anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
INTRODUCTION: Consensus Auditory Perceptual Evaluation of Voice (CAPE-V) is a widely used perceptual evaluation scale for voice assessment. It is adapted in many regional languages worldwide. This systematic review will help critically evaluate the methodologies used to adapt and establish CAPE-V as a valid and reliable tool.
METHOD: Authors reviewed literature in search engines (Scopus, Google Scholar, PubMed) to identify studies published in English between 2002-2020. The CAPE-V translated and adapted for linguistic or cultural variations were included for the review. The studies were compiled using the Mendeley Reference Manager and screened for title/abstract before shortlisting the studies.
RESULTS: The initial database had 3459 search results and after duplicates removal, 1535 articles were analysed. Thirteen studies were narrowed based on title/abstract screening. A final of ten studies were selected for the review.
DISCUSSION/CONCLUSION: This review provided a comprehensive understanding of the challenges encountered during cross-cultural adaptation and will help future researchers choose a suitable adaptation method.
The invention discloses a solid-gel ultra-refreshing fragrant refreshing agent and a preparation method thereof. The solid-gel ultra-refreshing fragrant refreshing agent is prepared from, by mass, 0.75-1.50% of an ultra-refreshing fragrance, 0.50-1.50% of solid gel, 8.00-10.00% of a high-efficiency solubilizer, 0.40-0.60% of a preservative, and balance of distilled water. The preparation method comprises ultra-refreshing fragrance preparation, ultra-refreshing fragrance solubilizing, preparation of solid gel with pH of 6-7, mixing of the solubilized ultra-refreshing fragrance and the solid gel with pH of 6-7, and the like, such that the solid-gel ultra-refreshing fragrant refreshing agent is finally obtained. The solid-gel ultra-refreshing fragrant refreshing agent is a pure natural, non-toxic, no-harm, and safe product with effects of fatigue dispelling, depression resisting, and emotion calming. The agent can be smeared on human skin, and can provide a refreshing effect. With the agent, refreshing, cooling, and pleasant fragrance can be continuously released.
BioWaveGO is a FDA 510(k) cleared high frequency neurostimulator. Patients that are first randomized to the BioWave arm will receive a 30 minute treatment in the clinic with a BioWaveGO device followed by a 30 minute washout and ending with a final 30 minute treatment. Data will be collected before, and after the final treatment. Patients will then be instructed to take the BioWaveGO device home and perform two 30 minute treatment sessions daily at home for 2 weeks. Follow-up in the clinic will be after the 2-week treatment period and the patients will be assessed in clinic for physiologic measures of pain response. A washout period of 2 weeks will follow, the patients will return to the clinic at week 4 and the patients will crossover to receive the TENS treatment (as described in the TENS arm).
Infants with large hemangiomas are often treated systemically with oral steroids (Prednisolone) to prevent complications. The best treatment for hemangiomas is not known and there are no medications approved by the FDA for treatment of hemangiomas. Also, the best method to measure the response of hemangioma to treatment is not known. Patients enrolling on this study will be randomly assigned to receive either daily Prednisolone by mouth or weekly Vincristine in a vein. Response to treatment will be monitored by clinical exams every two weeks and by an MRI at study entry and six and twelve weeks later. Patients with evidence of progressive disease (larger hemangiomas) on the week 6 MRI will be switched to the other drug to complete a total of 12 weeks of therapy. Side effects of each medication will be monitored closely determined from histories, physical exams, blood tests and other studies as necessary. Participation in this study will last up to 12 weeks and follow up for protocol.
Patients receive PCV 20 IM at week 0. Titers will be checked 4 weeks after this dose. Booster Vaccine: None. Titers will be checked at 12 weeks and then yearly for 5 years.
Arm I: Patients receive R-CHOP immunochemotherapy comprising rituximab IV, cyclophosphamide IV over 15 minutes, doxorubicin hydrochloride IV, and vincristine IV on day 1 and oral prednisone once daily on days 1-5. Treatment repeats every 21 days for 3 courses in the absence of disease progression or unacceptable toxicity. Patients then undergo restaging of their disease. Patients with disease progression proceed to salvage therapy off study. All other patients receive 3 more courses of R-CHOP.
This would be a cohort study including patients with locally advanced pancreatic cancer medically fit to receive chemotherapy. Eligible patients would receive gemcitabine (GNP; 28- day cycles). P-32 microparticles (OncoSil; OncoSil Medical) implantation will be planned at weeks 4-5. P-32 activity will be calculated from patients' tumor volume (TV) to deliver 100 Gy absorbed dose, with implantation assessment by EUS and Bremsstrahlung SPECT/CT imaging. The primary endpoint was safety and tolerability, graded using CTCAE v4.0. Response will be assessed using RECIST 1.1 with 8-weekly CT scans and FDG-PET scans at baseline and week 12. The outcome parameters include adverse events, response of the tumour, local progression free survival and overall survival (OS).
EGFR AS will be administered by direct intratumoral injection using direct visualization, endoscopy, or imaging-guidance (ultrasound) as clinically determined. Subjects will receive a total of up to 7 weekly intratumoral injections of EGFR antisense (or less if there is no identifiable tumor) starting 2 weeks prior to radiation. Patients will receive a total EGFR AS dose of 1.92 milligrams in 1.78 milliliters on each weekly treatment. This dose may be delivered equally in the same tumor site per weekly session, the primary tumor or cervical lymph nodes.
Participants receive NRT consisting of a patch, lozenges, or gum daily for 6 weeks in the absence of unacceptable toxicity. Participants who quit smoking continue treatment for 6 additional weeks in the absence of unacceptable toxicity. Participants also receive behavioral smoking cessation counseling.
BACKGROUND: Cutaneous neurotropic melanoma (NM) of the head and neck (H&N) is prone to local relapse, possibly due to difficulties widely excising the tumor. This trial assessed radiation therapy (RT) to the primary site after local excision.
METHODS: Participants from 15 international centers were randomized to observation or RT. The participants were required to have microscopically negative excision margins 5 mm wide or wider and no evidence of disease elsewhere. The primary outcome was time to local relapse. The secondary outcomes included time to any recurrence, overall survival (OS), and toxicity.
RESULTS: The trial ceased prematurely due to slow recruitment and the COVID-19 pandemic. During 2009-2020, 50 participants were randomized: 23 to observation and 27 to RT. The most common NM subsites were scalp (32%), midface (22%), and lip (20%). The median depth of invasion was 5 mm, and desmoplasia observed in 69%. The median duration from randomization to last contact was 4.8 years. Four participants (8%) experienced local relapse as a first recurrence during the study period: 3 in the observation arm and 1 in the RT arm (hazard ratio [HR] 0.29; 95% confidence interval [CI] 0.03-2.76; p = 0.279). No statistically significant difference in time to any relapse or OS was observed. More than 6 months after randomization, grade 3 or greater toxicity was experienced by 10% of the participants in the observation arm and 12.5% of the participants in the RT arm of the study.
CONCLUSION: Due to low accrual, the role of adjuvant RT for cutaneous NM of the H&N excised with microscopically negative margins 5 mm wide or wider remains undefined. Its routine use cannot be recommended. Local relapse might be less common than previously anticipated based on retrospective reports.
GFI is a simple questionnaire consisting of 15 items which are classified into 8 groups, consistent of 4 domains of functioning. A score of 4 or more indicates a higher risk for frailty and possible delirium.
OBJECTIVES: I. Determine the maximum tolerated dose and dose limiting toxicity of topotecan when combined with ifosfamide in patients with limited or extensive stage small cell lung cancer. II. Determine the pharmacokinetics of topotecan and correlate with toxicity or tumor response in these patients. III. Determine the effect of topotecan on apoptosis in tumor tissues and correlate the apoptosis-inducing effects with antitumor effects of topotecan in these patients. IV. Determine the response rate, time to progression, and survival of chemotherapy naive limited or extensive stage small cell lung cancer patients treated with ifosfamide and topotecan and then crossover consolidation/salvage therapy with carboplatin and etoposide. V. Determine the response rate, time to progression, and survival of pretreated limited or extensive stage small cell lung cancer patients treated with ifosfamide and topotecan as salvage therapy.

OUTLINE: This is a dose escalation study of topotecan (phase I). Patients are stratified by disease stage (extensive vs limited) and prior chemotherapy (naive vs pretreated) in phase II. Induction therapy: Patients receive topotecan IV over 72 hours and ifosfamide IV over 30 minutes every 3 weeks. Chemotherapy naive patients with complete or partial response after 3 courses, stable disease after 2 courses, or progressive disease at any time receive consolidation/salvage chemotherapy. Pretreated patients continue on induction regimen for a minimum of 6 courses unless disease progression or unacceptable toxicity. Phase I: Cohorts of 3-6 patients receive escalating doses of topotecan until the maximum tolerated dose (MTD) is determined. The MTD is defined as the dose preceding that at which 3 of 6 patients experience dose limiting toxicity. Salvage chemotherapy: Patients with extensive stage disease receive carboplatin IV over 30 minutes on day 1 and etoposide IV over 45 minutes on days 1, 2, and 3. Treatment repeats every 3 weeks for up to 4 to 6 courses. Patients with limited stage disease undergoing chest irradiation receive treatment every 28 days for the first course. Patients are followed every 2 months for 1 year, every 3 months for 1 year, and then every 4 months thereafter.

PROJECTED ACCRUAL: Approximately 15-20 patients will be accrued for phase I and approximately 35 patients will be accrued for phase II of this study.
BACKGROUND: We compared the spread of an injectate into the thoracic sympathetic chain resulting from a single-injection intertransverse process (ITP) block with that of a single-injection PV block at the T2 level.
METHODS: Sixteen soft-embalmed cadavers were used. The right hemithorax was randomly allocated to receive either an ultrasound-guided single-injection ITP block or ultrasound-guided single-injection PV block at the T2 vertebral level, with the opposite block administered to the other side. Approximately 10 mL of latex dye solution was injected into each hemithorax using a random allocation technique. The presence of dye at the nerve root in the sympathetic chain and intercostal nerves at the injection and additional levels was examined by dissection.
RESULTS: The injectate spread into the T2 sympathetic ganglion on both ITP (11/16, 68.8%) and PV (16/16, 100%) blocks. The ITP block demonstrated greater uniformity of dye staining in both the dorsal rami and dorsal root ganglion, which contrasts with the less consistent staining outcomes of the PV block in these regions.
CONCLUSIONS: At the T2 level, we observed a lower efficacy of the ITP block for analgesic coverage of the sympathetic nerve. This suggested a potential preference by clinicians for the application of the T2 PV block over the ITP block, specifically for the management of sympathetically maintained pain in the upper extremities. In addition, our findings may hint at the potential advantages of the ITP block in specific clinical contexts where targeted nerve involvement, such as the medial branch block or dorsal root ganglion block, is sought.
PURPOSE:To obtain pure IgM, useful as a remedy for bacterial infection, and capable of being an intravenous injection pharmaceutical, by fractionating a blood plasma fraction consisting essentially of IgM with polyethylene glycol (PEG) under weakly alkaline conditions, and separating kallikrein which is a factor for side effects. CONSTITUTION:A blood plasma fraction consisting essentially of IgM is fractionated with polyethylene glycol (PEG) under weakly alkaline conditions, preferably 7.5<pH<8.5. The reaction temperature is preferably 0-10 deg.C. A kallikrein- like active substance is contained in the resultant supernatant of the white deposited precipitates. The white precipitates are then redissolved to afford the aimed pure IgM. In the intravenous injection of the IgM pharmaceutical, the kallikrein- like active substance causing side effects, e.g. hypotension, can be separated, and the pure IgM fraction considered to be more desirable than the IgM for treating microbism can be obtained.
Lung cancer is the leading cause of mortality in the world. Previous study has shown that about 88% lung cancer cases belong to non-small cell lung cancer (NSCLC) in Taiwan (1). Approximately 50\~90% of NSCLC patients had expression (or described as overexpression) of EGFR in cancer (2,3). Although targeting the EGFR kinase domain using the inhibitors gefitinib (Iressa) and erlotinib (Tarceva) has no effect against solid tumors, it achieves impressive response in subgroup of NSCLC especially in Asian ethnic background, female sex, the absence of a history of smoking, and a tumor with histologic feature of adenocarcinoma (3,4,5). Molecular studies of highly responsive cases revealed high percentage of somatic mutation within the tyrosine kinase, ATP-binding domain of the EGFR gene (6). One possible explanation for this phenomenon is that the cancer cells are "addicted" to signaling via the mutant EGFRs and die when the mutant oncoprotein is inactivated (7). However, specific mechanisms underlying epidermal growth factor tyrosine kinase inhibitor (EGFR-TKI) induced cell death have not been well delineated (7).

Approximately 90% of mutations affect a few specific amino acids. In-frame deletions in exon 19 centered on codons 756 to 750 make up 45\~50% of mutations, and another 35\~45% consist of the missense mutation leucine to arginine at codon 858 (L858R) in exon 21 (8, 9, 10). The link between EGFR-TKI response and EGFR mutations have been confirmed, but the increased prevalence of mutations in Asian (25%to 50%) compared with North American and Western European patients (10%) is currently unexplained (6,8-12). The response rate to TKI treatment in mutations-positive is 77% (30% to 100% with most series \>60%) compared with 10% in mutation-negative cases (6). It is interesting that exon 19 deletion have increased response and survival with TKIs compared with L858R cases (10, 13, 14). This is in contrast to the natural history of patients, where those with exon 19 deletions appear to have shorter survival than those with L858R (8). The biological difference is still unknown and different mutations may have different biochemical signaling properties (15).

In this study, we will collect the pleural effusion from lung cancer patients. We will characterize the EGFR status of the cancer cell from malignant pleural effusion and try to establish the cancer cell lines from these patients. We hope to establish several cell lines with different mutations and then we can compare the difference responses and signal pathways in these cell lines. We can also explore the detailed mechanism of TKI responsive cancer cell and try to develop other agent to enhance the pathways.
This study is a clinical trial in patients with Parkinson's disease (PD), of a drug called exenatide, which is already licensed for the treatment of patients with type 2 diabetes. There have been several groups that have confirmed that exenatide has beneficial effects of nerve cells when tested in the laboratory, which raises the possibility that exenatide may slow down or stop the degeneration of PD. In an open label trial in patients with PD who self administered the drug for a period of 48 weeks, investigators have previously shown that the drug is well tolerated and shows encouraging effects on the movement and non-movement aspects of the disease. A double blind placebo controlled trial involving 60 participants was then conducted which indicated that exenatide may be a "neuroprotective" drug, i.e. one that stops the nerve cells dying in PD. The next step is therefore to confirm this "neuroprotective" effect and to see whether this effect can be reproduced in a multi-centre setting including a larger number of participants. An important objective is to explore whether any positive effects remain static or increase when the treatment is continued over a 96 week period.
PURPOSE:To enable efficient production of the title antibody for a group determining antigens having delicate difference which can recognized between human and human by using, as an immune animal, not human mammalian animal which is transformed with a recombinant gene into which HAL gene is introduced. CONSTITUTION:The HLA gene is introduced into a fertilized ovum of not human mammalian animal and the ovum is transferred into the uterus of the female animal as a tentative mother. Then, the tentative mother is fed for a certain period to give birth to the animal of which the gene is transformed. Then, HLA antigen is given to the mammalians expressing the HLA gene introduced as an immunogen. Then, the spleen is excised from the immunized animals, the spleen cells are fused with myeloma cells and the hybridoma producing the antibody is selected from the fused cells. Finally, the hybridoma is cultured to produce the subject antibody.
Despite epidermal turnover, the skin is host to a complex array of microbes, including viruses, such as HPV, which must infect and manipulate skin keratinocyte stem cells (KSCs) to survive. This crosstalk between the virome and KSC populations remains largely unknown. Here, we investigated the effect of HPV8 on KSCs using various mouse models. We observed that the HPV8 early region gene E6 specifically caused Lrig1+ hair follicle junctional zone KSC proliferation and expansion, which would facilitate viral transmission. Within Lrig1+ KSCs specifically, HPV8 E6 bound intracellular p300 to phosphorylate the STAT3 transcriptional regulatory node. This induced ΔNp63 expression, resulting in KSC expansion into the overlying epidermis. HPV8 was associated with 70% of human actinic keratoses. Together, these results define the "hit-and-run" mechanism for HPV8 in human actinic keratosis as an expansion of KSCs, which lack melanosome protection and are thus susceptible to sun light-induced malignant transformation.
Human Papillomavirus (HPV) is a widespread infection associated with various cancers, including cervical, oropharyngeal, anal, and genital cancers. This infection contributes to 5 % of global cancer cases annually, affecting approximately 625,600 women and 69,400 men. Cervical cancer remains the most prevalent HPV-linked cancer among females, with the highest incidence seen in low and middle-income countries (LMICs). While most HPV infections are transient, factors such as HPV variants, age, gender, and socioeconomic status influence transmission risks. HPV is categorized into high-risk (HR-HPV) and low-risk types, with strains like HPV 16 and 18 displaying distinct demographic patterns. The intricate pathogenesis of HPV involves genetic and epigenetic interactions, with HPV oncogenes (E6 and E7) and integration into host DNA playing a pivotal role in driving malignancies. Early diagnostics, utilizing HPV DNA testing with surrogate markers such as p16, and advanced molecular techniques like PCR, liquid biopsy, and NGS, significantly impact the management of HPV-induced cancers. Effectively managing HPV-related cancers demands a multidisciplinary approach, including immunotherapy, integrating current therapies, ongoing trials, and evolving treatments. Prevention via HPV vaccination and the inclusion of cervical cancer screening in national immunization programs by conventional Pap smear examination and HPV DNA testing remains fundamental.Despite the preventability of HPV-related cancers, uncertainties persist in testing, vaccination, and treatment. This review article covers epidemiology, pathogenesis, diagnostics, management, prevention strategies, challenges, and future directions. Addressing issues like vaccine hesitancy, healthcare disparities, and advancing therapies requires collaboration among researchers, healthcare providers, policymakers, and the public. Advancements in understanding the disease's molecular basis and clinical progression are crucial for early detection, proper management, and improved outcomes.
This will be a prospective, observational study in which patients in need of dental implants in the anterior regions of the maxilla or mandible will be treated with the Eztetic dental implant(s). Qualified patients will be those with one or more edentulous area in the anterior maxilla or mandible needing a single (restored as a single crown; if in the pre-molar region, it is recommended implant be splinted to another tooth or implant; no 2 adjacent edentulous sites). Qualified patients should have presence of posterior teeth or a stable posterior occlusion. All implants will be placed in a single-stage manner. A provisional abutment will be placed and a temporary crown will be placed (cemented or screw-retained) out of occlusion at implant placement surgery visit. Impressions for permanent prosthesis fabrication will take place at 6 weeks and prosthesis placement will take place at 2 months. Final prosthesis insertion will take place no later than 6 months following implant placement surgery. Resonance frequency assessment procedures will be done at implant placement surgery and at prosthesis insertion. Implant survival will be the primary study endpoint. Crestal bone regression will be the secondary study endpoint. Enrollment will continue until 20 patients have completed final prosthetic treatment at study center.
Initial dose is 0.4mg/kg/day, divided every 3-4 hours, given PO with feeds. Drug is required until symptoms of withdrawal no longer cause the infant feeding, behavior, or elimination problems, up to 3 months.
No prior studies have linked long-term air pollution exposure to incident sudden cardiac arrest (SCA) or its possible development trajectories. We aimed to investigate the association between long-term exposure to air pollution and SCA, as well as possible intermediate diseases. Based on the UK Biobank cohort, Cox proportional hazard model was applied to explore associations between air pollutants and SCA. Chronic obstructive pulmonary disease (COPD) and major adverse cardiovascular events (MACE) were selected as intermediate conditions, and multistate model was fitted for trajectory analysis. During a median follow-up of 13.7 years, 2884 participants developed SCA among 458 237 individuals. The hazard ratios (HRs) for SCA were 1.04-1.12 per interquartile range increment in concentrations of fine particulate matter, inhalable particulate matter, nitrogen dioxide, and nitrogen oxides. Most prominently, air pollutants could induce SCA through promoting transitions from baseline health to COPD (HRs: 1.06-1.24) and then to SCA (HRs: 1.16-1.27). Less importantly, SCA could be developed through transitions from baseline health to MACE (HRs: 1.02-1.07) and further to SCA (HRs: 1.12-1.16). This study provides novel and compelling evidence that long-term exposure to air pollution could promote the development of SCA, with COPD serving as a more important intermediate condition than MACE.