anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Cisplatin, a platinum-based chemotherapeutic, is effective against various solid tumors, but its use is often limited by its nephrotoxic effects. This study evaluated the protective effects of trametinib, an FDA-approved selective inhibitor of mitogen-activated protein kinase kinase 1/2 (MEK1/2), against cisplatin-induced acute kidney injury (AKI) in mice. The experimental design included four groups, control, trametinib, cisplatin, and a combination of cisplatin and trametinib, each consisting of eight mice. Cisplatin was administered intraperitoneally at a dose of 20 mg/kg to induce kidney injury, while trametinib was administered via oral gavage at 3 mg/kg daily for three days. Assessments were conducted 72 h after cisplatin administration. Our results demonstrate that trametinib significantly reduces the phosphorylation of MEK1/2 and extracellular signal-regulated kinase 1/2 (ERK1/2), mitigated renal dysfunction, and ameliorated histopathological abnormalities. Additionally, trametinib significantly decreased macrophage infiltration and the expression of pro-inflammatory cytokines in the kidneys. It also lowered lipid peroxidation by-products, restored the reduced glutathione/oxidized glutathione ratio, and downregulated NADPH oxidase 4. Furthermore, trametinib significantly inhibited both apoptosis and necroptosis in the kidneys. In conclusion, our data underscore the potential of trametinib as a therapeutic agent for cisplatin-induced AKI, highlighting its role in reducing inflammation, oxidative stress, and tubular cell death.
BACKGROUND: Microsatellite instability-high (MSI-H) tumors are distinct molecular subtypes in gastric cancer. However, a few studies have comprehensively reported the molecular features of MSI-H tumors and their prognostic factors in locally advanced gastric cancer. This study aimed to clarify the molecular features and prognostic factors of locally advanced MSI-H gastric cancer.
METHODS: This study included 499 patients with locally advanced gastric cancer who underwent radical gastrectomy. We evaluated the MSI status and compared with previously published whole-exome sequencing, panel sequencing, and gene expression profiling data. Clinicopathological characteristics and molecular profiles were compared between patients with MSI-H and microsatellite stable (MSS) gastric cancer. A subgroup analysis of survival was performed in patients with MSI-H gastric cancer.
RESULTS: MSI-H tumors were detected in 79 of 499 patients (15.8%). MSI-H tumors were associated with an increased tumor mutational burden, MLH1 downregulation, CD274 (PD-L1) upregulation, and enrichment of cell cycle pathways. Among patients with MSI-H gastric cancer, the disease-specific survival (DSS) tended to be better in the surgery plus tegafur, gimeracil, and oteracil potassium (S-1) adjuvant chemotherapy group than in the surgery alone group, especially for stage III patients. Furthermore, DSS was better in the T cell-inflamed gene expression signature-high group, and it tended to be worse in the non-solid type poorly differentiated adenocarcinoma group.
CONCLUSIONS: The molecular features and prognostic factors of locally advanced MSI-H gastric cancer were clarified. S-1 adjuvant chemotherapy appears to be beneficial, and the T cell-inflamed gene expression signature and histopathological type are prognostic factors in MSI-H tumors.
Patients should be advised that VISTIDE is not a cure for CMV retinitis, and that they may continue to experience progression of retinitis during and following treatment. Patients receiving VISTIDE should be advised to have regular follow-up ophthalmologic examinations. Patients may also experience other manifestations of CMV disease despite VISTIDE therapy.

HIV-infected patients may continue taking antiretroviral therapy, but those taking zidovudine should be advised to temporarily discontinue zidovudine administration or decrease their zidovudine dose by 50%, on days of VISTIDE administration only, because probenecid reduces metabolic clearance of zidovudine.

Patients should be informed of the major toxicity of VISTIDE, namely renal impairment, and that dose modification, including reduction, interruption, and possibly discontinuation, may be required. Close monitoring of renal function (routine urinalysis and serum creatinine) while on therapy should be emphasized.

The importance of completing a full course of probenecid with each VISTIDE dose should be emphasized. Patients should be warned of potential adverse events caused by probenecid (e.g., headache, nausea, vomiting, and hypersensitivity reactions). Hypersensitivity/allergic reactions may include rash, fever, chills and anaphylaxis. Administration of probenecid after a meal or use of antiemetics may decrease the nausea. Prophylactic or therapeutic antihistamines and/or acetaminophen can be used to ameliorate hypersensitivity reactions.

Patients should be advised that cidofovir causes tumors, primarily mammary adenocarcinomas, in rats. VISTIDE should be considered a potential carcinogen in humans (See Carcinogenesis, Mutagenesis, & Impairment of Fertility). Women should be advised of the limited enrollment of women in clinical trials of VISTIDE.

Patients should be advised that VISTIDE caused reduced testes weight and hypospermia in animals. Such changes may occur in humans and cause infertility. Women of childbearing potential should be advised that cidofovir is embryotoxic in animals and should not be used during pregnancy. Women of childbearing potential should be advised to use effective contraception during and for 1 month following treatment with VISTIDE. Men should be advised to practice barrier contraceptive methods during and for 3 months after treatment with VISTIDE.
HIV-1 infection elevates the risk of developing various cancers, including T-cell lymphoma. Whether HIV-1-encoded proteins directly contribute to oncogenesis remains unknown. We observe that approximately 1-5% of CD4+ T cells from the blood of people living with HIV-1 exhibit over-duplicated centrioles, suggesting that centrosome amplification underlies the development of HIV-1-associated cancers by driving aneuploidy. Through affinity purification, biochemical, and cellular analyses, we discover that Vpr, an accessory protein of HIV-1, hijacks the centriole duplication machinery and induces centrosome amplification and aneuploidy. Mechanistically, Vpr forms a cooperative ternary complex with an E3 ligase subunit, VprBP, and polo-like kinase 4 (Plk4). Unexpectedly, however, the complex enhances Plk4's functionality by promoting its relocalization to the procentriole assembly and induces centrosome amplification. Loss of either Vpr's C-terminal 17 residues or VprBP acidic region, the two elements required for binding to Plk4 cryptic polo-box, abrogates Vpr's capacity to induce these events. Furthermore, HIV-1 WT, but not its Vpr mutant, induces multiple centrosomes and aneuploidy in human primary CD4+ T cells. We propose that the Vpr•VprBP•Plk4 complex serves as a molecular link that connects HIV-1 infection to oncogenesis and that inhibiting the Vpr C-terminal motif may reduce the occurrence of HIV-1-associated cancers.
Due to the strong correlation between a significant decrease in CD4 count and the frequency and magnitude of OIs such as Pneumocystis carinii pneumonia (PCP), Mycobacterium avium complex (MAC), and severe bacterial infections, CD4 count has become the major criterion for initiating antimicrobial prophylaxis for OIs. However, despite the benefits of these antimicrobial drugs, all are associated with adverse side effects, and patients with reconstituted immune systems following antiretroviral therapy may be receiving prophylaxis unnecessarily. Benefits to stopping prophylaxis include: (1) elimination of adverse effects from drugs; (2) reduction in drug costs; and (3) removal of selective pressure for the development of drug-resistant microbes. These benefits must be weighed against the disadvantages, however, such as more frequent determinations of CD4 counts to assure maintenance of immunocompetence, more frequent occurrence of serious OIs otherwise preventable with prophylaxis in patients lost to follow-up, and possible occurrence of atypical PCP because of prior exposure to anti-PCP drugs. \[AS PER AMENDMENT 04/26/02: The extent of complete immune restitution has not yet been defined. An important corollary of an incomplete immune recovery is that vaccination schedules might need to be adjusted to obtain optimal responses in HIV-infected patients on highly active antiretroviral therapy (HAART). Therefore, a third dose of hepatitis A virus vaccine will be administered.\]

After pre-entry and entry laboratory studies, patients are followed every 8 weeks until the last patient has completed 104 weeks of study observation. Hepatitis A vaccination is administered at entry and Week 24 to measure responses to neoantigen. \[AS PER AMENDMENT 04/26/02: All patients (except those co-enrolled in P1024 on or after November 1, 2001) who have received 2 doses of hepatitis A virus vaccine during the study will be offered an opportunity to enroll in Step II of P1008. Patients in Step II receive a third dose of hepatitis A vaccination at Week 104 or later. Additional blood samples are taken 8 weeks later for antibody detection and peripheral blood mononuclear cell (PBMC) cryopreservation.\] All serious bacterial infections that are Grade 3 or higher and OI events are recorded and compared to historical event rates. Virologic and immunologic marker studies are done in all patients and correlated with the risk of developing serious bacterial infections or OI events. Patients are considered to have reached an endpoint if they develop PCP, 2 serious bacterial infections, other Category C OI diagnoses, or CD4% less than 15% and re-initiation of PCP prophylaxis.
BACKGROUND & AIMS: Some patients with irritable bowel syndrome (IBS) demonstrate low-grade inflammation in the intestine. Mesalamine, which has anti-inflammatory effects, may be an efficacious treatment for IBS, but studies are conflicting. We conducted a systematic review and meta-analysis to assess efficacy and safety of mesalamine in IBS.
METHODS: We searched the medical literature up to September 14, 2022, to identify randomized controlled trials (RCTs) of mesalamine in IBS. We judged efficacy and safety using dichotomous assessments of effect on global IBS symptoms, abdominal pain, bowel habit or stool frequency, and occurrence of any adverse event. We pooled data using a random effects model, with efficacy and safety reported as pooled relative risks (RRs) with 95% confidence intervals (CIs).
RESULTS: We identified 8 eligible RCTs (820 patients). Mesalamine was more efficacious than placebo for global IBS symptoms (RR of global symptoms not improving, 0.86; 95% CI, 0.79-0.95; number needed to treat = 10; 95% CI, 6-27), but not for abdominal pain or bowel habit or stool frequency. Subgroup analyses demonstrated efficacy of mesalamine in IBS with diarrhea for global IBS symptoms (RR, 0.88; 95% CI, 0.79-0.99), but not patients with other predominant bowel habits or those with post-infection IBS. Adverse event rates were no higher with mesalamine (RR, 1.20; 95% CI, 0.89-1.63) but were reported in only 5 trials.
CONCLUSIONS: Mesalamine may be modestly efficacious for global symptoms in IBS, particularly IBS with diarrhea, but quality of evidence was low. Adequately powered high quality RCTs of mesalamine in IBS are needed.
Dioclea violacea seed mannose-binding lectin (DvL) has attracted considerable attention because of its interesting biological activities, including antitumor, antioxidant, and anti-inflammatory activities. This study evaluated the cytotoxic effect of DvL on tumor and normal cells using the mitochondrial activity reduction (MTT) assay, the carcinogenic and anti-carcinogenic activity by the epithelial tumor test (ETT) in Drosophila melanogaster, and the anti-angiogenic effect by the chick embryo chorioallantoic membrane (CAM) assay. Data demonstrated that DvL promoted strong selective cytotoxicity against tumor cell lines, especially A549 and S180 cells, whereas normal cell lines were weakly affected. Furthermore, DvL did not promote carcinogenesis in D. melanogaster at any concentration tested, but modulated DXR-induced carcinogenesis at the highest concentrations tested. In the CAM and immunohistochemical assays, DvL inhibited sarcoma 180-induced angiogenesis and promoted the reduction of VEGF and TGF-β levels at all concentrations tested. Therefore, our results demonstrated that DvL is a potent anticancer, anti-angiogenic, and selective cytotoxic agent for tumor cells, suggesting its potential application as a prototype molecule for the development of new drugs with chemoprotective and/or antitumor effects.
A method for providing an optimized process in clinical research, comprising enabling research participant, site manager to input research participants' information by enrolment and retention module on research participant computing device, research site manager computing device. Identifying research participants' information stored in database and generating list of qualified research participants by list generating module. Enabling qualified research participants to schedule appointment with site manager by appointment scheduling module and assigning principal investigators to screen research participants. Enabling principal investigators to input screening data by primary source data capture module after screening research participants in real-time. Collecting screening data to calculate accounts receivable from sponsor by financial module and sending screening data to data review and reports generating module. Generating screening reports by data review and reports generating module and sending screening reports to invoice generating module thereby generating invoice. Sending invoice to sponsor computing device and enabling sponsor to review invoice.
Patients will have a Rocket Medical 16F ballooned chest drain inserted as per usual clinical guidelines. No other change to treatment will be made, and the drain is inserted in exactly the same way as a standard drain, using the Seldinger technique.
The present invention relates to a cell therapeutic agent or a pharmaceutical composition for cancer treatment, comprising, as an active ingredient, a transformed antigen-specific professional antigen presenting cell comprising a chimeric antigen receptor (CAR). In detail, the chimeric antigen receptor includes an antigen-binding domain binding specifically to HLA class II. The transformed cell according to the present invention comprises an enhanced chimeric signaling domain that induces the activity of the professional antigen presenting cell when the professional antigen presenting cell binds specifically to an antigen. For example, provided is a recombinant protein including extracellular domains 1-4 of LAG-3 that recognizes HLA class II (HLA-DP, HLA-DQ, and HLA-DR), and a novel synthetic intercellular signaling domain in which an immunoreceptor tyrosine-based activation motive (ITAM) of TLR-3, TLR-4, and an IgE receptor gamma chain (Fcε receptor I gamma chain, FcεRIγ), or an IgG receptor 2A alpha chain (Fcγ receptor 2A alpha chain, FcγR2Aα), or an IgE receptor beta chain (Fcε receptor I beta chain, FcεRIβ), which performs an important action in signaling of the professional antigen presenting cell, is used as a subunit, and three ITAMs are linked through a linker. In the case of a professional antigen presenting cell which has been transformed with a vector that can express the recombinant protein, the cell has cytotoxicity specifically with respect to cancer that expresses HLA class II (HLA-DP, HLA-DQ, and HLA-DR. Therefore, the professional antigen presenting cell that overexpresses the chimeric antigen receptor according to the present invention may be usefully utilized as an immunocellular therapeutic agent for the treatment of cancer that expresses HLA class II (HLA-DP, HLA-DQ, and HLA-DR).
Rationale: Cardiovascular disease (CVD) is a leading cause of morbidity and mortality among individuals with chronic obstructive pulmonary disease (COPD). Black women with COPD are at elevated risk of CVD-related mortality compared with White women. CVD risk factors are undertreated in Black men and women. However, barriers to CVD prevention from the perspective of Black individuals living with COPD have not been previously identified. Objectives: To identify barriers and facilitators for CVD prevention among Black individuals living with COPD. Methods: We conducted semistructured interviews with Black participants living with COPD and attending clinics at two urban hospitals. Participants were included if they had physician-confirmed COPD diagnoses and presence of CVD or CVD risk factors. Interviews were conducted until thematic saturation was reached, with additional interviews conducted to confirm saturation. Data were analyzed using thematic analysis, iteratively revising and updating the codebook by consensus of the study team. Codes were grouped into categories, subthemes, and themes. Themes were organized using the social ecological framework into individual, interpersonal, health system, and societal levels. Results: We interviewed 30 participants of mean age 67.8 ± 8.3 years; 17 (57%) were Black women and 13 (43%) were Black men. Individual-level themes were that living with COPD and resultant multimorbidity affects CVD prevention (theme 1) and that self-efficacy and advocacy affect care received (theme 2). At the interpersonal level, supportive relationships facilitate improved access to CVD prevention (theme 3). System-level themes were that health systems are not designed to support patients with COPD and CVD (theme 4) and that health systems do not deliver effective patient education (theme 5). At the societal level, structural barriers and racism prevent access to care and adoption of a healthy lifestyle (theme 6). Conclusions: We identified barriers to CVD prevention at all levels of the socioecological framework for Black individuals living with COPD. To maximize their impact, future interventions to prevent CVD among individuals with COPD can use these findings to target barriers at multiple levels.
Pain Modulation Index is a questionnaire that was developed in English for the assessment of chronic pain for qualities consistent with central sensitization. The English version of the questionnaire was translated into Turkish by two physicians than back translated into English by two separate bilingual translators. Initially 10 volunteers were asked to answer this first version of the questionnaire and report any difficulties in understanding the items. Their feedback was used to give the questionnaire its final shape. For the validation stage, patients that were diagnosed as having chronic non-cancer pain with more than 3 months duration were enrolled into the study. They answered the questions twice, 15 days apart. In addition to the Turkish version of the Pain Modulation Index, on the first visit, they were also asked to answer Pain Detect and Central Sensitization Inventory. Their answers were analysed to assess the validity and reliability of the Turkish version of Pain Modulation Index.
A computerized method for identification and notification of discrepancies in a medical setting from the time a medical provider orders a medical procedure to the time a medical claim is submitted. The computerized method focuses on the following discrepancies:
         1. Procedure scheduled is different from the procedure ordered by the medical provider   2. Procedure obtained Authorization for from the medical insurance company is different from the procedure ordered by the medical provider.   3. The Procedure Authorization is obtained under a diagnosis code different from the one under which the procedure was ordered by the medical provider.   4. The Procedure Authorization is obtained for a CPT (Current procedural terminology) code different from the one under which the procedure was ordered by the medical provider.   5. The Date of service (DOS) does not fall within the Procedure Authorization date span.   6. The patient medical insurance is different from the medical insurance from which the authorization was obtained,   7. The diagnosis code documented on the Operative note does not include the diagnosis code under which the procedure was ordered.   8. The CPT code on the medical claim is different from the CPT code for which the authorization was obtained from the medical insurance.   9. The medical insurance name on the medical claim is different from the medical insurance from which the authorization was obtained.   10. The Procedure authorization number on the medical claims is different from the authorization number obtained from the medical insurance.   11. The Date of service on the claim is different (does not fall within) the Procedure Authorization date span.       

     The computer program will make a recommendation to the user as part of notification on identification of an error. The computer program user can Override the recommendation. The program user will need to add Notes if she/he chooses to override the error generated. All the data related to Override will be logged along with details related to user, notes etc so that medical facility management can review user activity.
Ornithine Alpha Ketoglutarate for 4 weeks, followed by 2 week washout period. 4 weeks Glutamine, followed by 2 week washout period. 4 weeks Disodium Citrate, followed by 2 to 12 week washout period. Then continue an additional 30 weeks on Disodium Citrate (drug producing the best increment in plasma glutamine levels).
High myopia has become a major public concern globally, which is characterized by excessive axial elongation of the eyeball. Axial elongation is accompanied by mechanical stretching and thinning of the choroid and sclera, causing vision-threatening complications. Repeated low-level red-light (RLRL) therapy is an emerging effective and safe therapy for myopia control. Previous clinical trials in China have observed clinically significant axial shortening after RLRL treatment.

The purpose of this study is to investigate and identify possible mechanism for axial length (AL) shortening after 12-month RLRL therapy in highly myopic children and teenagers aged 8-18 years. In addition to single vision spectacles, subjects will receive RLRL treatment at home under supervision of the parents/guardians according to a standard protocol. Axial length, visual acuity, cycloplegic spherical equivalent refraction, slit lamp, fundus camera and optical coherence tomography/angiography will be measured at 1-, 3-, 6- and 12-month follow-up visits.
<P>PROBLEM TO BE SOLVED: To provide a Myrothecium sp. mycelium extract used for inhibiting the growth of cancer cells.  <P>SOLUTION: The Myrothecium sp. mycelium extract used for inhibiting the growth of cancer cells is particularly verrucarin A and verrucarin J isolated from Myrothecium sp. mycelium which effectively inhibit the cell growth of hepatic cancer, lung cancer, and prostate cancer. Here, the compounds of verrucarin A and verrucarin J can be applied to the inhibition of the growth of Hep3B and HepG2 of human hepatic cancer cells, A549 of a human lung cancer cell, and LNCaP and DU-145 of human prostate cancer cells and simultaneously can be used in a pharmaceutical composition for inhibiting the cell growth of hepatic cancer, lung cancer, and prostate cancer.  <P>COPYRIGHT: (C)2009,JPO&INPIT