Osteoarthritis of the Anterior Cruciate Ligament and Medial Tibial Plateau: A Cadaveric Study.

The objective of this study was to analyze morphometric anatomy and damages with aging in cadaveric knee specimens specific to the cruciate ligaments, the articular cartilage of the tibial plateau, and the menisci. Morphometric analyses to cadaveric anatomy of the knee were performed using Image-Pro® software on 3 age populations: <70 years old, 70 to 79 years old, and ≥80 years old. An average thickness of the cruciate ligaments was assessed with 5 circumferential measurements per specimen using nylon thread.

Anatomy of psoas muscle innervation: Cadaveric study.

Hip flexion weakness is relatively common after lateral transpsoas surgery. Persistent weakness may result from injury to the innervation of the psoas major muscles (PMMs); however, anatomical texts have conflicting descriptions of this innervation, and the branching pattern of the nerves within the psoas major, particularly relative to vertebral anatomy, has not been described. The authors dissected human cadavers to describe the branching pattern of nerves supplying the PMMs.

β-Adrenergic receptor signaling increases NAADP and cADPR levels in the heart.

Evidence suggests that β-Adrenergic receptor signaling increases heart rate and force through not just cyclic AMP but also the Ca(2+)-releasing second messengers NAADP (nicotinic acid adenine dinucleotide phosphate) and cADPR (cyclic ADP-ribose). Nevertheless, proof of the physiological relevance of these messengers requires direct measurements of their levels in response to receptor stimulation. Here we report that in intact Langendorff-perfused hearts β-adrenergic stimulation increased both messengers, with NAADP being transient and cADPR being sustained.

NAADP controls cross-talk between distinct Ca2+ stores in the heart.

In cardiac muscle the sarcoplasmic reticulum (SR) plays a key role in the control of contraction, releasing Ca(2+) in response to Ca(2+) influx across the sarcolemma via voltage-gated Ca(2+) channels. Here we report evidence for an additional distinct Ca(2+) store and for actions of nicotinic acid adenine dinucleotide phosphate (NAADP) to mobilize Ca(2+) from this store, leading in turn to enhanced Ca(2+) loading of the SR. Photoreleased NAADP increased Ca(2+) transients accompanying stimulated action potentials in ventricular myocytes.

Fundamental importance of Na+-Ca2+ exchange for the pacemaking mechanism in guinea-pig sino-atrial node.

Na+-Ca2+ exchange (NCX) current has been suggested to play a role in cardiac pacemaking, particularly in association with Ca2+ release from the sarcoplasmic reticulum (SR) that occurs just before the action potential upstroke. The present experiments explore in more detail the contribution of NCX to pacemaking. Na+-Ca2+ exchange current was inhibited by rapid switch to low-Na+ solution (with Li+ replacing Na+) within the time course of a single cardiac cycle to avoid slow secondary effects.