anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
The aim of the study is to examine the effects of distraction methods such as watching cartoons and ball squeezing on the level of pain and physiological parameters in the postoperative period in children aged 6-12 years who have outpatient surgery. The research is a randomized controlled trial. The sample number was determined as 40 children (total 120) in each group. Information Form, Physiological Parameters Follow-up Form, Wong-Baker Faces Pain Scale will be used to collect research data. In the initiative group, two attempts will be implemented, namely watching cartoons and squeezing the ball. Interventions will be implemented for a total of 15 minutes. Physiological Parameters Follow-up Form and Wong-Baker Faces Pain Scale will be filled in before the interventions are applied, 10 minutes during the intervention and 5 minutes after the intervention is completed. In the control group, the 10th and 20th minute physiological parameters and the Wong-Baker Faces Pain Scale will be evaluated after the child comes to the service after the operation and is prepared for the postoperative period (taking vital signs, putting on clothes, controlling bleeding, telling the feeding time, etc.). In the analysis of study data; chi-square test for descriptive statistics, chi-square test for repeated measurements, single factor analysis of variance, Mann-Whitney U test and Friedman will be used. In the study, values at the p\<0.05 level were considered statistically significant.
A tinted cosmetic composition is in the form of an aqueous gel comprising 0.1% to 20% by weight each of water dispersible polymer-treated pigment and a hydrophilic gelling agent. Glycerine is an optional component. Pigment is preferably a polyester or polyesteramide treated pigment. Typical pigments are iron oxides, talc, zeolite, kaolin and or -TiO2 or organic pigments e.g. phthalocyanines, toluidene red. Gellant may be a cellulose ether, PVP, PVA or a gum.
On day 1, high CHO dinner meal will provide 35% of participants total daily energy requirements. Meal will consist of pasta, meat ball and orange juice. On the day 2, participants will exercise for 60 minutes and then in 60 minutes will consume morning meal, providing 30% of their total daily energy requirements. Morning meal will consist of oats, skimmed-milk, banana and seedless raisins.
The formation of amyloid beta (Aβ) deposits (senile plaques) is one of the hallmarks of Alzheimer's disease (AD). This study investigates what processes are primarily responsible for their formation. A model is developed to simulate the diffusion of amyloid beta (Aβ) monomers, the production of free Aβ aggregates through nucleation and autocatalytic processes, and the deposition of these aggregates into senile plaques. The model suggests that efficient degradation of Aβ monomers alone may suffice to prevent the growth of senile plaques, even without degrading Aβ aggregates and existing plaques. This is because the degradation of Aβ monomers interrupts the supply of reactants needed for plaque formation. The impact of Aβ monomer diffusivity is demonstrated to be small, enabling the application of the lumped capacitance approximation and the derivation of approximate analytical solutions for limiting cases with both small and large rates of Aβ aggregate deposition into plaques. It is found that the rate of plaque growth is governed by two competing processes. One is the deposition rate of free Aβ aggregates into senile plaques. If this rate is small, the plaque grows slowly. However, if the rate of deposition of Aβ aggregates into senile plaques is very large, the free Aβ aggregates are removed from the intracellular fluid by deposition into the plaques, leaving insufficient free Aβ aggregates to catalyze the production of new aggregates. This suggests that under certain conditions, Aβ plaques may offer neuroprotection and impede their own growth. Additionally, it indicates that there exists an optimal rate of deposition of free Aβ aggregates into the plaques, at which the plaques attain their maximum size.
At the present time, heart transplant recipients must take anti-rejection medication to prevent rejection of the donated heart. Even with this medication, chronic rejection is the most common cause of late graft loss. The anti-rejection agents themselves are significantly toxic, with side effects including kidney damage, infection and an increased incidence of cancer. The goal of this study is to allow the patient to develop "tolerance" to the transplanted heart while maintaining a competent immune system. Tolerance enables the transplant recipient's body to recognize the transplanted organ as self rather than foreign tissue. The recipient will not try to reject the donor heart and the need for anti-rejection medication could be dramatically decreased or eliminated entirely. To accomplish this, patients in this study will receive specially treated bone marrow taken from their heart donor. Bone marrow transplant has been shown in animal studies and in humans to induce tolerance following organ transplant.

Two factors limit the application of donor marrow transplant to induce tolerance: 1) preparing the patient for transplant (conditioning); and 2) graft-versus-host disease (GVHD). Traditional conditioning destroys the recipient's immune system and requires that the marrow transplant be successful because the patient is unable to fight off infection if the donor cells do not survive. GVHD occurs when donor immune cells recognize the recipient's cells as foreign tissue and attack them. Severe GVHD can result in death. This study utilizes a new approach to conditioning which leaves the patient's immune system intact. The transplant product is depleted of GVHD-producing cells but retains tolerance-promoting facilitating cells, which are intended to ensure the donor and recipient cells coexists peacefully, a state called mixed chimerism. The toxicity of conditioning and transplantation is significantly reduced.

In this study, we will determine the appropriate cell dose to safely establish mixed chimerism following partial conditioning in heart transplant recipients. The study takes a gradual approach to increasing the cell dose to achieve mixed chimerism. We believe this study will provide a breakthrough in the approach to heart transplantation. Our goal is to evaluate the potential of safely establishing mixed chimerism to induce tolerance following heart transplant and reduce or eliminate the need for anti-rejection therapy.
Strategies to rapidly disseminate COVID-19 testing are urgently needed, particularly to address increasing health disparities among underserved communities. One promising approach to increase test uptake is the secondary distribution of self-tests, where an individual distributes test kits to contacts in their social network and encourages them to self-test. By decentralizing testing, this approach does not require individuals to have contact with medical systems, and can lower potential barriers to obtaining testing. This approach can increase case detection by facilitating testing among exposed individuals, and potentially ameliorate stigma, fear, and medical mistrust associated with COVID-19 among vulnerable populations because the testing process is decentralized.

The investigators will conduct a 1:1 randomized controlled trial randomizing individuals to receive either multiple self-test kits to distribute within their social circles, or referrals for standard clinic-based tests. All study participants will be offered testing upon enrollment. Study participants, deemed "Index Participants," will be randomized to receive multiple self-testing kits (intervention) or test referral cards and text messages (control) to encourage individuals in their social networks, deemed "network contacts" to test. Participants will complete a baseline evaluation and a follow-up evaluation at 8 weeks. We will measure network contact test uptake in both study arms. The central hypothesis of this trial is that distribution of self-test kits will increase test uptake compared with distribution of test referrals.
Patients received 1.0 g meropenem as an IV infusion every 8 hours (q8h). After a minimum of 4 days of IV meropenem, patients could switch to 250 or 500 mg oral levofloxacin for a total duration of 7 to 10 days (IV plus oral).
An implantable stimulator can control delivery of the neurostimulation to a patient according to a stimulation configuration and adjust the stimulation configuration by using a closed-loop control algorithm. In an example, the system may include a remote controller (RC) configured for use by the patient. The RC may transmit stimulator adjustment information to the implantable stimulator. The stimulator adjustment information may include direct control adjustment information for adjusting the stimulation configuration and adaptation adjustment information for adjusting the closed-loop control algorithm. The RC may generate the stimulator adjustment information based on patient adjustment instructions. The RC includes a user interface configured to receive a patient input and to determine the patient adjustment instructions by interpreting the patient input according to an RC configuration that is programmable for modifying capabilities of the RC in adjusting the stimulation configuration and adjusting the closed-loop control algorithm.
NEW MATERIAL:A compound expressed by formula I (R is lower alkyl; Sug is sugar residue after removing hydroxymethyl from sugars). EXAMPLE:3,8,13,18-Tetramethyl-2,7,12,17-tetra-(1,2,5,6-di-isopropylide ne-6-galacto) porphyrin. USE:A water-soluble and neutral therapeutic agent for cancer. PREPARATION:A compound expressed by formula II (R1 is lower alkyl) is reduced with a reducing agent such as LiAlH4 and then normally regulated to acidic conditions with p-toluenesulfonic acid, etc. The regulated compound is then subjected to dehydrating condensation in the presence of an oxidizing agent (e.g. p-chloranil or benzoxine).
The present invention relates to clothes with an anion emitting silicone patch, and a method of manufacturing the same. According to the present invention, the clothes with an anion emitting silicone patch comprise: clothes; and a silicone patch attached to the clothes and emitting anions. The silicone patch includes anion ore powder, and adhesion of the silicone patch is performed by pressing the silicone patch for 9-13 seconds at a pressure of 45-55 PSI in a temperature range of 170-180°C, and the silicone patch is attached to clothes in a non-sewing welding method. A numerical value of anions emitted from anion ore powder included in the silicone patch is formed to be 1000-2000 ion/cc. According to the present invention, a silicone patch is manufactured by using a material emitting anions, and the silicone patch is used by being attached to clothes. Therefore, blood circulation in a human body is improved by anions and the feeling of fatigue is relieved thereby at the same time. In addition, the silicone patch is used by being firmly attached to the clothes by silicone. After washing, the adhesive strength and washing fastness are excellent, a constant attachment state can be maintained regardless of time elapse, and a material emitting anions is not easily removed, and thus the clothes can be permanently used for a long period of time.
The invention discloses an anti-human Fc epsilon RI alpha subunit monoclonal antibody and application thereof. A hybridoma cell strain capable of producing the monoclonal antibody is preserved in China Center for Type Culture Collection and has the preservation number of CCTCC NO. C201326. The anti-human Fc epsilon RI alpha monoclonal antibody prepared by the invention can be bound with high-affinity receptor Fc epsilon RI alpha of human IgE and can be applied in detecting the expression of cell surface Fc epsilon RI alpha. The monoclonal antibody has important significance and relatively large clinical value for prevention and treatment of mast cell and basophilic granulocyte-related diseases, such as allergic dermatitis, dermatomyositis and psoriasis. The hybridoma cell strain disclosed by the invention grows well, and is bright and transparent, the cell body is uniform, the division is strong and the hybridoma cell strain has indefinitely divided proliferative capability.
Objective.This study aims to reveal longitudinal changes in functional network connectivity within and across different brain structures near chronically implanted microelectrodes. While it is well established that the foreign-body response (FBR) contributes to the gradual decline of the signals recorded from brain implants over time, how the FBR affects the functional stability of neural circuits near implanted brain-computer interfaces (BCIs) remains unknown. This research aims to illuminate how the chronic FBR can alter local neural circuit function and the implications for BCI decoders.Approach.This study utilized single-shank, 16-channel,100µm site-spacing Michigan-style microelectrodes (3 mm length, 703µm2 site area) that span all cortical layers and the hippocampal CA1 region. Sex balanced C57BL6 wildtype mice (11-13 weeks old) received perpendicularly implanted microelectrode in left primary visual cortex. Electrophysiological recordings were performed during both spontaneous activity and visual sensory stimulation. Alterations in neuronal activity near the microelectrode were tested assessing cross-frequency synchronization of local field potential (LFP) and spike entrainment to LFP oscillatory activity throughout 16 weeks after microelectrode implantation.Main results. The study found that cortical layer 4, the input-receiving layer, maintained activity over the implantation time. However, layers 2/3 rapidly experienced severe impairment, leading to a loss of proper intralaminar connectivity in the downstream output layers 5/6. Furthermore, the impairment of interlaminar connectivity near the microelectrode was unidirectional, showing decreased connectivity from Layers 2/3 to Layers 5/6 but not the reverse direction. In the hippocampus, CA1 neurons gradually became unable to properly entrain to the surrounding LFP oscillations.Significance. This study provides a detailed characterization of network connectivity dysfunction over long-term microelectrode implantation periods. This new knowledge could contribute to the development of targeted therapeutic strategies aimed at improving the health of the tissue surrounding brain implants and potentially inform engineering of adaptive decoders as the FBR progresses. Our study's understanding of the dynamic changes in the functional network over time opens the door to developing interventions for improving the long-term stability and performance of intracortical microelectrodes.
Acne is a multifactorial inflammatory disease with a robust microbial component and numerous correlations with dysbiosis states. Furthermore, various factors are recognized as triggers for skin dysbiosis, including the use of certain cosmetics. Based on these arguments, we hypothesized that using photoprotective formulations could trigger dysbiosis and the occurrence of acne manifestations. To verify this assumption, six volunteers between 19 and 23 years of age, meeting all the inclusion criteria, received two applications a day of a non-commercial sunscreen formulation developed with the sun filters ethylhexyl methoxycinnamate, ethylhexyl salicylate, methyl anthranilate, and octocrylene dispersed in a base gel, with an estimated protection factor of 28.8. The pure base gel was used as a control. The samples were applied to an area delimited by a standard template (15 cm2) in an amount corresponding to 30 mg (2 mg cm2) for ten days. At two points in time, pre- and post-sample applications, the facial skin surface was swabbed to collect extracted DNA and processed to verify divergent degrees of 16 S RNA coding sequences. The data obtained allowed us to determine the abundance of different bacterial entities at the genus and species levels. The results showed that critical species of the acne process, such as Cutibacterium acnes and Staphylococcus epidermidis, seem to tolerate the evaluated formulation well and are not significantly affected by the formulation, suggesting no interference of its use concerning dysbiosis induction. These findings refute the idea that photoprotectors may cause skin dysbiosis in men.
Methods and compositions useful for promoting and inhibiting natural killer (NK) cell-mediated lysis of activated T cells are provided. The methods and compositions relate more specifically to modulation of the interaction between major histocompatibility complex (MHC) class Ib molecule Qa-I or its human counterpart HLA-E, expressed on activated T cells, and the inhibitory receptor NKG2A, expressed on NK cells. Certain methods and compositions for promoting NK-cell-mediated lysis of activated T cells include the use of antibodies or fragments thereof that bind specifically to Qa-1 polypeptides. Methods for treating autoimmune disease, graft rejection, and graft- versus- host disease, as well as methods for reducing activated T cells are provided. Also provided are methods and compositions, based on increased expression of Qa-1 polypeptides, for inhibiting NK-cell-mediated lysis of activated T cells, thereby promoting a T-cell-mediated immune response. Methods for identifying additional agents useful for reducing activated T cells are also provided.
The Group B2 participants will consume a prepackaged dose of 25 peanuts. Along with Pre-breakfast but no post-dinner snack.
Disclosed herein are antimicrobial compositions that are substantially odorless. The antimicrobial compositions can comprise, for example, a first essential oil and a second essential oil, wherein the composition is substantially odorless. In some examples, the composition can further comprise a third essential oil. The compositions described herein can, for example, reduce the population of microbes, such as Staphylococcus aureus or Escherichia coli, by 5 log or more. Also disclosed herein are beverages and food products including the compositions disclosed herein. Also disclosed herein is milk including the compositions disclosed herein. Also disclosed herein are methods for treating or preventing a microbial infection in a subject, the methods comprising administering to the subject an effective amount of any of the compositions disclosed herein. Also disclosed herein are methods for combating bovine mastitis, the methods comprising applying any of the compositions disclosed herein to cow udders.
Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.

In two vehicle-controlled and one active-controlled U.S. clinical trials, treatment safety was monitored in 788 subjects who used twice-daily FINACEA Gel for 12 weeks (N=333) or 15 weeks (N=124), or the gel vehicle (N=331) for 12 weeks. In all three trials, the most common treatment-related adverse events were: burning/stinging/tingling (29%), pruritus (11%), scaling/dry skin/xerosis (8%) and erythema/irritation (4%). In the active-controlled trial, overall adverse reactions (including burning, stinging/tingling, dryness/tightness/scaling, itching, and erythema/irritation/redness) were 19.4% (24/124) for FINACEA Gel compared to 7.1% (9/127) for the active comparator gel at 15 weeks.

In patients using azelaic acid formulations, the following adverse events have been reported: worsening of asthma, vitiligo, depigmentation, small depigmented spots, hypertrichosis, reddening (signs of keratosis pilaris) and exacerbation of recurrent herpes labialis.

Local Tolerability Studies

FINACEA Gel and its vehicle caused irritant reactions at the application site in human dermal safety studies. FINACEA Gel caused significantly more irritation than its vehicle in a cumulative irritation study. Some improvement in irritation was demonstrated over the course of the clinical trials, but this improvement might be attributed to subject dropouts. No phototoxicity or photoallergenicity were reported in human dermal safety studies.
The ABCC1 gene belongs to the ATP-binding cassette membrane transporter superfamily, which plays a crucial role in the efflux of various endogenous and exogenous substances. Mutations in ABCC1 can result in autosomal dominant hearing loss. However, the specific roles of ABCC1 in auditory function are not fully understood. Through immunofluorescence, we found that ABCC1 was expressed in microvascular endothelial cells (ECs) of the stria vascularis (StV) in the murine cochlea. Then, an Abcc1 knockout mouse model was established by using CRISPR/Cas9 technology to elucidate the role of ABCC1 in the inner ear. The ABR threshold did not significantly differ between WT and Abcc1-/- mice at any age studied. After noise exposure, the ABR thresholds of the WT and Abcc1-/- mice were significantly elevated. Interestingly, after 14 days of noise exposure, ABR thresholds largely returned to pre-exposure levels in WT mice but not in Abcc1-/- mice. Our subsequent experiments showed that microvascular integrity in the StV was compromised and that the number of outer hair cells and the number of ribbons were significantly decreased in the cochleae of Abcc1-/- mice post-exposure. Besides, the production of ROS and the accumulation of 4-HNE significantly increased. Furthermore, StV microvascular ECs were cultured to elucidate the role of ABCC1 in these cells under glucose oxidase challenge. Notably, 30 U/L glucose oxidase (GO) induced severe oxidative stress damage in Abcc1-/- cells. Compared with WT cells, the ROS and 4-HNE levels and the apoptotic rate were significantly elevated in Abcc1-/- cells. In addition, the reduced GSH/GSSG ratio was significantly decreased in Abcc1-/- cells after GO treatment. Taken together, Abcc1-/- mice are more susceptible to noise-induced hearing loss, possibly because ABCC1 knockdown compromises the GSH antioxidant system of StV ECs. The exogenous antioxidant N-acetylcysteine (NAC) may protect against oxidative damage in Abcc1-/- murine cochleae and ECs.
The accumulation of senescent cells promotes ageing and age-related diseases, but molecular mechanisms that senescent cells use to evade immune clearance and accumulate in tissues remain to be elucidated. Here we report that p16-positive senescent cells upregulate the immune checkpoint protein programmed death-ligand 1 (PD-L1) to accumulate in ageing and chronic inflammation. We show that p16-mediated inhibition of cell cycle kinases CDK4/6 induces PD-L1 stability in senescent cells via downregulation of its ubiquitin-dependent degradation. p16-expressing senescent alveolar macrophages elevate PD-L1 to promote an immunosuppressive environment that can contribute to an increased burden of senescent cells. Treatment with activating anti-PD-L1 antibodies engaging Fcγ receptors on effector cells leads to the elimination of PD-L1 and p16-positive cells. Our study uncovers a molecular mechanism of p16-dependent regulation of PD-L1 protein stability in senescent cells and reveals the potential of targeting PD-L1 to improve immunosurveillance of senescent cells and ameliorate senescence-associated inflammation.