Journal of Personalized Medicine最新文献

Background: Artificial intelligence (AI) is transforming surgical practice by enhancing training, intraoperative guidance, decision-making, and postoperative assessment. However, its specific role in laparoscopic and robotic general surgery remains to be clearly defined. The objective is to systematically review the current applications of AI in laparoscopic and robotic general surgery and categorize them by function and surgical context. Methods: A systematic search of PubMed and Web of Science was conducted up to 22 June 2025, using predefined search terms. Eligible studies focused on AI applications in laparoscopic or robotic general surgery, excluding urological, gynecological, and obstetric fields. Original articles in English or Spanish were included. Data extraction was performed independently by two reviewers and synthesized descriptively by thematic categories. Results: A total of 152 original studies were included. Most were conducted in laparoscopic settings (n = 125), while 19 focused on robotic surgery and 8 involved both. The majority were technical evaluations or retrospective observational studies. Seven thematic categories were identified: surgical decision support and outcome prediction; skill assessment and training; workflow recognition and intraoperative guidance; object or structure detection; augmented reality and navigation; image enhancement; technical assistance; and surgeon perception and preparedness. Most studies applied deep learning, for classification, prediction, recognition, and real-time guidance in laparoscopic cholecystectomies, colorectal and gastric surgeries. Conclusions: AI has been widely adopted in various domains of laparoscopic and robotic general surgery. While most studies remain in early developmental stages, the evidence suggests increasing maturity and integration into clinical workflows. Standardization of evaluation and reporting frameworks will be essential to translate these innovations into widespread practice.

Background/Objectives: Major depressive disorder (MDD) and metabolic syndrome (MetS) are highly prevalent, bidirectionally linked conditions. Individuals with MetS are at increased risk of developing depression, while depression predisposes to metabolic dysfunction. Evidence suggests that comorbid MDD and MetS present a distinct psychopathological profile, with neurovegetative symptoms such as fatigue, sleep disturbances, and appetite dysregulation being more prominent. This study aimed to determine whether depressive symptom structures differ between MDD patients with and without MetS, applying Bayesian network methods to uncover probabilistic dependencies that may inform precision psychiatry. Methods: Data were drawn from 1779 adults with ICD-10-diagnosed MDD in the 2013-2020 National Health and Nutrition Examination Survey (NHANES). Using standard metabolic criteria, participants were categorized as MetS (n = 315) or non-MetS (n = 1464). Depressive symptoms were assessed with the Patient Health Questionnaire (PHQ-9). Directed Acyclic Graphs (DAGs) were estimated via a hill-climbing algorithm with 5000 bootstrap replications to ensure network stability. Results: MetS patients displayed a denser and more interconnected symptom network. Fatigue (PHQ4) emerged as a central hub linking sleep, appetite, cognition, and functional impairment. In contrast, non-MetS patients showed a more fragmented network dominated by affective symptoms (low mood, anhedonia) and negative self-cognitions. Conclusions: Depressive symptoms propagate differently depending on metabolic status. These results highlight the value of personalized medicine approaches, advocating for treatment strategies that address neurovegetative dysfunctions in MDD with MetS and affective-cognitive symptoms in non-MetS. Aligning interventions with individual symptom architectures and metabolic profiles may enhance therapeutic precision and improve clinical outcomes.

Despite recent progress in lymphoma immunotherapy, outcomes for patients with peripheral T cell lymphomas (PTCLs) remain poor. The challenge of PTCLs reflects the profound biological heterogeneity and relative rarity of this disease group and its resistance to conventional chemotherapy, as well as the formidable challenge of generating definitive clinical evidence. However, deepening insight into the immunogenomic and microenvironmental basis of PTCL has revealed diverse mechanisms of immune escape, spanning defects in antigen presentation, apoptotic signaling, adhesion, and extensive tumor microenvironmental remodeling. These vulnerabilities provide a sound rationale for novel immunotherapeutic strategies-checkpoint inhibitors, CAR-T and NK cell platforms, bispecific antibodies, oncolytic viruses, and immunomodulatory agents. Early studies show encouraging but inconsistent activity, and the variability in response highlights the urgent need for biomarker-driven stratification to deliver personalized approaches and clinically meaningful efficacy. This review synthesizes the current literature on the immune dysregulation of PTCLs, as well as advances in PTCL immunotherapy, outlining the biological rationale underpinning these approaches. We discuss approaches to molecular, transcriptomic, and microenvironmental profiling with circulating biomarkers that could enable adaptive trial designs and personalized treatment strategies. Together, these developments chart a path away from empiricism and toward precision therapy in PTCLs.

Background: Heart failure with preserved ejection fraction (HFpEF) is a major cause of hospitalization and mortality in older adults. Sudden cardiac arrest (SCA) is a leading cause of death in this population, yet national trends in incidence, outcomes, and disparities remain poorly defined. Methods: We performed a retrospective cohort study using the National Inpatient Sample from 2016 to 2020. Hospitalizations for patients aged ≥65 years with HFpEF and in-hospital cardiac arrest (CA) were identified using ICD-10-CM codes. Demographics, comorbidities, hospital outcomes, and temporal trends were examined. The primary outcome was in-hospital mortality. Secondary outcomes included length of stay, hospital charges, and discharge disposition. Results: Among 7,738,108 HFpEF admissions, 93,440 (1.2%) involved CA. Incidence rose from 1.1% in 2016 to 1.5% in 2020 (36% relative increase). The median age was 81 years; 54% were female, 70% White, 19% Black, and 8% Hispanic. CA incidence increased across all groups, with the largest relative rises among Native American (1.0% to 1.9%), Black (1.7% to 2.3%), and Hispanic patients (1.4% to 2.0%). In-hospital mortality was high, increasing from 58.2% to 61.7% over the study period (p < 0.001). Mortality rose most steeply among Black and low-income patients. Comorbidity patterns shifted toward greater metabolic complexity, including higher rates of complicated diabetes, hypertension, hyperlipidemia, and obesity. Conclusions: Elderly patients hospitalized with HFpEF are experiencing rising rates of in-hospital CA and persistently high mortality, with marked racial and socioeconomic disparities. These findings highlight the need for better risk stratification, targeted metabolic and inflammatory therapies, and more equitable care delivery.

Introduction. Over the past two decades, the αGal (Galα1-3Galβ1-4GlcNAc-R) epitope, a carbohydrate found in many non-primate mammals, has gained significant relevance in medicine due to its association with an increasing number of allergic reactions to animal-derived foods, drugs, and medical devices. Due to a mutated gene coding for α1,3-galactosyltransferase (α1-3GT), humans lack αGal and, therefore, naturally produce anti-α-Gal antibodies (IgM, IgA, and IgG), especially in the context of a xenotransplantation, which can lead to extreme immunological reactivity, including hyperacute rejection of the transplant. Recently, these uncontrollable immune reactions have driven demand for more accurate procedures to better detect αGal in animal-derived foods or bioprosthetics. The currently most widely used α-Gal-specific monoclonal antibody is an IgM antibody (clone M86), developed in Ggta1 KO mice and isolated from hybridoma tissue culture. As the IgM isotype has limited purification properties, specificity, and sensitivity, we aimed to produce a novel IgG antibody with high affinity and extensive applicability. Methods. An experimental murine IgG1 anti-αGal antibody (IgG-αGalomab) was developed by immunization of Ggta1 knockout (KO) mice, and its affinity was evaluated using ELISA, Western blot, flow cytometry, and immunohistochemistry/immunofluorescence. Results. Compared to IgM-M86, IgG-αGalomab demonstrated ~1200-fold higher binding potency and lower cross-reactivity with competitive molecules, i.e., bovine serum albumin, galactobiose, and lactose. Unlike IgM-M86, IgG-αGalomab showed an increasing affinity over time in the binding tests performed on xenogeneic tissues. Notably, high-affinity for αGal was detected by Western blot at high dilution [1:200,000] of IgG-αGalomab compared to IgM-M86 [1:1000]. By flow cytometry, specificity and dose-dependent response were confirmed using in vitro cultures of porcine and human fibroblasts. Finally, in immunofluorescence and immunohistochemistry analysis, αGal was demonstrated to be detectable by IgG-αGalomab at a dilution of [1:1000], while IgM-M86 was demonstrated to be detectable at [1:100]. Conclusions. Altogether, our newly developed antibody showed high sensitivity and specificity for α-Gal in various applications. Based on its potential binding capacity, IgG-αGalomab could have important applications in precision medicine for predicting, treating, and preventing immune-mediated phenomena of patients in different medical areas.

Introduction: Neurodevelopmental disorders (NDs), including autism spectrum disorder and related conditions, are increasingly recognized among women of reproductive age, yet their unique needs during pregnancy and childbirth remain poorly studied. Communication differences, sensory sensitivities, and co-occurring psychiatric conditions may complicate maternity care, leading to higher risks of adverse outcomes and ethical challenges in clinical practice. This study aimed to examine pregnancy complications, delivery outcomes, and postpartum characteristics in women with NDs, compared with a control group, and to identify specific barriers in perinatal care. Methods: A retrospective observational study was conducted at the National Medical Research Center for Obstetrics, Gynecology and Perinatology, Moscow, including 18 pregnant women with confirmed NDs and 21 matched controls with uncomplicated pregnancies. Data were extracted from medical records and included demographic parameters, pregnancy course, complications, labor management, neonatal outcomes, and documented communication or ethical issues. Comparative analyses were performed using chi-square or Fisher's exact tests for categorical variables and Student's t-test or Mann-Whitney U test for continuous variables. Results: Pregnant women with NDs had significantly higher rates of pelvic girdle pain (66.7% vs. 23.8%, p = 0.01), vaginal bleeding (44.4% vs. 14.3%, p = 0.04), anxiety (61.1% vs. 19.0%, p = 0.007), and depression (50.0% vs. 14.3%, p = 0.02) compared with controls. Persistent daily nausea was also more common (50.0% vs. 14.3%, p = 0.03). Attendance of prenatal physician visits was lower in the ND group (66.7% vs. 95.2%, p = 0.02). Cesarean delivery occurred in 83.3% of ND women versus 23.8% of controls (p < 0.001), with psychiatric recommendations often cited as the indication. Breastfeeding was declined in 94.4% of ND cases versus 4.8% of controls. Labor duration was prolonged, and neonatal anthropometrics were lower in the ND group. Communication difficulties were documented in 83.3% of ND participants, and postpartum depressive symptoms were identified in 77.8%. Conclusions: Pregnant women with NDs face a multidimensional vulnerability in maternity care, including higher frequencies of pain, bleeding, nausea, anxiety, and depression, prolonged labor, markedly increased cesarean rates, reduced breastfeeding initiation, and smaller neonatal anthropometrics. Frequent communication barriers, guardian decision-making, and postpartum separation further complicate care. These findings underscore the necessity of neurodiversity-informed, individualized perinatal strategies, integrating sensory accommodations, trauma-informed communication, and proactive mental health support to improve both clinical outcomes and patient experiences.

Background Facial clefts are rare congenital malformations, occurring in approximately 1 in 700 live births for cleft lip and palate and fewer than 1 in 100,000 for atypical Tessier clefts. They pose significant diagnostic and surgical challenges. While genetic, vascular, and environmental factors are well documented, growing embryological evidence suggests that the trigeminal nerve may also contribute to craniofacial development. This narrative review explores the association between trigeminal nerve development and facial clefts, aiming to provide a neurodevelopmental perspective with clinical implications, particularly in the context of personalized medicine, where patient-specific neuroanatomical and developmental factors can guide tailored care. Methods A narrative review of embryological, anatomical, and clinical data was conducted. Histological analyses of malformed fetuses and normal human embryos were integrated with published studies. Clinical findings were compared with Paul Tessier's facial cleft classification and mapped against trigeminal innervation territories. Results Two groups of facial clefts emerged according to the timing of trigeminal disruption. Early embryonic damage (before 10 weeks of gestation) produces superficial epidermal continuity with fibrotic tissue replacing normal deep structures. Later fetal damage results in complete clefts with full tissue discontinuity. The distribution of these clefts corresponds to trigeminal nerve terminal branch territories, supporting the hypothesis that trigeminal innervation exerts trophic effects on craniofacial morphogenesis through neurohormonal signaling. Conclusions Early impairment of trigeminal development may play a pivotal role in the pathogenesis of certain clefts. The spatial and temporal relationship between nerve development and morphogenesis should be considered in classification and surgical planning. However, limitations of this narrative approach include selective literature coverage and lack of quantitative synthesis. Future directions include single-cell transcriptomics, organoid models, and fetal MRI tractography to clarify trigeminal-mesenchyme interactions and inform therapeutic strategies. These advances may foster a personalized medicine approach, enabling more precise prenatal diagnosis, individualized surgical planning, and optimized long-term outcomes.

Background/Objectives: Evaluate outcomes and treatment patterns with 2 mg intravitreal aflibercept injection among patients who completed the phase 3 PANORAMA trial and enrolled in the VOYAGE (ClinicalTrials.gov identifier, NCT04708145; 12 January 2021) long-term extension study. Methods: During VOYAGE, patients were evaluated every 16 weeks and treated with 2 mg intravitreal aflibercept injection as needed depending on ophthalmoscopic examination findings. Those with no history of panretinal photocoagulation (PRP) received aflibercept if their clinician-determined diabetic retinopathy severity scale (DRSS) level was ≥47, corresponding to moderately severe non-proliferative diabetic retinopathy (NPDR). Patients with a history of PRP received aflibercept if active neovascularization was present. New or worsening diabetic retinopathy (DR) severity prompted more frequent treatment. Results: 320 patients (1 eye per patient) from 87 sites completed the PANORAMA trial. Of these, 41 patients (13% of PANORAMA completers) from 14 sites (16%) enrolled in VOYAGE after a mean interim period of 33.7 months, and 35 patients (85%) completed study visits through 1 year. At year 1 in VOYAGE, the mean number of anti-vascular endothelial growth factor (VEGF) injections increased from 1.1 per year during the interim period to 3.4 per year and was associated with stabilization or improvement in DRSS level in 81% (26/32) of patients. Mean best-corrected visual acuity (BCVA) remained relatively stable, and mean central subfield thickness (CST) improved by 24.4 µm to 269.5 μm through year 1 of VOYAGE. There were no unexpected safety events. Conclusions: Following a mean of 3 years of routine clinical care with associated declines in DRSS level, CST, and BCVA, stabilization of DRSS level and BCVA with reductions in CST was achieved through year 1 of the VOYAGE extension study, with a concurrent increase in aflibercept dosing frequency.

Background/Objectives: Many patients with breast cancer are treated with chemotherapy, including taxanes. These regimens bear a significant risk of potentially burdensome peripheral neuropathy. A scoring system supported by a neuropathy tracker, which can be self-administered by the patients, likely facilitates and speeds up the diagnosis of chemotherapy-induced peripheral neuropathy (CIPN). Before such a scoring system can be used, determination of the optimal cut-off score to discriminate between CIPN and no CIPN is necessary. The prospective NEURO-BREAC trial (NCT07148336) aims to identify the optimal cut-off score in patients treated with chemotherapy and adjuvant irradiation for breast cancer. Methods: The main goal of the NEURO-BREAC trial is to provide the optimal cut-off of a scoring system to discriminate between moderate to severe CIPN and no CIPN in breast cancer survivors previously treated with paclitaxel- or docetaxel-based chemotherapy and irradiation. The scores (0 to 44 points) are obtained by using a neuropathy tracker. This tracker is based on self-evaluation of symptoms and signs of CIPN by study participants. In addition, satisfaction of the patients with the scoring system is assessed. Twenty-four patients (sixteen patients with moderate to severe CIPN and eight patients without CIPN) are required for the Full Analysis Set. Assuming that about 5% of patients will not qualify for this set, 26 patients should be recruited for the NEURO-BREAC trial. The results of this trial are considered an important step for the development of a scoring system contributing to the identification of CIPN in breast cancer patients.

In recent years, the concept of personalized medicine has moved beyond a theoretical framework to become a tangible clinical imperative [...].