Nail psoriasis is common in patients with plaque psoriasis and is associated with morbidity, including onychomycosis, which can complicate psoriasis treatments and be difficult to differentiate. Matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry is a fast and simple technique for identifying microorganisms through protein analysis. This study aimed to determine the sensitivity and specificity of MALDI-TOF for diagnosing onychomycosis in patients with nail psoriasis, by using conventional mycological and histological methods as the reference standard.

A prospective study was conducted on 88 patients with clinically and histopathologically confirmed nail psoriasis. One hundred nail samples were obtained for direct examination, fungal culture, and mass spectrometry. None of the patients were receiving antifungal or systemic immunosuppressive therapy at the time of sampling.

Potassium hydroxide preparation and fungal culture were positive in 58 out of 100 nail samples from patients with psoriasis. MALDI-TOF identified onychomycosis in 68 out of 100 samples, distinguishing these cases from nail psoriasis without onychomycosis (32 out of 100). An excellent correlation (0.95) was found between MALDI-TOF and conventional onychomycosis diagnostic methods. The sensitivity and specificity of MALDI-TOF for diagnosing onychomycosis in patients with psoriatic nails were 95.4% and 97.5%, respectively.

MALDI-TOF can be used to accurately differentiate cases of nail psoriasis without infection from those with onychomycosis.

This review explores the complex interplay between the microbiome and human aging, highlighting how dysbiosis impacts host physiology and health, particularly in relation to genomic stability and telomere attrition. Recent advances in cellular and molecular biology have underscored the role of both intrinsic and extrinsic factors in human aging, with the microbiome emerging as a key determinant of host physiology and health. Dysbiosis—disruptions in microbiome composition—is linked to various age-related diseases and impacts genomic stability and telomere attrition, the progressive shortening of telomeres that limits cell division and contributes to aging. This review examines how microbiome dynamics influence aging by triggering inflammation, oxidative stress, immune dysregulation, and metabolic dysfunction, all of which affect two primary hallmarks of aging: genomic instability and telomere attrition. Understanding these interactions is essential for developing targeted interventions to restore microbiome balance and promote healthy aging, offering potential treatments to extend healthspan and alleviate aging-related diseases. The convergence of microbiome and aging research promises transformative insights and new avenues for improving global population well-being.

We reported a case of recurrent liver dysfunction in an adult patient with a history of abnormal liver enzymes persisting for over ten years. The primary abnormalities included elevated levels of gamma-glutamyl transferase and alkaline phosphatase. Despite conducting a series of extensive etiological tests to identify common causes of liver disease, the diagnosis remained unclear. However, whole-exome next-generation sequencing revealed a homozygous intronic mutation in the ferrochelatase gene (c.315-48T>C), which may be associated with the patient’s cholestasis.

Albumin is a major prognostic factor for patients with advanced liver disease, dependent on its concentration and biological activity. This study aimed to improve the method of active albumin detection and elucidate its predictive validity of albumin activity across hepatic disease progression and etiology.

This study synthesized a novel ratiometric fluorescent probe with an improved structure of 2′-FBPBN. The technique was used to detect native human albumin (HA) activity in 244 patients with hepatitis B cirrhosis (LC) and 66 patients with hepatocellular carcinoma (HCC). Clinical and laboratory data were also collected.

Patients with LC and HCC were divided into normal albumin and low albumin (LA) groups. The median levels of albumin and HA activity in LC patients were 41.44 g/L and 51.85%, 28.51 g/L and 53.89%, respectively, while in HCC patients, they were 43.19 g/L and 33.69%, 30.77 g/L and 43.63%, respectively. The levels of total bilirubin, prothrombin time, international normalized ratio, native HA activity, Child-Pugh score, model for end-stage liver disease score, and model for end-stage liver disease-Na score were significantly higher in the LA groups, while the levels of platelet, cholesterol, and cholinesterase were lower compared to the normal albumin group (P < 0.05). The LA groups were more likely to suffer from hepatic encephalopathy and ascites. Patients with normal active HA had significantly higher survival rates than those with low active HA.

Native HA activity may outperform albumin as a prognostic indicator for assessing the severity of liver disease.

Wilson’s disease (WD) is a rare autosomal recessive genetic disorder that can be treated with medications. The lack of a single, specific diagnostic indicator leads to diagnostic difficulties, which may result in disease progression to cirrhosis and even liver cancer. Thus, this study aimed to analyze the clinical data, imaging, histopathological manifestations, genetic testing results, and treatment effects of patients with WD hepatic type, and to explore the factors related to WD cirrhosis.

A single-center retrospective study was performed. 48 WD patients with a Leipzig score ≥ 4 were divided into a cirrhosis group and a non-cirrhosis group based on the presence of cirrhosis. Logistic regression analysis and odds ratios were used to describe the strength of association between risk factors and cirrhosis. The predictive value of the model for cirrhosis occurrence was evaluated by calculating the area under the receiver operating characteristic curve and the cutoff value.

All 48 patients diagnosed with WD had liver damage, with males accounting for 54.17%. The median age at diagnosis was 28 years (range: 10.25–40.5 years), and 39.58% of patients had cirrhosis. The most prevalent mutation was c.2333G>T (p.Arg778Leu), found in 41.30% (19/46) of cases. Imaging revealed fatty liver in 31.25% (15/48) of patients and “honeycomb-like” cirrhosis nodules in 73.68% (14/19). Compared with the non-cirrhosis group, the cirrhosis group had a higher positive rate for the Kayser-Fleischer (K-F) ring, older age at diagnosis, and higher levels of immunoglobulin G, but lower levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, white blood cells, and platelets (p < 0.05). Age at diagnosis (odds ratio = 1.072, 95% confidence interval = 1.007–1.142, p = 0.03) and the K-F ring (odds ratio = 18.657, 95% confidence interval = 1.451–239.924, p = 0.025) were independent risk factors for WD-related cirrhosis. The best values of area under the receiver operating characteristic curve for age at diagnosis combined with the K-F ring in predicting WD cirrhosis were 0.909. The average follow-up time for 33 patients was 48.6 months (range: 12–72 months). The biochemical recovery rate was over 60% after 12–72 months of treatment with zinc gluconate and/or penicillamine.

Age at diagnosis, combined with the K-F ring, is a simple and effective risk factor for WD-related cirrhosis. Zinc gluconate and penicillamine are safe and effective treatments.

Percutaneous endoscopic gastrostomy (PEG) tube placement is a common procedure used to provide medium- and long-term enteral nutrition to patients. Although generally considered safe, PEG tube placement can be associated with various potential complications. We report a case of gastrocolocutaneous fistula formation in a patient who presented with severe abdominal pain, new-onset diarrhea, and feculent emesis nine days after PEG tube placement. Awareness of this rare complication can facilitate the recognition of colonic perforation during gastrostomy tube placement and enable early detection of the complication post-procedurally. Additionally, we discuss various techniques that may be employed to prevent this complication during PEG tube placement.

The proto-oncogene c-Fos is known as a reliable marker of cell activation, which is immediately induced after a new stimulus in specific brain regions, depending on the nature of the stimulus applied. However, the expression of c-Fos is increased in Alzheimer’s disease (AD) and contributes to amyloid β-peptide-induced neurotoxicity. This review attempted to focus on the role of c-Fos in learning and memory in both healthy brain and AD, emphasizing on possible mechanisms. Comparing the available findings, regarding learning and memory, c-Fos expression leads to memory formation through ERK (extracellular signal-regulated kinase)/CREB (cAMP response element-binding protein) and long-term potentiation, while it is down regulated after the repetition and habituation of stimuli. However, its overexpression in neurons and glia of AD, contributes to cognitive deficits and neuronal loss, which represents a defect in its ability to habituate to repeated stimuli. Also, expression pattern in glial is associated with constitutive CREB activation following increasing amyloid beta (Aβ), activation transcription factor (ATF3), and cytochrome c in apoptosis pathways. Thus, two contradictory roles of c-Fos in the healthy brain and AD, reveal more complexity in c-Fos up and down stream signaling pathways, bioavailability, and sensitivity. Future studies focusing on c-Fos modulation, might offer promising strategies to mitigate cognitive decline in AD.

Inflammatory bowel disease (IBD) is an idiopathic intestinal inflammatory condition affecting the ileum, colon, and rectum, including ulcerative colitis and Crohn’s disease. Clinical symptoms include abdominal pain, diarrhea, and even bloody stools. The intestinal barrier is the first line of defense between the intestinal tract and the external environment, and maintaining its stability is essential for intestinal health. On one hand, it enables the digestion and absorption of water and nutrients; on the other, it plays a crucial role in reducing the absorption of toxins and the invasion of pathogens. Damage to the intestinal barrier has become one of the most important factors in the onset and progression of IBD. However, there is currently no literature that systematically reviews the mechanisms of the intestinal barrier in the pathogenesis of IBD and the factors influencing it. In this paper, we aimed to systematically elaborate on the role of the intestinal barrier in IBD through the perspectives of oxidative stress, intestinal flora, and cellular autophagy. Our goal was to explore the mechanisms of the intestinal barrier in IBD more deeply and to provide new insights for the diagnosis and treatment of IBD. This article will summarize the composition of the intestinal barrier, the factors affecting it, and strategies to protect it.

Protein disulfide isomerases (PDIs) are essential enzymes that facilitate the proper folding of proteins and maintain protein quality within the endoplasmic reticulum. Dysregulation of PDIs has been correlated with numerous disorders, including cancer and rheumatoid arthritis (RA). E64FC26 (EFC), a small molecule that inhibits a wide range of PDI family members, has shown promise as a therapeutic agent in oncology. However, its effects on RA have not yet been studied. This research investigates the efficacy of EFC as a potential treatment for RA.

To investigate EFC’s effects on RA fibroblast-like synoviocytes, several assays were employed, including Cell Counting Kit-8 for cell viability, EdU for cell proliferation, Transwell for migration and invasion, TUNEL for apoptosis, and in vitro tube formation assays for angiogenesis. Flow cytometry was used to assess apoptosis in detail. Cytokine production was analyzed using ELISA and real-time polymerase chain reaction. In vivo, a collagen-induced arthritis model was developed in DBA mice to evaluate EFC’s effects on inflammation, disease progression, and bone damage. RNA sequencing was utilized to identify the molecular pathways influenced by EFC treatment.

EFC exhibited significant anti-inflammatory effects on RA fibroblast-like synoviocytes, reducing cell proliferation, migration, invasion, angiogenic activity, and cytokine secretion, while simultaneously promoting apoptosis. In vivo experiments using the collagen-induced arthritis mouse model showed that EFC alleviated inflammation, slowed disease progression, and preserved joint and bone integrity. RNA sequencing data suggested that EFC acts through pathways associated with inflammation and apoptosis regulation.

The findings of this research underscore EFC’s therapeutic potential in managing RA. These results pave the way for the development of inhibitors targeting the PDI family as innovative treatments for RA.

Helicobacter pylori (H. pylori) infection can cause multiple secondary digestive disorders. Some studies have found that polymorphisms in Toll-like receptor (TLR) genes, including TLR10 rs10004195, may be associated with increased susceptibility to H. pylori infection. Despite conflicting reports, we conducted a meta-analysis to clarify the relationship between these factors.

We conducted an exhaustive review, encompassing all relevant literature up to February 2024, using databases such as PubMed, Embase, Web of Science, and the China National Knowledge Infrastructure. We screened studies based on specific criteria and evaluated their quality using the Newcastle-Ottawa scale. Heterogeneity testing and meta-analysis were performed using Stata 17.0 software, and SPSSAU was used for publication bias evaluation and sensitivity analysis.

Eight of the 487 identified studies met the inclusion criteria, comprising 3,004 and 2,140 individuals in the H. pylori-positive and negative control groups, respectively. Our results demonstrated that individuals carrying the AA genotype at the TLR10 rs10004195 locus had a significantly increased likelihood of H. pylori infection when analyzed using the recessive genetic model (OR: 1.64, CI: 1.04–2.58, p = 0.034). No statistically significant associations were found in the other four genetic models.

Our findings suggest that carrying the TLR10 rs10004195 AA genotype is associated with a significantly elevated risk of H. pylori infection. This information could be used to assess future risk of H. pylori infection in healthy individuals and provide personalized health guidance based on individual genetic polymorphisms.