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At present, there is no specific effective drug to prevent and treat Zika virus disease effectually. After receiving symptomatic treatment and antiviral treatments including Xiyanping injection, the patient's symptoms were relieved. Zika virus nucleic acid in blood and urine was negative. The patient was discharged. Combination of traditional Chinese medicine and Western medicine maybe a good method to prevent and treat Zika virus disease.
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Ibuprofen clearance values were 4.04 L/h (95% confidence interval [CI], 3.61-4.47 L/h), 2.79 L/h (95% CI, 2.07-3.52 L/h), and 0.40 L/h (95% CI, 0.37-0.43 L/h) for carriers of CYP2C8 genotypes *1/*1, *1/*3, and *3/*3, respectively, and 4.43 L/h (95% CI, 3.94-4.92 L/h), 3.26 L/h (95% CI, 2.53-3.99 L/h), 2.91 L/h (95% CI, 1.52-4.30 L/h), 2.05 L/h (95% CI, 0-6.37 L/h), 1.83 L/h (95% CI, 1.24-2.41 L/h), and 1.13 L/h (95% CI, 0.58-1.66 L/h) for carriers of the CYP2C9 genotypes *1/*1, *1/*2, *1/*3, *2/*2, *2/*3, and *3/*3, respectively. The P values for comparison across nonmutated, heterozygous, and homozygous genotypes were as follows: P <.001 for CYP2C8*3, P <.005 for CYP2C9*2, and P <.001 for CYP2C9*3. The main genetic factor for reduced clearance of R-(-)-ibuprofen is the CYP2C8*3 allele, whereas the clearance for S-(+)-ibuprofen is influenced by CYP2C8*3 and CYP2C9*3 alleles to a similar extent. The CYP2C9*2 allele was associated with low clearance only when it was present in combination with the CYP2C8*3 allele. As compared with individuals with no mutations, individuals with the common genotype CYP2C8*1/*3 plus CYP2C9*1/*2 (19% of the population) displayed decreased ibuprofen clearance (mean, 65% [95% CI, 42%-89%]; P <.001). Individuals homozygous or double-heterozygous for CYP2C8*3 and CYP2C9*3 variant alleles (8% of the population) had extremely low ibuprofen clearance rates, with values ranging from 7% to 27% of the mean clearance rates among noncarriers of mutations (P <.001). No enantiospecific reduction of ibuprofen clearance was observed.
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Embryo implantation is a critical step in both cows and humans. The use of ibuprofen lysinate to enhance implantation has been investigated in cattle with the specific aim of improving pregnancy rates after embryo transfer. In this study, heifers (n = 100) were assigned randomly to one of two groups: one group was treated i.m. with 5 mg ibuprofen lysinate kg(-1) body weight 1 h before embryo transfer and a control group received vehicle only. A single embryo was transferred into each recipient cow. There was a significant difference in the number of pregnancies after embryo transfer between cows in the treated (41 of 50; 82%) and control (28 of 50; 56%) groups (P < 0.05). These data indicate that ibuprofen lysinate may be an effective adjunctive treatment for assisted reproduction in cattle. Further studies are needed to clarify whether this effect is associated with the reduction of cyclooxygenase enzyme isoforms during embryo transfer or whether other mechanisms are involved.
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The list of all drugs purchased by the Health Ministry of Guatemala in 2004 was quantitatively and qualitatively analyzed both according to the number of units and value. All NSAIDs bought during that period were analyzed in order to find potential intervention areas which could be addressed to improve drug selection.
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The analgesic efficacy of a single dose of ketorolac or ibuprofen given preoperatively was assessed in healthy outpatients undergoing general anesthesia for laparoscopic tubal ligation. Fifty patients were randomized to receive either ketorolac 60 mg intravenously (i.v.), ibuprofen 800 mg orally, or placebo in a double-blind manner. Anesthesia was induced with fentanyl 2 micrograms/kg, thiopental 5 mg/kg, and either vecuronium 0.1 mg/kg or succinylcholine 1.5 mg/kg i.v. and was maintained with nitrous oxide 67% in oxygen and isoflurane. Patients were assessed at 15-min intervals in the postanesthesia care unit (PACU) and treated for pain with i.v. morphine by protocol. Patients were evaluated for pain, analgesic requirements, side effects, and recovery times. After discharge, patients completed questionnaires to assess pain, analgesic use, and side effects 6 and 24 h postoperatively. Parenteral morphine was required in 80% of patients in the control group, and 73% of patients in both treatment groups, and the difference was not statistically significant. The dose of parenteral morphine required in the PACU was not different between the control (7 +/- 1.2 mg), ibuprofen (5.7 +/- 1.4 mg), and ketorolac (6.1 +/- 1.4 mg) groups. There was no difference between groups in terms of pain visual analog scale (VAS) scores, fatigue VAS scores, recovery times, or the incidence of postoperative nausea and vomiting. The preoperative administration of either parenteral ketorolac or oral ibuprofen did not decrease postoperative pain or side effects when compared to placebo in this outpatient population.
In the absence of evidence of efficacy for oral aceclofenac in acute postoperative pain (at least at 150 mg single dose), its use in this indication is not justified. Because trials clearly demonstrating analgesic efficacy in the most basic of acute pain studies are lacking, use in other indications should be evaluated carefully. Given the large number of effective drugs available in this and similar classes of analgesics, there is no urgent research agenda required to demonstrate the effective dose of aceclofenac in acute postoperative pain.
Incidence of GI events and number of patients at specific time points were extracted.
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Sodium salts are often used in drug formulation but their partial solubility parameters are not available. Sodium alters the physical properties of the drug and the knowledge of these parameters would help to predict adhesion properties that cannot be estimated using the solubility parameters of the parent acid. This work tests the applicability of the modified extended Hansen method to determine partial solubility parameters of sodium salts of acidic drugs containing a single hydrogen bonding group (ibuprofen, sodium ibuprofen, benzoic acid and sodium benzoate). The method uses a regression analysis of the logarithm of the experimental mole fraction solubility of the drug against the partial solubility parameters of the solvents, using models with three and four parameters. The solubility of the drugs was determined in a set of solvents representative of several chemical classes, ranging from low to high solubility parameter values. The best results were obtained with the four parameter model for the acidic drugs and with the three parameter model for the sodium derivatives. The four parameter model includes both a Lewis-acid and a Lewis-base term. Since the Lewis acid properties of the sodium derivatives are blocked by sodium, the three parameter model is recommended for these kind of compounds. Comparison of the parameters obtained shows that sodium greatly changes the polar parameters whereas the dispersion parameter is not much affected. Consequently the total solubility parameters of the salts are larger than for the parent acids in good agreement with the larger hydrophilicity expected from the introduction of sodium. The results indicate that the modified extended Hansen method can be applied to determine the partial solubility parameters of acidic drugs and their sodium salts.
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In order to reduce the ulcerogenic effect of ibuprofen, its carboxylic group has been converted into 5-membered heterocyclic rings. Various 1,3,4-oxadiazoles (3-8, 16-21), 1,2,4-triazoles (22-27), 1,3,4-thiadiazoles (28-30), and 1,2,4-triazine (9) derivatives of ibuprofen were prepared by cyclization of 2-(4-i-butylphenyl) propionic acid hydrazide (2) and N1-[2-(4-i-butylphenyl)-propionyl]-N4-alkyl/aryl-thiosemicarbazides (10-15) under various reaction conditions. The cyclized derivatives were screened for their anti-inflammatory activity by the carrageenan induced rat paw edema method and showed 50 to 86% inhibition, whereas the standard drug ibuprofen showed 92% inhibition at the same oral dose. Five compounds, 7, 16, 18, 22 and 30 that showed more than 80% anti-inflammatory activity were selected to study their analgesic, ulcerogenic and lipid peroxidation activities. All the tested compounds showed a significant reduction in ulcerogenic activity compared to ibuprofen through the severity index 0.5 to 0.8, vs. ibuprofen 1.8. The compounds, that showed less ulcerogenic effect also produced less malondialdehyde content in gastric mucosa, which is one of the end products of lipid peroxidation. The results of biological studies showed that oxadiazole derivative 16 as the lead molecule with maximum anti-inflammatory, analgesic and minimum ulcerogenic and lipid peroxidation activities.
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Proinflammatory cytokines, altered connective tissue metabolism, and overexpression of matrix metalloproteinases (MMPs) such as stromelysin compared to tissue inhibitors of metalloproteinases (TIMPs) result in synovial inflammation and erosion of arthritic cartilage. Tumor necrosis factor alpha (TNF-alpha) is a major synovial inflammatory mediator responsible for inhibiting extracellular matrix (ECM) synthesis and stimulating degradation of cartilage ECM by activated MMPs in arthritic joints. To suppress these effects and to gain insight into the mechanism of TNF-alpha action, we identified the inhibitors of TNF-alpha stimulation of stromelysin gene expression. In bovine synovial fibroblasts, TNF-alpha did not affect a recently identified inhibitor, TIMP-3, but induced stromelysin mRNA expression in a dose- and time-dependent fashion (3- to 5-fold) which required de novo protein synthesis. Stimulation by TNF-alpha was potently inhibited (99-100%) by the synthetic glucocorticoid, dexamethasone. Sodium salicylate dose-dependently inhibited (100%) the TNF-alpha action. Indomethacin and ibuprofen were partially inhibitory. Free radical scavenger antioxidant, N-acetylcysteine (but not other antioxidants) also suppressed the TNF-alpha induction (36-100%) of stromelysin suggesting involvement of reactive oxygen species in the induction process. TNF-alpha induction of stromelysin gene expression can therefore be inhibited at the gene expression level by several pharmacological agents which are likely to function via arachidonic acid metabolites, free radical scavenging or interference with the activator protein 1, polyoma virus enhancer A-binding protein 3, and nuclear factor kappaB classes of transcription factors. Our results may help to elucidate the mechanism of TNF-alpha action and explain the beneficial role of these agents in the treatment of inflammatory diseases.
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Inflammatory pain impacts adversely on the quality of life of patients, often resulting in motor disabilities. Therefore, we studied the effect of peripheral inflammation induced by intraplantar administration of complete Freund's adjuvant (CFA) in mice on a particular form of voluntary locomotion, wheel running, as an index of mobility impairment produced by pain. The distance traveled over 1 hour of free access to activity wheels decreased significantly in response to hind paw inflammation, peaking 24 hours after CFA administration. Recovery of voluntary wheel running by day 3 correlated with the ability to support weight on the inflamed limb. Inflammation-induced mechanical hypersensitivity, measured with von Frey hairs, lasted considerably longer than the impaired voluntary wheel running and is not driving; therefore, the change in voluntary behavior. The CFA-induced decrease in voluntary wheel running was dose-dependently reversed by subcutaneous administration of antiinflammatory and analgesic drugs, including naproxen (10-80 mg/kg), ibuprofen (2.5-20mg/kg), diclofenac (1.25-10mg/kg), celecoxib (2.5-20mg/kg), prednisolone (0.62-5mg/kg), and morphine (0.06-0.5mg/kg), all at much lower doses than reported in most rodent models. Furthermore, the doses that induced recovery in voluntary wheel running did not reduce CFA-induced mechanical allodynia, indicating a greater sensitivity of the former as a surrogate measure of inflammatory pain. We conclude that monitoring changes in voluntary wheel running in mice during peripheral inflammation is a simple, observer-independent objective measure of functional changes produced by inflammation, likely more aligned to the global level of pain than reflexive measures, and much more sensitive to analgesic drug effects.
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Despite their high effectiveness, progestin-only contraceptives are considered less than ideal by the many women who experience disruption of their normal vaginal bleeding pattern when using these methods. Current treatments to control these bleeding irregularities are not sufficiently effective.
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Compared with controls, P-I 400 mg/kg/day inhibited the growth of MDA-MB231 xenografts by 266%, while the growth of MCF-7 xenografts was inhibited 51% byP-I 300 mg/kg/day and 181% by Lipo-P-I 300 mg/kg/day. In both cell lines, P-I induced oxidative stress and suppressed the thioredoxin system (oxidized Trx-1 and decreased its expression; inhibited thioredoxin reductase activity). These changes triggered downstream redox signaling: the activity of NF-κB was suppressed and the Trx-1-ASK1 complex was dissociated, activating the p38 and JNK mitogen-activated protein kinase cascades. Trx-1 knockdown abrogated the anti-cancer effect of P-I in vitro and in vivo.
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Infants treated for hsPDA showed significant higher levels of urinary NT-proBNP and UNBCR on postnatal day 14 whereas similar results were determined on postnatal day 28. Cut-off level of NT-proBNP was 567pg/mL with a sensitivity of 79% and a specificity of 71%.
In this study, we evaluated the effect of high dose ibuprofen in closure of PDA in term neonates.
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New insights into the biological properties of cyclooxygenase-2 (COX-2) and its response pathway challenge the hypothesis that COX-2 is simply pro-inflammatory and inhibition of COX-2 solely prevents the development of inflammation and ameliorates inflammatory pain. The present study performed a comprehensive analysis of gene/protein expression induced by a selective inhibitor of COX-2, rofecoxib, compared with a non-selective COX inhibitor, ibuprofen, and placebo in a clinical model of acute inflammatory pain (the surgical extraction of impacted third molars) using microarray analysis followed by quantitative RT-PCR verification and Western blotting. Inhibition of COX-2 modulated gene expression related to inflammation and pain, the arachidonic acid pathway, apoptosis/angiogenesis, cell adhesion and signal transduction. Compared to placebo, rofecoxib treatment increased the gene expression of ANXA3 (annexin 3), SOD2 (superoxide dismutase 2), SOCS3 (suppressor of cytokine signaling 3) and IL1RN (IL1 receptor antagonist) which are associated with inhibition of phospholipase A(2) and suppression of cytokine signaling cascades, respectively. Both rofecoxib and ibuprofen treatment increased the gene expression of the pro-inflammatory mediators, IL6 and CCL2 (chemokine C-C motif ligand 2), following tissue injury compared to the placebo treatment. These results indicate a complex role for COX-2 in the inflammatory cascade in addition to the well-characterized COX-dependent pathway, as multiple pathways are also involved in rofecoxib-induced anti-inflammatory and analgesic effects at the gene expression level. These findings may also suggest an alternative hypothesis for the adverse effects attributed to selective inhibition of COX-2.
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The aim of this paper is to design initial salt screening procedures for manufacturing ibuprofen. Salt forms of a pharmaceutical acid racemic (R,S)-(+/-)-ibuprofen and their "developable" synthetic routes were ferreted out simultaneously through the screening of seven bases of sodium hydroxide, potassium hydroxide, L-arginine, L-histidine, L-lysine, diethanolamine, and tris(hydroxymethyl)aminomethane (THAM), and the match with the use of nine organic solvents of methanol, dimethyl sulfoxide, ethanol, N, N-dimethylformamide, acetonitrile, isopropyl alcohol, 1,4-dioxane, acetone, and tetrahydrofuran mainly in the presence of water in 20 mL scintillation vials. Racemic (R,S)-(+/-)-sodium ibuprofen dihydrate, a well-known ibuprofen salt and the newly discovered racemic (R,S)-(+/-)-THAM ibuprofen, appeared as white-squared powders with a molecular weight of 327.42 g/mol, a melting point of 160.17 degrees C, and the apparent solubility product, K'(sp), of 6.0 x 10(-4) M(2) at 25 degrees C were successfully synthesized by the initial salt screening methods. The new amine salt of ibuprofen was monoclinic and had a space group of P2(1)/c and lattice parameters of a = 17.578(8) degrees, b = 10.428(4) degrees, c = 9.991(4) A, alpha = 90.00 degrees , beta = 97.17(1) degrees, gamma = 90.00 degrees, and V = 1,817.05(244) A(3). The aspect ratio of the amine salt crystals of ibuprofen of approximately 1.0 implied that the crystals had a better flowability than the sodium salt counterparts. This amine salt of ibuprofen was more stable in moist or dried atmospheres and was more hydrophobic than the sodium salt of ibuprofen. Moreover, the slow dissolution of this amine salt of ibuprofen might have made it less bitter and more suitable as a sustained release drug than the sodium salt of ibuprofen. The future work is to search for the different polymorphs of this amine salt of ibuprofen and to extend the initial salt screening working logics to the formation of co-crystals.
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Ocular inflammation was elicited by topical application of sodium arachidonate. Inflammation was quantified according to a modified Draize test. The protein level and the number of polymorphonuclear leukocytes in the aqueous humor were assessed after 2 h from arachidonate instillation. The ibuprofen concentration in the aqueous humor was evaluated by HPLC assay. The physico-chemical properties of nanoparticles were also evaluated.
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We conclude that the net effect of ibuprofen on neutrophils is antiapoptotic, especially in the presence of hypoxia or LPS. This effect may be mediated, in part, by increased production of TNF-alpha by peripheral blood mononuclear cells. These data suggest that treatment of infants with ibuprofen, in the presence of infection and/or tissue hypoperfusion/hypoxia, may contribute to the development of inflammatory diseases.
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For TOTPAR-3, all active treatments were superior to placebo; no statistically significant difference between the three active treatments could be detected. A similar pattern was also observed with regard to TOTPAR-6 (6h evaluation time), > or =50%maxTOTPAR at 3 and 6h, weighted pain intensity difference at 3 and 6h (SPID-3; SPID-6), percentage of patients with complete headache relief at 2h, end of study global evaluation and time to rescue medication. The number-needed-to-treat (NNT) at 6h was 4.5 (2.9-9.2) in the ibuprofen 400mg group, 4.0 (2.8-7.3) in the diclofenac-K 12.5mg group and 3.9 (2.7-7.1) in the diclofenac-K 25mg group. These differences were not statistically significant.
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Ibuprofen caused significantly (P <0.001) greater gastrointestinal blood loss (geometric mean ratio of 5.2, 95% confidence interval [CI]: 4.2 to 6.3) than the 25-mg dose of rofecoxib (2.6, 95% CI: 2.2 to 3.1), the 50-mg dose of rofecoxib (2.6, 95% CI: 2.2 to 3.0), or placebo (2.1, 95% CI: 1.8 to 2.5). In contrast, gastrointestinal blood loss with both doses of rofecoxib were equivalent to placebo by a predetermined clinical similarity bound.
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Over the last years, continuous manufacturing has created significant interest in the pharmaceutical industry. Continuous filtration at low flow rates and high solid loadings poses, however, a significant challenge. A commercially available, continuously operating, dynamic cross-flow filtration device (CFF) is tested and characterized. It is shown that the CFF is a highly suitable technology for continuous filtration. For all tested model active pharmaceutical ingredients, a material-specific strictly linear relationship between feed and permeate rate is identified. Moreover, for each tested substance, a constant concentration factor is reached. A one-parameter model based on a linear equation is suitable to fully describe the CFF filtration performance. This rather unexpected finding and the concentration polarization layer buildup is analyzed and a basic model to describe the observed filtration behavior is developed.
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Ventilator-induced lung injury-(VILI-) induced endothelial permeability is regulated through the Rho-dependent signaling pathway. Ibuprofen inhibits Rho activation in animal models of spinal-cord injury and Alzheimer's disease. The study aims to investigate ibuprofen effects on high tidal volume associated VILI.
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The study cohort included 672 subjects of 1444 potential participants (46% response rate). The mean age of the patients was 7.9 ± 3.6 years. Narcotics were prescribed in 71.9%, and 70.4% were told to use ibuprofen. Children who took ibuprofen alone were significantly younger (P < .001). Pain was significantly less on postoperative days 2 and 3 in the ibuprofen-only group as compared with the groups taking narcotics only (P < .001) and ibuprofen with narcotics (P = .002). Those taking ibuprofen alone returned to normal activity (P < .001) and diet (P = .026) sooner than those taking ibuprofen with narcotics. No difference was seen in pain control on subgroup analysis comparing oxycodone and hydrocodone.
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The total cost of care per patient receiving nabumetone was estimated to be between 25 pounds sterling (Pound) and 41 Pounds more expensive than ibuprofen. In a hypothetical cohort of 100,000 patients, there were between 690 and 821 more major adverse effects using ibuprofen than nabumetone. The cost per life-year gained (LYG) from using nabumetone rather than ibuprofen ranged between 1880 Pounds and 2517 Pounds (1995 values), depending upon the management of adverse effects.
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The anti-pyretic activity of alminoprofen (AP), a non-steroidal anti-inflammatory agent, and its mode of action were investigated in conscious febrile rabbits. A fever was evoked by i.v. injection of lipopolysaccharide (LPS), intracisternal (i.c.) injection of leukocytic pyrogen (LP) or i.c. injection of arachidonic acid (AA). The amount of PGE2 or AP in the cerebrospinal fluid (CSF) after i.v. LPS was estimated using an RIA or HPLC method. AP (3-30 mg/kg, p.o.) dose-dependently inhibited the LPS (0.5 micrograms/kg, i.v.)-induced fever; AP, ibuprofen, indomethacin and pranoprofen had ED50 values of 9.64, 26.45, 4.41 and 11.91 mg/kg, p.o., respectively. PGE2 in the CSF was markedly increased during the elevation of body temperature after i.v. LPS (0.5 microgram/kg). AP (30 mg/kg, p.o.) markedly inhibited the increase in PGE2 that was observed in the CSF during fever developed in response to i.v. LPS (0.5 micrograms/kg). The AP concentration in the CSF 2 hr after AP (30 mg/kg, p.o.) was 2.86 x 10(-6) (1.15-4.57 x 10(-6) M, a concentration too low to inhibit PG synthesis. A dose-dependent fever was observed after i.c. LP (1-8 unit) or AA (10-100 micrograms). AP (30 mg/kg, p.o.) shifted the dose-response curves for the i.c. LP-induced fever to the right, but did not have any effect on the i.c. AA-induced fever. These results suggest that AP has a relatively potent anti-pyretic activity, and its mechanism of action involves competition with LP at a site in the CNS, but does not involve an inhibition of cyclooxygenase at a central site, which has been considered as an anti-pyretic mechanism of nonsteroidal anti-inflammatory drugs.
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PPD was determined from arterial photoplethysmography signals (pulse waves) measured by infrared sensors routinely used for pulse oximetry in 56 premature infants less than 32 weeks gestation. Only infants with significant PDA (sPDA) diagnosed by echocardiography were treated with ibuprofen (for 3 days). Patients were classified according to whether or not they responded (Success/Failure) to this treatment. The Control group was composed of infants in whom ductus had already closed spontaneously at the time of the first echocardiography. The 3 groups were compared in terms of PPD at the beginning (T1) and at the end (T2) of the study. For patients in the Failure (n = 17) and Success groups (n = 18), T1 corresponded to the first day of treatment and T2 to the day after completion of the course of ibuprofen. In the Control group (n = 21), T1 corresponded to 1 to 3 days of life (DOL), and T2 to 4-6 DOL.