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Presents an algorithm for the production of a graphical diagram from a matrix formula in such a way that its components are logically and hierarchically arranged. The algorithm, which relies on the matrix equations of J. McArdle and R. McDonald (1984), calculates the individual path components of expected covariance between variables and recognizes feedback loops. (SLD)

Study design:Longitudinal.Objective:We identified changes in the association of somatic and non-somatic symptoms (as measured by the Patient Health Questionnaire-9, PHQ-9) between inpatient rehabilitation after spinal cord injury (SCI) and 1 year after discharge.Setting:A specialty hospital in the Southeastern USA.Methods:A total of 584 adults with traumatic SCI were administered the PHQ-9 during inpatient rehabilitation. Of them, 227 completed the PHQ-9 by survey at 1-year follow-up. We performed time-lagged regression between times of measurement for somatic and non-somatic factors of the PHQ-9.Results:The non-somatic factor at baseline was significantly predictive of the non-somatic (r=0.67, P=0.002) and somatic factors at follow-up (r=0.53, P=0.019). The somatic factor did not significantly predict either the somatic (r=0.10, n.s.) or non-somatic factors at follow-up (r=−0.01, NS). Factor analysis also indicated changing factor structure between inpatient rehabilitation and follow-up.Conclusions:Our results question the interpretation of somatic items during inpatient rehabilitation, as they are not predictive of either somatic or non-somatic symptoms at follow-up. [ABSTRACT FROM AUTHOR]

Glucosensing neurons in the ventromedial hypothalamic nucleus (VMN) were studied using visually guided slice-patch recording techniques in brain slices from 14- to 21-day-old male Sprague-Dawley rats. Whole-cell current-clamp recordings were made as extracellular glucose levels were increased (from 2.5 to 5 or 10 mmol/l) or decreased (from 2.5 to 0.1 mmol/l). Using these physiological conditions to define glucosensing neurons, two subtypes of VMN glucosensing neurons were directly responsive to alterations in extracellular glucose levels. Another three subtypes were not directly glucose-sensing themselves, but rather were presynaptically modulated by changes in extracellular glucose. Of the VMN neurons, 14% were directly inhibited by decreases in extracellular glucose (glucose-excited [GE]), and 3% were directly excited by decreases in extracellular glucose (glucose-inhibited [GI]). An additional 14% were presynaptically excited by decreased glucose (PED neurons). The other two subtypes of glucosensing neurons were either presynaptically inhibited (PIR; 11%) or excited (PER; 8%) when extracellular glucose was raised to > 2.5 mmol/l. GE neurons sensed decreased glucose via an ATP-sensitive K(+) (K(ATP)) channel. The inhibitory effect of increased glucose on PIR neurons appears to be mediated by a presynaptic gamma-aminobutyric acid-ergic glucosensing neuron that probably originates outside the VMN. Finally, all types of glucosensing neurons were both fewer in number and showed abnormal responses to glucose in a rodent model of diet-induced obesity and type 2 diabetes. [ABSTRACT FROM AUTHOR]

Hippocampal neurones were freshly isolated from the brain of adult mice and voltage-dependent K+ currents were recorded with the whole-cell patch-clamp technique. Three components of transient K+ current (IA) were isolated when analyzing data with exponential functions or treating neurones with a variety of voltage protocols and pharmacologic agents. Subtraction of the delayed rectifier current ( IK) from the K+ currents elicited after prepulses to –120 mV of varying duration revealed fast (IAf) and slow (IAs) components with decay time constants of 45 ± 8 and 612 ± 140 ms, respectively; the corresponding time constants for the removal of inactivation were 12.3 and 189.6 ms. Both tetraethylammonium and dendrotoxin selectively inhibited IAs. 4-Aminopyridine (4-AP) specifically blocked IAf and 40% of IAs with different affinities. Therefore, the properties of a 4-AP-resistant (IAsR) and a 4-AP-sensitive (IAsS) component of IAs were compared. These data suggest that three distinct subtypes of K+ currents contribute to the IA of mature murine hippocampal neurones. [ABSTRACT FROM AUTHOR]