Hyperuricemia (HU), characterized by elevated uric acid (UA) levels in the blood, is a global health concern associated with various conditions, including cardiovascular diseases, gout, hypertension, metabolic syndrome, renal dysfunction, and neurodegenerative diseases. Recent studies highlight the multifaceted origins of HU, implicating genetic predisposition, dietary patterns, lifestyle choices, and environmental influences. Genetic variations affecting enzymes and transporters involved in purine metabolism and UA excretion have been identified, paving the way for personalized treatment strategies. Advances in diagnostic imaging and omics technologies provide enhanced precision in detecting and evaluating risks. While pharmacological interventions remain central to managing HU, persistent challenges such as treatment resistance necessitate the exploration of novel drug targets and lifestyle modifications. Chinese herbal medicines present a potential alternative with fewer side effects. Emerging research on the impact of gut microbiota on UA metabolism opens new therapeutic avenues. Despite progress, challenges such as optimizing treatment duration and understanding long-term effects remain. Collaborative efforts are essential to address these challenges and advance our comprehension of HU. Integrating precision medicine and holistic patient care approaches holds promise for improving outcomes and enhancing the quality of life for individuals with HU. This review provided a contemporary analysis of HU, covering its causes, associated health risks, diagnosis, treatment, and future outlook.

Cyclin-dependent kinase inhibitor 2A/2B (CDKN2A/2B) deletions are frequently identified in patients with biliary tract cancer; however, standard treatment options for this genetic alteration are lacking. Here, we present the case of a 64-year-old woman diagnosed with intrahepatic cholangiocarcinoma and hilar lymph node metastasis who underwent radical surgery. Postoperative pathology confirmed moderately differentiated adenocarcinoma. The tumor recurred during the second cycle of adjuvant chemotherapy following surgery, and the metastatic sites included the cranial region, right lung, and right adrenal gland. Genetic analysis revealed a CDKN2A/2B deletion, indicating palbociclib sensitivity. Subsequently, the patient received palbociclib plus lenvatinib as systemic therapy, along with stereotactic radiotherapy for the intracranial lesion. Notably, the right pulmonary metastasis significantly regressed after 12 months of treatment, with the complete disappearance of the intracranial tumor. However, the disease progressed at 32.2 months, with significant enlargement of the right adrenal gland metastasis and new metastasis in the right lung. The progression-free survival and overall survival were 32.2 months and 34.4 months, respectively. In conclusion, our case demonstrates that palbociclib plus lenvatinib is a promising chemotherapy-free second-line treatment for intrahepatic cholangiocarcinoma with a CDKN2A/2B deletion.

Proper nutritional management has been shown to reduce complications and lead to better clinical outcomes. However, inaccurate nutritional screening and assessment, inappropriate nutrition support, and deviations from suggested guidelines were observed in clinical practice. We aimed to investigate the nutritional status and support of hospitalized patients with neurological diseases to identify deficiencies in nutritional assessment and treatment.

A self-designed questionnaire, developed through a literature review, group discussions, and expert consultation, was converted into an electronic form to conduct a cross-sectional survey in a tertiary-level general hospital. The patients’ basic information and the first nutrition assessment were filled out upon admission. The final nutrition assessment were logged at discharge, transfer out, or death. Two-person cross-entry was used to ensure the accuracy of data input.

A total of 620 patients were enrolled in this study. Of these, 24.4% were at nutritional risk upon admission, and 22.7% were identified as at nutritional risk in the final assessment. There were no statistically significant differences in nutritional status between the first and final assessments, except for serum albumin concentration. A total of 118 patients (19.0%) received nutrition therapy. Complications occurred in 35 (45.5%) patients treated with enteral nutrition and 29 (30.5%) patients treated with parenteral nutrition.

The incidence of nutritional risk in inpatients with neurological diseases enrolled in this study was relatively low. However, nutritional treatment in this study was not sufficiently standardized. Nurses are needed to receive relevant professional training to improve quality of nutritional interventions.

Acupuncture treatment on the DU channel has shown therapeutic effects for Alzheimer’s disease (AD), but the underlying mechanisms are not yet clear. The purpose of this study was to comprehensively observe the protective effects of acupuncture on different brain regions in AD model mice, providing laboratory evidence for clinical acupuncture intervention in AD.

Eleven senescence-resistant strain 1 male mice were used as the normal control group. The senescence-accelerated prone strain 8 (SAMP8) male mice were used as AD model mice. Thirty-three SAMP8 mice were randomly divided into three groups: AD model group (group M), drug treatment group, and acupuncture treatment group (group A). The effect of acupuncture on learning and memory capabilities of SAMP8 mice was assessed by the Morris water maze test. Nissl staining was employed to provide a general view of the brain structure in AD model mice. Additionally, Western blot analysis was used to quantify Caspase-3 and tau protein levels.

In the spatial navigation test, the ratio of time mice spent in the goal quadrant in group M remained low, even lower than 25%. The ratio of time spent in the goal quadrant by mice in the acupuncture group on day 4 was higher than that on day 1 (P < 0.01). There was a trend indicating that the time ratio of mice in the acupuncture group during the probe trial was higher than in group M, though there was no statistically significant difference. Most traces of mice in group A were in the goal platform quadrant and across the platform in different, yet effective, ways. Compared to group M, most of the cells in the frontal cortex, hippocampus, and temporal cortex of mice in group A were round with clear stratification, regular arrangement, and increased Nissl bodies. The content of Caspase-3 in the frontal cortex and hippocampus of mice in the acupuncture group was lower than in group M (P < 0.01, P < 0.05). The content of tau in the hippocampus and temporal cortex of mice in group A was lower than in group M (P < 0.05; P < 0.01).

Acupuncture at the DU channel can improve learning and memory abilities to a certain degree by reducing apoptosis in the frontal cortex and hippocampus and decreasing tau deposition in the hippocampus and temporal cortex of AD model mice.

Waist circumference (WC) is closely associated with metabolic diseases, including diabetes mellitus (DM), metabolic syndrome, and mortality. However, the correlation between WC and mortality varies across populations and has rarely been examined specifically in patients with DM. In this study, we explored the relationships between WC and both all-cause and cardiovascular mortalities among individuals with DM.

Participants from the National Health and Nutrition Examination Survey 2003–2018 included 3,151 women and 3,473 men with DM who had baseline WC measurements. Survival data were collected from enrollment until December 31, 2019. Cox proportional hazard models were adjusted for demographic features and other confounders. Restricted cubic spline curves and threshold effect analyses were performed separately for men and women. Sensitivity analyses were conducted to minimize reverse causality.

Among 6,624 participants with DM, 621 women and 871 men died during median follow-ups of 6.8 and 6.3 years, respectively. WC demonstrated a U-shaped association with all-cause and cardiovascular mortalities in women, and a J-shaped trend in men. The optimal WC thresholds for minimizing mortality risk were 107.0 cm for women and 89.0 cm for men. For women, adjusted hazard ratios for all-cause mortality were 0.97 (95% confidence interval (CI): 0.96–0.98, P < 0.001) for WC below 107.0 cm and 1.04 (95% CI: 1.02–1.05, P < 0.001) for WC above 107.0 cm. In men, the corresponding ratios were 0.94 (95% CI: 0.90–0.97, P < 0.001) for WC below 89.0 cm and 1.03 (95% CI: 1.02–1.05, P < 0.001) for WC above 89.0 cm.

WC showed a U-shaped association with all-cause and cardiovascular mortalities in women and a J-shaped association in men among U.S. adults with DM from the National Health and Nutrition Examination Survey. Further research is needed to explore the underlying mechanisms rather than promoting preconceived notions about an optimal WC.

Free radicals are produced in the body during normal cellular metabolic activities, and their excessive accumulation can overwhelm the natural antioxidant mechanisms. This leads to oxidative stress, which is associated with the development and progression of non-communicable diseases (NCDs) such as liver and kidney diseases, cardiovascular diseases, neurodegenerative diseases, cancer, and diabetes. Enzymes play a significant role in maintaining a balance between antioxidants and free radicals by either enhancing the production of antioxidants or slowing down the generation of free radicals in the body. There is no up-to-date review on how antioxidant-enzyme interactions modulate the development and progression of NCDs. This review, therefore, discusses the mechanisms of antioxidant-enzyme interactions in the control of oxidative stress, as well as the implications and prospects of these interactions in the management of NCDs. Therapeutic strategies targeting antioxidant-enzyme interactions in the natural defense mechanisms of the body against oxidative stress can provide targeted benefits in the management of various NCDs. The mechanisms of interaction of some antioxidants with catalase, superoxide dismutase, glutathione reductase, glutathione peroxidase, glutathione S-transferases, thioredoxin protein, and thioredoxin reductase suggest their strong involvement in mitigating the development and progression of NCDs. Moreover, understanding the specific interactions and signaling pathways involved in antioxidant-enzyme interactions could facilitate the emergence of novel and effective therapeutic strategies for the management of NCDs and should be considered a primary goal of future studies. This study provides the necessary template, encourages discussion, and creates more opportunities for the next stage in the development of antioxidant therapies.

The number of molecular abnormalities identified in hematopoietic and lymphocytic neoplasms has grown exponentially over the past decades. Patients with genetic biomarker-matched targeted therapies have experienced significantly improved survival rates. Modern molecular laboratories, equipped with advanced technologies such as next-generation sequencing, can simultaneously test hundreds of genes and thousands of hotspots in a single run with multiple samples analyzed side by side. Bioinformatics tools provide seamless, evidence-based information to determine whether the detected mutations are benign or pathogenic, somatic or germline, druggable or diagnostic. This review is divided into five sections, each aiming to provide a comprehensive overview of the genetic landscape of myeloid and lymphocytic neoplasms. It highlights the challenges and proposes potential solutions to facilitate interpretation and maximize the clinical utility of molecular profiling results.

Clostridioides difficile infection (CDI) is associated with significant morbidity and mortality and carries a high risk of recurrence. Given the substantial healthcare burden and the evolving nature of CDI, understanding the role of emerging treatment strategies is essential. While oral vancomycin remains a mainstay of CDI treatment, the past decade has brought several notable advances in agents and practices that may be used for CDI treatment and prevention. Fidaxomicin or vancomycin are now recommended for an initial episode of CDI, with several guidelines giving preference to fidaxomicin based on its demonstrated ability to reduce recurrent CDI. Promising developments have emerged regarding the use of fecal microbiota-based therapies in the management of CDI, including conventional fecal microbiota transplantation and the approved live biotherapeutic products, Rebyota and Vowst. These therapies help restore the microbiota of the colon to treat severe CDI and prevent recurrence in select patients. Several strategies have emerged to prevent recurrent CDI, including bezlotoxumab, a single-dose, weight-based IgG1 monoclonal antibody that may be given to patients at high risk of recurrence. Additional pipeline therapies, such as vaccines, beta-lactamases, and bacteriophages, may provide future opportunities for CDI management. This narrative review aimed to summarize societal guideline recommendations for CDI management, describe the evidence for key therapies used in CDI treatment, and review recent updates on emerging treatment modalities.

Glioblastoma is the most common primary tumor of the central nervous system, characterized by an infiltrative growth pattern, which results in the most unfavorable prognosis. The average survival time of patients after diagnosis of this tumor is typically several months, with complete recovery from glioma being very rare. In recent years, significant involvement of exosomes in the development of cancer, including malignant brain tumors, has been discovered. Exosomes are extracellular vesicles that carry signaling molecules and participate in communication between cells. They influence cell survival, proliferation, migration, and increased neoangiogenesis, all of which significantly contribute to tumor recurrence. Molecules carried by exosomes are considered potential diagnostic markers, enabling early diagnosis of cancer and prompt implementation of appropriate treatment. Of particular diagnostic importance are microRNA molecules, which promote increased cell proliferation and inhibition of apoptosis. Equally important exosomal transmitters include proteins such as PSMD2 and EGFR, which enhance tumor invasiveness and resistance to chemotherapeutic agents. Recent studies suggest the possibility of using exosomes as carriers for new anticancer drugs, potentially improving the therapeutic treatment of cancers resistant to standard treatment methods. This review aimed to provide a comprehensive analysis of recent research on glioblastoma, the role of exosomes in its progression, the potential of exosomes as diagnostic biomarkers, and their use as therapeutic targets for patients who have not responded to conventional treatments.

Ectopic or heterotopic pancreases are normal pancreatic tissues located outside the pancreas. The ectopic pancreas has its own vascular and ductal systems and does not communicate with the normal pancreas. The prevalence of ectopic pancreas ranges from 0.6% to 15% among all autopsies. Many types of tumors, including intraductal papillary mucinous neoplasms (IPMNs), have been reported in the ectopic pancreas. However, little is known about the synchronous occurrence of IPMNs in both ectopic and orthotopic pancreas. In this study, we report, for the first time, two cases of concurrent IPMNs in an ectopic pancreas and an orthotopic pancreas. One patient had IPMNs both in the pancreas and in ectopic pancreatic tissue in the jejunum. Another patient had IPMNs in both the pancreas and ectopic pancreatic tissue in the duodenum. These cases may provide valuable insights into the etiological factors of IPMNs.

The refusal of blood transfusions and blood derivatives compels surgeons to face clinical and ethical challenges. We reviewed our perioperative and long-term outcomes of Jehovah’s Witnesses undergoing colon cancer surgery to evaluate the feasibility of bloodless procedures.

We retrospectively analyzed data from patients with colon cancer and Jehovah’s Witnesses who underwent surgery between January 2014 and December 2023. A protocol was systematically followed to optimize hemoglobin levels and other parameters according to the Enhanced Recovery After Surgery guidelines.

Sixteen patients underwent colon surgery, with a median age of 69 years and an equal gender distribution. Thirty-seven and a half percent had preoperative anemia and were managed by a hematologist. All procedures were performed in accordance with oncological standards. Postoperative treatment included low molecular weight heparin, and hemoglobin levels temporarily decreased postoperatively. No blood transfusions were needed during hospitalization. Two patients required surgical intervention due to postoperative hemorrhage. Complications included anastomotic dehiscence and perforation, with an overall morbidity rate of 25% and no 90-day mortality.

This study highlights the challenges in managing patients who reject blood products during colon cancer surgeries; however, the outcomes show results comparable to those of the general population with appropriate protocols. Preoperative optimization is crucial to reduce blood loss. Treatment of postoperative hemorrhage requires a lower threshold for intervention due to limited alternatives to blood products. Despite the limitations of the study, the findings advocate for careful monitoring and intervention. Larger studies are needed to validate these findings and improve care for this group of patients.

Breast cancer is the most common cancer among women, with hormone receptors playing a crucial role, not only in cancer cell growth but also as primary targets in breast cancer treatment. This systematic literature review aimed to summarize the current evidence on estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) discordance rates between primary and recurrent breast cancer. Additionally, it seeks to identify how discordance affects prognosis, metastasis, and the potential evidence of primary tumor heterogeneity.

The databases Web of Science, Scopus, MEDLINE, and PubMed were searched for publications of original research in English from 2013 to 2023. Studies with paired histopathology from primary and recurrent breast cancer that employed immunohistochemistry and fluorescence in situ hybridization were included. Ten studies were deemed eligible for inclusion.

Concordance between primary and recurrent breast cancer was high for ER (80%), PR (65%), and HER2 (85%). Average discordance rates were: ER 19%, PR 34%, and HER2 15%, with PR discordance consistently being the highest. Loss of ER and PR receptors was observed more frequently than gain, while the opposite trend was noted for HER2. Loss of ER and PR was associated with a worse prognosis. Discordance was also observed in cases of tumor metastasis.

Discordance in receptor expression between primary and recurrent breast cancer was common, highlighting the importance of re-biopsy in recurrent or metastatic breast cancer, if possible. Patients who lost hormone receptors experienced worse outcomes, suggesting the development of treatment-resistant tumor clones.

Poor bioavailability and a short half-life limit the therapeutic efficacy of ibuprofen. This study developed floating nanoballoons to enhance ibuprofen’s bioavailability and sustain its anti-inflammatory effects through improved gastric retention.

Ibuprofen-loaded nanoballoons were synthesized using solvent evaporation with ethyl cellulose as the polymer matrix. The formulation was characterized for morphology, buoyancy, drug loading, and release kinetics. In vivo studies assessed the anti-inflammatory efficacy in acute and chronic inflammation models using male Sprague-Dawley rats.

The nanoballoons exhibited optimal characteristics, including 96% buoyancy and a drug loading efficiency of 96.54 ± 1.32%. Scanning Electron Microscopy revealed a spherical morphology with a porous structure. Drug release followed a biphasic pattern: an initial release of 35.23 ± 2.13% over 2 h, followed by sustained release reaching 97.54 ± 1.30% at 12 h. In acute inflammation studies, the nanoballoon formulation showed superior edema inhibition (68.12%) compared to pure ibuprofen (51.67%). Chronic inflammation studies demonstrated significant improvements in inflammatory markers: reduced TNF-α (19.12 ± 0.48 vs. 31.11 ± 1.23 pg/mL), hs-CRP (201.7 ± 11.02 vs. 232.12 ± 11.33 ng/mL), and IL-6 (100.01 ± 18.40 vs. 135 ± 11.22 pg/mL), with increased anti-inflammatory IL-10 (507.18 ± 10.11 vs. 276.11 ± 19.16 pg/mL).

The developed floating nanoballoon system significantly enhanced ibuprofen’s bioavailability and anti-inflammatory efficacy, presenting a promising gastro-retentive delivery platform for poorly water-soluble drugs.

Incomplete immune reconstitution is characterized by chronic immune activation and systemic inflammation, which are not fully reversed by antiretroviral therapy. Dihydroartemisinin (DHA) has demonstrated anti-inflammatory and immunosuppressive properties, which may benefit individuals with incomplete immune reconstitution. This study aimed to investigate the biological mechanisms underlying incomplete immune reconstitution and evaluate the therapeutic potential of DHA in modulating immune activation in immunological non-responders (INRs). This study aimed to investigate the biological mechanisms underlying incomplete immune reconstitution and evaluate the therapeutic potential of DHA in modulating immune activation in immunological non-responders (INRs).

RNA sequencing data (GSE106792) was retrieved from the Gene Expression Omnibus database. R software and Bioconductor packages were used to identify differentially expressed genes (DEGs) among INRs, immune responders (IRs), and healthy controls (HCs). Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses, along with protein-protein interaction (PPI) network construction, were performed. Potential DHA-binding proteins were predicted using the STITCH server and molecular docking studies. Validation experiments were conducted on peripheral blood mononuclear cells from 18 INRs. Cells were treated with varying concentrations of DHA, and CD4+ and CD8+ T cell activation markers (CD38 and HLA-DR) were measured via flow cytometry.

Enrichment and PPI network analysis identified 119, 56, and 189 DEGs in the INR vs. HC, INR vs. IR, and IR vs. HC comparisons, respectively. Enrichment and PPI analyses showed that DEGs were mainly involved in immune response pathways. DHA was predicted to interact with multiple target proteins, indicating anti-inflammatory effects. In vitro, DHA significantly reduced the frequency of CD38− HLA-DR+ CD4+ T cells and CD38+ HLA-DR+ CD8+ T cells at 1,000 µM and 500 µM compared to the control.

This study provides insights into the biological mechanisms underlying incomplete immune reconstitution and supports DHA’s potential as a therapeutic agent. DHA effectively inhibits T cell activation in INRs, presenting a novel and promising treatment strategy.

Breast cancer is one of the leading causes of mortality among women worldwide. Tumor necrosis factor α-induced protein 3-interacting protein 1 (TNIP1) is a ubiquitin-binding protein that is widely expressed, but its function in breast cancer cells remains unknown. This study aimed to elucidate the molecular mechanism of TNIP1 regulation in the proliferation and apoptosis of breast cancer cells.

A colony formation assay was conducted on MCF-7 and T47D cells stably transfected with TNIP1/cyclin G1 (CCNG1) short hairpin RNAs. Quantitative polymerase chain reaction was performed to assess the relative abundances of TNIP1, CCNG1, and cyclin D1 (CCND1) messenger RNAs. Immunoprecipitation and immunoblotting were used to detect the expression of TNIP1, CCNG1, CCND1, and related proteins. A dual-luciferase reporter assay was employed to explore the molecular mechanism of TNIP1 in signal transduction. Caspase activity in MCF-7 and T47D cells transfected with TNIP1 short hairpin RNAs was measured using the Caspase-Glo 3/7 assay.

Ablation of TNIP1 induced growth arrest in breast cancer cells. TNIP1 directly interacted with CCNG1, and TNIP1 knockdown increased the ubiquitination of CCNG1. CCNG1 knockdown also induced growth arrest in MCF-7 and T47D cells. Furthermore, TNIP1 knockdown activated the NF-κB pathway and induced apoptosis in these cells.

TNIP1 regulates the proliferation and apoptosis of breast cancer cells, suggesting that TNIP1 may serve as a potential biomarker for breast cancer.

Liquid biopsy (LB) represents a promising strategy for the early diagnosis and treatment of lung cancer. However, relying solely on single-biomarker immunohistochemistry for predictive purposes has shown limited efficacy, often leading to suboptimal responses in certain patients. LB provides a complementary or alternative approach to immunohistochemistry by aiding in the identification of patients better suited for immunotherapy, thereby improving treatment precision. This review highlights key LB targets, including circulating tumor cells, exosomes, and small protein molecules, and explores the predictive and prognostic value of LB in immunotherapy for lung cancer and other tumors. These biomarkers play complex and multifaceted roles in liquid biopsies. Consequently, researchers have developed numerous targeted detection methods to study and identify key factors among multiple biomarkers in lung cancer and other tumor diseases. In addition, the limitations and future directions of LB are examined, aiming to advance its clinical application and support the development of personalized and precise immunotherapy. The integration of LB with artificial intelligence holds significant clinical potential for guiding immunotherapy and advancing precision medicine in lung cancer and other tumors.