anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with a high tendency for developing a recurrent disease. Circulating micro-RNAs (cmiRNAs) obtained through liquid biopsy are potential prognostic biomarkers for the assessment of TNBC recurrence risk. In this study, we sequenced cmiRNAs from the serum samples of 14 recurrent and 19 non-recurrent TNBC cases and compared expression profiles in relation to recurrence status, survival data and miRNA expression in matched tumor samples. Differential expression analysis between recurrent and non-recurrent cases identified ten differentially expressed (DE) cmiRNAs, of which cmiRNAs miR-21-5p (p = 0.030, HR = 1.87, 95% CI 1.06-3.30), miR-16-5p (p = 0.032, HR = 0.53, 95% CI 0.30-0.95), and miR-26b-5p (p = 0.023, HR = 0.52, 95% CI 0.29-0.91) were associated with recurrence-free survival in multivariable survival analysis. Expression profiles of matched tumor and serum samples were shown to correlate with each other. DE cmiRNAs were associated with common cancer-related signaling pathways and improved the overall predictive performance of the logistic regression model assessing the recurrence risk. Our results indicate that recurrent and non-recurrent TNBC differ in their cmiRNA expression profiles, and that three specific cmiRNAs can be used to assess the risk of recurrence in TNBC.
Due to the different mechanisms of action of the long-acting insulin analog insulin glargine and both a GLP-1 analog (exenatide) and a DPP-4-inhibitor (sitagliptin), it could be a promising approach to combine insulin glargine with either exenatide or sitagliptin for optimum control of fasting and postprandial blood glucose values. Thus, in the present study the influence of either exenatide or sitagliptin as a 4-week adjunctive therapy to a basal insulin (insulin glargine) was investigated versus insulin glargine alone as active comparator in subjects with type 2 diabetes. Preexisting metformin was continued, sulfonylureas, if any, were stopped. In particular, the effects on postprandial blood glucose excursion following ingestion of a standard breakfast, assessed after 4 weeks of treatment, the effects on mean daily blood glucose, on self-measured 7-point profiles, the percentage of subjects reaching ADA treatment goals (HbA1c \< 7.0%) at the end of treatment, on fasting lipid profile, on HOMA index, weight, hypoglycemic episodes and general safety were assessed. The study consisted of a screening visit, a 4-8 week (depending on pre-treatment) run-in period, a 4-week treatment period, and a follow-up visit. There were weekly visits at the site and twice weekly telephone contacts.
Conventional 18F-FDG PET/CT has important diagnostic value in cell metabolism level, early metastasis, judging malignant potential and prognosis of tumors. It has been routinely used for staging and restaging of most tumors, but there are still some tumors with low uptake of 18F-FDG PET/CT. Receptor imaging with a single target also has some limitations in clinical application. For example, not all diseased cells express a large amount of single receptor on the surface, which greatly affects the judgment of the nature of the lesion. The dual-target molecular imaging based on GRPr expressed in the lesion site and integrin αvβ3 receptor highly expressed on the surface of the lesion neovascularization will overcome the above limitations and make full use of the advantages of the dual-target molecular imaging, which will greatly assist the diagnosis of malignant tumors such as breast\\brain\\prostate tumor which have high GRPr and αvβ3 receptor expression . In this study, a novel dual-target imaging agent 68Ga-RM26-RGD was used for PET/CT imaging of breast\\brain\\prostate cancer, compared with conventional 18F-FDG, or single target imaging agent 68Ga-RGD or 68Ga-RM26 PET/CT imaging.
After the enrollment and lead in period, subjects will be given a sham device to sleep with every night for a month. They will be asked to fill out their pain and analgesic use logs, and undergo the bi weekly assessments. After a month they will be crossed over to an active "Painshield SAW patch device" and will continue to complete their pain and analgesic use logs as well as undergo biweekly assessments for months two and 3.
BACKGROUND: Traumatic brain injury (TBI) leads to acute gastrointestinal dysfunction and mucosal damage, resulting in feeding intolerance. C-C motif chemokine receptor 2 (Ccr2 + ) monocytes are crucial immune cells that regulate the gut's inflammatory response via the brain-gut axis. Using Ccr2 ko mice, we investigated the intricate interplay between these cells to better elucidate the role of systemic inflammation after TBI.
METHODS: A murine-controlled cortical impact model was used, and results were analyzed on postinjury days 1 and 3. The experimental groups included (1) sham C57Bl/6 wild type (WT), (2) TBI WT, (3) sham Ccr2 ko , and (4) TBI Ccr2 ko . Mice were euthanized on postinjury days 1 and 3 to harvest the ileum and study intestinal dysfunction and serotonergic signaling using a combination of quantitative real-time polymerase chain reaction, immunohistochemistry, fluorescein isothiocyanate-dextran motility assays, and flow cytometry. Student's t test and one-way analysis of variance were used for statistical analysis, with significance achieved when p < 0.05.
RESULTS: Traumatic brain injury resulted in severe dysfunction and dysmotility of the small intestine in WT mice as established by significant upregulation of inflammatory cytokines iNOS , Lcn2 , TNFα , and IL1β and the innate immunity receptor toll-like receptor 4 ( Tlr4 ). This was accompanied by disruption of genes related to serotonin synthesis and degradation. Notably, Ccr2 ko mice subjected to TBI showed substantial improvements in intestinal pathology. Traumatic brain injury Ccr2 ko groups demonstrated reduced expression of inflammatory mediators ( iNOS , Lcn2 , IL1β , and Tlr4 ) and improvement in serotonin synthesis genes, including tryptophan hydroxylase 1 ( Tph1 ) and dopa decarboxylase ( Ddc ).
CONCLUSION: Our study reveals a critical role for Ccr2 + monocytes in modulating intestinal homeostasis after TBI. Ccr2 + monocytes aggravate intestinal inflammation and alter gut-derived serotonergic signaling. Therefore, targeting Ccr2 + monocyte-dependent responses could provide a better understanding of TBI-induced gut inflammation. Further studies are required to elucidate the impact of these changes on brain neuroinflammation and cognitive outcomes.
Fusarium head blight (FHB) is a devastating wheat disease. Fhb1, the most widely applied genetic locus for FHB resistance, is conferred by TaHRC of an unknown mode of action. Here, we show that TaHRC alleles distinctly drive liquid-liquid phase separation (LLPS) within a proteinaceous complex, determining FHB susceptibility or resistance. TaHRC-S (susceptible) exhibits stronger LLPS ability than TaHRC-R (resistant), and this distinction is further intensified by fungal mycotoxin deoxynivalenol, leading to opposing FHB symptoms. TaHRC recruits a protein class with intrinsic LLPS potentials, referred to as an "HRC-containing hub." TaHRC-S drives condensation of hub components, while TaHRC-R comparatively suppresses hub condensate formation. The function of TaSR45a splicing factor, a hub member, depends on TaHRC-driven condensate state, which in turn differentially directs alternative splicing, switching between susceptibility and resistance to wheat FHB. These findings reveal a mechanism for FHB spread within a spike and shed light on the roles of complex condensates in controlling plant disease.
A device and method for the infusion of medicinal fluid at a controlled flow rate to a wound site or the blood stream of a patient is disclosed. A pump delivers fluid under pressure from a fluid source through a continuous and substantially constant flow path and through a supplemental bolus dose flow path. A large volume bolus dose reservoir accumulates a large quantity of fluid from the bolus dose flow path and holds the fluid under pressure. A flow regulator controls the fill rate of the large volume bolus reservoir. The large volume supplemental bolus dose is released from the bolus reservoir upon patient activation of a valve. The release rate of the bolus dose is controlled by the decompression of an elastomeric sphere or spring chamber, by the pressure gradient at the valve and/or by optional flow control tubing. In one embodiment, a source of fluid under pressure is pumped at a continuous and substantially constant rate to a wound site or the blood stream of a patient and into a bolus syringe, which is capable of holding a large quantity of fluid under pressure. A plunger on the bolus syringe may be depressed to release a bolus dose of fluid into a chamber accumulator and then to the patient at a controlled release rate.
Phenotype D-- is associated with severe hemolytic transfusion reactions and hemolytic disease of the fetus and newborn. It is typically caused by defective RHCE genes. In this study, we identified a D-- phenotype proband and verified Rh phenotypes of other 6 family members. However, inconsistent results between the phenotypic analysis and Sanger sequencing revealed intact RHCE exons with no mutations in the D-- proband, but the protein was not expressed. Subsequent whole-genome sequencing by Oxford Nanopore Technologies of the proband revealed an inversion with ambiguous breakpoints in intron 2 and intron 7 and copy number variation loss in the RHCE gene region. Given that the RHCE gene is highly homologous to the RHD gene, we conducted a comprehensive analysis using Pacific Biosciences long-read target sequencing, Bionano optical genome mapping, and targeted next-generation sequencing. Our findings revealed that the proband had 2 novel recombinant RHCE haplotypes, RHCE∗Ce(1-2)-D(3-10) and RHCE∗Ce(1-2)-D(3-10)-Ce(10-8)-Ce(3-10), with clear-cut breakpoints identified. Furthermore, the RH haplotypes of the family members were identified and verified. In summary, we made, to our knowledge, a novel discovery of hereditary large inversion and recombination events occurring between the RHD and RHCE genes, leading to a lack of RhCE expression. This highlights the advantages of using integrated genetic analyses and also provides new insights into RH genotyping.
AIM OF THE STUDY: The purpose of this study is to conduct a comparative analysis of the microbiological profiles in periprosthetic joint infections (PJIs) after total knee arthroplasty (TKA) between diabetic and non-diabetic patients. The study aims to address what are the variations in microbial colonization and infection patterns between diabetic and non-diabetic patients undergoing total knee arthroplasty.
METHODS: A retrospective analysis of 2,569 culture-positive cases of PJIs post-TKA was conducted, comparing outcomes between diabetic (n = 321) and non-diabetic (n = 2,248) patients. Demographic, clinical, and microbiological data were collected and analyzed using descriptive statistics, chi-squared tests, logistic regression, and other statistical tests.
RESULTS: Diabetic patients exhibited distinct microbial colonization patterns, with a higher prevalence of pathogens such as Staphylococcus aureus (p = 0.033), Pseudomonas aeruginosa (p < 0.001), Streptococcus spp. (Streptococcus agalactiae and Streptococcus dysgalactiae; p = 0.010, 0.016 respectively), Candida spp. (p = 0.010), and Corynebacterium spp. (p = 0.024). Additionally, diabetic patients were at increased risk of polymicrobial infections. Comorbidities associated with diabetes, including chronic pulmonary disease, renal insufficiency, and peripheral artery disease, were significantly more prevalent in diabetic patients and further complicated PJI outcomes.
CONCLUSION: This study underscores the importance of tailored perioperative antimicrobial strategies and vigilant infection control measures in diabetic patients undergoing TKA. Understanding the differential microbial profiles and associated comorbidities can inform targeted interventions to mitigate the risk of PJIs and improve outcomes in this high-risk population. Further research is warranted to elucidate the underlying mechanisms and optimize management strategies for diabetic patients undergoing TKA.
INTRODUCTION: Kinesin family member 20A (KIF20A) is essential for cell proliferation and is implicated in promoting tumor progression, but its role in hepatocellular carcinoma (HCC) remains poorly studied.
METHODS: Through the analysis of bulk RNA-sequencing (bulk RNA-seq) and single-cell RNA sequencing (scRNA-seq) data, the expression of KIF20A and its relationship with diagnosis, prognosis, and the immune microenvironment were examined. The association between KIF20A and the malignant progression and metastasis of HCC was confirmed through in vitro and in vivo experiments. Furthermore, patient re-staging was performed using Recursive Partitioning Analysis (RPA) to enhance clinical benefit.
RESULTS: In this study, we firstly found KIF20A was overexprerssed in HCC both by bulk RNA-seq and scRNA-seq, and then the overexpression of KIF20A significantly promoted the proliferation, invasion, and metastasis in vitro. In vivo, the overexpression of KIF20A promoted the growth and lung metastasis of HCC. Furthermore, gene set variation analysis of bulk RNA-seq and scRNA-seq revealed that KIF20A might be associated with cell cycle related signaling pathways of E2F and G2M, and overexpression of KIF20A inhibited the activity of p21 and bax, as well as shortened G2 phase. Importantly, we found that KIF20A could induce T cell exhaustion via the SPP1-CD44 axe using scRNA-seq. Additionally, KIF20A was also correlated with the expression of immune checkpoint inhibitors (ICIs), and KIF20Ahigh subgroup might be benefited from the ICIs therapy.
CONCLUSION: KIF20A emerges as a pivotal driver of HCC progression, intricately regulating cell cycle pathways and modulating immune responses, which position KIF20A as a promising target for HCC management.
The comparator arm is treatment as usual. For each monthly crossover, 12 students in a cluster are eligible to receive C2T in a stepped wedge study design. Student outcomes prior to receiving C2T will be compared to outcomes after receiving C2T.
This home-based randomized clinical trial is designed to test the efficacy of ZA-5 mg in Parkinson's disease (PD) and parkinsonism patients. This trial will also address barriers to treatment of patients with PD and parkinsonism by providing rigorous evidence about whether ZA reduces fracture risk in patients with PD and parkinsonism, simplifying treatment by giving ZA at home without extra medical visits and BMD testing, and overcoming poor persistence with oral therapies because one infusion may prevent bone loss for at least 2 years. The outcome of this trial will demonstrate how a home-based fracture prevention can reach older PD patients who would not otherwise receive treatment to reduce their high risk of fractures.

Patients with PD will be recruited throughout the US by participating neurologists and health networks as well as the Parkinson's Foundation. Patients may also self-refer to the study. Interested patients can access study information on a study website (topaz.eurekaplatform.org) as well as through the Parkinson's Foundation Helpline. Patients who wish to enroll will be directed to an interactive electronic consent (eConsent). Following eConsent, participants complete a screening questionnaire (to confirm eligibility), followed by a baseline questionnaire. If a participant is determined to be eligible following these steps, they may be scheduled for a Telemedicine assessment to further confirm the PD or parkinsonism diagnosis, unless they have been referred directly from a participating neurologist. If confirmed, the participant will be mailed a supply of vitamin D3 800-1000 IU and instructed to take one vitamin D tablet every day for 2 months. Lastly, a Nurse Home Visit will be scheduled and conducted to confirm final eligibility, randomization, and administration of the study drug, if appropriate. Participants who are randomized will be contacted every 4 months for at least 2 years to determine if they have had any fractures.
Acute respiratory distress syndrome (ARDS) is regarded as a type of respiratory failure. Emerging evidence has demonstrated the significant roles of microRNAs in various disorders. Nevertheless, the role of miR-202-3p in ARDS is unclear. Forty male C57BL/6 mice treated with phosphate buffer saline/lipopolysaccharide (PBS/LPS) and administrated with NC/miR-202-3p agomir were divided into four groups. A reverse transcription-quantitative polymerase chain reaction was used to evaluate the level of miR-202-3p, its target genes, and proinflammatory factors. Hematoxylin‑eosin was utilized for histological observation of the lung tissues. The Wet/Dry ratio, myeloperoxidase activity, and total protein concentration in bronchoalveolar lavage fluid were assessed to determine pulmonary edema. Western blotting was used for quantifying protein levels of proinflammatory factors, nuclear factor kappa B (NF-κB), and NLR family pyrin domain containing 3 (NLRP3) signaling-associated proteins. Calmodulin 1 (Calm1) protein expression in murine lung tissues was evaluated by immunohistochemistry. The binding relation between miR-202-3p and Calm1 was assessed by luciferase reporter assay. The results showed that miR-202-3p was lowly expressed in the lung tissues of ARDS mice. Overexpressed miR-202-3p relieved LPS-induced edema, reduced proinflammatory factors, and inactivated NF-κB/NLRP3 signaling in murine lung tissues. Calm1 was targeted by miR-202-3p and displayed a high level of LPS-induced ARDS. In conclusion, miR-202-3p targets Calm1 and suppresses inflammation in LPS-induced ARDS, thereby inhibiting the pathogenesis of ARDS in a mouse model.
Disclosed in the present invention is a new protein template for generating a non-antibody targeted binding molecule. The protein template and a targeted binding molecule derived therefrom are able to form a fusion protein or protein conjugate with a polypeptide, protein or chemically functional molecule. Thus, the latter may have the property of an adjustable targeting or half life while retaining structural stability and the original activity of the functional molecule, with a wide application prospect in the fields of pharmacy and molecular diagnosis. Also disclosed in the present invention are a series of GLP-1 receptor agonist fusion proteins, wherein a macromolecule comprises a GLP-1 receptor agonist polypeptide and a targeting peptide. The targeting peptide is a peptide capable of reversibly binding to a serum albumin after artificial modification. The macromolecule may also comprise a linker molecule between the targeting peptide and the GLP-1 receptor agonist polypeptide. Such macromolecule agents are able to retain the activity of the GLP-1 receptor agonist polypeptide while having a longer in vivo half-life, with a better prospect in the fields of treating diabetes, obesity, neurodegenerative diseases and the like.
BACKGROUND: Acute nutrition-related adverse outcomes are common in head and neck cancer patients undergoing radiotherapy. Predictive models can assist in identifying high-risk patients to enable targeted intervention. We aimed to systematically evaluate predictive models for predicting severe acute nutritional symptoms, insufficient intake, tube feeding, sarcopenia, and weight loss.
METHODS: We searched PubMed, Web of Science, EBSCO, Embase, WanFang, CNKI, and SinoMed. We selected studies developing predictive models for the aforementioned outcomes. Data were extracted using a predefined checklist. Risk of bias and applicability assessment were assessed using the Prediction model Risk of Bias Assessment Tool. A narrative synthesis was conducted to summarize the model characteristics, risk of bias, and performance.
RESULTS: A total of 2941 studies were retrieved and 19 were included. Study outcome measure were different symptoms (n = 11), weight loss (n = 5), tube feeding (n = 3), and symptom or tube feeding (n = 1). Predictive factors mainly encompassed sociodemographic data, disease-related data, and treatment-related data. Seventeen studies reported area under the curve or C-index values ranging from 0.610 to 0.96, indicating moderate to good predictive performance. However, candidate predictors were incomplete, outcome measures were diverse, and the risk of bias was high. Most of them used traditional model development methods, and only two used machine learning.
CONCLUSIONS: Most current models showed moderate to good predictive performance. However, predictors are incomplete, outcome are inconsistent, and the risk of bias is high. Clinicians could carefully select the models with better model performance from the available models according to their actual conditions. Future research should include comprehensive and modifiable indicators and prioritize well-designed and reported studies for model development.
The invention provides an oral Chinese patent medicine used for preventing and treating chilblain and frostbite. People who have suffered from chilblain suffer from chilblain again when staying in an environment with a temperature lower than 0 DEG C for a long time each year. Chilblain mainly occurs on the hand and the ear; and curing of chilblain on the hand is the most difficult. The primary symptoms of chilblain comprise lumps and redness; then one with chilblain feels extremely itching at night and is difficult to sleep; then swelling is aggravated, and blisters are formed; and after the blisters are broken, pus flows out, anabrosis or ulcer is formed, and pain occurs. An oral Chinese patent medicine prepared from red sage root and rose paprika and used for preventing and treating chilblain in the prior art has good treatment effect on chilblain on the hand and needs a short treatment course; however, the oral Chinese patent medicine has poor effect on chilblain on the ear. The oral Chinese patent medicine provided by the invention additionally comprises Chinese angelica, Ligusticum wallichii or pseudo-ginseng, and red date compared with the oral Chinese patent medicine in the prior art, and is capable of preventing and treating chilblain on the hand and on the ear and capable of preventing and treating frostbite. According to results of verification by more than one thousand of patients for more than ten years, the oral Chinese patent medicine provided by the invention can prevent chilblain if one takes the oral Chinese patent medicine when about to suffer from chilblain; and the oral Chinese patent medicine can cure patients with chilblain within 3 to 7 d as long as the skins of the patients are not broken. The oral Chinese patent medicine also has prevention and treatment effects on common cold due to wind-cold, arteriosclerosis, thrombotic diseases, coronary heart diseases, etc. and has no toxic and side effect on ordinary people.