A reaction route graph analysis of the electrochemical hydrogen oxidation and evolution reactions

The reaction route (RR) graph approach recently developed by us for complex, non-linear kinetic mechanisms is applied to the hydrogen oxidation and evolution reactions. A corresponding RR graph is constructed and translated into an equivalent electrical circuit network by associating each elementary step with a characteristic resistance for the steady-state case and considering the overall reaction as a power source. It is further shown that the steady-state kinetics of the reaction can be investigated employing the conventional methods of the electrical network theory. Using a set of rate constants for the hydrogen evolution reaction (her) in alkaline solutions from the literature, the dominant RRs are identified and simplified mechanisms and kinetics derived.     

Transplantation of microencapsulated bovine chromaffin cells reduces lesion-induced rotational asymmetry in rats

Surrounding bovine chromaffin cells by a semipermeable membrane may protect the transplanted cells from a host immune response and shield them from the inflammatory process resulting from the surgical trauma. Encapsulation of the chromaffin cells was achieved by inter-facial adsorption of a polycation on a polyanionic colloid matrix in which the chromaffin cells were entrapped. Basal and potassium-evoked release of catecholamines from encapsulated bovine chromaffin cells was analyzed over a 4-week period in vitro. Norepinephrine and dopamine release remained constant over time whereas epinephrine release significantly decreased. The chromaffin cells also retained the capacity for depolarization-elicited catecholamine release 4 weeks following the encapsulation procedure. Morphological analysis revealed the presence of intact chromaffin cells with well-preserved secretory granules. Striatial implantation of chromaffin cell-loaded capsules significantly reduced apomorphine-induced rotation compared to empty polymer capsules in animals lesioned with 6-hydroxydopamne frr at least 4 weeks. Intact chromaffin cells expressing tyrosine hydroxylase and dopamine-β-hydroxylase were observed in all capsules implanted in the striatum for 4 weeks. The assessment of the clinical potential of transplanting encapsulated adrenal chromaffin cells of either allo- or xenogeneic origin for Parkinson's disease will require long-term behavioral studies. The present study suggests, however, that the polymer encapsulation procedure may offer an alternative to adrenal autografts as a source of dopaminergic tissue.     

Toward a more viable model of grieving and consequences for older persons

Most theories of grieving derive from Sigmund Freud and Erich Lindemann's understanding of mourning and include two assumptions: (a) Grieving is time limited; the process should be completed or resolved after a year or two; and (b) The main task of grieving is to achieve “decathexis.” One should detach oneself from emotional ties to the deceased so as to be able to form new relationships. This study presents evidence that these assumptions are flawed and that modern theories of grieving fall short of explaining the complicated reality of the mourning process. An alternative model is presented arguing that when a “high-grief” death occurs, a griever may be able to adapt and adjust to loss, but the grieving continues indefinitely. Implications of this model for older grievers are explored.     

UVA solarium versus UVB phototherapy of atopic dermatitis: a paired-comparison study

In a paired-comparison study, 21 patients suffering from atopic dermatitis were treated with fluorescent tubes radiating mainly ultraviolet A (UVA) on one half of the body and with tubes radiating mainly UVB on the other. Treatment was given three times a week for up to 8 weeks. Eight variables reflecting disease status were recorded and the sum of these comprised the total score. The total score and the overall evaluation score were better with UVA therapy (P less than 0.02 and P = 0.01, respectively). No statistically significant difference for the pruritus score was found. The reduction in extent of dermatitis, seen with both therapies, was more pronounced with UVA (P less than 0.05). Differences in the healing score were not statistically significant. Treatment with UVA resulted in healing or considerable improvement in 15 patients and 13 patients showed improvement when treated with UVB. A better result was found with UVA in 10 subjects and with UVB in two subjects. Equal results occurred with both UVA and UVB in nine of the patients although most preferred UVA treatment.     

Steroids in Duchenne muscular dystrophy--deflazacort trial

We conducted a double blind controlled trial in 28 Duchenne muscular dystrophy (DMD) patients with Deflazacort (DF), an oxazoline derivative of prednisolone which reduces its side-effects. Myometric muscle strength measurements, Scott Score and timed tests showed statistically significant improvement for the treated group (P less than 0.05). Side-effects after 9 months of treatment included mild cushingoid appearance in four patients (28%) and moderate in only one (7%), increased appetite in seven (50%), increased body hair in four (28%), irritability and hyperactivity in three (21%). Increased body weight was not prominent and was controlled with dietary measures. No patient had to be withdrawn from medication. More research and long-term follow-up are needed in order to establish the mechanism of improvement and the consequences of long-term steroid administration in DMD. In this regard DF appears as an alternative to prednisone preserving its benefits but with fewer side-effects.     

Possible mechanisms of morphine analgesia.

The body has an endogenous analgesic system that prevents excess pain from interfering with the normal body functions. Depression of pain sensations occurs within the dorsal horn of the spinal cord where the primary pain fibers, which transmit pain sensations from the periphery, synapse with neurons that transmit pain to the higher centers. There appear to be two mechanisms by which the transmission of pain sensations are depressed; these include hyperpolarization of interneurons within the dorsal cord and depressing the release of the neurotransmitters associated with pain transmission. Activation of the analgesic mechanisms results from an interaction between specific neurotransmitters, such as enkephalin, serotonin, or norepinephrine, and specific receptors located on the neurons that transmit pain. The spinal analgesic mechanisms can be activated by either pain or nonpainful sensations arriving from the periphery or by supraspinal mechanisms. The supraspinal mechanisms originate in specific structures within the brainstem that include the periaqueductal gray matter, locus ceruleus, and nuclei in the medulla. These systems are activated either by ascending pain impulses or by higher centers such as the cortex or hypothalamus that, in turn, activate the spinal analgesic systems. There are three systems associated with activation of the supraspinal mechanisms. These include the opioid system associated with the release of the endorphins, the adrenergic system associated with the release of norepinephrine, and the serotonergic system associated with the release of serotonin. The interaction between these systems activates the spinal analgesic system. When the endogenous analgesic systems fail to control pain, analgesic drugs can be used to enhance the endogenous systems. Opiate drugs, such as morphine, interact with opioid receptors and produce analgesia by the same mechanisms as enkephalin, i.e., hyperpolarization of interneurons and depressing the release of transmitters associated with transmission of pain. In addition, morphine can interact with opioid receptors located in the supraspinal structures and activate the supraspinal system. Adrenergic drugs that interact with specific receptors also produce analgesia and it has been suggested that morphine interacts with the adrenergic system to produce analgesia.     

Basicranial diastematomyelia: a case report

Diastematomyelia is a congenital dysraphism of the spinal cord in which the affected segment is longitudinally divided by a band of fibrous tissue, cartilage, or bone. Diastematomyelia has been well described in the cervical, thoracic, lumbar, and sacral spinal cord; this paper presents a case involving the basicranium. Based on the early embryologic development of the basicranium and brain, this case demonstrates that the same mechanisms proposed as the origin of spinal diastematomyelia may also operate at a more cephalad level.