anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND: Being obese can lead to various complications during pregnancy, such as Gestational Diabetes Mellitus (GDM), pregnancy induced hypertension (PIH), Pre-Eclampsia (PE), and Large Gestational Age (LGA). Although bariatric surgery is an effective way to treat obesity, it can also result in complications and may be linked to having small for gestational age (SGA) babies. This cohort study protocol aims to compare the maternal and fetal/neonatal outcomes of two groups of Iranian pregnant women: those who have undergone bariatric surgery and those who are obese but have not had bariatric surgery.
METHODS: In this study Pregnant women (< 14 weeks' gestation) (n = 38 per group) are recruited either from one of the obesity clinic (exposure group = with a history of bariatric surgery) or primary healthcare clinics in Tehran city (comparison group = pregnant women with obesity and and no history of bariatric surgery). Dietary intake and nutrient status are assessed at < 14, 28, and 36 weeks. Maternal and fetal/neonatal outcomes are compared between the two groups, including gestational diabetes, preeclampsia, preterm labor, intrauterine growth restriction, severe nausea and vomiting, abortion, placenta previa and abruption, venous thrombosis, vaginal bleeding, cesarean delivery, meconium aspiration, and respiratory distress. Maternal serum levels of ferritin, albumin, zinc, calcium, magnesium, selenium, copper, vitamins A, B9, B12, and 25-hydroxy Vit D are checked during 24th to 28th weeks. Maternal and neonatal outcomes, including height, weight, head circumference, fetal abnormality, infection, small or large fetus, low birth weight, macrosomia, NICU admission, and total weight gain during pregnancy, are measured at birth. Maternal and offspring outcomes, including weight, height, head circumference, total weight gain during pregnancy, newborn diseases, postpartum bleeding, breastfeeding, and related problems, are assessed 6 weeks after delivery. Child's weight, height, and head circumference are followed at 2, 4, 6, 8, 10, and 12 months after birth. Maternal stress, anxiety, and depression are assessed with the DASS-21 questionnaire, and physical activity is evaluated using the PPAQ questionnaire in the first and third trimesters.
DISCUSSION: By assessing the levels of micronutrients in the blood of pregnant women along with the evaluation of pregnancy outcomes, it is feasible to gain a more accurate understanding of how bariatric surgery affects the health and potential complications for both the mother and the fetus/newborn. This information can help specialists and patients make more informed decisions about the surgery. Additionally, by examining issues such as stress, anxiety, and depression in women undergoing surgery, this study can contribute to recognizing these problems, which can also affect pregnancy outcomes.
Liraglutide, a glucagon-like peptide-1 (GLP-1) analog, is approved for obesity treatment, but the specific neuronal sites that contribute to its therapeutic effects remain elusive. Here, we show that GLP-1 receptor-positive (GLP-1R-positive) neurons in the lateral septum (LSGLP-1R) play a critical role in mediating the anorectic and weight-loss effects of liraglutide. LSGLP-1R neurons were robustly activated by liraglutide, and chemogenetic activation of these neurons dramatically suppressed feeding. Targeted knockdown of GLP-1 receptors within the LS, but not in the hypothalamus, substantially attenuated liraglutide's ability to inhibit feeding and lower body weight. The activity of LSGLP-1R neurons rapidly decreased during naturalistic feeding episodes, while synaptic inactivation of LSGLP-1R neurons diminished the anorexic effects triggered by liraglutide. Together, these findings offer critical insights into the functional role of LSGLP-1R neurons in the physiological regulation of energy homeostasis and delineate their instrumental role in mediating the pharmacological efficacy of liraglutide.
Pre-breakfast insulin will be given as a Super Bolus 15 minutes before the high-glycemic index meal (cornflakes and milk). The Super Bolus will be calculated based on individual ICR increased to 150% and basal insulin will be suspended for 2 hours at the same time.
INTRODUCTION: Dystonia can present in primary and secondary forms, depending on co-occurring symptoms and syndromic associations. In contrast to primary dystonia, secondary forms of dystonia are often associated with lesions in the putamen or globus pallidus. Such disorders are commonly neurodegenerative or neurometabolic conditions which produce varied neurologic as well as systemic manifestations other than dystonia. Chemo-denervation with botulinum toxin has been successfully used for focal or segmental dystonia. However, studies evaluating the effect of BoNT therapy on patients with secondary dystonia are sparse, given the heterogeneity in etiology and presentation.
METHODS: We present a series of patients with secondary dystonia who were managed with botulinum toxin therapy. Patients included in this series had a confirmed neurometabolic cause of dystonia.
RESULTS: A total of 14 patients, with ages ranging from 17 to 36 years, with disorders including Wilson's disease, pantothenate kinase-associated neurodegeneration (PKAN), Niemann-Pick disease type C (NPC), glutaric aciduria type 1, Sanfilippo syndrome (Mucopolysaccharidosis Type IIIb), and GM2 gangliosidosis (Sandhoff disease) are presented. Most patients experienced a mild to moderate improvement in treated dystonia with benefits ranging from 6 to 12 weeks, with the median length of the benefits lasting approximately eight weeks, without any significant adverse effects.
CONCLUSION: Although the secondary causes of dystonia are complex and diverse, our presented data and the available reports of the use of botulinum toxin support the conclusion that chemo-denervation plays an important role in symptom alleviation.
FIELD: medicine, pharmacy. SUBSTANCE: invention relates to development of the novel pharmaceutical composition containing bacterial collagenase. Pharmaceutical composition has collagenase from Streptomycins lavendulae taken in the amount 3-10 U/100 g of product and also antiseptic myramistin, proxanol and polyethylene glycol. New bacterial collagen-base pharmaceutical composition shows nontoxic nonallergenic properties that can be used for healing and cleaning the wound, burn and other damages of skin. EFFECT: enhanced effectiveness of composition. 2 cl, 4 tbl, 2 ex
Participants will complete 1 session of education about the treatment. After completion of treatment education and baseline questionnaires, participants will complete sessions 2 through 12 of virtual treatment for anorexia nervosa and mobile assessments.
A system for enabling the delivery of healthcare services is provided. The system has a server with a database that stores an electronic community care record (ECCR). The system also has a directing workstation. The directing workstation has a user interface for allowing a licensed healthcare professional to access the ECCR.  The system further has a mobile device. The mobile device has a user interface for allowing a healthcare assistant to access the ECCR.  The ECCR has an entity history index that contains data corresponding to an action performed on the user interface of the directing workstation and the mobile device.
PROBLEM TO BE SOLVED: To provide a method for suppressing rejection after a transplant.SOLUTION: The inhibitor for cytotoxic T cell induction includes an IL-6 inhibitor as an active component. The IL-6 inhibitor is an antibody that recognizes an IL-6. The IL-6 inhibitor is an antibody that recognizes an IL-6 receptor. The antibody is a monoclonal antibody. The antibody is an antibody that recognizes a human IL-6 or a human IL-6 receptor. The antibody is a recombinant antibody. The antibody is a chimeric antibody, a humanized antibody or a human antibody.
Ibandronate sodium is a nitrogen-containing bisphosphonate that inhibits osteoclast-mediated bone resorption. The chemical name for ibandronate sodium is 3-(N-methyl-N-pentyl) amino-1-hydroxypropane-1,1diphosphonic acid, monosodium salt, with the molecular formula C9H22NO7P2Na and a molecular weight of 341. Ibandronate sodium is an off-white to white colored powder. It is sparingly soluble in water. Ibandronate sodium has the following structural formula:

Ibandronate sodium tablets are available as a white, capsule shaped 150-mg coated tablets for once-monthly oral administration. One 150 mg coated tablet contains 160.33 mg ibandronate sodium, equivalent to 150 mg of ibandronic acid. Ibandronate sodium tablets also contains the following inactive ingredients: colloidal silicon dioxide, crospovidone, croscarmellose sodium, lactose monohydrate, microcrystalline cellulose, povidone, and sodium stearyl fumarate. The tablet coating contains hypromellose, polyethylene glycol 400, and titanium dioxide. Imprinting ink contains: ammonium hydroxide, black iron oxide, propylene glycol and shellac.
A 12-week supervised exercise program consisting of 3 days a week on a stationary bike or treadmill. In addition, at the time of enrollment patients are provided educational materials focusing on breathing and energy conservation.
Methods, devices, systems and computer program products determine suitability of an individual for participation in a drug trial. One method for assessment of suitability of an individual for participation in a drug trial includes receiving a message that provides an identity of an individual and a request for a drug trial suitability assessment for the individual. In response, medical, health or drug-related data is obtained from a plurality of data sources. One or more of the data sources is a real-time data source that is updated on a continual basis. The method further includes filtering the information to produce a customized data set based on the individual's identity and a phase of drug assessment trial. Such customized data set is changeable based on real-time changes in the information obtained from the data sources.
Novel antigen-presenting cells, including but not limited to dendritic cells (DC), that are loaded with antigens from dead or dying cells including allogenic cell lines, and the methods for making such antigen-presenting cells are described. These loaded antigen-presenting cells are useful to induce both prophylactic immune responses and therapeutic immune responses in humans. In particular, such loaded antigen-presenting cells are useful in the management of cancer and infectious diseases. Alternatively, the loaded antigen-presenting cells can be used to eliminate undesired immune responses such as autoimmune responses and graft versus host disease or host versus graft reaction, i.e., graft rejection in organ and bone marrow transplantation. Antigen-presenting cells useful in the present invention include but are not limited to dendritic cells at various differentiation stages (precursors, immature dendritic cells and mature dendritic cells), dendritic cells derived from blood precursors including but not limited to monocytes, dendritic cells derived from CD34-hematopoetic progenitor cells, subsets of dentritic cells such as Langerhans cells, interstitial DCs and lymphoid DCs. The antigen-presenting cells and the precursors of cytotoxic cells are derived from healthy volunteers or from tumor-bearing patients. Antigen-loaded dendritic cells prepared as described here can also prime naïve T cells to differentiate into effector cells able to  recognize multiple and/or shared tumor antigens that are expressed either on the tumor cells that are used to load the dentritic cells and/or on other tumor cells. The cytotoxic T cells generated by exposure to antigen-loaded dendritic cells prepared as described here can also be used in adoptive therapy. This induction of responses against multiple antigens shared between different cells, for instance tumor cells, as described here is important as it leads to broad immune responses. In the present invention, the T cells that are exposed to dendritic cells loaded with killed cells can be tolerized against the antigen(s) expressed on the killed cells. That can be achieved by manipulation of loaded dentritic cells that allows  presentation of the antigen but inhibits the expression of co-stimulatory molecules.
The safety and effectiveness of EMFLAZA for the treatment of DMD have been established in patients 2 years of age and older. Use of EMFLAZA in pediatric patients is supported by a multicenter, randomized, double-blind, placebo- and active-controlled study in 196 males 5 to 15 years of age  [see Clinical Studies (14)]. Use of EMFLAZA in patients 2 years to less than 5 years of age is supported by the findings of efficacy and safety in patients 5 years and older with DMD.

Safety and effectiveness in pediatric patients below the age of 2 years have not been established.

EMFLAZA Oral Suspension contains benzyl alcohol and is not approved for use in pediatric patients less than 2 years of age. Serious adverse reactions including fatal reactions and “gasping syndrome” occurred in premature neonates and low birth weight infants in the neonatal intensive care unit who received drugs containing benzyl alcohol as a preservative. In these cases, benzyl alcohol dosages of 99 to 234 mg/kg/day produced high levels of benzyl alcohol and its metabolites in the blood and urine (blood levels of benzyl alcohol were 0.61 to 1.378 mmol/L). Additional adverse reactions included gradual neurological deterioration, seizures, intracranial hemorrhage, hematologic abnormalities, skin breakdown, hepatic and renal failure, hypotension, bradycardia, and cardiovascular collapse. Preterm, low-birth weight infants may be more likely to develop these reactions because they may be less able to metabolize benzyl alcohol.

When prescribing EMFLAZA Oral Suspension consider the combined daily metabolic load of benzyl alcohol from all sources including EMFLAZA Oral Suspension (EMFLAZA Oral Suspension contains 10.45 mg of benzyl alcohol per mL; EMFLAZA Tablets do not contain benzyl alcohol) and other drugs containing benzyl alcohol. The minimum amount of benzyl alcohol at which serious adverse reactions may occur is not known. At the recommended dose of 0.9 mg/kg/day of EMFLAZA Oral Suspension, patients would receive approximately 0.4 mg/kg/day of benzyl alcohol [see Warnings and Precautions (5.13)].

Juvenile Animal Toxicity Data   
Oral administration of deflazacort (0, 0.1, 0.3, and 1.0 mg/kg/day) to juvenile rats from postnatal day (PND) 21 to 80 resulted in decreased body weight gain and adverse effects on skeletal development (including decreased cellularity of growth plate and altered bone distribution) and on lymphoid tissue (decreased cellularity). A no-effect dose was not identified. In addition, neurological and neurobehavioral abnormalities were observed at the mid and/or high dose. Plasma 21-desDFZ exposure (AUC) at the lowest dose tested (0.1 mg/kg/day) was lower than that in humans at the recommended human dose of EMFLAZA (0.9 mg/kg/day).
Chylothorax is not uncommon following congenital heart surgery. It often results in prolonged chest tube drainage and hospital stays. Due to the feeding difficulties, it often results in malnutrition and the need for central hyperalimentation. In addition, it results in a depressed immune system with the possibility of subsequent infection. Chylothorax can be a significant contributor to post-operative morbidity and mortality.

The primary aims are to determine at risk populations - certain congenital heart defects or certain operative procedures, to define the associated morbidity secondary to chylothorax - prolonged chest tube drainage, prolonged hospital stay, need for central access and hyperalimentation, subsequent infection and to review our current treatment methods - change formulas, hyperalimentation, somatostatin. The secondary aims are to determine ways to prevent chylothorax, determine the most successful treatment method, and to discover better treatment methods. This study will be conducted through a retrospective chart review.
CD40L-CD40-TRAF signaling plays a role in atherosclerosis progression and affects the pathogenesis of coronary heart disease (CHD). We tested the hypothesis that CD40L-CD40-TRAF signaling is a potential therapeutic target in hyperlipidemia, diabetes, and hypertension. In mouse models of hyperlipidemia plus diabetes (db/db mice) or hypertension (1 mg/kg/d angiotensin-II for 7 days), TRAF6 inhibitor treatment (2.5 mg/kg/d for 7 or 14 days) normalized markers of oxidative stress and inflammation. As diabetes and hypertension are important comorbidities aggravating CHD, we explored whether the CD40L-CD40-TRAF signaling cascade and their associated inflammatory pathways are expressed in CHD patients suffering from comorbidities. Therefore, we analyzed vascular bypass material (aorta or internal mammary artery) and plasma from patients with CHD with diabetes and/or hypertension. Our Olink targeted plasma proteomic analysis using the IMMUNO-ONCOLOGY panel revealed a pattern of step-wise increase for 13/92 markers of low-grade inflammation with significant changes. CD40L or CD40 significantly correlated with 38 or 56 other inflammatory targets. In addition, specific gene clusters that correlate with the comorbidities were identified in isolated aortic mRNA of CHD patients through RNA-sequencing. These signaling clusters comprised CD40L-CD40-TRAF, immune system, hemostasis, muscle contraction, metabolism of lipids, developmental biology, and apoptosis. Finally, immunological analysis revealed key markers correlated with comorbidities in CHD patients, such as CD40L, NOX2, CD68, and 3-nitrotyrosine. These data indicate that comorbidities increase inflammatory pathways in CHD, and targeting these pathways will be beneficial in reducing cardiovascular events in CHD patients with comorbidities.
Single-agent TAS102 (trifluridine/tipiracil) and regorafenib are FDA-approved treatments for metastatic colorectal cancer (mCRC). We previously reported that regorafenib combined with a fluoropyrimidine can delay disease progression in clinical case reports of multidrug-resistant mCRC patients. We hypothesized that the combination of TAS102 and regorafenib may be active in CRC and other gastrointestinal (GI) cancers and may in the future provide a treatment option for patients with advanced GI cancer. We investigated the therapeutic effect of TAS102 in combination with regorafenib in preclinical studies employing cell culture, colonosphere assays that enrich for cancer stem cells, and in vivo. TAS102 in combination with regorafenib has synergistic activity against multiple GI cancers in vitro including colorectal and gastric cancer, but not liver cancer cells. TAS102 inhibits colonosphere formation and this effect is potentiated by regorafenib. In vivo anti-tumor effects of TAS102 plus regorafenib appear to be due to anti-proliferative effects, necrosis and angiogenesis inhibition. Growth inhibition by TAS102 plus regorafenib occurs in xenografted tumors regardless of p53, KRAS or BRAF mutations, although more potent tumor suppression was observed with wild-type p53. Regorafenib significantly inhibits TAS102-induced angiogenesis and microvessel density in xenografted tumors, as well inhibits TAS102-induced ERK1/2 activation regardless of RAS or BRAF status in vivo. TAS102 plus regorafenib is a synergistic drug combination in preclinical models of GI cancer, with regorafenib suppressing TAS102-induced increase in microvessel density and p-ERK as contributing mechanisms. The TAS102 plus regorafenib drug combination may be further tested in gastric and other GI cancers.
A polyketide synthase ("PKS") of Type I is a complex multienzyme including a loading domain linked to a multiplicity of extension domains. Ths first extension module receives an acyl starter unit from the loading domain and each extension module adds a further ketide unit which may undergo processing (e.g. reduction). We have found that the Ksq domain possessed by some PKS's has decarboxylating activity, e.g. generating (substituted) acyl from (substituted) malonyl. The CLF domain of type II PKS's has similar activity.  By inserting loading modules including such domains into PKS's not normally possessing them it is possible to control the starter units used.
The invention relates to a microneedle membrane containing a breathable substrate material and a preparation method thereof. The microneedle membrane comprises a breathable substrate material layer and a microneedle body layer, and the two layers are mutually embedded. The breathable substrate material layer is made of natural fibers, chemical fibers or yarn materials of different materials. The microneedle membrane can be used for preparing dissolvable microneedles and swelling microneedle products, various functional components can be contained in the microneedle body layer, and the microneedle membrane can be applied to the fields of medical products, health-care products and beauty and skin care products. The invention solves the problem of complicated preparation procedures of the traditional microneedle membranes, and the integrated microneedle membranes are prepared by directly using the breathable base material. In addition, the method can be used for preparing large-area microneedle membranes, has simple process, can realize rapid mass production, can well meet the industrial production requirements of large-area microneedle membranes, and has higher application and popularization values and huge market potential.
The mechanism of action of ingenol mebutate for actinic keratosis(AK) treatment involves a rapid induction of necrosis followed by neutrophil-mediated, antibody-dependent cellular cytotoxicity (ADCC) of residual lesion. As the ingenol mebutate infiltrates the cell membrane, it increases intracellular Ca2+ concentration which leads to mitochondrial swelling and disruption of mitochondrial membrane within hours. The release of intra-mitochondrial Ca2+ into the cytoplasm leads to depletion of adenosine triphosphate (ATP) and a rapid induction of cell death by necrosis. This process occurs within 1 hour of application, which explains why the treatment period requires only 2 or 3 days of treatment. As the next phase, the cellular necrosis is accompanied by a robust inflammatory response through the release of proinflammatory cytokines from skin cells and tumor cells undergoing necrosis. The release of these proinflammatory cytokines into the dysplastic cells mediates the process of neutrophil recruitment through paracrine signaling and activation of endothelial cells. Here, the neutrophil mediated ADCC occurs, where activated neutrophils attach to the fragment, crystallized (Fc) parts of antibodies of dysplastic cells and destroys the residual dysplastic epidermal cells. In this way, the ingenol mebutate eradicates any residual tumor cells and prevents recurrence of actinic keratosis.As described above, the rapid effect and dual mechanism of action of ingenol mebutate gel allows not only a short-course therapy (2 or 3 days of application) for the elimination of actinic keratosis but also, the benefit for eradication of any residual lesions preventing the recurrence and the progression of AK into squamous cell carcinoma (SCC).