anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
For Treatment of Toxoplasmosis: The dosage of pyrimethamine for the treatment of toxoplasmosis must be carefully adjusted so as to provide maximum therapeutic effect and a minimum of side effects. At the dosage required, there is a marked variation in the tolerance to the drug. Young patients may tolerate higher doses than older individuals. Concurrent administration of folinic acid is strongly recommended in all patients. 

The adult starting dose is 50 to 75 mg of the drug daily, together with 1 to 4 g daily of a sulfonamide of the sulfapyrimidine type, e.g. sulfadoxine. This dosage is ordinarily continued for 1 to 3 weeks, depending on the response of the patient and tolerance to therapy. The dosage may then be reduced to about one half that previously given for each drug and continued for an additional 4 to 5 weeks. The pediatric dosage of pyrimethamine is 1 mg/kg/day divided into 2 equal daily doses; after 2 to 4 days this dose may be reduced to one half and continued for approximately 1 month. The usual pediatric sulfonamide dosage is used in conjunction with pyrimethamine.
Alzheimer's disease (AD) stands as the most prevalent neurodegenerative ailment, presently lacking a definitive cure. Given that primary medications for AD patients in the early or middle stages demonstrate optimal efficacy, it becomes crucial to delve into the identification of risk genes associated with early onset. In our study, we compiled and integrated three transcriptomics datasets (GSE48350, GSE36980, GSE5281) originating from the hippocampus of 37 AD patients and 66 healthy controls (CTR) for comprehensive bioinformatics analysis. Comparative analysis with CTR revealed 25 up-regulated genes and 291 down-regulated genes in AD. Those down-regulated genes were notably enriched in processes related to the transmission and transport of synaptic signals. Intriguingly, 27 differentially expressed genes implicated in AD were also correlated with the Braak stage, establishing a connection with various immune cell types that exhibit differences in AD, including cytotoxic T cells, neutrophils, CD4 T cells, Th1, Th2, and Tfh. Significantly, a Cox model, constructed using nine feature genes, effectively stratified AD samples (HR = 2.72, 95% CI 1.94 ~ 3.81, P = 3.6e-10), highlighting their promising potential for risk assessment. In conclusion, our investigation sheds light on novel genes intricately linked to the onset and progression of AD, offering potential biomarkers for the early detection of this debilitating condition. This study contributes valuable insights toward enhancing the strategies for preventing and treating AD.
Mother-infant interactions are the foundation for the organization of the infant's neurobiological, sensory, perceptual, emotional, physical, and relational systems (Hofer, 1987). For the developing infant, one of the most critical sources of regulatory input is through contact with the mother and her nurturing behavior. The infant's responses to the mother provide feedback that shapes her behavior as well. There are many co-regulatory processes embedded in these synchronous and reciprocal interactions which cross neurophysiological and neurobehavioral domains (Als, 1999). A necessary but detrimental separation between mother and infant is created at a critical period when mother-infant co-regulation should be developing. Regardless of NICU or well-baby nursery care, the physiological challenges associated with being born too soon, along with disturbances in normal mother-infant interactions are key factors underlying the risks of early and late preterm infants for a broad range of early and midlife disorders (DeBoer, et al., 1984 if this does not include late preterm, find another reference). This study compares common early interventions such as occupational, physical, and speech therapy with a Family Nurture Intervention (FNI), instituted at age 3 to 4 for preschool aged children with developmental delays. This is a developmental time point at which delays including deficits in emotion regulation, language, cognition, and attention are identifiable. The investigators hypothesize that the Family Nurture Intervention will alter a wide range of physiological regulatory capacities and will result in improved indices of mother psychological and child neurobehavioral outcomes.
Hallucinations can have rather heterogeneous aetiology and presentation. This inspired the concept of different subtypes based on symptom profiles, especially in the field of auditory hallucinations. As many people experience hallucinations in more than one sensory modality, it seems important to investigate potential hallucination subtypes across different sensory modalities. We assessed the content of hallucinations as part of a large survey among the general Dutch population (n = 10,448) using the Questionnaire for Psychotic Experiences. Based on their descriptions, thematic categories were created in a data-driven cluster analysis. 2594 participants who experienced hallucinations over the past week that contained at least 2 different thematic categories were selected. Clustering of their hallucination content was performed with the HDBSCAN method. We identified 4 clusters, i.e., subtypes, which can be typified as 1. hallucinations of foul odors, 2. complex visual scenes, 3. a vast variety of rather common hallucinations possibly related to heightened alertness, and 4. possibly bereavement hallucinations. The bereavement subtype showed an increase in emotional loneliness and the presence of delusions. Our findings suggest that the content of hallucinations can be informative, especially when investigated across sensory modalities. Such subtypes may help to better understand their underlying mechanisms.
Active TENS is delivered for 30mins at a frequency of 100 Hz and pulse duration of 100μsec using the EMPI Select TENS unit (calibrated using an oscilloscope prior to study). The intensity will be increased until patients feel a "maximally strong but comfortable sensation" to ensure an analgesic effect.
Alzheimer's Disease (AD) is a neurodegenerative disease characterized by profound memory impairments, synaptic loss, neuroinflammation, and hallmark pathological markers. High-fat diet (HFD) consumption increases the risk of developing AD even after controlling for metabolic syndrome, pointing to a role of the diet itself in increasing risk. In AD, the complement system, an arm of the immune system which normally tags redundant or damaged synapses for pruning, becomes pathologically overactivated leading to tagging of healthy synapses. While the unhealthy diet to AD link is strong, the underlying mechanisms are not well understood in part due to confounding variables associated with long-term HFD which can independently influence the brain. Therefore, we experimented with a short-term diet regimen to isolate the diet's impact on brain function without causing obesity. This project investigated the effect of short-term HFD on 1) memory, 2) neuroinflammation including complement, 3) AD pathology markers, 4) synaptic markers, and 5) in vitro microglial synaptic phagocytosis in the 3xTg-AD mouse model. Following the consumption of either standard chow or HFD, 3xTg-AD and non-Tg mice were tested for memory impairments. In a separate cohort of mice, levels of hippocampal inflammatory markers, complement proteins, AD pathology markers, and synaptic markers were measured. For the last set of experiments, BV2 microglial phagocytosis of synapses was evaluated. Synaptoneurosomes isolated from the hippocampus of 3xTg-AD mice fed chow or HFD were incubated with equal numbers of BV2 microglia. The number of BV2 microglia that phagocytosed synaptoneurosomes was tracked over time with a live-cell imaging assay. Finally, we incubated BV2 microglia with a complement receptor inhibitor (NIF) and repeated the assay. Behavioral analysis showed 3xTg-AD mice had significantly impaired long-term contextual and cued fear memory compared to non-Tg mice that was further impaired by HFD. HFD significantly increased inflammatory markers and complement expression while decreasing synaptic marker expression only in 3xTg-AD mice, without altering AD pathology markers. Synaptoneurosomes from HFD-fed 3xTg-AD mice were phagocytosed at a significantly higher rate than those from chow-fed mice, suggesting the synapses were altered by HFD. The complement receptor inhibitor blocked this effect in a dose-dependent manner, demonstrating the HFD-mediated increase in phagocytosis was complement dependent. This study indicates HFD consumption increases neuroinflammation and over-activates the complement cascade in 3xTg-AD mice, resulting in poorer memory. The in vitro data point to complement as a potential mechanistic culprit and therapeutic target underlying HFD's influence in increasing cognitive vulnerability to AD.
The purpose of this three year study is to evaluate Me \& You: Building Healthy Relationships, a classroom- and computer-based healthy relationships and dating violence prevention curriculum for 6th grade students, in a large, urban public school district in Southeast Texas. This curriculum was adapted from an existing effective sex education and relationship curriculum, It's Your Game...Keep it Real (IYG), which was enhanced to more explicitly address teen dating violence (TDV) and encompass multiple levels of the social-ecological model (e.g., youth, family, school staff). A randomized two-arm, nested design was conducted among 6th grade students, where students receiving the curriculum were compared to students receiving usual care. Ten middle schools participated in the study, five schools were randomly assigned to receive the curriculum and five to receive usual care. Outcomes were assessed at baseline, immediately following the intervention, and 12 months after baseline. Parental permission and student assent were obtained prior to administration of the surveys. The primary hypothesis is that students who receive the curriculum will have significantly lower TDV perpetration than those who do not receive the curriculum.
Introduction: The close relationship between inflammatory processes and epileptic seizures is already known, although the exact pathophysiological mechanism is unclear. In this study, the anticonvulsant capacity of piroxicam, an anti-inflammatory drug, was evaluated. A rat pentylenetetrazole kindling model was used.Methods: Male Wistar rats, 8-9 weeks old, received piroxicam (0.15 and 0.30 mg/kg), diazepam (2 mg/kg) or saline for 14 days, and PTZ, on alternate days. Intraperitoneal was chosen as the route of administration. The intensity of epileptic seizures was assessed using a modified Racine scale. The open field test and object recognition analysis were performed at the beginning of the study to ensure the safety of the drugs used. At the end of the protocol, the animals were euthanized to measure the levels of inflammatory (TNF-a and IL-6) and anti-inflammatory (IL-10) cytokines in the cortex, hippocampus, and serum.Results:There were no changes in the open field test and object recognition analysis. Piroxicam was found to decrease Racine scale scores at both concentrations. The reported values for IL-6 levels remained steady in all structures, whereas the TNF-alpha level in the cortex was higher in animals treated with piroxicam than in the saline and diazepam subjects. Finally, animals treated with the anti-inflammatory drug presented reduced IL-10 levels in the cortex and hippocampus.onclusions: Using inflammation as a guiding principle, the anticonvulsant effect of PIRO could be associated with the hippocampal circuits, since this structure showed no increase in inflammatory cytokines.
The invention discloses a kidney-invigorating and body-strengthening buccal tablet. The kidney-invigorating and body-strengthening buccal tablet comprises functional components, an excipient, a condiment and de-ionized water. The kidney-invigorating and body-strengthening buccal tablet is characterized in that the functional components comprise Morinda officinalis extract and mixed extract; the Morinda officinalis extract accounts for 10-25% of the total weight of the buccal tablet while the mixed extract accounts for 15-25% of the total weight of the buccal tablet; and the mixed extract is extracted from a mixture of Chinese dodder seeds, barks of eucommia and herbs of sagittate epimedium in a ratio of 3: 3: 2. The preparation method disclosed by the invention has the following advantages: the extraction technology is high in efficiency, so that the buccal tablet is high in active-ingredient content and good in effect. The buccal tablet can be conveniently and rapidly used as well as directly contained in the mouth. The buccal tablet is capable of invigorating the kidney and strengthening the body in long-term use, so that the buccal tablet is good for body health.
Hypoxia/reoxygenation caused by chronic intermittent hypoxia (CIH) plays an important role in cognitive deficits in patients with obstructive sleep apnea. However, the precise underlying mechanism remains unclear. This study investigated whether the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is involved in CIH-induced spatial learning and memory impairment in mice, and the possible underlying upstream and downstream mechanisms. The C57BL/6 male mice were exposed to CIH (21% O2-6% O2, 4 min/cycle, 8 h/day) for 9 weeks to investigate the role of NLRP3 in CIH-induced spatial learning and memory impairment in mice. BV2 cells were exposed to intermittent hypoxia (21% O2-1% O2, 90 min/cycle) for 48 h to investigate the possible mechanisms in vitro. We found that: 1) inhibition of NLRP3 inflammasome activation improved CIH-induced spatial learning and memory impairment in mice. 2) CIH damaged hippocampal neurons but increased the number of microglia in mice hippocampi; CIH activated microglia-specific NLRP3 inflammasome, leading to upregulation of matured IL-1β and N-GSDMD. 3) intermittent hypoxia activated NLRP3 inflammasome via the ROS-NF-κB signaling pathway to promote the release of matured IL-1β from microglia in a GSDMD-dependent manner without pyroptosis. 4) The IL-1β released from microglia might impair the synaptic plasticity of hippocampal CA3-CA1 synapses by acting on IL-1 receptors in hippocampal neurons. Our findings reveal that ROS-NF-κB-NLRP3 inflammasome-GSDMD dependent IL-1β release from microglia may participate in CIH-induced spatial learning and memory impairment by acting on hippocampal neuronal IL-1 receptor, leading to synaptic plasticity impairment.
A mechanism of macrophage-induced T cell suppression is the selective elimination of tryptophan and/or increase in one or more tryptophan metabolites within the local macrophage microenvironment. Studies demonstrate that expression of IDO can serve as a marker of suppression of T cell activation, and may play a significant role in allogeneic pregnancy and therefore other types of transplantation, and that inhibitors of IDO can be used to activate T cells and therefore enhance T cell activation when the T cells are suppressed by pregnancy, malignancy or a virus such as HIV. Inhibiting tryptophan degradation (and thereby increasing tryptophan concentration while decreasing tryptophan metabolite concentration), or supplementing tryptophan concentration, can therefore be used in addition to, or in place of, inhibitors of IDO. Similarly, increasing tryptophan degradation (thereby, decreasing tryptophan concentration and increasing tryptophan metabolite concentration), for example, by increasing IDO concentration or IDO activity, can suppress T cells. Although described particularly with reference to IDO regulation, one can instead manipulate local tryptophan concentrations, and/or modulate the activity of the high affinity tryptophan transporter, and/or administer other tryptophan degrading enzymes. Regulation can be further manipulated using cytokines such as macrophage colony stimulating factor, interferon gamma, alone or in combination with antigen or other cytokines.
More than half of patients with typical gastroesophageal reflux symptoms such as heartburn are considered to have non-erosive reflux disease (NERD), which is characterized by a lack of clinically defined damage to the esophagus. One approach to maintain control of these symptoms is to have medication available "on-demand." This is a double-blind, placebo-controlled study of the effectiveness of "on-demand" rabeprazole in the long-term maintenance of heartburn control in NERD patients, for whom heartburn was resolved with short-term, daily rabeprazole therapy. The study has two phases: an acute phase (4 weeks) during which patients receive rabeprazole medication daily, and an "on-demand" phase (6 months) during which patients take medication (rabeprazole or placebo) as needed. Only patients who have complete resolution of heartburn at the end of the acute phase are eligible to continue in the "on-demand" phase. Efficacy assessments include the proportion of patients discontinuing treatment in the "on-demand" phase because of insufficient heartburn control, and the severity of heartburn and patient satisfaction determined at the beginning and end of "on-demand" phase. Safety assessments include incidence of adverse events throughout the study, physical examination at study initiation, and vital signs at the beginning and the end of the study. The study hypothesis is that "on-demand" therapy with rabeprazole is superior to placebo in maintaining heartburn control and is well tolerated by the patients with NERD. Rabeprazole tablet (10 milligrams\[mg\]) once daily in the morning for 4 weeks. Rabeprazole tablets (10mg) once daily on an "on-demand" basis for the following 6 months.
Mannitol will be administered (IV) during the hemodialysis session at a maximum rate of 0.25g/kg/hour (maximum rate 25g/hour; maximum 75g per session; maximum volume 375mLs per session). Administration will be discontinued 30 minutes before the end of the hemodialysis session.
<P>PROBLEM TO BE SOLVED: To provide intraluminal medical devices related to the administration of therapeutic agents for the prevention and treatment of vascular disease, and more particularly to intraluminal medical devices in combination with therapeutic agents for the prevention and treatment of vascular disease such as restenosis while substantially improving thrombosis resistance.  <P>SOLUTION: Medical devices, and in particular implantable medical devices, may be coated to minimize or substantially eliminate a biological organism's reaction to the introduction of the medical device to the organism. The medical devices may be coated with any number of biocompatible materials. Therapeutic drugs, agents or compounds may be mixed with the biocompatible materials and affixed to at least a portion of the medical device. These therapeutic drugs, agents or compounds may also further reduce a biological organism's reaction to the introduction of the medical device to the organism. In addition, these therapeutic drugs, agents and/or compounds may be utilized to promote healing, including the formation of blood clots. Various materials and coating methodologies may be utilized to maintain the drugs, agents or compounds on the medical device until delivered and positioned.  <P>COPYRIGHT: (C)2007,JPO&INPIT
Rats or rabbits administered oral haloperidol at doses of 0.5 to 7.5 mg/kg, which are approximately 0.2 to 7 times the maximum recommended human dose (MRHD) of 20 mg/day based on mg/m2 body surface area, showed an increase in incidence of resorption, reduced fertility, delayed delivery and pup mortality. No fetal abnormalities were observed at these doses in rats or rabbits. Cleft palate has been observed in mice administered oral haloperidol at a dose of 0.5 mg/kg, which is approximately 0.1 times the MRHD based on mg/m2 body surface area. 

There are no adequate and well-controlled studies in pregnant women. There are reports, however, of cases of limb malformations observed following maternal use of haloperidol along with other drugs which have suspected teratogenic potential during the first trimester of pregnancy. Causal relationships were not established with these cases. Since such experience does not exclude the possibility of fetal damage due to haloperidol, haloperidol decanoate should be used during pregnancy or in women likely to become pregnant only if the benefit clearly justifies a potential risk to the fetus. 

### Non-Teratogenic Effects 

Neonates exposed to antipsychotic drugs (including haloperidol) during the third trimester of pregnancy are at risk for extrapyramidal and/or withdrawal symptoms following delivery. There have been reports of agitation, hypertonia, hypotonia, tremor, somnolence, respiratory distress, and feeding disorder in these neonates. These complications have varied in severity; while in some cases symptoms have been self-limited, in other cases neonates have required intensive care unit support and prolonged hospitalization. 

Haloperidol decanoate should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
FIELD: medicine. SUBSTANCE: substituent of living skin is used for treatment of damaged skin layers at burns and wounds that consists of suspension of cells covered with microspheres. It can be applied on the damaged skin as paste or ointment. Skin implant can be adopted to the changes of skin damage of the vast areas and does not demand sutures or clamps application. Microspheres can be made of the different biocompatible material resorbing in vitro. EFFECT: enhanced effectiveness of skin substituent.
Mothers in the neonatal kit clusters will receive a neonatal kit and training on how to use the kit components during their third trimester of pregnancy. The kit will contain a clean birth kit to be used at the time of delivery either at home or in a facility, 4% chlorhexidine (CHX) lotion, sunflower oil emollient, ThermoSpot, a Mylar infant sleeve, and a reusable, non-electric, heating device. Community Health Workers will be equipped with a hand-held battery operated scale to identify low birth weight newborns.