anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
A mild glucose-lowering effect first appeared following single oral doses as low as 0.5-0.6 mg in healthy subjects. The time required to reach the maximum effect (i.e., minimum blood glucose level [Tmin]) was about 2 to 3 hours. In noninsulin-dependent (Type 2) diabetes mellitus (NIDDM) patients, both fasting and 2-hour postprandial glucose levels were significantly lower with glimepiride (1, 2, 4, and 8 mg once daily) than with placebo after 14 days of oral dosing. The glucose-lowering effect in all active treatment groups was maintained over 24 hours. 

In larger dose-ranging studies, blood glucose and HbA1c were found to respond in a dose-dependent manner over the range of 1 to 4 mg/day of glimepiride. Some patients, particularly those with higher fasting plasma glucose (FPG) levels, may benefit from doses of glimepiride up to 8 mg once daily. No difference in response was found when glimepiride was administered once or twice daily.

In two 14-week, placebo-controlled studies in 720 subjects, the average net reduction in HbA1c for glimepiride tablets patients treated with 8 mg once daily was 2.0% in absolute units compared with placebo-treated patients. In a long-term, randomized, placebo-controlled study of Type 2 diabetic patients unresponsive to dietary management, glimepiride therapy improved postprandial insulin/C-peptide responses, and 75% of patients achieved and maintained control of blood glucose and HbA1c. Efficacy results were not affected by age, gender, weight, or race.

In long-term extension trials with previously-treated patients, no meaningful deterioration in mean fasting blood glucose (FBG) or HbA1c levels was seen after 2 1/2 years of glimepiride therapy. 

Combination therapy with glimepiride and insulin (70% NPH/30% regular) was compared to placebo/insulin in secondary failure patients whose body weight was >130% of their ideal body weight. Initially, 5-10 units of insulin were administered with the main evening meal and titrated upward weekly to achieve predefined FPG values. Both groups in this double blind study achieved similar reductions in FPG levels but the glimepiride/insulin therapy group used approximately 38% less insulin.

Glimepiride therapy is effective in controlling blood glucose without deleterious changes in the plasma lipoprotein profiles of patients treated for Type 2 diabetes.
SCLC is the most aggressive and deadly subtype of lung cancer. Indeed, despite the novel treatment strategies, patients with ES SCLC still have a dismal prognosis. The most relevant therapeutic progress that occurred in the last decades in the treatment of this disease consists in the combination of immunotherapy (anti PD-L1 monoclonal antibodies) with standard cytotoxic chemotherapy as the first-line treatment. However, in clinical trials that led to the registration of currently used chemoimmunotherapy combination regimens, the addition of immunotherapy to chemotherapy approaches only led to a marginal increase in patient PFS and OS. Therefore, novel therapeutic strategies are needed to increase the efficacy of chemo-immunotherapy approaches. Pre-clinical and translational evidence suggests that patients with ES SCLC receiving anti-PD-1/PD-L1 agents may benefit from the combination of cyclic, short-term calorie restriction to immunotherapy both for reasons related to the metabolic vulnerabilities of SCLC cells (e.g., enhanced glycolysis) and their potential sensitivity to glucose-lowering strategies, and to the potential synergistic antitumor effects resulting from the combination of immunotherapy with cyclic calorie restriction. Based on these data, we design the FASTIMMUNE trial, a single center, open-label, single arm, phase II clinical study with a Simon's two-stage design. The study consists of 2 phases: an induction phase and an experimental maintenance treatment phase. Participants will undergo an experimental maintenance treatment with triweekly cycles of 5-day calorie restriction (on days -2 through 2 of each cycle) in combination with atezolizumab (at a dose of 1200 mg, administered intravenously on day 0 of each cycle) until the occurrence of unacceptable toxic effects, disease progression, consent withdrawal or patient death. Patients interrupting cyclic calorie restriction for any reason other than disease progression may continue the maintenance treatment with atezolizumab alone, if clinically indicated.
In controlled clinical trials, edema was reported more frequently in patients treated with pioglitazone tablets than in placebo-treated patients and is dose-related . In postmarketing experience, reports of new onset or worsening edema have been received. [see ] Adverse Reactions (6.1)

Pioglitazone tablets should be used with caution in patients with edema. Because thiazolidinediones, including pioglitazone tablets, can cause fluid retention, which can exacerbate or lead to congestive heart failure, pioglitazone tablets should be used with caution in patients at risk for congestive heart failure. Patients treated with pioglitazone tablets should be monitored for signs and symptoms of congestive heart failure , . [see Boxed Warningand ] Warnings and Precautions (5.1)Patient Counseling Information (17.1)
Nutropin AQ (somatropin) injection, for subcutaneous use is a human growth hormone (hGH) produced by recombinant DNA technology. Nutropin AQ has 191 amino acid residues and a molecular weight of 22,125 daltons. The amino acid sequence of the product is identical to that of pituitary-derived hGH. Nutropin AQ may contain not more than fifteen percent deamidated GH at expiration. The deamidated form of GH has been extensively characterized and has been shown to be safe and fully active.

Nutropin AQ is a sterile liquid intended for subcutaneous administration. The product is nearly isotonic at a concentration of 5 mg of GH per mL and has a pH of approximately 6.0.

Each pen cartridge or NuSpin contain either 5 mg, 10 mg or 20 mg of somatropin formulated in 17.4 mg sodium chloride, 5 mg phenol, 4 mg polysorbate 20, and 10 mM sodium citrate [see How Supplied/Storage and Handling (16)].
PROBLEM TO BE SOLVED: To produce a prescription of therapeutic exercise by only inputting basic data for a patient. SOLUTION: This medical care prescription preparing system comprises a basic data inputting means for inputting basic data for patients; a basic data analyzing means to analyze the basic data for the patient on the basis of calorie calculation; and a prescription preparing means for producing prescription for therapeutic exercise, on the basis of the analysis result. In addition, this system comprises an exercise level adjusting means to make the level of exercise intensity of the patient fluctuate around a standard value for adjustment. Basic data for the patient includes the height, weight, gender and birth date or age of the patient. The basic data also includes at least one data item selected from among blood sugar level, blood pressure value, cholesterol value and neutral fat level of the patient.  In addition, this system has a database registering means for registering the basic data for the patient to a database.
Pro-inflammatory signals generated after intracerebral hemorrhage (ICH) trigger a form of regulated cell death known as pyroptosis in microglia. White matter injury (WMI) refers to the condition where the white matter area of the brain suffers from mechanical, ischemic, metabolic, or inflammatory damage. Although the p2Y purinoceptor 6 (P2Y6R) plays a significant role in the control of inflammatory reactions in central nervous system diseases, its roles in the development of microglial pyroptosis and WMI following ICH remain unclear. In this study, we sought to clarify the role of P2Y6R in microglial pyroptosis and WMI by using an experimental mouse model of ICH. Type IV collagenase was injected into male C57BL/6 mice to induce ICH. Mice were then treated with MRS2578 and LY294002 to inhibit P2Y6R and phosphatidylinositol 3-kinase (PI3K), respectively. Bio-conductivity analysis was performed to examine PI3K/AKT pathway involvement in microglial pyroptosis. Quantitative Real-Time PCR, immunofluorescence staining, and western blot were conducted to examine microglial pyroptosis and WMI following ICH. A modified Garcia test, corner turning test, and forelimb placement test were used to assess neurobehavior. Hematoxylin-eosin staining (HE) was performed to detect cells damage around hematoma. Increases in the expression of P2Y6R, NLRP3, ASC, Caspase-1, and GSDMD were observed after ICH. P2Y6R was only expressed on microglia. MRS2578, a specific inhibitor of P2Y6R, attenuated short-term neurobehavioral deficits, brain edema and hematoma volume while improving both microglial pyroptosis and WMI. These changes were accompanied by decreases in pyroptosis-related proteins and pro-inflammatory cytokines both in vivo and vitro. Bioinformatic analysis revealed an association between the PI3K/AKT pathway and P2Y6R-mediated microglial pyroptosis. The effects of MRS2578 were partially reversed by treatment with LY294002, a specific PI3K inhibitor. P2Y6R inhibition alleviates microglial pyroptosis and WMI and ameliorates neurological deficits through the PI3K/AKT pathway after ICH. Consequently, targeting P2Y6R might be a promising approach for ICH treatment.
Distant metastasis is a prevalent cause of mortality in gastric cancer (GC) patients. Anoikis, a process that induces cell death when cells get detached from the extracellular matrix (ECM), acts as a barrier to tumor metastasis. To survive in the circulatory system and metastasize, tumor cells must acquire anoikis resistance. It is crucial to identify the molecular processes that cause resistance to anoikis in GC since this might lead to the discovery of novel treatment targets and improve the long-term survival of GC patients. In this study, we employed quantitative proteomics to identify growth differentiation factor 15 (GDF15) as a key factor in GC anoikis resistance. We found that GDF15 enhances protective autophagy, thereby promoting anoikis resistance in GC cells. Furthermore, through DNA pull down assay, activating transcription factor 2 (ATF2) was found to be a critical regulator of GDF15 expression, acting as a transcriptional activator of GDF15. Collectively, these discoveries indicate that ATF2 and GDF15 have great potential as target candidates for developing therapeutic strategies to address the metastasis of GC.
<P>PROBLEM TO BE SOLVED: To provide a medical treatment fee automatic charging system which dispenses with a medical fee document.  <P>SOLUTION: A medical institution transmits to an examination mechanism an electronic chart prepared in accordance with operations of a doctor as it is (S104 to S106). The examination mechanism extracts the benefit for medical treatment from the electronic chart (S205) and attaches a medical treatment fee mark to the benefit (S206). The examination mechanism determines whether the extracted benefit for the medical treatment is doubtful (S207), transmits to the medical institution a medical treatment fee mark with a doubt when the benefit is doubtful (S208) and transmits to the medical institution only the medical treatment fee mark when the benefit has no doubts (S209). The examination mechanism prepares a medical examination cost invoice on the basis of the given medical treatment fee mark and transmits the medical examination cost invoice to an insurer.  <P>COPYRIGHT: (C)2004,JPO
UNLABELLED: Intratumoral hypoxia correlates with metastasis and poor survival in patients with sarcoma. Using an impedance sensing assay and a zebrafish intravital microinjection model, we demonstrated here that the hypoxia-inducible collagen-modifying enzyme lysyl hydroxylase PLOD2 and its substrate collagen type VI (COLVI) weaken the lung endothelial barrier and promote transendothelial migration. Mechanistically, hypoxia-induced PLOD2 in sarcoma cells modified COLVI, which was then secreted into the vasculature. Upon reaching the apical surface of lung endothelial cells, modified COLVI from tumor cells activated integrin β1 (ITGβ1). Furthermore, activated ITGβ1 colocalized with Kindlin2, initiating their interaction with F-actin and prompting its polymerization. Polymerized F-actin disrupted endothelial adherens junctions and induced barrier dysfunction. Consistently, modified and secreted COLVI was required for the late stages of lung metastasis in vivo. Analysis of patient gene expression and survival data from The Cancer Genome Atlas (TCGA) revealed an association between the expression of both PLOD2 and COLVI and patient survival. Furthermore, high levels of COLVI were detected in surgically resected sarcoma metastases from patient lungs and in the blood of tumor-bearing mice. Together, these data identify a mechanism of sarcoma lung metastasis, revealing opportunities for therapeutic intervention.
SIGNIFICANCE: Collagen type VI modified by hypoxia-induced PLOD2 is secreted by sarcoma cells and binds to integrin β1 on endothelial cells to induce barrier dysfunction, which promotes sarcoma vascular dissemination and metastasis.
Experimental: Nivolumab Nivolumab 40 mg IV over 60 minutes on day 1. Treatment repeats every 14 days for up to 24 courses in the absence of disease progression or unacceptable toxicity.
10.1 Symptoms

Acute overdose of codeine is characterized by respiratory depression (a decrease in respiratory rate and/or tidal volume, Cheyne-Stokes respiration, cyanosis), extreme somnolence progressing to stupor or coma, miosis (mydriasis may occur in terminal narcosis or severe hypoxia), skeletal muscle flaccidity, cold and clammy skin, and sometimes bradycardia and hypotension. In severe overdosage, apnea, circulatory collapse, cardiac arrest, and death may occur.

Codeine sulfate may cause miosis, even in total darkness. Pinpoint pupils are a sign of opioid overdose but are not pathognomonic (e.g., pontine lesions of hemorrhagic or ischemic origin may produce similar findings). Marked mydriasis rather than miosis may be seen with hypoxia in overdose situations.

10.2 Treatment

Primary attention should be given to the re-establishment of adequate respiratory exchange through provision of a patent airway and institution of assisted or controlled ventilation as necessary. Supportive measures (including oxygen and vasopressors) should be employed in the management of circulatory shock and pulmonary edema accompanying overdose as indicated. Cardiac arrest or arrhythmias may require cardiac massage or defibrillation. Induction of emesis is not recommended because of the potential for CNS depression and seizures. Activated charcoal is recommended if the patient is awake and able to protect his/her airway. In persons who are at risk for abrupt onset of seizures or mental status depression, activated charcoal should be administered by medical or paramedical personnel capable of airway management to prevent aspiration in the event of spontaneous emesis. Severe agitation or seizures should be treated with an intravenous benzodiazepine. 

The opioid antagonist naloxone hydrochloride is a specific antidote against respiratory depression resulting from overdosage or unusual sensitivity to opiate agonists, including codeine. Therefore, an appropriate dose of naloxone hydrochloride (see prescribing information for naloxone hydrochloride) should be administered, preferably by the intravenous route, simultaneously with efforts at respiratory resuscitation. Since the duration of action of codeine may exceed that of the antagonist, the patient should be kept under continued surveillance and repeated doses of the antagonist should be administered as needed to maintain adequate respiration. A narcotic antagonist should not be administered in the absence of clinically significant respiratory or cardiovascular depression secondary to codeine sulfate overdose. 

In an individual physically dependent on opioids, administration of the usual dose of the antagonist will precipitate an acute withdrawal syndrome. The severity of the withdrawal symptoms experienced will depend on the degree of physical dependence and the dose of the antagonist administered. Use of an opioid antagonist should be reserved for cases where such treatment is clearly needed. If it is necessary to treat serious respiratory depression in the physically dependent patient, administration of the antagonist should be initiated with care and titrated with smaller than usual doses.
Methods and systems for measuring and using the oxidation-reduction characteristics of a biological sample are provided. The system generally includes a test strip and a readout device. A fluid sample is placed in the test strip, and the test strip is in turn operatively connected to the readout device. The readout device provides a controlled current that is sent across the fluid in the sample chamber. In addition, the readout device identifies an inflection point or transition time at which the voltage between contacts of the test strip is changing at the highest rate. The oxidation-reduction capacity of the sample is taken as the integral of the current profile from the time at which current begins to be supplied to the sample to the identified transition time.
An erosion-controlled active agent release system contains at least one low solubility active agent (I) opt. together with high solubility active agents (II), having delayed release for (I) and, if incorporated, only slightly delayed release for (II) characterised in that the active agents are combined with at least one adjuvant (III) capable of swelling and at least one adjuvant (swelling controller (IV)) having higher affinity to water than the adjuvant (III) and opt. also further conventional  adjuvants. (III) may be e.g. microcrystalline cellulose or starch. (IV) may be, e.g. a cellulose deriv., polyethylene glycol or K2SO4. The compsns. may also contain e.g. fatty acids, metal salts of fatty acids and/or silicones as hydrophobising adjuvants.
AIM: Mitochondrial dysfunction, a characteristic pathological feature of renal Ischemic/reperfusion injury (I/RI), predisposes tubular epithelial cells to maintain an inflammatory microenvironment, however, the exact mechanisms through which mitochondrial dysfunction modulates the induction of tubular injury remains incompletely understood.
METHODS: ESI-QTRAP-MS/MS approach was used to characterize the targeted metabolic profiling of kidney with I/RI. Tubule injury, mitochondrial dysfunction, and fumarate level were evaluated using qPCR, transmission electron microscopy, ELISA, and immunohistochemistry.
RESULTS: We demonstrated that tubule injury occurred at the phase of reperfusion in murine model of I/RI. Meanwhile, enhanced glycolysis and mitochondrial dysfunction were found to be associated with tubule injury. Further, we found that tubular fumarate, which resulted from fumarate hydratase deficiency and released from dysfunctional mitochondria, promoted tubular injury. Mechanistically, fumarate induced tubular injury by causing disturbance of glutathione (GSH) hemostasis. Suppression of GSH with buthionine sulphoximine administration could deteriorate the fumarate inhibition-mediated tubule injury recovery. Reactive oxygen species/NF-κB signaling activation played a vital role in fumarate-mediated tubule injury.
CONCLUSION: Our studies demonstrated that the mitochondrial-derived fumarate promotes tubular epithelial cell injury in renal I/RI. Blockade of fumarate-mediated ROS/NF-κB signaling activation may serve as a novel therapeutic approach to ameliorate hypoxic tubule injury.
Immediately prior to ECT study patients will be administered intravenous ketamine for anesthesia at a dose of 0.5 -1.0 mg/kg given as a bolus dose. Hyperventilation will be administered (20 breaths in 30 seconds) by face mask immediately prior to ECT.
PHASE II STUDY D: Patients with PD-L1 expression \< 50% after 4 cycles of induction chemotherapy with pembrolizumab, receive CIMAvax IM and pembrolizumab IV over 30 minutes. Treatment repeats every 4 weeks for 2 years in the absence of disease progression or unacceptable toxicity.
The present invention provides for aminoaryl oxazolidinone N-oxide compounds of Formula Iwherein the variables are as defined herein. These compounds are exceedingly water soluble which is useful in preparing pharmaceutical formulations of these compounds. They are also rapidly converted back to the parent amines in vivo, making them useful as prodrugs of the parent amines. They are effective against a number of human and veterinary pathogens, including gram-positive aerobic bacteria such as multiply-resistant staphylococci, streptococci and enterococci as well as anaerobic organisms, such as Bacteroides spp. and Clostridia spp. species, and acid-fast organisms such as Mycobacterium tuberculosis, Mycobacterium avium and Mycobacterium spp., and in organisms such as Mycoplasma spp.
The liver cancer resisting gene medicine composition includes antisense fup1 gene and/or small molecular interfering RNA and pharmaceutically acceptable supplementary material. The antisense fup1 gene has the DNA sequence of SEQ ID No. 2 in the sequence list, while the small molecular interfering RNA includes the RNA sequence of SEQ ID No. 3 in the sequence list. The present invention also provides the liver cancer resisting gene medicine screening method to design small molecular interfering RNA based on fup1 encoding area via adopting ambion web site provided RNAi design software. The present invention further provides liver cancer resisting small molecule include RNA sequence of SEQ ID No. 3 in the sequence list. The present invention adopts gene fup1 high expressed in liver cancer cell as medicine target to design the antagonistic molecule to provide powerful measure for the gene treatment of liver cancer and excellent platform for further screening liver cancer resisting gene medicine.
PCT No. PCT/FR95/01213 Sec. 371 Date May 21, 1996 Sec. 102(e) Date May 21, 1996 PCT Filed Sep. 20, 1995 PCT Pub. No. WO96/09281 PCT Pub. Date Mar. 28, 1996Polyiodinated derivatives of formula:   <IMAGE>   in which A is a moiety from an aromatic or aliphatic molecule, Za, Zb, Zc and Zd is Tz-Qz-Vz wherein Tz and Vz are O, COND or NDCO, and D is H or C1 to C6 alkyl or hydroxyalkyl and Qz is C1 to C6 alkylene or hydroxyalkylene or wherein Vz has the above meanings and Qz and/or Tz do not exist, Xa, Xb, Xc and Xd, which are identical or different, have formula    <IMAGE>  II  in which Ar and Ar' are tri- or tetraiodinated phenyl groups carrying one or two amide groups substituted by optionally hydroxylated alkyls and T, Q and V have one of the meanings of the Tz, Qz and Vz, or X have, formula e formula II and the T, Q and V groups have one of the meanings of the Tz, Qz and Vz. Use of these products as contrast agents in X-ray radiology.