anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Body temperature of the patients will be measured in the pre-operative service and in the waiting room. Sociodemographic characteristics form, preoperative, intra and postoperative evaluation forms will be completed. Body temperature, blood pressure, respiratory rate, heart rate and O2 saturation of the patients will be monitored every 15 minutes during the operation and postoperative 2 hours and data will be recorded on the data collection form.
Catecholamine-depleting drugs: Catecholamine-depleting drugs (e.g., reserpine) may have an additive effect when given with beta-blocking agents or monoamine oxidase (MAO) inhibitors. Observe patients treated with metoprolol plus a catecholamine depletor for evidence of hypotension or marked bradycardia, which may produce vertigo, syncope, or postural hypotension. In addition, possibly significant hypertension may theoretically occur up to 14 days following discontinuation of the concomitant administration with an irreversible MAO inhibitor. 

Digitalis glycosides and beta blockers: Both digitalis glycosides and beta blockers slow atrioventricular conduction and decrease heart rate. Concomitant use can increase the risk of bradycardia. Monitor heart rate and PR interval. 

Calcium channel blockers: Concomitant administration of a beta-adrenergic antagonist with a calcium channel blocker may produce an additive reduction in myocardial contractility because of negative chronotropic and inotropic effects. 

CYP2D6 Inhibitors:Potent inhibitors of the CYP2D6 enzyme may increase the plasma concentration of metoprolol which would mimic the pharmacokinetics of CYP2D6 poor metabolizer (see Pharmacokinetics section). Increase in plasma concentrations of metoprolol would decrease the cardioselectivity of metoprolol. Known clinically significant potent inhibitors of CYP2D6 are antidepressants such as fluvoxamine, fluoxetine, paroxetine, sertraline, bupropion, clomipramine, and desipramine; antipsychotics such as chlorpromazine, fluphenazine, haloperidol, and thioridazine; antiarrhythmics such as quinidine or propafenone; antiretrovirals such as ritonavir; antihistamines such as diphenhydramine; antimalarials such as hydroxychloroquine or quinidine; antifungals such as terbinafine. 

Hydralazine: Concomitant administration of hydralazine may inhibit presystemic metabolism of metoprolol leading to increased concentrations of metoprolol. 

Alpha-adrenergic agents: Antihypertensive effect of alpha-adrenergic blockers such as guanethidine, betanidine, reserpine, alpha-methyldopa or clonidine may be potentiated by beta-blockers including metoprolol. Beta- adrenergic blockers may also potentiate the postural hypotensive effect of the first dose of prazosin, probably by preventing reflex tachycardia. On the contrary, beta adrenergic blockers may also potentiate the hypertensive response to withdrawal of clonidine in patients receiving concomitant clonidine and beta-adrenergic blocker. If a patient is treated with clonidine and metoprolol concurrently, and clonidine treatment is to be discontinued, stop metoprolol several days before clonidine is withdrawn. Rebound hypertension that can follow withdrawal of clonidine may be increased in patients receiving concurrent beta-blocker treatment. 

Ergot alkaloid: Concomitant administration with beta-blockers may enhance the vasoconstrictive action of ergot alkaloids. 

Dipyridamole: In general, administration of a beta-blocker should be withheld before dipyridamole testing, with careful monitoring of heart rate following the dipyridamole injection.
No intervention given during the randomized controlled portion of the study (through week 12). After week 12, subjects will receive pegcetacoplan treatment.
BACKGROUND: Along with environmental components, genetic factors play an essential role in the pathophysiology and progression of acute myocardial infarction (AMI). There is limited and conflicting data on the influence of the AGT M235T genetic variant on coronary atherosclerosis and death in AMI patients.
METHODS: We carried out a prospective cohort study among 504 Vietnamese AMI patients selected between January 2020 and May 2021. All patients underwent invasive coronary angiography, had AGT M235T genetic variant genotyped using the polymerase chain reaction method, and were followed up for 12-month all-cause mortality.
RESULTS: The proportions of the MM, MT, and TT genotypes were 0.4%, 20.8%, and 78.8%, respectively. There was no significant difference between the TT genotype and the MM + MT genotype groups regarding the position and number of stenosed coronary artery branches and the Gensini score. The AGT M235T genetic variant did not affect 12-month mortality (hazard ratio of TT vs. MM + MT: 1.185; 95% confidence interval: 0.596-2.354; P = 0.629). Subgroup analyses by age, sex, hypertension, diabetes mellitus, dyslipidemia, obesity, smoking, and angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker therapy also did not reveal an association between the AGT M235T variant and all-cause mortality.
CONCLUSION: In summary, the AGT M235T genetic variant was not found to be associated with coronary atherosclerosis characteristics and 12-month mortality in Vietnamese patients with AMI. Further multicenter studies with larger sample sizes and extended follow-up periods are needed to investigate this issue.
OBJECTIVE: Deep gluteal syndrome is a clinical condition in which discomfort may arise due to the pathoanatomy of the subgluteal space. We conducted an anatomical exploration to categorize the relationship of the piriformis muscle, sciatic nerve (SN), and pudendal nerve (PN) to the ischial spine (IS) and sacrospinous ligament.
METHODS: We analyzed 22 cadavers. The piriformis muscle, SN, and PN were exposed through either a transgluteal approach or a gluteal flap. The relationship of the neural structures to the IS, sacrospinous ligament, and ischial bone as they exit the greater sciatic foramen was observed, and the exit zones were classified as zone A, medial to the IS (entirely on sacrospinous ligament); zone B, on the IS; and zone C, lateral to the IS (entirely on ischial bone).
RESULTS: The SN was observed either in zone B or zone C in all specimens. The PN was found to be in either zone A or zone B in 97.6% of specimens. The most common combinations were SN in zone B and PN in zone A (type I), and SN in zone C and PN in zone B (type II).
CONCLUSIONS: The results from this study show clear anatomical differences in the SN-PN relationship, which may play a role in pain seen in deep gluteal syndrome. Moreover, classification of the SN-IS and PN-IS relationships described in this article will help describe different pathologies affecting the deep gluteal area.
The invention relates to the technical field of medicines, discovers an application of juglone for adjusting immune states of mice and oxidizing reactions, and mainly researches medicinal composition juglone. A chemical name of the juglone is 5-hydroxy-1,4-naphthoquinone and 5-hydroxy-1,4-naphthalene diketone. An English name of the juglone is Juglone, walnuts quinine, 5-hydroxy-1,4-naphthoquinone and 5-hydroxynaphthalene, regianin, Nucin. A molecular formula of the juglone is C10H6O3. A relative molecular weight is 174.15. An immunocompromised model is built through systematic pharmacological tests and by using KM mice and adopting dexamethasone sodium phosphate injecta, a mouse immunostimulation model is built by using sheep red blood cells (SRBC) to induce the mice to produce SRBC immune bodies and cyclophosphamide, a fact that the juglone can recover low immunologic functions to a normal level is proved, the immunostimulation states are improved, self stability of an organism is maintained, and both-way immunoregulation functions are displayed. The juglone displays functions of adjusting organism immune system functions by adjusting oxidative stress reactions in the organism.
Colorectal cancer accounts for approximately 10% of all annually diagnosed cancers and cancer-related deaths worldwide. With progress of developing countries, it is predicted that the incidence of colorectal cancer worldwide will increase to 2.5 million new cases in 2035. The majority of colorectal cancer is thought to arise from precancerous lesions through the adenoma-carcinoma pathway. Detecting and removing of colorectal advanced adenomas can reduce incidence of colorectal cancer. Although colonoscopy is currently considered the most effective method for detecting advanced adenomas, individuals may be reluctant to undergo colonoscopy due to the uncomfortable feeling and the relatively high cost of colonoscopy. Conversely, stool tests are relatively cheap and more readily accepted. Annual fecal immunochemical test (FIT), one of the preferred methods of colorectal cancer screening, is economic and easy to use. However, the existing commercially available qFIT is insufficiently sensitive to the minor hemorrhage of advanced adenomas, and the sensitivity is about only 27% to 47%. To improve diagnostic accuracy in detecting colorectal advanced adenoma, an improved technology of qFIT, which have a higher sensitivity in extremely low concentration of hemoglobin in stool compared with existing commercially available qFIT, is developed. The investigators design this research to prove the diagnostic accuracy of the new qFIT in detecting colorectal advanced adenoma.
Adipose tissue (AT) adapts to overnutrition in a complex process, wherein specialized immune cells remove and replace dysfunctional and stressed adipocytes with new fat cells. Among immune cells recruited to AT, lipid-associated macrophages (LAMs) have emerged as key players in obesity and in diseases involving lipid stress and inflammation. Here, we show that LAMs selectively express transmembrane 4 L six family member 19 (TM4SF19), a lysosomal protein that represses acidification through its interaction with Vacuolar-ATPase. Inactivation of TM4SF19 elevates lysosomal acidification and accelerates the clearance of dying/dead adipocytes in vitro and in vivo. TM4SF19 deletion reduces the LAM accumulation and increases the proportion of restorative macrophages in AT of male mice fed a high-fat diet. Importantly, male mice lacking TM4SF19 adapt to high-fat feeding through adipocyte hyperplasia, rather than hypertrophy. This adaptation significantly improves local and systemic insulin sensitivity, and energy expenditure, offering a potential avenue to combat obesity-related metabolic dysfunction.
Generic febuxostat tablets were listed in China's third-round centralized drug procurement program. However, there are no sufficient data available on the use of febuxostat in a real-world setting. This study aimed to compare the efficacy, safety, and cost of selected generic febuxostat with original febuxostat in primary gout and hyperuricemia. Medical records at 3 tertiary hospitals from January 2014 to February 2022 were retrospectively analyzed. Propensity score matching was used to balance the distribution of baseline characteristics. The proportion of patients achieving target serum uric acid (SUA) levels at 12 weeks, the percent changes from baseline in SUA, adverse drug reactions, and the cost of febuxostat therapy were assessed. A total of 221 patients were recruited and 57 pairs of patients were 1:1 matched in the 2 groups. There was no statistically significant difference in the proportion of patients achieving a target SUA levels below 300 μmol/L, the percent changes of SUA decreased from baseline, and the incidence of adverse drug reactions between the 2 groups (all P > .05). The daily febuxostat cost in the generic group were significantly lower than that in original group (P < .05). Based on the results of this study, the clinical efficacy of selected generic febuxostat is comparable to that of original febuxostat for gout with hyperuricemia. No serious adverse reactions were reported in the 2 groups, and generic febuxostat is more economical than the original febuxostat.
Patients will be advised on split-dose bowel preparation (as per option 1), but will also receive instructions on day before bowel preparation. The instructions will indicate that split-dose bowel preparation is the optimal preparation for cleansing the bowel and for visualizing polyps, but they may choose day before bowel preparation if the split dose preparation is too difficult for them.
PURPOSE:To enable the control of crosslinking rate and prepare a gel with a little change in crosslinking degree with time by using a specific crosslinker in producing the gel mainly comprising polyacrylic acid and/or a salt thereof. CONSTITUTION:In producing a gel mainly comprising polyacrylic acid and/or a salt thereof, an ethylenediaminetetraacetic acid-polyvalent metal complex salt in a dissolved state is used as a crosslinker. The crosslinker is prepd. by adding a small amt. of an aq. soln. of ethylenediaminetetraacetic acid to a dil. aq. soln. of a polyvalent metal salt such as calcium chloride, aluminum chloride, aluminum tartrate, or alum. Pref. contents of polyacrylic acid and/or the salt thereof, the polyvalent metal salt and ethylenediaminetetraacetic acid are 3 to 20, 0.001 to 0.1 and 0.01 to 0.5wt.%, respectively.
In this study, we report a rare case of tick paralysis in a cat induced by Otobius megnini infestation. An 11-month-old female cat was admitted to a private veterinary clinic in Luling Texas, USA presenting with depression, tachycardia, and flaccid paralysis of the entire body. The four recovered ticks were morphologically and molecularly identified as O. megnini nymphs. Following initial tick removal and treatment with 0.1% milbemycin oxime in the ear canal on the first day of hospitalization, and additional tick removal and topical selamectin treatment on the second day of hospitalization the animal gradually improved. The recovery of the cat after tick removal supports the diagnosis of tick toxicosis. While tick antiserum is not available in North America, prevention of tick infestation and tick-induced paralysis can be effectively accomplished using repellent collars and the compliant use of other ectoparasiticide products year-round.
###  Pregnancy Category C.

Animal studies have shown reproductive toxicity in rats and rabbits. Cyclosporine gave no evidence of mutagenic or teratogenic effects in the standard test systems with oral application (rats up to 17 mg/kg and rabbits up to 30 mg/kg per day orally). Cyclosporine Oral Solution, USP has been shown to be embryo- and fetotoxic in rats and rabbits when given in doses 2-5 times the human dose. At toxic doses (rats at 30 mg/kg/day and rabbits at 100 mg/kg/day), Cyclosporine Oral Solution, USP was embryo- and fetotoxic as indicated by increased pre- and postnatal mortality and reduced fetal weight together with related skeletal retardations. In the well-tolerated dose range (rats at up to 17 mg/kg/day and rabbits at up to 30 mg/kg/day), Cyclosporine Oral Solution, USP proved to be without any embryolethal or teratogenic effects.

There are no adequate and well-controlled studies in pregnant women and therefore, cyclosporine should not be used during pregnancy unless the potential benefit to the mother justifies the potential risk to the fetus.

In pregnant transplant recipients who are being treated with immunosuppressants, the risk of premature birth is increased. The following data represent the reported outcomes of 116 pregnancies in women receiving cyclosporine during pregnancy, 90% of whom were transplant patients, and most of whom received cyclosporine throughout the entire gestational period. Since most of the patients were not prospectively identified, the results are likely to be biased toward negative outcomes. The only consistent patterns of abnormality were premature birth (gestational period of 28 to 36 weeks) and low birth weight for gestational age. It is not possible to separate the effects of cyclosporine on these pregnancies from the effects of the other immunosuppressants, the underlying maternal disorders, or other aspects of the transplantation milieu. Sixteen fetal losses occurred. Most of the pregnancies (85 of 100) were complicated by disorders; including, preeclampsia, eclampsia, premature labor, abruptio placentae, oligohydramnios, Rh incompatibility and fetoplacental dysfunction. Preterm delivery occurred in 47%. Seven malformations were reported in 5 viable infants and in 2 cases of fetal loss. Twenty-eight percent of the infants were small for gestational age. Neonatal complications occurred in 27%. In a report of 23 children followed up to 4 years, postnatal development was said to be normal. More information on cyclosporine use in pregnancy, please write to: Apotex Corp., Consumer Affairs, 2400 N. Commerce Parkway, Suite 400, Weston, FL 33326.

A limited number of observations in children exposed to cyclosporine in utero are available, up to an age of approximately 7 years. Renal function and blood pressure in these children were normal.
Risk Summary

The ZOMACTON 5mg diluent contains benzyl alcohol. Because benzyl alcohol is rapidly metabolized by a lactating woman, benzyl alcohol exposure in the breastfed infant is unlikely. However, adverse reactions have occurred in premature neonates and low birth weight infants who received intravenously administered benzyl alcohol-containing drugs [see Warnings and Precautions (5.13) and Use in Specific Populations (8.4)]. If ZOMACTON 5mg is needed during lactation, reconstitute with 0.9% sodium chloride injection, use only one dose per vial, and discard after use or use a ZOMACTON 10 mg benzyl alcohol-free formulation.

There is no information regarding the presence of somatropin in human milk. Limited published data indicate that exogenous somatropin does not increase normal breastmilk concentrations of growth hormone. No adverse effects on the breastfed infant have been reported with somatropin. The developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for ZOMACTON and any potential adverse effects on the breastfed child from ZOMACTON or from the underlying maternal condition.
Participants with CFRD on elexacaftor/tezacaftor/ivacaftor who meet criteria and agree to participation in the study will be placed on metformin 500 mg twice daily on study week 0 after undergoing study procedures through week 14. They will then undergo a two week washout period. For the second half of the study metformin will be resumed and, if tolerated, dose will be increased by 500mg on weeks 17 and 18 to a final dose of 1000 mg twice daily through end of study (week 30).
The origin of breast cancer (BC) has traditionally been a focus of medical research. It is widely acknowledged that BC originates from immortal mammary stem cells and that these stem cells participate in two division modes: symmetric cell division (SCD) and asymmetrical cell division (ACD). Although both of these modes are key to the process of breast development and their imbalance is closely associated with the onset of BC, the molecular mechanisms underlying these phenomena deserve in-depth exploration. In this review, we first outline the molecular mechanisms governing ACD/SCD and analyze the role of ACD/SCD in various stages of breast development. We describe that the changes in telomerase activity, the role of polar proteins, and the stimulation of ovarian hormones subsequently lead to two distinct consequences: breast development or carcinogenesis. Finally, gene mutations, abnormalities in polar proteins, modulation of signal-transduction pathways, and alterations in the microenvironment disrupt the balance of BC stem cell division modes and cause BC. Important regulatory factors such as mammalian Inscuteable mInsc, Numb, Eya1, PKCα, PKCθ, p53, and IL-6 also play significant roles in regulating pathways of ACD/SCD and may constitute key targets for future research on stem cell division, breast development, and tumor therapy.
Days 1 to 7: Patients will receive placebo in divided doses BID for 7 days. Days 8 to 14: Patients will continue to receive placebo in divided doses. Days 15 to 21: Patients will receive continue to receive placebo in divided doses.
INTRODUCTION: There has been an almost 100% increase in referrals to breast cancer diagnostic clinics in the past decade. Breaching of the two-week cancer referral target is now commonplace, potentially delaying diagnoses of breast malignancy in many women. Almost one in five of these referrals are women with mastalgia, not a symptom linked to breast cancer. The objective of the study was the safe introduction of an advanced nurse practitioner-led telephone service for women with mastalgia to improve the service for women and create capacity for those with "red flag" breast symptoms.
METHODS: Referrals to clinic were triaged, women with mastalgia only were directed to a telephone-based assessment clinic and symptoms evaluated using a multidisciplinary created proforma.
RESULTS: Within 23 months, 1,427 women were assessed in the breast pain telephone assessment clinic: 863 (61%) were aged over 40 and 564 (39%) aged under 40. A total of 1,238 underwent telephone assessment. Reassurance and discharge only was needed for 365 (26%). The aetiology of pain was identified as musculoskeletal in 1,104/1,238 (89%) of patients, with only 39/1,238 (3.2%) identified as having true breast pain. Additional symptoms were mentioned by 264 women (18%) during the consultation; all immediately redirected back to a diagnostic clinic. Mammography was undertaken in 609 women (43%). Seven women (0.6%) were diagnosed with a breast malignancy. Patient survey indicated that 93% of patients were satisfied with the care received and 97% said they would recommend the service to a family member or friend.
CONCLUSIONS: Although face-to-face assessments for breast pain remain the standard practice in many breast units, data indicating the safety of a telephone assessment clinic, along with high levels of patient satisfaction, question whether services can be delivered differently.