anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
The present application provides diagnostic methods for determining the fertility status of a male individual by evaluating his DEFB-126 phenotypic and genotypic status. The present invention relates to a dinucleotide deletion polymorphism in the protein coding sequence of a DEFB-126 nucleic acid. The amino acid sequence of this variant has a significantly altered the carboxyl terminal, carbohydrate-containing domain of DEFB-126 in comparison to a wild-type DEFB-126 polypeptide. This variant results in aberrant protein function and structure, leading to reduced sperm function and fertility. The present invention provides methods for analyzing the genotype of individuals with respect to the gene encoding DEFB-126 in order to determine whether that individual has reduced fertility. Such determination will provide an individual knowledge of whether their genotype is associated with a risk of reduced fertility and to allow that individual to receive appropriate fertility treatment options. The present invention further provides kits that are useful for diagnosing increased risk or probability of infertility based on the presence or absence of the DEFB-126 deletion polymorphism. The application also provides therapeutic methods and compositions for restoring sperm functionality (e.g., to effect conception) in sperm from an individual who expresses insufficient levels of DEFB-126.
1436566 α-Hydrazisobenzyl penicillins ISF SpA 2 Nov 1973 [10 Nov 1972 15 May 1973] 50944/73 Heading C2C Novel compounds (I) and salts thereof in which R is hydrogen or C 1 -C 6  alkyl are prepared by (I) reaction of 6-aminopenicillanic acid or a salt or protected derivative thereof (preferably trimethysilyl ester) with a compound II in which Hal is chlorine or bromine or (2) reaction of 6-amino-penicillanic acid with a compound IV  in which X is -O-CO-OEt imidazolyl or 2,4-diatrophenoxy and Y is carbobenzyloxy, CCl 3 CO- or Me 3 Si- and removal of the protecting Y group by hydrolysis or hydrogenolysis. Compounds I are formed as racemates and enantiomers; the R(-) and S(+) form of compound I (R = H) being prepared. Compounds II are prepared by reacting α-chloro or bromo-phenylacetic acid with a hydrazine R-NH.NH 2  and reacting the hydrazino acid hydrochloride or hydrobromide produced with the appropriate phosphorus pentahalide. α-(l-Methyl-2-benzyloxycarbonylhydrazino) - phenylacetic acid is prepared by reaction of benzyl chloroformate with the appropriate hydrazine acid. α-(2-Benzyl oxycarbonyl - 1 - pentyl - hydrazino)phenylacetic acid is prepared by reaction of α-bromophenylacetic acid with 1-pentyl-2-benzyloxycarbonylhydrazine. Compounds I have antibiotic activity and form with an excipient a pharmaceutical composition.
BACKGROUND: Diabetes mellitus is a significant risk factor for cardiovascular events and mortality in dialysis patients. The impact of different dialysis modalities on the risk of new onset diabetes mellitus (NODM) remains a subject of debate. Previous studies did not adequately account for critical confounding factors such as pre-dialysis glycemic status, medication use, and nutritional status, which may influence the association between dialysis modality and NODM risk.
METHODS: We conducted a retrospective cohort study of 1426 non-diabetic end-stage renal disease (ESRD) patients who underwent either hemodialysis (HD) or peritoneal dialysis (PD) at a single medical center. We used different statistical methods, adjusting for potential confounding factors, and accounted for competing risk of death.
RESULTS: Over 12 years, 331 patients (23 %) developed NODM. After adjusting for potential confounding factors and mortality, PD patients had a significantly higher risk of NODM compared to HD patients (adjusted HR 1.52, p = 0.001). A propensity-matched cohort sensitivity analysis yielded similar results. Among patients with prediabetes, those receiving PD had a 2.93 times higher risk of developing NODM than those receiving HD (p for interaction <0.001), whereas no significant difference was observed among euglycemic patients. NODM was also associated with a 1.78 times increased risk of major cardiovascular events.
CONCLUSION: Our study provides evidence that PD treatment may increase the risk of NODM in ESRD patients, particularly among those with preexisting prediabetes. These findings highlight the importance of personalized treatment approaches, and nephrologists should consider prediabetes when choosing the dialysis modality for their patients.
One of the extracellular matrix proteins, tenascin-C (TN-C), is known to be upregulated in age-related inflammatory diseases such as cancer and cardiovascular diseases. Expression of this molecule is frequently detected, especially in the macrophage-rich areas of atherosclerotic lesions; however, the role of TN-C in mechanisms underlying the progression of atherosclerosis remains obscure. Previously, we found a hidden bioactive sequence termed TNIIIA2 in the TN-C molecule and reported that the exposure of this sequence would be carried out through limited digestion of TN-C by inflammatory proteases. Thus, we hypothesized that some pro-atherosclerotic phenotypes might be elicited from macrophages when they were stimulated by TNIIIA2. In this study, TNIIIA2 showed the ability to accelerate intracellular lipid accumulation in macrophages. In this experimental condition, an elevation of phagocytic activity was observed, accompanied by a decrease in the expression of transporters responsible for lipid efflux. All these observations were mediated through the induction of excessive β1-integrin activation, which is a characteristic property of the TNIIIA2 sequence. Finally, we demonstrated that the injection of a drug that targets TNIIIA2's bioactivity could rescue mice from atherosclerotic plaque expansion. From these observations, it was shown that TN-C works as a pro-atherosclerotic molecule through an internal TNIIIA2 sequence. The possible advantages of clinical strategies targeting TNIIIA2 are also indicated.
Serious, life-threatening, or fatal respiratory depression has been reported with the use of modified-release opioids, even when used as recommended. Respiratory depression from opioid use, if not immediately recognized and treated, may lead to respiratory arrest and death. Management of respiratory depression may include close observation, supportive measures, and use of opioid antagonists, depending on the patient’s clinical status [see Overdosage (10)]. Carbon dioxide (CO2) retention from opioid-induced respiratory depression can exacerbate the sedating effects of opioids. 

While serious, life-threatening, or fatal respiratory depression can occur at any time during the use of ZOHYDRO ER, the risk is greatest during the initiation of therapy or following a dose increase. Closely monitor patients for respiratory depression when initiating therapy with ZOHYDRO ER and following dose increases.

To reduce the risk of respiratory depression, proper dosing and titration of ZOHYDRO ER are essential [see Dosage and Administration (2)]. Overestimating the ZOHYDRO ER dose when converting patients from another opioid product can result in fatal overdose with the first dose. 

Accidental ingestion of even one dose of ZOHYDRO ER, especially by children, can result in respiratory depression and death due to an overdose of hydrocodone.
Participation will last 3 months from enrollment. Demographic data will be retrieved from the electronic health record and the Generalized Anxiety Disorder-7 (GAD-7) Anxiety Questionnaire will be administered at baseline. Participants will repeat the GAD-7 in 3 months and an additional qualitative survey on their experience including an evaluation of the structured anxiety reduction program.
All patients will be instructed to wear the device for 23 weeks for 12 weeks after being instructed on how to use the appropriate compression orthosis. The patient's relatives will be asked to keep a book in order to monitor their use. Patients who have not used the device for 5 consecutive days will be excluded from the study. The first group will be given awareness training on using one session orthosis and posture correction.
Participants first received AVICOD 200 mg FT manufactured by Pharma Plant in a fasting state. After a washout period of 24 hours, they then received Avigan FT200 mg manufactured by Toyama Chemical Industry Co.Ltd./Japan in a fasting state.
Professionals: meeting methodological of 30 minutes duration. Patients: Usual clinical practice. Health education individually on nursing consultation.
The present invention relates to recombinant proteins, compositions thereof and methods of stabilizing the same. The invention relates in particular to stable recombinant proteins of SEQ ID NO. 1 and compositions comprising recombinant proteins of SEQ ID NO. 1. The invention also relates to a method for preparing, storing and stabilizing the recombinant protein of SEQ ID NO. 1 and to compositions thereof for extending shelf life.
The immune system recognizes a multitude of innocuous antigens from food and intestinal commensal microbes toward which it orchestrates appropriate, non-inflammatory responses. This process requires antigen-presenting cells (APCs) that induce T cells with either regulatory or effector functions. Compromised APC function disrupts the T cell balance, leading to inflammation and dysbiosis. Although their precise identities continue to be debated, it has become clear that multiple APC lineages direct the differentiation of distinct microbiota-specific CD4+ T cell programs. Here, we review how unique APC subsets instruct T cell differentiation and function in response to microbiota and dietary antigens. These discoveries provide new opportunities to investigate T cell-APC regulatory networks controlling immune homeostasis and perturbations associated with inflammatory and allergic diseases.
The rapidly aging population is consuming more alcohol, leading to increased alcohol-associated acute pancreatitis (AAP) with high mortality. However, the mechanisms remain undefined, and currently there are no effective therapies available. This study aims to elucidate aging- and alcohol-associated spatial transcriptomic signature by establishing an aging AAP mouse model and applying Visium spatial transcriptomics for understanding of the mechanisms in the context of the pancreatic tissue. Upon alcohol diet feeding and caerulein treatment, aging mice (18 months) developed significantly more severe AAP with 5.0-fold increase of injury score and 2.4-fold increase of amylase compared to young mice (3 months). Via Visium spatial transcriptomics, eight distinct tissue clusters were revealed from aggregated transcriptomes of aging and young AAP mice: five acinar, two stromal, and one islet, which were then merged into three clusters: acinar, stromal, and islet for the comparative analysis. Compared to young AAP mice, > 1300 differentially expressed genes (DEGs) and approximately 3000 differentially regulated pathways were identified in aging AAP mice. The top five DEGs upregulated in aging AAP mice include Mmp8, Ppbp, Serpina3m, Cxcl13, and Hamp with heterogeneous distributions among the clusters. Taken together, this study demonstrates spatial heterogeneity of inflammatory processes in aging AAP mice, offering novel insights into the mechanisms and potential drivers for AAP development. KEY MESSAGES: Mechanisms regarding high mortality of AAP in aging remain undefined. An aging AAP mouse model was developed recapturing clinical exhibition in humans. Spatial transcriptomics identified contrasted DEGs in aging vs. young AAP mice. Top five DEGs were Mmp8, Ppbp, Serpina3m, Cxcl13, and Hamp in aging vs. young AAP mice. Our findings shed insights for identification of molecular drivers in aging AAP.
Etonogestrel and ethinyl estradiol vaginal ring is a non-biodegradable, flexible, transparent, colorless to almost colorless, combination contraceptive vaginal ring containing two active components, a progestin, etonogestrel (13-ethyl-17-hydroxy-11-methylene-18,19-dinor-17α-pregn-4-en-20-yn-3-one) and an estrogen, ethinyl estradiol (19-nor-17α-pregna-1,3,5(10)-trien-20-yne-3,17-diol). When placed in the vagina, each ring releases on average 0.120 mg/day of etonogestrel and 0.015 mg/day of ethinyl estradiol over a three-week period of use. Etonogestrel and ethinyl estradiol vaginal ring is made of ethylene vinylacetate copolymers (28% and 9% vinylacetate) and magnesium stearate and contains 11.7 mg etonogestrel and 2.7 mg ethinyl estradiol. Etonogestrel and ethinyl estradiol vaginal ring is not made with natural rubber latex. Etonogestrel and ethinyl estradiol vaginal ring has an outer diameter of 54 mm and a cross-sectional diameter of 4 mm. The molecular weights for etonogestrel and ethinyl estradiol are 324.46 and 296.40, respectively.   
The structural formulas are as follows:
FIELD: medicine. ^ SUBSTANCE: invention relates to medicine, namely to dermatocosmetology and can be used for face and neck skin rejuvenation in women. For this purpose plasmapheresis in mode of discontinuous flow separation with sampling of 800-1000 ml of blood is carried out. In course of carrying out plasmapheresis after the first cycle, native plasma is taken and immediately introduced intradermally papularly on Langer lines. Diametre of papules is 0.5-1 cm, distance between them is 1.5-2.5 cm. Total volume of introduced plasma is 5-10 ml. Course consists of 2-3 procedures after 12-16 days. ^ EFFECT: method allows to increase efficiency of face and neck skin rejuvenation in women due to combination of local and systemic impact of plasma, which possesses high tropism to skin cells, which ensures formation of new collagen in skin. ^ 3 tbl, 2 ex
STRATAGRAFT is applied in appropriate aseptic conditions by a trained healthcare provider. 

Follow the steps below for topical application of STRATAGRAFT:

  1. If utilizing fibrin glue to anchor STRATAGRAFT, apply prior to placing the meshed STRATAGRAFT on the prepared wound bed. If utilizing anchoring methods other than fibrin glue, start with step 2.
  2. Place the meshed STRATAGRAFT with the dermal (shiny) side down in contact with the patient's prepared wound bed. Ensure the epidermal (matte) side is facing up. Abut the constructs when placing multiple STRATAGRAFT constructs. Overlapping the STRATAGRAFT construct edges is not required.  
Note: If the area to be treated is smaller than one construct, trim excess STRATAGRAFT before or after anchoring to the wound bed. Ensure that STRATAGRAFT has contact across the entire surface of the wound bed. Do not stretch or expand STRATAGRAFT, as doing so may degrade the structural integrity of STRATAGRAFT.
  3. Anchor STRATAGRAFT with staples, tissue adhesive such as cyanoacrylate, or sutures to keep STRATAGRAFT from dislodging. Place a porous, nonadherent contact dressing over STRATAGRAFT and leave the dressing in place for one week before changing.
  4. Place a second layer of dressing that does not contain silver [see Drug Interactions (7.2)].
  5. Placement of an outer bolster or wrap that keeps STRATAGRAFT from moving as clinically appropriate is at the discretion of the physician.
The invention discloses a method for preparing tetanus human immune globulin by double virus inactivation. The method comprises separating and purifying blood plasma from healthy people containing high-potency tetanus antibody by a low-temperature ethanol protein-separating method, and inactivating virus at the pH value of 4.0 after incubation at 23-25 DEG C for 21 days and treating with DV50 nanometer anti-virus membrane for double virus inactivation. The method of the invention has the beneficial effects that the tetanus human immune globulin prepared by double virus inactivation can greatly reduce disease transmitted by blood products, and the quality of products fully complies with the requirement of Pharmacopoeia of People's Republic of China. Through a test using the pseudorabies virus, Sindbis virus and human immunodeficiency virus (HIV), the virus titer (TCID50) can be decreased by at least 4.00log. The safety and reliability of the products are ensured. The tetanus human immune globulin is particularly suitable for people allergic to tetanus antitoxin (TAT).
Overdoses (up to 10-fold of the prescribed dose) occurred in patients treated with intravenous topotecan. The primary complication of overdosage is bone marrow suppression. The observed signs and symptoms of overdose are consistent with the known adverse reactionsassociated with topotecan hydrochloride for injection for intravenous use [see Adverse Reactions (6.1, 6.2)].

In addition, elevated hepatic enzymes and mucositis have been reported following overdose. One patient received a single dose of 40 mg/m2 of intravenous topotecan and developed gastrointestinal toxicity, skin toxicity, and myelosuppresion leading to septic shock. Another patient received a single dose of 35 mg/m2 and experienced severe, reversible neutropenia. 

There is no known antidote for overdosage with topotecan hydrochloride for injection. If an overdose is suspected, monitor the patient for bone marrow suppression and institute supportive-care measures (such as prophylactic G-CSF and antibiotic therapy) as appropriate.
PURPOSE OF REVIEW: Despite established effectiveness in overactive bladder and nonobstructive retention, neuromodulation's application in interstitial cystitis/bladder pain syndrome (IC/BPS) remains a topic of ongoing research. The purpose of this article is to review recent developments in neuromodulation as treatment of IC/BPS offering guidance for healthcare practitioners dealing with IC/BPS cases.
RECENT FINDINGS: Recent research underlines the promising role of sacral, tibial and pudendal neuromodulation in management of IC/BPS symptoms. Studies reveal encouraging outcomes, particularly in alleviating urgency and frequency symptoms. However, while urgency and frequency symptoms tend to improve, comprehensive pain relief remains a challenge. Percutaneous tibial nerve stimulation (PTNS) and transcutaneous tibial nerve stimulation (TTNS) stand out due to their minimal invasive nature. Existing literature points to the need for larger prospective studies with extended follow-up periods to validate the efficacy and sustainability of neuromodulation.
SUMMARY: Neuromodulation is a promising treatment modality for refractory IC/BPS. Due to the minimal invasive nature, they should be tried before rigorous surgery. However, the limited quantity of available data and the variability in pain relief outcomes necessitate cautious interpretation. The review emphasizes the need for further research.
In the arm which IHC showed CD8 ≥10%, this arm will be subdivided into 6 sub-arms, in which Arm 5A-4D, we choose the patients who had CDK4/6 inhibitor before while in Arm 5E, we choose the patients who secondarily resistant to adjuvant endocrine therapy , and in Arm 5FF, we choose the patients who is in stage IV without precious treatment or sensitively recurrence. A patient would receive SHR1210(PD-1 antibody) ,nab-paclitaxel and Faminitib in Arm-5A. A patient would receive SHR1210(PD-1 antibody) and VEGF inhibitor in Arm-5B. A patient would receive SHR1701(PD-L1/TGF-βRII inhibitor) in Arm-5C. A patient would receive SHR1701(PD-L1/TGF-βRII inhibitor) and SHR6390(CDK4/6 inhibitor) in Arm-5D. A patient would receive SHR1210(PD-1 antibody) and SHR6390(CDK4/6 inhibitor) and SERD in Arm-5E. A patient would receive SHR1210(PD-1 antibody) and SHR6390(CDK4/6 inhibitor) and AI in Arm-5F.
PURPOSE: To obtain high decomposition activity for fat with little side effect and to improve the muscle/fat ratio of agricultural cattle such as ruminant animals and poultry by feeding cattle with a compsn. containing a specified compd. CONSTITUTION: A compsn. containing a compd. expressed by formula I as a phenylalkylamino deriv. or its salt with addition of acid, or containing a compd. expressed by formula II or its salt with addition of acid is fed to an animal to increase the muscle/fat ratio, especially of a cow and sheep. In formula I, R1 is a phenylalkyl group having a phenyl group which may have substituents such as 1 to 3C alkyl, hydroxy or methoxy groups, or a thienylalkyl group having 1 to 3C alkyl groups, and R2 , R3 are methyl or ethyl groups. In formula II, n is 1 to 3, Ar is a thienyl or phenyl group which may have substituents of hydroxy or methoxy groups.
Chronic obstructive pulmonary disease(COPD) is a gradually worsening and fatal heterogeneous lung disease characterized by airflow limitation and increasingly decline in lung function. Currently, it is one of the leading causes of death worldwide. The consistent feature of COPD is airway inflammation. Several inflammatory factors are known to be involved in COPD pathogenesis; however, anti-inflammatory therapy is not the first-line treatment for COPD. Although bronchodilators, corticosteroids and roflumilast could improve airflow and control symptoms, they could not reverse the disease. The cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) signaling pathway plays an important novel role in the immune system and has been confirmed to be a key mediator of inflammation during infection, cellular stress, and tissue damage. Recent studies have emphasized that abnormal activation of cGAS-STING contributes to COPD, providing a direction for new treatments that we urgently need to develop. Here, we focused on the cGAS-STING pathway, providing insight into its molecular mechanism and summarizing the current knowledge on the role of the cGAS-STING pathway in COPD. Moreover, we explored antagonists of cGAS and STING to identify potential therapeutic strategies for COPD that target the cGAS-STING pathway.
The invention relates to the field of ophthalmic treatment medicines, in particular to application of pidotimod in preparing a medicine for treating diabetic retinopathy. The invention has the advantages that: the invention provides application of PG545 in preparing a medicament for treating diabetic retinopathy, and solves the problem that no effective method for treating diabetic retinopathy exists at present. PG545 is injected intraperitoneally, and avoids intraocular complications such as intraocular hypertension and endophthalmitis which may be caused by multiple intravitreal injections. PG545 slows the weight gain and fasting blood glucose levels in diabetic mice. Intraperitoneal injection of PG545 alleviates retinal edema and inflammatory cell infiltration caused by diabetes. Intraperitoneal injection of PG545 reduces levels of proinflammatory factors IL-1 beta and TNF-alpha mRNA and protein in retinal tissue in diabetic mice. In addition, PG545 decreases the permeability of human retinal endothelial cells under high glucose conditions.
Maintaining genomic stability is a prerequisite for proliferating NPCs to ensure genetic fidelity. Though histone arginine methylation has been shown to play important roles in safeguarding genomic stability, the underlying mechanism during brain development is not fully understood. Protein arginine N-methyltransferase 5 (PRMT5) is a type II protein arginine methyltransferase that plays a role in transcriptional regulation. Here, we identify PRMT5 as a key regulator of DNA repair in response to double-strand breaks (DSBs) during NPC proliferation. Prmt5F/F; Emx1-Cre (cKO-Emx1) mice show a distinctive microcephaly phenotype, with partial loss of the dorsal medial cerebral cortex and complete loss of the corpus callosum and hippocampus. This phenotype is resulted from DSBs accumulation in the medial dorsal cortex followed by cell apoptosis. Both RNA sequencing and in vitro DNA repair analyses reveal that PRMT5 is required for DNA homologous recombination (HR) repair. PRMT5 specifically catalyzes H3R2me2s in proliferating NPCs in the developing mouse brain to enhance HR-related gene expression during DNA repair. Finally, overexpression of BRCA1 significantly rescues DSBs accumulation and cell apoptosis in PRMT5-deficient NSCs. Taken together, our results show that PRMT5 maintains genomic stability by regulating histone arginine methylation in proliferating NPCs.