Flexion-relaxation response to gravity

The objective of this report was to study the influence of the orientation of gravitational loading on the behavior of anterior and posterior trunk muscles during anterior trunk flexion-extension. Participants (N=13) performed five (5) cycles of trunk flexion-extension while standing with gravity parallel to the body axis and five (5) cycles while in the supine condition (e.g. sit-ups) with gravity perpendicular to the body axis. Surface electromyographic (EMG) patterns from lumbar paraspinal, rectus abdominis, external oblique, rectus femoris, semimembranosis, and biceps femoris muscles were analyzed during each condition. EMG signals were synchronized with lumbar flexion and trunk inclination angles. Flexion-extension from the standing position resulted in a myoelectric silent period of the lumbar posterior muscles (e.g. flexion-relaxation phenomena (FRP)) as well as the hamstring muscles through deep angles during which activity was observed in abdominal muscles. Flexion-extension during sit-ups, however, resulted in a myoelectric silent period of the abdominal muscles and the quadriceps through deep angles during which the lumbar posterior muscles were active. In this condition, the FRP was not observed in posterior muscles. The new findings demonstrate the profound impact of the orientation of the gravity vector on the FRP, the abdominal muscles reaction to gravitational loads during sit-ups and its relationships with lumbar antagonists and thigh musculature. The new findings suggest that gravitational moments requirements dominate the FRP through the prevailing kinematics, load sharing and reflex activation-inhibition of muscles in various conditions. Lumbar kinematics or fixed sensory motor programs by themselves, however, are not the major contributor to the FRP. The new findings improve our insights into spinal biomechanics as well as understanding and evaluating low back disorders.     

Biochemical response to cadmium

The effect of daily oral administration of ethanol (2.5, 5, or 10% in drinking water for 8 wk), lead (10 mg/kg, po, once daily for 8 wk), or their combination on tissue trace-metal concentration and hematopoietic and hepatic biochemical indices was investigated in male rats. Ethanol (10%) ingestion enhanced the hepatic lipid peroxidation and decreased the calcium and magnesium content of blood and liver. Coexposure to lead and ethanol (5 and 10%) produced a more pronounced elevation of blood zinc protoporphyrin (ZPP) and hepatic lipid peroxidation. Combined lead-ethanol exposure also lowered the concentration of blood and hepatic magnesium and calcium and increased the amount of lead in the blood, liver, and brain compared to a group treated with lead alone. The results suggest that chronic alcohol ingestion results in calcium and magnesium loss. However, coexposure to lead and ethanol could result in more serious depletion of calcium and magnesium, and this could be the cause of suspected synergism between alcohol consumption and lead poisoning.     

A response to Purdy

The authors respond to Laura Purdy's article, "Surrogate mothering: exploitation or empowerment?," in the same issue of Bioethics. They contend that focusing on what is necessarily wrong with surrogate motherhood contracts allows Purdy to overlook the contingent features of classist, patriarchal society that make such contracts morally wrong and to marginalize feminist concerns. Theoretical fallacies within Purdy's consequentialist framework create too individualistic and narrow a discussion of the possible harms of surrogate contracts, ignoring influences upon women as a group and the psychological risks to the surrogate mother. If surrogacy contracts have the potential to empower women, then we must see some specific changes that would make this a reality, given that Purdy does not mean surrogacy as it is currently practised.     

Dihydroceramide-based response to hypoxia

To understand the mechanisms of ceramide-based responses to hypoxia, we performed a mass spectrometry-based survey of ceramide species elicited by a wide range of hypoxic conditions (0.2-5% oxygen). We describe a rapid, time-dependent, marked up-regulation of dihydroceramides (DHCs) in mammalian cells and in the lungs of hypoxic rats. The increase affected all DHC species and was proportional with the depth and duration of hypoxia, ranging from 2- (1 h) to 10-fold (24 h), with complete return to normal after 1 h of reoxygenation at the expense of increased ceramides. We demonstrate that a DHC-based response to hypoxia occurs in a hypoxia-inducible factor-independent fashion and is catalyzed by the DHC desaturase (DEGS) in the de novo ceramide pathway. Both the impact of hypoxia on DHC molecular species and its inhibitory effect on cell proliferation were reproduced by knockdown of DEGS1 or DEGS2 by siRNA during normoxia. Conversely, overexpression of DEGS1 or DEGS2 attenuated the DHC accumulation and increased cell proliferation during hypoxia. Based on the amplitude and kinetics of DHC accumulation, the enzymatic desaturation of DHCs fulfills the criteria of an oxygen sensor across physiological hypoxic conditions, regulating the balance between biologically active components of ceramide metabolism.     

miRNA response to DNA damage

Faithful transmission of genetic material in eukaryotic cells requires not only accurate DNA replication and chromosome distribution but also the ability to sense and repair spontaneous and induced DNA damage. To maintain genomic integrity, cells undergo a DNA damage response using a complex network of signaling pathways composed of coordinate sensors, transducers and effectors in cell cycle arrest, apoptosis and DNA repair. Emerging evidence has suggested that miRNAs play a crucial role in regulation of DNA damage response. In this review, we discuss the recent findings on how miRNAs interact with the canonical DNA damage response and how miRNA expression is regulated after DNA damage.