anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Participants receive printed exercise programme to complete twice per week. Exercises can be a combination of aerobic, strengthening and balance exercises. Participants receive a weekly phone call from a physiotherapist for the first two weeks to check on progress. Participants complete a paper exercise diary and after the first 2 weeks if they require a progression to their exercise programme they contact their physiotherapist.
Group 1 will begin with a 3-4-month preparation phase and up to 12 sessions in the gravity neutral device (GND) will occur. The training sessions in the GND will be used to obtain the optimal stimulation parameters. Next, participants will enter Intervention Phase 1 where they will receive training sessions 3 days/week for approximately 2 hours. This will be done in the GND in the presence of stimulation. Afterwards, Intervention 2 will include the same training procedures with the addition of Buspirone or Placebo in a cross-over fashion halfway through this phase.
LUNESTA is a CNS depressant and can impair daytime function in some patients at the higher doses (2 mg or 3 mg), even when used as prescribed. Prescribers should monitor for excess depressant effects, but impairment can occur in the absence of symptoms (or even with subjective improvement), and impairment may not be reliably detected by ordinary clinical exam (i.e., less than formal psychomotor testing). While pharmacodynamic tolerance or adaptation to some adverse depressant effects of LUNESTA may develop, patients using 3 mg LUNESTA should be cautioned against driving or engaging in other hazardous activities or activities requiring complete mental alertness the day after use. 

Additive effects occur with concomitant use of other CNS depressants (e.g., benzodiazepines, opioids, tricyclic antidepressants, alcohol), including daytime use. Downward dose adjustment of LUNESTA and concomitant CNS depressants should be considered [see Dosage and Administration (2.4)].

The use of LUNESTA with other sedative-hypnotics at bedtime or the middle of the night is not recommended. 

The risk of next-day psychomotor impairment is increased if LUNESTA is taken with less than a full night of sleep remaining (7- to 8 hours); if higher than the recommended dose is taken; if coadministered with other CNS depressants; or coadministered with other drugs that increase the blood levels of eszopiclone [see Dosage and Administration (2.3) and Clinical Studies (14.3)].

Because Lunesta can cause drowsiness and a decreased level of consciousness, patients, particularly the elderly, are at higher risk of falls.
Long noncoding RNAs (lncRNAs) serve pivotal roles in cancer biology. The present study investigated the oncogenic roles of lncRNAs in renal cell carcinoma (RCC) and their potential as prognostic biomarkers. The lncRNA leucine‑rich repeat containing 75 A‑antisense RNA1 (LRRC75A‑AS1) was identified through lncRNA microarray as a potential lncRNA that may predict the efficacy of immune checkpoint inhibitor therapy and cancer progression in RCC. The present study subsequently assessed the expression of LRRC75A‑AS1 in 212 patients with clear cell RCC (ccRCC) who underwent nephrectomy, and performed in vitro functional analysis of LRRC75A‑AS1 in RCC cell lines. Additionally, the interactions between LRRC75A‑AS1, microRNA (miR)‑370‑5p and ADAMTS5 were explored. LRRC75A‑AS1 was revealed to be significantly upregulated in ccRCC tissues compared with in adjacent normal tissues, and high LRRC75A‑AS1 expression was associated with poor prognosis, including lower progression‑free survival, in patients with RCC. The knockdown of LRRC75A‑AS1 in RCC cell lines resulted in reduced cell proliferation and invasion, highlighting its role in promoting tumorigenesis. Furthermore, the interaction among LRRC75A‑AS1, miR‑370‑5p and ADAMTS5 was suggested as a regulatory mechanism underlying RCC progression. These findings indicated that LRRC75A‑AS1 may function as an oncogene in RCC, promoting cell proliferation and invasion. Its significant upregulation in ccRCC tissues and association with poor prognosis underscore its potential as a prognostic biomarker for RCC. Understanding the regulatory interactions among LRRC75A‑AS1, miR‑370‑5p and ADAMTS5 may provide new insights into the molecular mechanisms underlying RCC and facilitate the identification of novel therapeutic targets.
The invention, the Image Viewer system, represents a new way to store and access medical images such as scans and X-rays. The invention is comprised of the web portal design, including the web browser layout, and the software application. A patient's medical images, created during an imaging session, are stored at a central location, a web portal, by medical personnel who catalog and code the images using the software application or a web browser. The images stored at the portal can be accessed by any networked device with a web browser or the software application from any connection to the Internet. The connection to the Internet can be wired or wireless, such as WiFi or cellular. Networked devices include PCs, tablets, laptops and smart phones. Physicians with a network device can retrieve images and enter data in the web portal, including diagnoses and personal information. Patients with a networked device can access the portal to download images or to enter their personal profile.
* For adult patients with baseline (start of treatment) WBC greater than or equal to 3 x10 9/L, ANC greater than or equal to 1.5 x10 9/L, and platelets greater than or equal to 75 x10 9/L, adjust the dose as follows, based on nadir counts for any given cycle: 


  * For adult patients whose baseline counts are WBC less than 3 x10 9/L, ANC less than 1.5 x10 9/L, or platelets less than 75 x10 9/L, base dose adjustments on nadir counts and bone marrow biopsy cellularity at the time of the nadir as noted below, unless there is clear improvement in differentiation (percentage of mature granulocytes is higher and ANC is higher than at onset of that course) at the time of the next cycle, in which case continue the current dose. 



If a nadir as defined in the table above has occurred, give the next course 28 days after the start of the preceding course, provided that both the WBC and the platelet counts are greater than 25% above the nadir and rising. If a greater than 25% increase above the nadir is not seen by day 28, reassess counts every 7 days. If a 25% increase is not seen by day 42, reduce the scheduled dose by 50%.

Pediatric use information is approved for Celgene Corporation’s Vidaza ®(azacitidine for injection). However, due to Celgene Corporation’s marketing exclusivity rights, this drug product is not labeled with that information.
The invention relates to a polypeptide capable of binding SARS-CoV-2, comprising 3 complementarity determining regions CDR1-3, wherein the sequence of CDR1 is or comprises one of the sequences shown in SEQ ID NO. 1-9, the sequence of CDR2 is or comprises one of the sequences shown in SEQ ID NO. 10-20, and the sequence of CDR3 is or comprises one of the sequences shown in SEQ ID NO. 21-38. The invention carries out nano antibody drug development aiming at SARS-CoV-2, and through immune alpaca, platform technology which utilizes phage library to display nano monoclonal antibody, etc., nano antibody which is specifically combined with receptor structural domain on S protein of virus is screened, CDR sequence is identified, and humanized antibody C9NB is constructed; evaluating the efficacy of C9NB in treating the viral infection using a virus neutralization assay; simultaneously, an AAV vector was used to load the expression sequence encoding C9 NB. The present invention provides a new potential nano antibody medicine for the clinical prevention, treatment and detection of SARS-CoV-2.
Phase 1: Endotracheal intubation using the videolaryngoscope with blade 0 or 1 according to weight of infant. videolaryngoscope will be used to proceed to endotracheal intubation indirectly with the use of the video monitor for guidance. Phase 2: Endotracheal intubation using the classic laryngoscope with Miller blade 0 or 1 according to weight of infant.
Liver disease is a common and serious threat to human health. The progression of liver diseases is influenced by many physiologic processes, including oxidative stress, inflammation, bile acid metabolism, and autophagy. Various factors lead to the dysfunction of these processes and basing on the different pathogeny, pathology, clinical manifestation, and pathogenesis, liver diseases are grouped into different categories. Specifically, Sirtuin1 (SIRT1), a member of the sirtuin protein family, has been extensively studied in the context of liver injury in recent years and are confirmed the significant role in liver disease. SIRT1 has been found to play a critical role in regulating key processes in liver injury. Further, SIRT1 seems to cause divers outcomes in different types of liver diseases. Recent studies have showed some therapeutic strategies involving modulating SIRT1, which may bring a novel therapeutic target. To elucidate the mechanisms underlying the role of sirtuin1 in liver injury and its potentiality as a therapeutic target, this review outlines the key signaling pathways associated with sirtuin1 and liver injury, and discusses recent advances in therapeutic strategies targeting sirtuin1 in liver diseases.
In the WHIMS estrogen-alone ancillary study of WHI, a population of 2,947 hysterectomized women 65 to 79 years of age was randomized to daily CE (0.625 mg)-alone or placebo.

After an average follow-up of 5.2 years, 28 women in the estrogen-alone group and 19 women in the placebo group were diagnosed with probable dementia. The relative risk of probable dementia for CE-alone versus placebo was 1.49 (95 percent CI, 0.83–2.66). The absolute risk of probable dementia for CE-alone versus placebo was 37 versus 25 cases per 10,000 women-years. (See CLINICAL STUDIES and PRECAUTIONS, Geriatric Use.)

In the WHIMS estrogen plus progestin ancillary study of WHI, a population of 4,532 postmenopausal women 65 to 79 years of age was randomized to daily CE (0.625 mg) plus MPA (2.5 mg) or placebo.

After an average follow-up of 4 years, 40 women in the CE plus MPA group and 21 women in the placebo group were diagnosed with probable dementia. The relative risk of probable dementia for CE plus MPA versus placebo was 2.05 (95 percent CI 1.21–3.48). The absolute risk of probable dementia for CE plus MPA versus placebo was 45 versus 22 cases per 10,000 women-years. (See CLINICAL STUDIES and PRECAUTIONS, Geriatric Use.)

When data from the two populations in the WHIMS estrogen-alone and estrogen plus progestin ancillary studies were pooled as planned in the WHIMS protocol, the reported overall relative risk for probable dementia was 1.76 (95 percent CI, 1.19–2.60). Since both substudies were conducted in women 65 to 79 years of age, it is unknown whether these findings apply to younger postmenopausal women. (See PRECAUTIONS, Geriatric Use.)
PRIMARY OBJECTIVES: I. Determine the overall response rate (ORR), including complete responses (CR) and partial responses (PR), with combined lenalidomide and panobinostat in patients with relapsed or refractory Hodgkin's lymphoma. SECONDARY OBJECTIVES: I. Assess the safety and tolerability of combined lenalidomide and panobinostat in patients with previously treated Hodgkin's lymphoma. II. Determine progression-free survival (PFS) in patients with previously treated Hodgkin's lymphoma receiving combined lenalidomide and panobinostat. III. Evaluate changes in natural killer (NK) cell number and function, plasma cytokines, gene expression profile of peripheral blood, and plasma proteins via proteomics, before, during, and after lenalidomide and panobinostat therapy. IV. Determine levels of histone acetylation before and after treatment with panobinostat. V. Determine the pharmacokinetics of lenalidomide in the presence of panobinostat. VI. To collect deoxyribonucleic acid (DNA) samples for potential later analysis of associations between outcomes and polymorphisms in genes coding for drug metabolizing enzymes, transporters and molecular targets of lenalidomide or panobinostat. OUTLINE: Patients receive panobinostat orally (PO) on days 1, 3, and 5 of weeks 1-4 and lenalidomide PO on days 1-7 of weeks 1-3. Courses repeat every 28 days in the absence of disease progression or unacceptable toxicity. After completion of study treatment, patients are followed up at least every 3 months for 2 years, and then every 6 months for 3-5 years
Radiopharmaceuticals is currently used for the treatment of metastatic cancer date. While radiopharmaceuticals are generally well tolerated, one of its most devastating long-term toxicities is the development of therapy related myeloid neoplasms (t-MN), an umbrella term for myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). PRRT (Receptor Radionuclide Therapy) is a targeted radiopharmaceutical therapy (RPT) used to treat neuroendocrine tumors. RPTs use drugs to attack cancer cells while reducing harm to healthy tissue. PRRT delivers high doses of radiation to tumors in the body to destroy or slow their growth and reduce disease side effects.

While PRRT is generally well tolerated, one of its long-term side effects is the development of therapy related myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). The identification of genetic changes that lead to the development of MDS and AML during PRRT is a growing area of research. It is now known that the genetic changes that lead to progression into AML typically occur through many years of pre-leukemic hematopoietic stem cell clonal evolution, before development of late mutations that lead to malignant disease. The short interval between exposure to PRRT and appearance of MDS and AML would suggest some patients are already at high risk of developing AML and are potentially detectable. The ability to identify individuals predisposed to developing MDS/AML could improve patient selection for PRRT and design strategies to mitigate the development of MDS/AML.

This research proposes to study the genetic changes that occur pre-PRRT and post-PRRT using blood samples obtained from a patient population at Princess Margaret Hospital. Cohort A will consist of 20 patients that have had PRRT within the past 4 years. Cohort B will consist of 20 patients planned for PRRT. Cohort C will consist of 1-5 patients post PRRT, diagnosed with t-MN.
AAT deficiency is a genetic disorder associated with emphysema. Spirometry, the lung function test that measures how well the lungs exhale air, is used to diagnose and track the progression of emphysema. Some studies have suggested that forced expiratory volume in 1 second (FEV1) measurements, a type of spirometry test, may lack accuracy in detecting disease progression in cases of severe AAT deficiency. Another method, high resolution chest CT scans, may be more accurate at measuring the progression of emphysema. The purpose of this study is to determine if high resolution CT scans are better at detecting the progression of emphysema than lung function tests. Results from this study may lead to the development of a more accurate way to assess lung tissue loss and may improve the understanding of lung destruction in AAT deficiency.

This study will last 4 years and will enroll people with AAT deficiency who have nearly normal lung function test results. Study visits, each lasting about 4 hours, will occur at baseline and months 6, 12, 18, 24, and 36. At each visit, participants will undergo lung function tests, a CT scan, blood collection, and a physical exam. Female participants will have urine collected for a pregnancy test. All participants will also complete questionnaires to assess health status and lung function. Study researchers will call participants every 2 months to collect information on lung disease symptoms and medication changes.
INTRODUCTION: Planar lymphoscintigraphy (PL) is commonly used in mapping before sentinel lymph node biopsy (SLNB) for invasive cutaneous melanoma. Recently, single-photon emission computed tomography (SPECT)/ computed tomography (CT) has been utilized, in addition to PL, for detailed anatomic information and detection of sentinel lymph nodes (SLNs) outside of the primary nodal basin in truncal and head and neck melanoma. Following a protocol change due to COVID-19, our institution began routinely obtaining both PL and SPECT-CT imaging for all melanoma SLN mapping. We hypothesized that SPECT-CT is associated with higher instances of SLNBs from "nontraditional" nodal basins (NTNB) for extremity melanomas.
METHODS: Patients with extremity melanoma (2017-2022) who underwent SLNB were grouped into SPECT-CT with PL versus PL alone. Outcomes were total SLNs removed, + or-SLN status, total NTNB sampled, and postoperative complication rate. Poisson regression and logistic regression models were used to assess association of SPECT-CT with patient outcomes.
RESULTS: Of 380 patients with extremity melanoma, 42.11% had SPECT-CT. There were no differences between the groups with regards to age at diagnosis or sex. From 2020 to 2022, all patients underwent SPECT-CT. SPECT-CT was associated with increased odds of SLNB from an NTNB, (odds ratio = 2.39 [95% confidence interval: 1.25-4.67]). There was no difference in odds of number of SLNs sampled, SLN positivity rate, or postoperative complication rate with SPECT-CT.
CONCLUSIONS: Routine SPECT-CT was associated with higher incidence of SLNB in NTNB but did not increase number of SLNs removed or SLN positivity rate. The added value of routine SPECT-CT in cutaneous melanoma of the extremities remains to be defined.
Pitocin (oxytocin injection, USP) is a sterile, clear, colorless aqueous solution of synthetic oxytocin, for intravenous infusion or intramuscular injection. Pitocin is a nonapeptide found in pituitary extracts from mammals. It is standardized to contain 10 units of oxytocic hormone/mL and contains 0.5% Chlorobutanol, a chloroform derivative as a preservative, 1.65 mg acetic acid and 0.16 mg ammonium acetate as buffers, and with the pH adjusted with acetic acid to achieve a targeted pH of 3.5. Pitocin may contain up to 16% of total impurities. The hormone is prepared synthetically to avoid possible contamination with vasopressin (ADH) and other small polypeptides with biologic activity. Pitocin has the empirical formula C43H66N12O12S2 (molecular weight 1007.19). The structural formula is as follows:
This is a single arm prospective, monocentric, open, experimental pilot study. The response to NAC in breast cancer is extremely heterogeneous. The study and the identification of factors that can predict the response to treatment is therefore a priority, constituting a relevant "clinical unmet need".Modern molecular biology techniques as well as imaging diagnostics could be valuable tools for characterizing the response to NAC toward the definition of more personalized therapies.The prediction of therapy response after two cycle of chemotherapy rather than at the end of six cycles using non-invasive procedures will spare unwanted toxicity to the patients and resources to the Regional and National Health system. This study will also provide the patients, their familiar and all the stakeholders involved in the cure of Breast Cancer new important information regarding the management of breast cancer patients.This is a non-interventional study; therefore, the treatment will be as per physician choice according to the most appropriate therapeutic opportunities available for each patients' based on the type and stage of disease and the patients' performance status.Currently, the NAC regimens commonly used at CRO-Aviano for NAC are Epirubicine 90 mg/mq + Ciclophosphamide 600 mg/mq d1 q21 or q14 (EC)(dose dense) followed by weekly Paclitaxel 80 mg/mq for a total of 12 administrations. Occasionally, due to patients and tumor features only weekly Paclitaxel is used, and usually in this case up to 24 administrations may be given. Only in the case of HER2 positive BC trastuzumab 2 mg/kg is added to weekly Paclitaxel. Given the low response rate of hormone-based neoadjuvant therapy, only in rare cases (e.g. patients not amenable of surgery due to comorbidities), this approach is used.
Introduction. The relationship between obesity and alcohol consumption is a topic of significant interest to public health. Alcoholic beverages contribute additional calories to the diet, which could be a relevant factor to the overweight risk. However, its association with weight gain is controversial and influenced by multiple factors. Objective. To analyze the relationship between moderate alcohol intake and body mass index, considering the variables that may influence this relationship. Materials and methods. The sample consisted of 155 individuals from Puerto Madryn (Argentina). Each participant completed a questionnaire about health, lifestyle, demographic, and socioeconomic factors. Anthropometric measurements were taken, and polymorphisms of 18 genes related to alcohol metabolism were genotyped. Results. We found that moderate alcohol consumption is associated with a lower body mass index, particularly in females. An increase of 14 grams of alcohol was associated with a risk of 0.68 for obesity and 0.71 for overweight. The T variant of the marker rs4646543 (ALDH1A1), a gene involved in alcohol metabolism and adipogenesis, was associated with a higher frequency of alcohol consumption. Conclusion. The findings of this study suggest that moderate alcohol consumption does not significantly contribute to body weight in the sample studied. Furthermore, the association with genetic variants, such as those of the ALDH1A1 gene, may provide a biological explanation for the inverse relationship observed between weight and alcohol consumption.
The present invention relates to single chain antibody (ScFv) of antihuman vascular endothelial growth factor (VEGF) for curing tumor of human body. Its aesign and preparation. It prepares VEGF synthetic peptide to establish antihuman VEGF monoclonal antibody (MAb) hybridoma cell strain. SAid MAb possesses stable bioactivity and obvious tumor-inhibiting action. Said invention make RT-PCR amplificatino of light and heavy chain genes of MAb variable region, and uses DNA fragment to implement connection to constitute antihuman VEGF ScFv gene and finally obtain the high-effective expres of ScFv. The tests show that said antihuman VEGF ScFv is small in molecular weight, possesses strong power for penetrating tumor ittue, its immunogenicity is low, so that it possesses the tumor-resisting function.
The pulmonary heart disease is a disease caused by weak lung Qi and disabled discharging of phlegm accumulated in lung. The heart disease has the symptom of weak and slow pulse and arrhythmia caused by deficiency of heart-Yang and weak heart Qi. When in treatment, crystal sugar phlegmatic diarrhea broth and heart-enhancing broth are used so as to play the effect on curing the pulmonary heart disease. Taboos are remembered when taking the crystal sugar phlegmatic diarrhea broth and wet phlegm in the lung and human body can be rapidly discharged so as to cure the lung disease. When taking the heart-enhancing broth, the heart disease can be rapidly cured. By adopting the above two ways, the heart disease can be rapidly cured.
PURPOSE:To obtain the title compound useful as a physiologically active substance such as antimicrobial agent and an index substance concerned in dynamic mechanism of in vivo tissue, etc. by reacting alpha,beta-unsaturated aldehyde with a primary amine compound. CONSTITUTION:An alpha,beta-unsaturated aldehyde (e.g. aldol condensate) is allowed to react with a primary amine compound (e.g. aliphatic amine, amino acid, amino acid ester, etc.) to provide a quaternary pyridinium compound. The compound obtained by the above-mentioned method can readily be converted into a pyridine compound useful as various kinds of medicines, agricultural chemicals or intermediates thereof by subjecting the compound to pyrolysis, namely Hofmann degradation.