Inflammation is associated with skeletal muscle dysfunction and atrophy in patients with chronic obstructive pulmonary disease (COPD). Theophylline has an anti-inflammatory role in COPD. However, the effects of theophylline on inflammation in skeletal muscle in COPD have rarely been reported. The aims of this study were to explore whether theophylline has an anti-inflammatory effect on skeletal muscle in a mouse model of emphysema and to investigate the molecular mechanism underlying this effect. In mice, cigarette smoke (CS) exposure for 28 weeks resulted in atrophy of the gastrocnemius muscle. Histone deacetylase 2 (HDAC2) and nuclear factor-κBp65 (NF-κBp65) mRNA and protein levels were significantly decreased and increased, respectively, in gastrocnemius muscle. This effect was revered by aminophylline. The exposure of murine skeletal muscle C2C12 cells to cigarette smoke extract (CSE) significantly increased IL-8 and TNF-α levels as well as NF-κBp65 mRNA and protein levels and NF-κBp65 activity. This effect was reversed by theophylline. HDAC2 knockdown enhanced the activity of NF-κBp65 and increased IL-8 and TNF-α levels in C2C12 cells. CSE significantly inhibited the interaction of HDAC2 with NF-κBp65 in C2C12 cells. These data suggest that theophylline has an anti-inflammatory effect on skeletal muscle in a mouse model of emphysema by upregulating HDAC2 expression and decreasing NF-κBp65 activation.

Three new isosteroidal alkaloids, frititorines A-C (1-3), were isolated from the bulbs of Fritillaria tortifolia, together with ten known ones (4-13). Their structures were elucidated by extensive spectroscopic analyses, chemical methods, and single-crystal X-ray crystallographic analysis. Compound 1 is the first 5β-cevanine alkaloid with a cis A/B ring junction from the Fritillaria genus. Compound 2 is the first example of glycosylated isosteroidal alkaloid N-oxide. Compound 1 showed significant relaxant effect on Ach-induced tracheal contraction with pA2 and EC50 values equivalent to those of aminophylline.

The present study aims to analyze the risk factors for metabolic bone disease (MBD) of prematurity.A total of 238 preterm infants who were born at <34 weeks of gestation and were hospitalized for at least 6 weeks in the Department of Neonatology, Fujian Maternity and Children Hospital between January 1, 2011 and November 30, 2015 were enrolled in the study. Sixteen preterm infants diagnosed with MBD were selected as the case group, and 32 non-MBD preterm infants were matched 2:1 at admission into the study. The 2 groups were compared to examine the differences in maternal obstetric conditions, conditions during parturition, neonatal conditions, and neonatal diseases and treatments. The risk factors for MBD of prematurity were analyzed using t tests, χ tests, and a logistic regression model.The mean gestational age and birth weight of the case group were significantly lower (P < .05) than those of the control group. Compared with the control group, the case group had a significantly higher ratios of small-for-gestational-age infants, antenatal maternal corticosteroids use, sedative use, ventilator use, aminophylline use, diuretic use, liver function impairment, vitamin D (VitD) supplementation at more than 14 days of age, achievement of total enteral nutrition (TEN) beyond 28 days of age, and feeding intolerance.Logistic regression analysis showed that birth at <30 weeks of gestation, VitD supplementation at >14 days of age, and achievement of TEN beyond 28 days of age were independent risk factors for MBD (P < .05).Level of Evidence: IV.

The latest aminophylline shortage has prompted a need for alternative reversal agents for pharmacological stress testing. Cardiac stress testing is common for diagnosis and prognosis in patients with coronary heart disease. Options for pharmacological stress test agents include adenosine, regadenoson, dipyridamole, and dobutamine, whereas aminophylline is the recommended reversal agent. Adenosine and dobutamine can be used as alternatives to regadenoson and dipyridamole to decrease or eliminate the use of aminophylline. Alternatives to aminophylline include theophylline and caffeine. It is important to efficiently identify alternatives during a drug shortage to maintain optimal patient outcomes.

Objective To investigate the effect of the pre-administration with aminophylline on the occurrence of post-dural puncture headache (PDPH) in women undergoing caesarean section by combined spinal-epidural anaesthesia (CSEA). Methods The study enrolled women undergoing elective caesarean sections with CSEA and randomly allocated them into two groups; for 30 min immediately after the infant was delivered, group A received 250 mg aminophylline intravenously and group B received an equal volume of normal saline. Demographic data, operation time, intraoperative blood loss, intraoperative transfusion volume and the occurrence of PDPH during the first 7 days after the operation were recorded. Side-effects such as hypersensitivity, convulsion and arrhythmia were also recorded in the patients and infants in group A within 24 h after aminophylline administration. Results A total of 120 patients aged 24-38 years (pregnancy range, 38-42 weeks) were randomly allocated into two groups ( n = 60). The incidence of PDPH in group A was significantly lower than group C (two of 59 [3.4%] versus 10 of 58 [17.2%], respectively). There were no related side-effects within 24 h after aminophylline administration in group A. Conclusions Intraoperative intravenous infusion of 250 mg aminophylline reduced the incidence of PDPH after caesarean section under CSEA with no side-effects.

While alveolar liquid clearance (ALC) mediated by the β2-adrenergic receptor (β2-AR) plays an important role in lung edema resolution in certain models of lung injury, in more severe lung injury models, this response might disappear. Indeed, we have shown that in an ischemia-reperfusion-induced lung injury model, β2-agonists do not enhance ALC. The objective of this study was to determine if downregulation of the β2-AR could explain the lack of response to β2-agonists in this lung injury model. In an in vivo canine model of lung transplantation, we observed no change in β2-AR concentration or affinity in the injured transplanted lungs compared to the native lungs. Furthermore, we could not enhance ALC in transplanted lungs with dcAMP + aminophylline, a treatment that bypasses the β2-adrenergic receptor and is known to stimulate ALC in normal lungs. However, transplantation decreased αENaC expression in the lungs by 50%. We conclude that the lack of response to β2-agonists in ischemia-reperfusion-induced lung injury is not associated with significant downregulation of the β2-adrenergic receptors but is attributable to decreased expression of the ENaC channel, which is essential for sodium transport and alveolar liquid clearance in the lung.