anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
The present invention relates to compositions forming a low viscosity mixture of: a) 20-80 wt. % of at least one diacyl glycerol and/or a tocopherol; b) 20-80 wt. % of at least one phosphatidyl choline (PC); c) 5-20 wt. % of at least one biocompatible, organic mono-alcoholic solvent; d) up to 20 wt. % polar solvent e) at least one peptide active agent; f) optionally at least one antioxidant; wherein the ratio of components a:b is in the range 40:60 to 54:46; wherein the pre-formulation forms, or is capable of forming, at least one liquid crystalline phase structure upon contact with excess aqueous fluid. The invention further relates to methods of treatment comprising administration of such compositions, and to pre-filled administration devices and kits containing the formulations.
This protocol is designed to examine those growth potentiating and inhibiting factors which regulate mast cell number and survival in patients with mastocytosis, and to explore the molecular basis of the disease process in hopes of improving therapy. Patients will carry the diagnosis of mastocytosis based on abnormal bone marrow biopsy and aspirate, abnormal skin biopsy, presence of urticaria pigmentosa, and if available, elevated serum tryptase level \> 20 ng/ml and the presence of aberrant mast cell morphology and surface markers of CD2 and CD25. Mastocytosis patients will include children and adults from zero years to 80 years of age. Unaffected relatives (age 2 to 80 years) may also be enrolled. The protocol is designated for up to a 1-year enrollment period; with only a small number of enrolled patients that will stay on study for more than one visit, based on investigator assessment of contribution to study objectives. Participants will undergo standard physical exam, medical history review, and blood collection for clinical and research laboratory evaluations. We will collect clinical data and biological specimens for research evaluation from individuals undergoing clinically indicated diagnostic procedures. Some patients may participate in research evaluations including buccal swab collection, dietary intake assessment, stool collection, exercise challenge, microbiome studies, and activity tracking. These studies are optional. Patients may be asked to re-enter this protocol at a later time for further follow-up.
The present invention discloses the preparation of placenta tissue derived CD106high CD151+Nestin+ mesenchymal stem cells (MSCs). In a first aspect, the invention relates to a particular method to prepare these cells at industrial scale and the cell population generated thereby. In a second aspect, the invention relates to a cell culture obtained by said particular method, containing placental CD106high CD151+Nestin+ MSCs expressing the vascular cell adhesion molecule 1 (VCAM-1) marker. The present application shows that said placental CD106high CD151+Nestin+ MSCs are capable of inducing angiogenesis in vitro and in vivo. The herein presented results also show that administering said placental CD106high CD151+Nestin+ MSCs to individuals suffering from an ischemic disease or from a disorder of the circulatory system results in a detectable improvement of one or more symptoms of said disease or disorder. Therefore, in a third aspect, the invention relates to placental CD 106high CD151+Nestin+ MSCs for use as a medicament for treating subjects suffering from an ischemic disease, a disorder of the circulatory system, an immune disease, an organ injury or an organ function failure.
PURPOSE: Provided are compositions for suppression of appetite and desire for carbohydrates and method thereof using precursors of neurotransmitter such as sertonin, dopamine, epinephrine and histamine. CONSTITUTION: A composition containing precursors of neurotransmitter such as sertonin,dopamine, epinephrine and histamine. The precursors contain amino groups and comprise tryptophan for serine, phenylalanine and tyrosine for dopamine and epinephrine, and histidine for histidine. The precursors improve appetite suppression of the neurotransmitter by combination with one another or xanthin. The xanthin is provided from a natural source of supply. Especially, cocoa provides combination of xanthin containing theobromine and caffeine, and amine, especially, phenylamine in an organism. Tryptophan is administrated in the form of hydrolyzed protein by protease.
In clinical studies in RA patients with the 4 mg per kg and 8 mg per kg intravenous doses or the 162 mg weekly and every other weekly subcutaneous doses of tocilizumab, decreases in levels of C-reactive protein (CRP) to within normal ranges were seen as early as week 2. Changes in pharmacodynamic parameters were observed (i.e., decreases in rheumatoid factor, erythrocyte sedimentation rate (ESR), serum amyloid A, fibrinogen and increases in hemoglobin) with doses, however the greatest improvements were observed with 8 mg per kg tocilizumab. Pharmacodynamic changes were also observed to occur after tocilizumab administration in GCA, PJIA, and SJIA patients (decreases in CRP, ESR, and increases in hemoglobin). The relationship between these pharmacodynamic findings and clinical efficacy is not known. 

In healthy subjects administered tocilizumab in doses from 2 to 28 mg per kg intravenously and 81 to 162 mg subcutaneously, absolute neutrophil counts decreased to the nadir 3 to 5 days following tocilizumab administration. Thereafter, neutrophils recovered towards baseline in a dose dependent manner. Rheumatoid arthritis and GCA patients demonstrated a similar pattern of absolute neutrophil counts following tocilizumab administration [see Warnings and Precautions (5.4)].
BACKGROUND: Predicting chemorefractory disease in advanced epithelial ovarian cancer (EOC) remains challenging. This study aimed to identify clinicopathological factors and hemogram data as predictive markers for chemorefractory EOC and to explore potential therapeutic approaches that may mitigate these unfavorable conditions.
METHODS: We conducted a retrospective analysis of patients with advanced EOC treated with chemotherapy. Hemogram data and clinicopathological variables were collected. We employed logistic regression to assess factors associated with chemorefractory EOC and used the Kaplan-Meier method for survival analysis.
RESULTS: Among the 191 patients analyzed, suboptimal surgery, lymphocyte count < 1440/mm3, systemic immune-inflammation index (SII) ≥ 2350, and lack of bevacizumab therapy were independently associated with chemorefractory EOC (OR 19.30, 95% CI 7.01-53.12; OR 9.07, 95% CI 2.76-29.82; OR 12.45, 95% CI 3.87-40.07; OR 6.61, 95% CI 2.01-21.78, respectively). Elevated SII was also identified as a risk factor for poor progression-free (PFS) and overall survival (OS). Specifically, patients with high SII who did not receive bevacizumab had a significantly higher probability of chemorefractory EOC and poorer survival outcomes compared to those who received bevacizumab.
CONCLUSIONS: Our findings suggest that hemogram parameters and clinicopathological factors such as suboptimal surgery, lymphocyte count, SII, and bevacizumab therapy status are predictive markers for chemorefractory disease in advanced EOC. Elevated SII emerged as a predictor for poorer PFS and OS outcomes, particularly in the absence of bevacizumab therapy.
BAG3 is a multifaceted protein characterised by having WW domain, PXXP motif and BAG domain. This protein gets upregulated during malignant transformation of cells and has been associated with poorer survival of patients. Procancerous activity of BAG domain of BAG3 is well documented. BAG domain interacts with ATPase domain of Hsp-70 preventing protein delivery to proteasome. This impediment results in enhanced cell survival, proliferation, resistance to apoptosis and chemoresistance. Besides BAG domain other two domains/motifs of BAG3 are under research vigilance to explore its further oncogenic role. This review summarises the role of different structural determinants of BAG3 in elevating oncogenesis. Based on the already existing findings, more interacting partners of BAG3 are anticipated. The anticipated partners of BAG3 can shed a wealth of information into the mechanistic insights of its proproliferative role. Proper insights into the mechanistic details adopted by BAG3 to curtail/elaborate activity of anticipated interacting partners can serve as a potent target for development of therapeutic interventions.
Before surgery, patients no need to treat with PD-1 and apatinib. Sequential therapy with PD-1 and apatinib when patients accepted surgery.
Completed Sample of all patients admitted to the Mitchells Plain Hospital of Hope COVID-19 Field Hospital between January 1st and February 29th 2021. All patients were diagnosed with COVID-19 prior to admission to the hospital and were transferred directly from a referring hospital.
Despite the increasing incidence and prevalence of amputation across the globe, individuals with acquired limb loss continue to struggle with functional recovery and chronic pain. A more complete understanding of the motor and sensory remodeling of the peripheral and central nervous system that occurs postamputation may help advance clinical interventions to improve the quality of life for individuals with acquired limb loss. The purpose of this article is to first provide background clinical context on individuals with acquired limb loss and then to provide a comprehensive review of the known motor and sensory neural adaptations from both animal models and human clinical trials. Finally, the article bridges the gap between basic science researchers and clinicians that treat individuals with limb loss by explaining how current clinical treatments may restore function and modulate phantom limb pain using the underlying neural adaptations described above. This review should encourage the further development of novel treatments with known neurological targets to improve the recovery of individuals postamputation.Significance Statement In the United States, 1.6 million people live with limb loss; this number is expected to more than double by 2050. Improved surgical procedures enhance recovery, and new prosthetics and neural interfaces can replace missing limbs with those that communicate bidirectionally with the brain. These advances have been fairly successful, but still most patients experience persistent problems like phantom limb pain, and others discontinue prostheses instead of learning to use them daily. These problematic patient outcomes may be due in part to the lack of consensus among basic and clinical researchers regarding the plasticity mechanisms that occur in the brain after amputation injuries. Here we review results from clinical and animal model studies to bridge this clinical-basic science gap.
KRN23 administered subcutaneously (SC) every 4 weeks for 48 weeks. The dose varies according to serum phosphorus level which include 0.3,0.6,1.0,1.4 and 2.0 mg/kg.
BACKGROUND: Single limb support phase of the gait-cycle in patients who are treated for a pertrochanteric fracture is characterized by transversal loads acting on the lag screw, tending to block its dynamization. If the simultaneous axial force overcomes transversal loads of the sliding screw, the dynamization can still occur.
METHODS: Biomechanical investigation was performed for three types of dynamic implants: Gamma Nail, and two types of Selfdynamizable Internal Fixators (SIF) - SIF-7 (containing two 7 mm non-cannulated sliding screws), and SIF-10 (containing one 10 mm cannulated sliding screw). Contact surface between the stem and the sliding screws is larger in SIF implants than in Gamma Nail, as the stem of Gamma Nail is hollow. A special testing device was designed for this study to provide simultaneous application of a controlled sliding screws bending moment and a controlled transversal load on sliding screws (Qt) without using of weights. Using each of the implants, axial forces required to initiate sliding screws dynamization (Qa) were applied and measured using a tensile testing machine, for several values of sliding screws bending moment. Standard least-squares method was used to present the results through the linear regression model.
RESULTS: Positive correlation between Qt and Qa was confirmed (p < 0.05). While performing higher bending moments in all the tested implants, Qa was higher than it could be provided by the body weight. It was the highest in Gamma Nail, and the lowest in SIF-10.
CONCLUSIONS: A larger contact surface between a sliding screw and stem results in lower forces required to initiate dynamization of a sliding screw. Patients treated for a pertrochanteric fracture by a sliding screw internal fixation who have longer femoral neck or higher body weight could have different programme of early postoperative rehabilitation than lighter patients or patients with shorter femoral neck.
PPARδ was identified as a target of APC suppression through the analysis of global gene expression profiles in human colorectal cancer cells. PPARδ expression is elevated in primary colorectal cancers and significantly repressed by APC in colorectal cancer cells. This repression is mediated by two Tcf-4-responsive elements in the PPARδ promotor. Reporters containing PPARδ-responsive elements are repressed by sulindac, a non-steroidal anti-inflammatory (NSAID) agent which can reduce the size and number of colon tumors in humans and animals with APC mutations. Furthermore, sulindac is able to specifically disrupt the ability of PPARδ to bind its cognate recognition sequences. These findings suggest a model wherein NSAIDs inhibit tumorigenesis through post-transcriptional modification of a gene that is normally regulated by APC. This novel molecular target for NSAIDs can be used to develop more effective chemopreventive agents for colorectal tumors.
In some embodiments, the system integrates different unique identifiers from agencies and organizations and associated the different unique identifiers with each other in a table. In some embodiments, the table links all different unique identifiers to a single individual so that a search for any one identifier returns links to all records and data associated with the individual. In some embodiments, the system collects the different unique identifiers from organizations such as patient medical services, local and federal law enforcement databases, and private company records. In some embodiments, the system parses each component of each identifier and stores them as variations. In some embodiments, each parsed identifier is associated with a master identifier. In some embodiments, the system links the master identifier to all records and data across multiple organizations and agencies.
The intervention will be performed as a group activity twice a week during a 12-week period. Each group will include 4-6 participants under the guidance of two instructors, and a related party if needed or wanted from the participant. The exercise is partly accompanied with calm music and recorded nature sounds and partly made in silence listening to one's own bodily rhythm. The exercise consists of tasks related to cardio and strength training, balance, conscious breathing, body awareness, mental imagery (nature visualizations), flexibility, emotional expression, and movement anticipation together with the facilitator and fellow participants. All the tasks are practiced during a flow of 45- to 60-minute exercise without any major breaks. Complexity and physical intensity of the tasks will gradually increase over the 12-week intervention period.
BACKGROUND: Atrial fibrosis is associated with the pathogenesis of atrial fibrillation (AF). This study aims to discuss the function of circ_0079480 in atrial fibrosis and its underlying mechanism.
METHODS: In vitro and in vivo models of atrial fibrosis were established by using angiotensin II (Ang II) to treat human atrial fibroblasts (HAFs) and C57/B6J mice. qRT-PCR and western blot were used to examine the mRNA and protein expression levels. CCK-8, EdU, cell strach, and transwell assays were performed to determine the proliferation and migration of HAFs. Dual-luciferase reporter and RIP/RNA pull-down assays were explored to identify the interaction of miR-338-3p and circ_0079480/THBS1. HE and Masson's trichrome staining experiments were performed to analyze the histopathological change in mice atrial tissues.
RESULTS: Circ_0079480 expression was increased in AF patients' atrial tissues and Ang II-treated HAFs. Silencing circ_0079480 inhibited cell proliferation and migration and reduced fibrosis-associated gene expression in Ang II-treated HAFs. Circ_0079480 could target miR-338-3p to repress its expression. MiR-338-3p inhibitor blocked the inhibitory effects of circ_0079480 knockdown on HAFs proliferation, migration, and fibrosis. Thrombospondin-1 (THBS1) was confirmed as a downstream target of miR-338-3p, and circ_0079480 could sponge miR-338-3p to upregulate THBS1 expression. Moreover, silencing THBS1 suppressed Ang II-induced proliferation, migration, and fibrosis in HAFs. More importantly, depletion of circ_0079480 inactivated the THBS1/TGF-β1/Smad3 signaling by upregulating miR-338-3p. Mice experiments also confirmed the suppression of circ_0079480 knockdown on atrial fibrosis.
CONCLUSION: Circ_0079480 acts as a sponge of miR-338-3p to upregulate THBS1 expression and activate the TGF-β1/Smad3 signaling, finally promoting Ang II-induced atrial fibrosis.
Mitoxantrone Injection, USP (concentrate) should be administered under the supervision of a physician experienced in the use of cytotoxic chemotherapy agents.

Mitoxantrone Injection, USP (concentrate) should be given slowly into a freely flowing intravenous infusion. It must never be given subcutaneously, intramuscularly, or intra-arterially. Severe local tissue damage may occur if there is extravasation during administration. (See ADVERSE REACTIONS, General, Cutaneous and DOSAGE AND ADMINISTRATION, Preparation and Administration Precautions).

NOT FOR INTRATHECAL USE. Severe injury with permanent sequelae can result from intrathecal administration. (See WARNINGS, General)

Except for the treatment of acute nonlymphocytic leukemia, mitoxantrone therapy generally should not be given to patients with baseline neutrophil counts of less than 1,500 cells/mm3. In order to monitor the occurrence of bone marrow suppression, primarily neutropenia, which may be severe and result in infection, it is recommended that frequent peripheral blood cell counts be performed on all patients receiving mitoxantrone.
Patients receive MVA-209-FSPs IM at week 52. Patients undergo endoscopy with biopsy as well as blood sample collection on the trial.
Vanishing bile duct syndrome (VBDS) is characterized by bile duct degeneration and necrosis, which result in bile duct loss and bile stasis. A 70-year-old man had malaise after receiving celecoxib. Laboratory tests revealed elevated hepatobiliary enzymes. His condition worsened without response to medical treatment, and he was transferred to our hospital. A liver biopsy revealed severe bile duct injury and mild cholestasis. He was diagnosed with celecoxib-induced VBDS and underwent bilirubin adsorption therapy. However, his condition continued to deteriorate, and he died. An autopsy showed that liver regeneration was poor, and bile duct loss was exacerbated. The pathological autopsy findings were consistent with VBDS.
BACKGROUND: In patients with steroid-resistant nephrotic syndrome (SRNS), the presence of monogenic variants influences therapeutic strategies. Large cohort studies reported the detection of monogenic variants in approximately 30% of patients with SRNS. However, these cohorts included many patients, such as those with symptomatic proteinuria, who did not meet the strict diagnostic criteria for pediatric nephrotic syndrome (NS). Therefore, we investigated the proportion of causative monogenic variants detected in patients who strictly met the diagnostic criteria of SRNS and explored their clinical characteristics.
METHODS: We examined pediatric SRNS cases with genetic analysis conducted in our hospital. Cases satisfying all of the following criteria were included: (1) age at onset 1-18 years, (2) serum albumin at onset ≤ 2.5 g/dl, (3) persistent heavy proteinuria, and (4) no complete remission after 4 weeks of steroid monotherapy.
RESULTS: The proportion of detected monogenic variants was 12% (22/185) among all patients. The proportion was only 7% (9/129) in patients with edema at disease onset compared with 38% (9/24) in those without (p < 0.0001). Monogenic variants were rare in patients with acute kidney injury associated with NS (1% (1/11)) or a history of complete remission (4% (2/51)).
CONCLUSIONS: Our study revealed a monogenic cause in 12% of individuals with strictly defined SRNS, a much smaller proportion than previously reported. The presence or absence of edema at the onset was an important factor to distinguish SRNS with monogenic cause from SRNS without. Our results provide further evidence of the SRNS types attributable to monogenic causes.
The most common adverse reactions (≥ 3%) are diarrhea, abdominal pain, dysmenorrhea, and twitch.

The adverse reactions to pyridostigmine bromide are typically of two varieties: muscarinic and nicotinic. Muscarinic adverse reactions include abdominal cramps, bloating, flatulence, diarrhea, emesis, increased peristalsis, nausea, hypersalivation, urinary incontinence, increased bronchial secretion, diaphoresis, miosis, and lacrimation. Nicotinic adverse reactions are comprised chiefly of muscle cramps, fasciculations, and weakness.

Pyridostigmine bromide is a quaternary ammonium compound and does not readily cross the blood-brain barrier. Compared to the peripheral effects of pyridostigmine bromide, central nervous system manifestations are less frequent and less serious, primarily consisting of headache and vertigo, with minor and clinically insignificant changes in heart rate, blood pressure, and respiratory function.

Extremely high doses may produce central nervous system (CNS) symptoms of agitation, restlessness, confusion, visual hallucinations, and paranoid delusions. Electrolyte abnormalities, possibly resulting from high serum bromide concentrations, also have been reported. Death may result from cardiac arrest or respiratory paralysis and pulmonary edema.

As with any compound containing bromide, a skin rash may be observed in an occasional patient, which usually subsides promptly upon discontinuance of the medication.
The new medicament "Oxytocin" is for the treatment of diabetes mellitus type I patients who have none or insufficient oxytocin in the blood. The presumption that the low sugar level owing to a low adrenalin level is caused by an insufficient production of tyrosine. Tyrosine production is dependent on oxytocin. Therefore administration of oxytocin will produce tyrosine and hence adrenalin. Adrenalin should then mobilise glycogen for an increase in the blood sugar level causing the secretion of insulin. USE - Oxytocin is used for the treatment of juvenile type I diabetes mellitus. The blood sugar level is thereby increased to 80 to 120 mg/100 ml so that insulin is produced for the removal of blood glucose.
PROBLEM TO BE SOLVED: To obtain the subject medicine capable of reducing toxicity of β- alanine used in a large amount, by including sesame as an active ingredient. SOLUTION: This medicine comprises sesame or its extract as an active ingredient. Sesame is used as a food from old times, has high safety and newly shows inhibitory actions on absorption of β-amino acid, mainly β-alanine. A dose of sesame or its extract is 0.5-50 g per adult daily in the case of oral administration. Some β-amino acid has toxicity in excessive administration, causes histopathological damage in brain and induces nervous disorder such as epilepsy and drowsiness by competition of GABA of inhibitory amino acid in a nerve cell and its receptor. The competition is related to mental unhealthiness such as irritation, anxiety and impatience in stress society. Since β-alanine is synthesized by decomposition of a pyrimidine base or decarboxylation of aspartic acid optionally in vivo, β-alanine is not deficient even by inhibition of the absorption.