogramming and epigenetic regulation in malignant tumors, including gynecological malignancies. Both lactate and lactylation play critical roles in the tumor microenvironment, ultimately promoting tumor proliferation, metastasis, and drug resistance. Therapies targeting lactate production and transport show considerable anticancer potential, particularly through the inhibition of lactate dehydrogenase and monocarboxylate transporters. These inhibitors can also act as immunotherapy potentiators, producing a synergistic therapeutic effect when combined with immunotherapy. This review emphasizes how lactate and lactylation drive the malignant progression of gynecological cancers and explores promising perspectives on potential therapeutic targets.

It is established that administration of the COVID-19 vaccine may be associated with an exaggerated immune response leading to enlargement of several lymph nodes. Although most cases are benign and self-limiting, some have been reported in the literature as B-cell or T-cell lymphomas, with no reported cases of chronic lymphocytic leukaemia (CLL). We report two cases of follicular lymphoma and CLL that occurred a few weeks after COVID-19 vaccination. Case 1 is a 48-year-old woman who noticed two significantly palpable masses, one in each axilla, 48 h after receiving the first dose of the Pfizer-BioNTech BNT162b2 vaccine for COVID-19. Seven days later, she noticed another mass on the right side of her neck, which was biopsied within 48 hours. Case 2 is a 75-year-old man who presented with localized swellings in the axilla and on the neck, noted 24 h after the first dose of the Moderna messenger RNA-1273 COVID-19 vaccine. Neither patient reported any constitutional or associated symptoms. Surgical biopsy of the axillary lymph node in case 1 revealed a non-Hodgkin lymphoma, confirmed via immunohistochemistry as CD20-positive B-cell follicular lymphoma. The patient also had multiple pre- and para-aortic lymph nodes. In case 2, complete blood count showed lymphocytosis (total white blood cell – 148 × 109/L; lymphocyte differential – 92%), while peripheral blood film showed lymphocytosis with a predominance of small, mature-looking lymphocytes, both suggesting CLL. Although requested, immunophenotyping and molecular testing were not performed due to patient-related challenges. Although a chance occurrence is possible, lymphoid malignancies should be considered a strong differential. The vaccination history of patients presenting with clinical manifestations suggestive of a lymphoid malignancy should be thoroughly investigated, while ruling out other possible differentials such as a benign, self-limiting inflammatory process.

Amoebiasis, or amoebic dysentery, is a gastrointestinal disorder caused by the parasite Entamoeba histolytica. The disease is endemic in parts of Africa, Asia, North and South America, leading to several deaths annually. Reported adverse effects associated with the current first-line treatment for amoebiasis, coupled with the evolution of resistance to it, call for the need to search for plant-based alternatives. This study systematically reviews medicinal plants with activity against Entamoeba histolytica.

The PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines were followed to retrieve scholarly literature. The study reviewed 70 articles from 7 popular databases: Google Scholar, PubMed, ScienceDirect, Booksc.org, Emerald, Scopus, and MEDLINE, highlighting several plants with anti-amoebic properties.

The primary parts of the plant used in the treatment of Entamoeba histolytica were the leaves (61%), followed by rhizomes (13%), roots (8%), seeds (8%), stems (4%), and fruits (4%). The families Asteraceae (18%) and Zingiberaceae (18%) contain most plants that are effective against Entamoeba histolytica. These medicinal plants families are rich in phytochemicals such as terpenoids and flavonoids that have anti-entamoeba histolytica activity. Maceration is the most commonly used extraction method.

The results suggest that plants are a promising source of new agents to combat amoebiasis caused by Entamoeba histolytica. The most frequently used plant parts were leaves (61%), and the maceration method was the most common extraction technique due to its simplicity and cost-effectiveness. The majority of studies were limited to in vitro models, with only one plant (Adenophyllum aurantium) tested in vivo. Further research is needed to establish their mechanisms of action, toxicities, and clinical potential.

Mitochondrial respiratory complexes (Complexes I–V) and their assembly into respiratory supercomplexes (SCs) are fundamental to liver bioenergetics, redox homeostasis, and metabolic adaptability. Disruption of these systems contributes to major liver diseases, including non-alcoholic fatty liver disease, alcoholic liver disease, drug-induced liver injury, viral hepatitis, and hepatocellular carcinoma, by impairing adenosine triphosphate synthesis, increasing oxidative stress, and altering metabolic pathways. Recent advances have clarified the structural-functional interdependence of individual complexes within SCs, revealing their dynamic remodeling in response to physiological stress and pathological injury. These insights open opportunities for clinical translation, such as targeting SC stability with pharmacological agents, nutritional strategies, or gene therapy, and employing mitochondrial transplantation in cases of severe mitochondrial failure. Precision medicine approaches, incorporating multi-omics profiling and patient-derived models, may enable individualized interventions and early detection using SC integrity as a biomarker. By linking molecular mechanisms to therapeutic strategies, this review underscores the potential of mitochondrial-targeted interventions to improve outcomes in patients with liver disease.