anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND: Liver fibrosis is a common pathological process of chronic liver disease, characterized by excessive deposition of extracellular matrix (ECM). Mesenchymal stem cells (MSCs) have been found to have potential therapy effect on liver fibrosis, but the mechanism involved was still unclear. The objective of this study is to investigate the therapeutic efficacy of adipose-derived mesenchymal stem cells (ADMSCs) on the treatment of liver fibrosis, with particular emphasis on elucidating the underlying mechanism of action through which ADMSCs inhibit the activation of hepatic stellate cells (HSCs).
METHODS: ADMSCs were isolated from adipose tissue and injected intravenously into hepatic fibrosis model of rats. The histopathological changes, liver function, collagen deposition, the expression of fibroin and Hippo pathway were evaluated. In vitro, ADMSCs were co-cultured with HSCs activated by transforming growth factor beta 1 (TGF-β1), and the inhibitor of Hippo pathway was used to evaluate the therapeutic mechanism of ADMSCs transplantation.
RESULTS: The results showed that after the transplantation of ADMSCs, the liver function of rats was improved, the degree of liver fibrosis and collagen deposition were reduced, and the Hippo signaling pathway was activated. In vitro, ADMSCs can effectively inhibit the proliferation and activation of HSCs induced by TGF-β1 treatment. However, the inhibitory effect of ADMSCs was weakened after blocking the Hippo signaling pathway.
CONCLUSIONS: ADMSCs inhibit HSCs activation by regulating YAP/TAZ, thereby promoting functional recovery after liver fibrosis. These findings lay a foundation for further investigation into the precise mechanism by which ADMSCs alleviate liver fibrosis.
Five very low birth weight (VLBW) infants enrolled within 2 days of birth, with a weight \< 1300 g and gestational age \< 29 weeks and without any malformation or metabolic disease at birth were supplemented with two daily doses of a mixture of "Bifidobacterium breve" and "Lactobacillus salivarius" , probiotic strains isolated from human milk during their first weeks of life. The lyophilized powder has contained at least 1x10\^9 colony forming units (CFU) per doses of each one of the probiotic bacteria.
<P>PROBLEM TO BE SOLVED: To provide a composition and a method for stimulating or inhibiting the angiogenesis and/or cardiovascularization of mammals including human.  <P>SOLUTION: The pharmaceutical composition is based on polypeptides or antagonists thereto identified for one or more of those uses. Disorders that can be diagnosed, prevented or treated by the composition include trauma such as wounds, various cancers, and disorders of the vessels including atherosclerosis and cardiac hypertrophy. In addition, the present invention is directed to new polypeptides and to nucleic acid molecules encoding those polypeptides. Also provided herein are vectors and host cells comprising those nucleic acid sequences, chimeric molecules comprising the polypeptides fused to heterologous polypeptides, antibodies binding to the polypeptides and a method for producing the polypeptides.  <P>COPYRIGHT: (C)2009,JPO&INPIT
MI (myocardial infarction) often triggers severe heart failure and is one of the leading causes of death worldwide. Receptor expression-enhancing protein 5 (REEP5), a member of REEPs, acts as regulators of endoplasmic reticulum (ER) affecting cardiac functions. Based on GSE114695 profile data, REEP5 was decreased in the left ventricle of MI mice. However, its role and potential mechanism in MI remain to be investigated. In the present study, the mouse MI model was established by ligation of the left anterior descending artery. REEP5 expression was downregulated in the infarct penumbra area of MI mice. Next, its role during MI was explored by gain-of-function. Interestingly, REEP5 overexpression improved left ventricular function of mice with MI, accompanied with reduced infarct size. In cardiomyocytes, REEP5 overexpression inhibited ER stress, accompanied with repressive phosphorylation of PERK and IRE1α, and the decreased nuclear translocation of ATF6. Subsequently, REEP5 overexpression downregulated the levels of Chop and cleaved caspase-12, further alleviating ER stress-induced apoptosis, which was consistent with the in vivo results. Moreover, REEP5 was found to bind to C-type lectin member 5 A (CLEC5A), a protein that triggers cardiac dysfunction. CLEC5A, whose expression was elevated in hypoxia-induced cell models, led to cardiomyocyte apoptosis. Noteworthily, REEP5 overexpression markedly abolished the effects of CLEC5A on ER stress-induced apoptosis. Taken together, REEP5 mediated the function of CLEC5A to relieve MI via inhibiting ER stress-induced apoptosis in vivo and in vitro. REEP5 may be a promising target for treating MI.
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.

Based on multicenter cooperative group ALL trials, the most common adverse reaction occurring in > 20% of patients was myelosuppression, including anemia, neutropenia, lymphopenia and thrombocytopenia. Adverse reactions occurring in 5% to 20% of patients included anorexia, nausea, vomiting, diarrhea, malaise and rash. Adverse reactions occurring in < 5 % of patients included urticaria, hyperuricemia, oral lesions, increased transaminases, hyperbilirubinemia, hyperpigmentation, infections, and pancreatitis. Oral lesions resemble thrush rather than antifolic ulcerations. Delayed or late adverse reactions include hepatic fibrosis, hyperbilirubinemia, alopecia, pulmonary fibrosis, oligospermia and secondary malignancies [see Warnings and Precautions (5.1, 5.2)].

Drug fever has been reported with mercaptopurine.

Additional adverse reactions that have been reported in patients who have received mercaptopurine include photosensitivity, hypoglycemia, and portal hypertension.
This is a prospective, double-masked, randomized, controlled, parallel-group trial designed to compare the impact of Systane Complete PF lipid-based artificial tears (the Treatment solution under study) on tear lipid layer thickness compared with a non-lipid Control solution, Refresh Relieva PF. Secondarily, the study will compare changes in tear lipid layer thickness, lipid layer uniformity, tear film thinning dynamics, and symptoms between the Treatment solution, the non-lipid Control solution, and 2 other available lipid-based solutions (Active Comparators: Refresh Optive Mega-3 PF and CVS Health Lubricant Eye Drop (PG 0.6%)). The study will include 4 clinic visits, and require 1 week of single-masked run-in with Systane Ultra PF (an over-the-counter non-lipid-based solution) followed by 3 months of study treatment dosing. All subjects will complete a screening interview, then an in-clinic baseline ocular health examination and study eligibility determination followed by dispensing of the Control solution to all subjects for 1 week of run-in. After that week, subjects will be randomized to 1 of the 4 artificial tear solutions and have an in-clinic ocular examination and dispense of the assigned solution to use for 3 months. An in-clinic follow-up examination is completed after 1 month of study solution use, followed by a phone interview at 2 months, and a final in-clinic examination at 3 months post-dispensing.
The 10-week intervention will include twice weekly 1-2 hours sessions with multiple professional team members to undergo education and exercise sessions. The multidisciplinary team will consist of a rheumatologist, rheumatology nurse, dietitian, physiotherapist, a trained exercise therapist, a physiologist who specializes in pain management, a psychiatrist and a mental health clinician. All intervention team members have expertise in working with individuals with chronic pain conditions. General disease information, current best practices and techniques such as self-pain management, pacing, sleep hygiene, approach to a healthy lifestyle and weight loss will be discussed. The total number of hours for the 10 week intervention is 31 hours.
Varicose veins of lower extremities are common chronic diseases. The main clinical manifestations are lower extremity weakness, heaviness, burning sensation, itching, swelling or pain, and severe cases are often accompanied by complications such as changes in skin color, ulceration and hemorrhage. Venous ulceration is one of the main complications of lower extremity varicose veins, accounting for more than 75% of all lower extremity ulcers. Venous ulceration are difficult to heal and prone to recurrence. Studies have shown that the recurrence rate of venous ulceration is as high as 67%. The refractory and high recurrence rate of venous ulceration not only have a serious impact on the quality of patients' life, but also bring a heavy economic burden on society.

Venous ulceration in varicose veins of lower extremities patients may linked to different causes, including past medical history, comorbidity, inflammatory response, etc. The purpose of this study is to collect demographic characteristics, lifestyle characteristics, laboratory indicators, past history, comorbidity and other information by using the data set of patients with varicose veins of lower extremities based on the Shandong Provincial Qianfoshan Hospital Healthcare Big Data Platform. To explore the potential risk factors of venous ulceration in patients with varicose veins of lower extremities through case-control study.
The recommended starting dose for patients whose HbA1c is less than 8% is 0.5 mg orally before each meal. For patients whose HbA1c is 8% or greater the starting dose is 1 or 2 mg orally before each meal.

The recommended dose range is 0.5 mg to 4 mg before meals, with a maximum daily dose of 16 mg. The patient’s dose should be doubled up to 4 mg with each meal until satisfactory glycemic control is achieved. At least one week should elapse to assess response after each dose adjustment.

Instruct patients to take PRANDIN within 30 minutes before meals. PRANDIN may be dosed 2, 3, or 4 times a day in response to changes in the patient’s meal pattern.

In patients who skip meals, instruct patients to skip the scheduled dose of PRANDIN to reduce the risk of hypoglycemia. In patients who experience hypoglycemia, the dose of PRANDIN should be reduced [see Warnings and Precautions (5.1)].
BACKGROUND: Focal nodular hyperplasia is a common nonmalignant liver mass. This nonvascular lesion is an uncommon mass in children, especially those with no predisposing factors, namely radiation, chemotherapy, and hematopoietic stem cell therapy. Exophytic growth of the lesion further than the liver margins is not common and can complicate the diagnosis of the lesion. This report observes a focal nodular hyperplasia as a pedunculated lesion in a healthy child.
CASE PRESENTATION: We describe a 9-year-old healthy Persian child who was born following in vitro fertilization complaining of abdominal pain lasting for months and palpitation. Employing ultrasound and computed tomography, a mass was detected in the right upper quadrant compatible with focal nodular hyperplasia imaging features. The child underwent surgery and the mass was resected.
CONCLUSION: Diagnosing focal nodular hyperplasia, especially pedunculated form can be challenging, although magnetic resonance imaging with scintigraphy is nearly 100% sensitive and specific. Thus, a biopsy may be needed to rule out malignancies in some cases. Deterministic treatment in patients with suspicious mass, remarkable growth of lesion in serial examination, and persistent symptoms, such as pain, is resection, which can be done open or laparoscopic.
This invention is related to the method of preparing enteric-coated pancreatin granules, by which the activity of enzymes including amylase, lipase and protease can be maintained at a level of higher than 90%. Basically, pancreatin powder is only granulated with water with or without adding any pharmaceutical excipients. After screening and drying, the powder is then granulating with water again. The wet mass is extruded and sized to obtain pancreatin granules. An enteric materials, such as Eudragit L30D, is applied on the outer surface of granules to protect from the deterioration of acid on the enzyme's activity. Therefore, an enteric-coated pancreatin granular dosage form is obtained.
Pregnancy — Patients should be advised to notify their physician if they become pregnant or intend to become pregnant during therapy. Fluoxetine should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus [see Use in Specific Populations (8.1)].

Nursing Mothers — Patients should be advised to notify their physician if they intend to breast-feed an infant during therapy. Because fluoxetine is excreted in human milk, nursing while taking fluoxetine is not recommended [see Use in Specific Populations (8.3)].

Pediatric Use of fluoxetine — Fluoxetine is approved for use in pediatric patients with MDD and OCD [see BOX WARNING and Warnings and Precautions (5.1)]. Limited evidence is available concerning the longer-term effects of fluoxetine on the development and maturation of children and adolescent patients. Height and weight should be monitored periodically in pediatric patients receiving fluoxetine. [see Warnings and Precautions (5.6) and Use in Specific Populations (8.4)].
PURPOSE: A composition for improving stem cell differentiation potency is provided to produce a large amount of stem cells, especially multipotent mesenchymal stem cells by effectively improving the differentiation rate of the stem cells and to be used in various clinical fields. CONSTITUTION: A composition for improving stem cell differentiation potency contains an Epimedii herba extract. The extract is prepared from Epimedii herba using water, methanol, ethanol, or a mixture thereof. The stem cells are totipotent stem cells or multipotent stem cells. The stem cells are mutipotent mesenchymal stem cells, multipotent hematopoietic stem cells, multipotent nerve stem cells, multipotent liver stem cells, multipotent pancreatic stem cells, or multipotent epidermal stem cells. A method for improving differentiation potency of the stem cells comprises the step of treating the stem cells with the extract.
Individuals received usual care provided by nurses from the time the premature infant was admitted to the NICU until discharge. The usual care process is carried on between the nurse and the mother. Mothers are allowed to perform limited care practices (bottom cleaning, breastfeeding) that the nurse considers appropriate. Mothers of babies who are planned to be discharged start staying in the hospital approximately 2 days before. Fathers are not included in the care and process. They are not allowed to stay in the hospital. Fathers are only informed and not included in the care.
INTRODUCTION: Chronic myeloid leukemia (CML) prevalence is currently increasing due to the great efficacy of tyrosine kinase inhibitor (TKI) therapy. Discontinuation of treatment in the long-term, owing to avoid off-target side effects or treatment-free remission (TFR), has become an additional treatment goal in CML patients who achieved a deep molecular response (DMR). Second-generation TKIs (2 G-TKIs) have a significantly higher rate of DMR than imatinib. Hence, especially in young patients with a strategy of TFR, 2 G-TKIs are becoming the most frequently used TKIs and may increase TFR attempts in the future.
AREAS COVERED: In this review, the main findings extrapolated from clinical trials and real-life evidence regarding 2 G-TKIs discontinuation were discussed, through broad research on Medline, Embase, and archives from EHA and ASH congresses.
EXPERT OPINION: Overall, TFR rate after 2 G-TKIs is ranging from 40% to 60% for selected patients with sustained DMR and it can be considered a safe procedure, that have become, nowadays, a daily practice. However, many crucial aspects regarding treatment choices, timings, as well as predictive factors, patient communication, and optimal strategies need to be better clarified to improve successful TFR rate.
The present invention relates to methods for modulating progestagen signaling for treating neurological disorders or neurodegenerative disease, or preventing or delaying its onset in individuals deemed by competent observation and testing to be susceptible thereto. Progestagens can be administered to elevate serum and brain levels of progestagens and induce neurogenesis. Progestagen therapy may prevent some of the neurodegenerative and cognitive changes associated with developmental and aging associated neurological disorders and neurodegenerative diseases. Progestagen therapy together with suppression of GnRH, kisspeptin, LH and/or FSH signaling also may be used for treating neurological disorders or neurodegenerative diseases. The invention also relates to methods for inhibiting or delaying blastulation during embryogenesis, and neurogenesis during embryogenesis, fetal, neonatal, childhood, puberty or adult life. Blocking progestagen, estrogen and/or opioid signaling with receptor antagonists will inhibit neurogenesis. The invention also relates to using progestagens in vitro to induce neurogenesis in embryonic or adult stem cells.
Disclosed are peptides having non-canonical amino acids. These peptides are useful, for example, as protein binding agents. Libraries of such peptides can be used, for example to screen and select protein binding agents. The broader chemical space of the disclosed peptides can provide peptide with different, improved, more specific, and/or pharmaceutically compatible peptides and protein binding agents. In some forms, the peptides can have the following structure (I):including stereoisomers, pharmaceutically acceptable salts and prodrugs thereof, wherein R, R1, L1, L2, G, M, Y1 Y2 and SEQ are as defined herein. Methods associated with preparation and use of such peptides, as well as pharmaceutical compositions comprising such peptides, are also disclosed.
The IQ101 is the first generation of the non invasive cardiograph. This device uses impedance to a micro-electric field passing from the electrodes. The NcIQ uses Radio frequencies and the same 3 dimensional signal averaging algorithm used in the IQ101 to generate hemodynamic data. The radio waves enables the device to work without the contact lead arrays used in the IQ2 and can take measurements without even contacting the patient, hence can be applied through clothing and is simple to apply. This makes the potential use by first responders a possibility. The device measures the change in the radio wave reflection during the cardiac cycle to estimate ardiac function. Specifically, it measures cardiac output, the amount of blood pumped per minute, and other hemodynamic parameters previously only measurable with invasive catheters. The data us used to generate a LIFESCORE and can measure and report dangerous trends to the caretaker. The device has a companion device to download the data for the hospital providers to create a seamless transfer of care. The new device uses technology similar to the previous generation machine but has been miniaturized, given updated operating system, and newer computer technology that helped make the device smaller, and faster. The underlying patented algorithm was not changed. Therefore, it is expected to provide the same degree of accuracy and precision as the predicate device.

The IQ101 is the first generation of the non invasive cardiograph. This device uses impedance to a micro-electric field passing from the electrodes. The device can use the impedance and the change in the impedance during the cardiac cycle to estimate thoracic fluid volumes and cardiac function. Specifically, it measures cardiac output, the amount of blood pumped per minute, and other hemodynamic parameters previously only measurable with invasive catheters. There are many studies documenting the device's performance. The new device uses the same technology but has been modernized with updated operating system, and newer computer technology that helped make the device smaller, and faster. The device has also been redesigned to make operator use simpler and reduce the number wires involved. The underlying patented algorithm was not changed. Therefore, it is expected to provide the same degree of accuracy and precision as the predicate device with simplified user interface and lighter, smaller, more portable housing to improve ease of use.
The invention discloses a soap pod saponin extract, a preparation method thereof and an application for curing lung cancer, liver cancer, stomach cancer, colorectal cancer and leukemia. The soap pod saponin extract uses fructus gleditsiae or fructus gleditsiae sinensis as the raw material and is prepared by the extraction of ethanol, and the separation and the purification of macroporous resin, and the content of total saponin of the extract is more than 60 percent. The saponin extract mainly comprises various pentacyclic triterpene saponin compounds, has obvious lethal effect on the clone of the leukemia progranulocyte HL-60 and the stomach cancer transferring lymphocyte SGC7901 of people, and has remarkably inhibited effect on the tumor of mice S180 and mice having the liver cancer. When capsules prepared by the extract are used for curing 40 examples having liver cancer, lung cancer, stomach cancer and colorectal cancer, the partial remission rate is 45 percent, and the partial remission and stabilization rate is 72.5 percent. When the capsules are used for curing 30 patients who have leukemia, the complete remission rate is 66.7 percent, and the total remission rate is 90 percent which is better than that of a single chemo-treatment group. The extract can obviously lighten the toxic side effect caused by the chemo-treatment.
INTRODUCTION: The advent of therapeutic recombinant factor VIII (FVIII) and factor IX (FIX) protein infusions revolutionized the care of persons with haemophilia in the 1990s. It kicked off an era with the increasing use of prophylactic factor infusions for patients and transformed conversations around the ideal trough activity levels as well as the ultimate goals in tailored, individualized care. Our knowledge surrounding the immunologic basis of inhibitor development and treatment derives from a time when patients were receiving frequent factor infusions and focused on immune tolerance induction following inhibitor development.
DISCUSSION: More recently, care was revolutionized again in haemophilia A with the approval of emicizumab, a bispecific antibody mimicking activated FVIII function, to prevent bleeding. The use of emicizumab prophylaxis has resulted in a significantly slower accumulation of factor exposure days and continued effective prophylaxis in the case of inhibitor development. While emicizumab is effective at reducing the frequency of bleeding events in patients with haemophilia A, management of breakthrough bleeds, trauma, and surgeries still requires additional treatment. Ensuring that FVIII is a therapeutic option, particularly for life-threatening bleeding events and major surgeries is critical to optimizing the care of persons with haemophilia A. Other novel non-factor concentrate therapies, including rebalancing agents, will dramatically change the landscape for persons with haemophilia B with inhibitors.
CONCLUSION: This review discusses the changing landscape regarding the timing of inhibitor development and management strategies after inhibitor development, stressing the importance of education across the community to continue to vigilantly monitor for inhibitors and be prepared to treat persons with inhibitors.