anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Methods and apparatus to form a biometric based information communication system are described. In some examples, the biometric based information communication system comprises biomedical devices with sensing means, wherein the sensing means produces a biometric result.  In some examples the biometric based information communication system may comprise a user device such as a smart phone paired in communication with the biomedical device. A biometric measurement result may trigger a communication of a biometric based information communication message. The biometric based information communication message may comprise an advertisement. In some examples, the advertisement may include a means to link to an electronic purchasing or e-procurement vehicle.
In the morning, this group brushed with Tartarase for 30 seconds, spit, but did not rinse and repeated the process. In 30 minutes they brushed with Crest. They repeated this routine before bed. This routine was repeated daily for 4 weeks.
BACKGROUND: Tuberculosis (TB) is still the main cause of mortality due to a single transfectant, Mycobacterium tuberculosis (MTB). Latent tuberculosis infection (LTBI) is a condition characterized by the presence of tuberculosis (TB) that is not clinically apparent but nonetheless shows a sustained response to MTB. Presently, tuberculin skin test (TST) and interferon gamma (IFN-γ) release assays (IGRAs) are mainly used to detect LTBI via cell-mediated immunity of T-cells. For people with end-stage renal disease (ESRD), the diagnosis of patients infected with MTB is difficult because of T-cell dysfunction. To get more accurate diagnosis results of LTBI, it must compensate for the deficiency of IGRA tests.
METHODS: Sixty-seven hemodialysis (HD) patients and 96 non-HD patients were enrolled in this study and the study population is continuously included. IFN-γ levels were measured by the QuantiFERON-TB Gold In-Tube (QFT-GIT) test. Kidney function indicators, blood urea nitrogen (BUN), serum creatinine (Cr), and estimated glomerular filtration rate (eGFR) were used to compensate for the declined IFN-γ levels in the IGRA test.
RESULTS: In individuals who were previously undetected, the results of compensation with serum Cr increased by 10.81%, allowing for about 28% more detection, and compensation with eGFR increased by 5.41%, allowing for approximately 14% more detectable potential among them and employing both of them could enhance the prior shortcomings of IGRA tests. when both are used, the maximum compensation results show a sensitivity increase rate of 8.81%, and approximately 23% of patients who were previously undetectable may be found.
CONCLUSION: Therefore, the renal function markers which are routine tests for HD patients to compensate for the deficiency of IGRA tests could increase the accuracy of LTBI diagnosis.
The present invention includes nucleic acids of the Bartonella henselae virB  virulence operon and polypeptides encoded by the nucleic acids. The invention includes expression vectors containing the nucleic acids and transformed cell lines containing the expression vectors. The invention includes detection methods for B. henselae infection, and kits for performing these methods. The methods comprise detecting the nucleic acids or polypeptides of the invention, or antibodies against the polypeptides, in patient fluids. Also included in the invention are therapeutic compositions, such as vaccines, for treating Bartonella henselae infection. Furthermore, the invention includes antibodies against the polypeptides encoded by the B. henselae virB operon. Finally, the invention includes methods of producing polypeptides encoded by the B.  henselae virB operon.
Puccinia striiformis f. sp. tritici (Pst) has a wide range and serious damage, which severely threatens global wheat production. In this study, we focused on an effector protein Pst3180.3, which was induced to be highly expressed during the Pst infection stage. The N-terminal 19 amino acid of Pst3180.3 was verified to function as a signal peptide and transferred to cytoplasm and nucleus of wheat following Pst infection. Transient overexpression of Pst3180.3 in Nicotiana benthamiana inhibited programmed cell death triggered via BAX. The instantaneous silencing of Pst3180.3 by BSMV- HIGS significantly reduced the number of uredinia and increased accumulation of reactive oxygen species. Those results indicated that Pst3180.3 is an important pathogenic factor of Pst. Interaction of Pst3180.3 with a transcription factor TaMYB4L in host was confirmed through yeast two-hybrid, luciferase complementation, and co-immunoprecipitation. Virus-induced gene silencing of TaMYB4L weakened the resistance to Pst, indicated that TaMYB4L may be involved in the positive regulation of plant immunity. Dual-luciferase assays revealed that Pst3180.3 inhibited the transcriptional activity of TaMYB4L. Meanwhile, molecular docking analysis identified the key residue sites for the interaction and binding between Pst3180.3 and MYB4L. Those results demonstrated that Pst3180.3 binds to TaMYB4L and interacts to inhibit wheat resistance to Pst infection.
A consent block is a type of block that may be stored in a blockchain. Each consent block has an owner and may store an owner consent contract, i.e., a smart contract containing owner-specified access rules that determine who may access data assets that are stored in other blocks of the blockchain and owned by the same owner. The consent block may alternatively store a global consent contract containing global access rules that supersede owner-specified access rules. The consent block also stores a hash value determined from the consent contract and a previous hash value of the block immediately preceding the consent block. The consent contract and the position of the consent block in the blockchain are verifiable from the hash value. Each consent block, once added to the blockchain, becomes part of the immutable record of data stored in the blockchain, and therefore leaves an auditable trail.
Use of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor for the treatment and/or prevention of coxsackievirus infection and adenoviral infection, or diseases caused by coxsackievirus and/or adenovirus, is claimed. An independent claim is also included for a pharmaceutical composition comprising at least one HMG-CoA reductase inhibitor. ACTIVITY : Cardiant; Antiinflammatory; Neuroprotective; Gastrointestinal-Gen; Ophthalmological; Antiallergic; Respiratory-Gen; Antidiarrheic; Cytostatic; Virucide. MECHANISM OF ACTION : HMG-CoA reductase inhibitor. The ability of lovastatin (HMG-CoA reductase inhibitor) to reduce the concentration of coxsackie-adenovirus receptor (CAR) mRNA expression was tested in human umbilical vein endothelial cells. The results showed that lovastatin at a concentration of 5 mu M decreases the concentration of CAR mRNA expression by 76%.
Hemorrhage occurred in 51% of patients with cervical cancer treated with TIVDAK across clinical trials. The most common all grade hemorrhage adverse reaction was epistaxis (33%). Grade 3 hemorrhage occurred in 4% of patients.

The median time to onset of hemorrhage was 0.3 months (range, 0-10.4). Of the patients who experienced hemorrhage, 71% had complete resolution and 12% had partial resolution (defined as a decrease in severity by one or more grades from the worst grade) at last follow-up.

Monitor patients for signs and symptoms of hemorrhage. For patients experiencing pulmonary or CNS hemorrhage, permanently discontinue TIVDAK. For grade ≥2 hemorrhage in any other location, withhold until bleeding has resolved, blood hemoglobin is stable, there is no bleeding diathesis that could increase the risk of continuing therapy, and there is no anatomical or pathologic condition that can increase the risk of hemorrhage recurrence. After resolution, either resume treatment or permanently discontinue TIVDAK [see Dosage and Administration (2.3)].
Participants will receive combined oral contraceptive NOMAC-E2 2.5 mg/1.5 mg tablet for 13 consecutive 28-day cycles. Each 28-day cycle with consist of 24 active tablets and 4 placebo tablets taken at approximately the same time each day.
For the treatment group, education sessions will be conducted during the baseline visit on carb counting and bolus calculator methods, installation, and usage instructions for DIA:CONN P8 and DIA:CONN app, as well as CGM and CGM app. During the 12-week, for basal insulin, the treatment group will input and inject the dosage using the DIA:CONN P8, using only the insulin injection and injection recording functions, same as the blind CGM period. For bolus insulin, when the carbohydrate counting is entered or the type of meal is selected into the DIA:CONN P8 application, the insulin dosage is automatically calculated and set using the entered information and other indicators. Subjects inject the insulin at that calculated dosage using the DIA:CONN P8. Insulin injection dosage, time stamps, and other related details will be recorded into DIA:CONN P8 device and app.
Stroke is the leading cause of long-term disability in the U.S. Individuals with hemiparesis due to stroke often have difficulty bearing weight on the paretic lower extremity and transferring weight from one leg to the other. Impaired weight transfer and limb loading contribute to lateral instability and are associated with decreased walking speed and increased risk of falling. Consequently, restoring limb loading ability is an important goal for rehabilitation post-stroke. Despite considerable rehabilitation efforts aimed at enhancing paretic limb loading, their effectiveness on improving neuromotor and functional outcomes remains limited possibly due to poorly understood limb loading mechanisms and the reluctance to use the paretic limb. The coordination of neuromuscular actions to regulate loading force during weight acceptance is an important component of functional limb loading. Because altered neuromuscular control is common in persons with stroke, it is possible that these abnormalities may impair limb loading ability. The long-term objective of this project is to develop a mechanism-based framework for designing and testing the effectiveness of novel rehabilitation interventions to enhance lower limb weight transfer and limb loading to improve balance and mobility. This project aims to (1) identify the neuromuscular and biomechanical abnormalities in limb loading responses in individuals post-stroke, (2) determine the underlying mechanisms responsible for the deficits in limb loading, and (3) test the short-term effectiveness of a 6-week perturbation-induced limb load training program on improving limb loading responses and mobility function. The investigators propose to apply a sudden unilateral lowering of the supporting surface to induce lateral weight transfer that forces limb loading. Kinetic, kinematic, and lower extremity muscle activation patterns will be recorded. The investigators expect that, compared to healthy controls, individuals with stroke will show increased muscle co-activation of the knee musculature with decreased knee flexion and torque production, and irregular impact force regulation during loading that will disrupt weight transfer and loading of the paretic limb. Furthermore, the investigators hypothesize that compared to a conventional clinical weight-shift rehabilitation training program, the imposed limb loading group will show greater improvements during voluntary stepping and walking following training. Specifically, the investigators expect the knee muscle co-activation duration will be reduced, with increased knee joint torque, and the paretic single stance/double support time will increase, reflecting improved paretic limb loading ability during gait following training.
Dacomitinib 45 mg will be administered orally daily. Treatment cycles will consist of 28 days.
The present invention relates to a personal care composition. The personal care composition comprises a surfactant phase. The surfactant phase comprises a surfactant of about 3% to about 12%, by weight of the personal care composition and a co-surfactant of about 4% or less by weight of the personal care composition. The surfactant includes sodium trideceth sulfate. The surfactant phase further comprises a structuring system. The structuring system comprises about 0.05% to about 5%, by weight of the personal care composition, of a crosslinked associative polymer and an electrolyte. The crosslinked associative polymer comprises a hydrophobic modification of less than 10% and can be hydrophobically modified with greater than a C6 alkyl. The personal care composition further comprises a benefit phase comprising a hydrophobic benefit material of about 1% to about 50%, by weight of the personal care composition.
BACKGROUND: Hepatocellular senescence may be a causal factor in the development and progression of non-alcoholic steatohepatitis (NASH). The most effective currently available treatment for NASH is lifestyle intervention, including dietary modification. This study aimed to evaluate the effects of dietary intervention on hallmarks of NASH and molecular signatures of hepatocellular senescence in the Gubra-Amylin NASH (GAN) diet-induced obese (DIO) and biopsy-confirmed mouse model of NASH.
METHODS: GAN DIO-NASH mice with liver biopsy-confirmed NASH and fibrosis received dietary intervention by switching to chow feeding (chow reversal) for 8, 16 or 24 weeks. Untreated GAN DIO-NASH mice and chow-fed C57BL/6J mice served as controls. Pre-to-post liver biopsy histology was performed for within-subject evaluation of NAFLD Activity Score and fibrosis stage. Terminal endpoints included blood/liver biochemistry, quantitative liver histology, mitochondrial respiration and RNA sequencing.
RESULTS: Chow-reversal promoted substantial benefits on metabolic outcomes and liver histology, as demonstrated by robust weight loss, complete resolution of hepatomegaly, hypercholesterolemia, elevated transaminase levels and hepatic steatosis in addition to attenuation of inflammatory markers. Notably, all DIO-NASH mice demonstrated ≥ 2 point significant improvement in NAFLD Activity Score following dietary intervention. While not improving fibrosis stage, chow-reversal reduced quantitative fibrosis markers (PSR, collagen 1a1, α-SMA), concurrent with improved liver mitochondrial respiration, complete reversal of p21 overexpression, lowered γ-H2AX levels and widespread suppression of gene expression markers of hepatocellular senescence.
CONCLUSIONS: Dietary intervention (chow reversal) substantially improves metabolic, biochemical and histological hallmarks of NASH and fibrosis in GAN DIO-NASH mice. These benefits were reflected by progressive clearance of senescent hepatocellular cells, making the model suitable for profiling potential senotherapeutics in preclinical drug discovery for NASH.
The starting dose of Erythropoietin is 60 (50-100) IU/kg body weight/week for naïve patients. Administration dose for patients who are treated with erythropoietin is similar dose of previously administered amount (IV or SC without any change). After then, dose adjustment will be done based on patients' response. In addition to main intervention, Nephrovit tablet/day and vitamine B12 100 mcg/month will be prescribed for patients.
Forkhead box M1 (FOXM1) is a key regulator of mitosis and is identified as an oncogene involved in several kinds of human malignancies. However, how it induces carcinogenesis and related therapeutic approaches remains not fully understood. In this study, we aimed to identify a regulatory axis involving FOXM1 and its target gene DEP domain containing 1 (DEPDC1) and investigate their biological functions. FOXM1 bound to the promoter and transcriptionally induced DEPDC1 expression, in turn, DEPDC1 physically interacted with FOXM1, promoted its nuclear translocation, and reinforced its transcriptional activities. The FOXM1/DEPDC1 axis was indispensable for cancer cells, as evidenced by the fact that DEPDC1 rescued cell growth inhibition caused by FOXM1 knockdown, and silencing DEPDC1 efficiently attenuated tumor growth in a murine hepatocellular carcinoma model. Furthermore, strong positive associations between FOXM1/DEPDC1 axis and poor clinical outcome were observed in human hepatocellular carcinoma samples, further indicating their significance for hepatocarcinogenesis. Finally, we attempted to exploit immunotherapy approaches to target the FOXM1/DEPDC1 axis. Several HLA-A24:02-restricted T-cell epitopes targeting FOXM1 or DEPDC1 were identified through bioinformatic analysis. Then, T cell receptor (TCR)-engineered T cells targeting FOXM1262-270 or DEPDC1294-302 were successfully established and proved to efficiently eradicate tumor cells. Our findings highlight the significance of the FOXM1/DEPDC1 axis in the process of oncogenesis and indicate their potential as immunotherapy targets.
Recent research found artesunate could inhibit ocular fibrosis; however, the underlying mechanisms are not fully known. Since the ocular fibroblast is the main effector cell in fibrosis, we hypothesized that artesunate may exert its protective effects by inhibiting the fibroblasts proliferation. TGF-β1-induced ocular fibroblasts and glaucoma filtration surgery (GFS)-treated rabbits were used as ocular fibrotic models. Firstly, we analyzed fibrosis levels by assessing the expression of fibrotic marker proteins, and used Ki67 immunofluorescence, EdU staining, flow cytometry to determine cell cycle status, and SA-β-gal staining to assess cellular senescence levels. Then to predict target genes and pathways of artesunate, we analyzed the differentially expressed genes and enriched pathways through RNA-seq. Western blot and immunohistochemistry were used to detect the pathway-related proteins. Additionally, we validated the dependence of artesunate's effects on HO-1 expression through HO-1 siRNA. Moreover, DCFDA and MitoSOX fluorescence staining were used to examine ROS level. We found artesunate significantly inhibits the expression of fibrosis-related proteins, induces cell cycle arrest and cellular senescence. Knocking down HO-1 in fibroblasts with siRNA reverses these regulatory effects of artesunate. Mechanistic studies show that artesunate significantly inhibits the activation of the Cyclin D1/CDK4-pRB pathway, induces an increase in cellular and mitochondrial ROS levels and activates the Nrf2/HO-1 pathway. In conclusion, the present study identifies that artesunate induces HO-1 expression through ROS to activate the antioxidant Nrf2/HO-1 pathway, subsequently inhibits the cell cycle regulation pathway Cyclin D1/CDK4-pRB in an HO-1-dependent way, induces cell cycle arrest and senescence, and thereby resists periorbital fibrosis.
Although the past two decades have seen substantial proportional growth of home hemodialysis in the United States, the absolute number of patients treated with home hemodialysis remains small. Currently available stationary hemodialysis devices for use in the home have inherent limitations that represent barriers for more widespread adoption by a larger proportion of individuals with kidney failure. These limitations include device weight and bulk, ergonomics considerations, technical complexity, vascular access challenges, and limited remote patient monitoring. Recent years have witnessed a resurgence in research and development of prototype wearable kidney replacement devices incorporating innovations in miniaturization, new biomaterials, and new methods for toxin clearance and dialysate regeneration. Recent work has built on five decades of incremental innovation in wearable dialysis concepts and prototypes, starting from the work by Kolff in the 1970s. Wearable dialysis devices that successfully overcome key persistent barriers to successful development and adoption of these technologies will radically reshape the landscape of kidney replacement therapies and have the potential to dramatically improve the lives of individuals living with kidney failure.
Mesencephalic astrocyte-derived neurotrophic factor (MANF) has cytoprotective effects on various injuries, including cerebral ischemia, and it can promote recovery even when delivered intracranially several days after ischemic stroke. In the uninjured rodent brain, MANF protein is expressed almost exclusively in neurons, but post-ischemic MANF expression has not been characterized. We aimed to investigate how endogenous cerebral MANF protein expression evolves in infarcted human brains and rodent ischemic stroke models. During infarct progression, the cerebral MANF expression pattern both in human and rat brains shifted drastically from neurons to expression in inflammatory cells. Intense MANF immunoreactivity took place in phagocytic microglia/macrophages in the ischemic territory, peaking at two weeks post-stroke in human and one-week post-stroke in rat ischemic cortex. Using double immunofluorescence and mice lacking MANF gene and protein from neuronal stem cells, neurons, astrocytes, and oligodendrocytes, we verified that MANF expression was induced in microglia/macrophage cells in the ischemic hemisphere. Embarking on the drastic expression transition towards inflammatory cells and the impact of blood-borne inflammation in stroke, we hypothesized that exogenously delivered MANF protein can modulate tissue recovery processes. In an attempt to enhance recovery, we designed a set of proof-of-concept studies using systemic delivery of recombinant MANF in a rat model of cortical ischemic stroke. Intranasal recombinant MANF treatment decreased infarct volume and reduced the severity of neurological deficits. Intravenous recombinant MANF treatment decreased the levels of pro-inflammatory cytokines and increased the levels of anti-inflammatory cytokine IL-10 in the infarcted cortex one-day post-stroke. In conclusion, MANF protein expression is induced in activated microglia/macrophage cells in infarcted human and rodent brains, and this could implicate MANF's involvement in the regulation of post-stroke inflammation in patients and experimental animals. Moreover, systemic delivery of recombinant MANF shows promising immunomodulatory effects and therapeutic potential in experimental ischemic stroke.
The invention discloses traditional Chinese medicine oil for treating burns, scalds and cauma. The traditional Chinese medicine oil comprises the following raw materials in parts by weight: 300-500 parts of lithospermum, 50-100 parts of rhizoma bletillae, 50-100 parts of garden burnet and 50-100 parts of borneol. The raw materials are cleaned and then 500-800 parts of sesame oil are added. The traditional Chinese medicine oil is reasonable and simple in formula, wide in medicinal herb resource and convenient for industrialization. For various burns, scalds and cauma with wound thickness smaller than 1cm, the burning pain can be mostly or completely relieved after applying the traditional Chinese medicine oil for 30 minutes. The traditional Chinese medicine oil is definite in effect, capable of detoxifying, eliminating swelling, relieving pain, promoting tissue regeneration and promoting wound healing, short in curing time and low in treatment cost.
We plan to identify patients planning to undergo conservative surgery for endometrioma at the University of Oklahoma private practice OB/GYN clinic and at the University of Oklahoma Resident Women's clinic. After clear and appropriate consent and discussion regarding options, we plan to randomize patients to monophasic OCPs vs. placebo following surgery. We plan to enroll 35 patients in each arm and follow them for 24 months following the surgery. Surveillance with pelvic exam and transvaginal ultrasonography will occur at 2, 6 and 12 months. The patients surgery will be done prior to enrolling in our study. We will use information from their surgery only to confirm the diagnosis of endometrioma. The only procedure the subjects will undergo during the protocol are periodic transvaginal ultrasonography.