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Biomedical subjects

B D Johnson

Publications and source records attributed to B D Johnson.

At least 73 records · Page 4Linked to original sources
PubMed1997

Effective group behavioral intervention for older periodontal patients.

A randomized clinical trial assessed the effect of a group-based behavior modification intervention on oral hygiene skills, adherence and clinical outcomes for older periodontal patients. Subjects (n = 107) were aged 50-70 yr with moderate periodontal disease. They were randomly assigned to usual care or intervention. Intervention consisted of 5 weekly, 90-min sessions that included skill training, self-monitoring, weekly feedback about bleeding points and group support focused on long-term habit change. Four-month follow-up indicated significant improvements in the intervention versus the usual periodontal maintenance group for oral hygiene skills and self-reported flossing (p < 0.001), plaque, gingival bleeding, bleeding upon probing throughout the mouth, and pocket depth for sulcus depths that measured between 3 and 6 mm at baseline (p < 0.009). Group oral health intervention provides an effective and relatively inexpensive means of helping patients improve their self-care skills and achieve high levels of adherence to an effective self-care regimen.

Aged↗
PubMed1997

Molecular determinants of drug binding and action on L-type calcium channels.

The crucial role of L-type Ca2+ channels in the initiation of cardiac and smooth muscle contraction has made them major therapeutic targets for the treatment of cardiovascular disease. L-type channels share a common pharmacological profile, including high-affinity voltage- and frequency-dependent block by the phenylalkylamines, the benz(othi)azepines, and the dihydropyridines. These drugs are thought to bind to three separate receptor sites on L-type Ca2+ channels that are allosterically linked. Results from different experimental approaches implicate the IIIS5, IIIS6, and IVS6 transmembrane segments of the alpha 1 subunits of L-type Ca2+ channels in binding of all three classes of drugs. Site-directed mutagenesis has identified single amino acid residues within the IIIS5, IIIS6, and IVS6 transmembrane segments that are required for high-affinity binding of phenylalkylamines and/or dihydropyridines, providing further support for identification of these transmembrane segments as critical elements of the receptor sites for these two classes of drugs. The close proximity of the receptor sites for phenylalkylamines, benz(othi)azepines, and dihydropyridines raises the possibility that individual amino acid residues may be required for high-affinity binding of more than one of these ligands. Therefore, we suggest that phenylalkylamines and dihydropyridines bind to different faces of the IIIS6 and IVS6 transmembrane segments and, in some cases, bind to opposite sides of the side chains of the same amino acid residues. The results support the domain interface model for binding and channel modulation by these three classes of drugs.

Amino Acid Sequence↗
PubMed1996

The sigma subunit of Escherichia coli RNA polymerase senses promoter spacing.

The promoters recognized by sigma 70, the primary sigma of Escherichia coli, consist of two highly conserved hexamers located at -10 and -35 bp from the start point of transcription, separated by a preferred spacing of 17 bp. sigma factors have two distinct DNA binding domains that recognize the two hexamer sequences. However, the component of RNA polymerase recognizing the length of the spacing between hexamers has not been determined. Using an equilibrium DNA binding competition assay, we demonstrate that a polypeptide of sigma 70 carrying both DNA binding domains is very sensitive to promoter spacing, whereas a sigma 70 polypeptide with only one DNA binding domain is not. Furthermore, a mutant sigma, selected for increasing transcription of the minimal lac promoter (18-bp spacer), has an altered response to promoter spacing in vivo and in vitro. Our data support the idea that sigma makes simultaneous, productive contacts at both the -10 and the -35 regions of the promoter and discerns the spacing between these conserved regions.

Base Sequence↗
PubMed1996

Sequential assessment of exercise tolerance in heart transplantation compared with coronary artery bypass surgery after phase II cardiac rehabilitation.

To investigate the improvement in exercise capacity of transplant patients after an early postoperative (phase II) cardiac rehabilitation program during the first year after surgery, we analyzed retrospectively exercise capacity within 3 months (at the completion of phase II rehabilitation) and 1 year after surgery in 17 orthotopic heart transplantation patients (15 men and 2 women) and 17 age- and gender-matched coronary artery bypass graft (CABG) patients. All patients participated in a phase II cardiac rehabilitation exercise program followed by a home-based exercise program. At the completion of phase II cardiac rehabilitation, mean peak oxygen (VO2) adjusted for body weight in heart transplant patients was not significantly different from that in CABG patients (19.7 +/- 3.7 vs 21.9 +/- 4.1 ml/kg/min), and oxygen pulse at peak exercise did not differ between the 2 groups (11.5 +/- 2.5 vs 12.6 +/- 2.4 ml/beat). Between 3 months and 1 year after surgery, CABG patients had a marked increase in exercise time, increase in heart rate from rest to peak exercise (heart rate reserve), peak VO2, and oxygen pulse. In contrast, heart transplant patients had a significant but only modest increase in peak VO2, and were much more limited in exercise capacity at 1 year than were CABG patients (21.3 +/- 3.9 vs 27.4 +/- 4.7 ml/kg/min, p <0.0001). In our limited patient population, usual phase I rehabilitation with subsequent home-based exercise training was inadequate to improve the exercise capacity of heart transplant patients, and different rehabilitation protocols, such as long-term supervised exercise training, specific to this patient group may be indicated.

Blood Pressure↗
PubMed1996

Respiratory muscle fatigue during exercise: implications for performance.

Heavy whole-body exercise, requiring a 10- to 15-fold increase in minute ventilation, encroaches on the capacities of the respiratory muscle system to respond. Recently, using the technique of bilateral phrenic nerve stimulation, it has been shown that heavy endurance exercise (> 85% of VO2max) lasting > 8-10 min causes diaphragmatic fatigue (15-30% reduction in transdiaphragmatic pressures when electrically stimulated at low frequencies [1-20 Hz] supramaximally). The fatigue appears to be due to an interaction of diaphragmatic work (i.e., pressure production) combined with effects related to exercise intensity (i.e., increased blood flow competition with the locomotor muscles and increased production of metabolic by-products) and requires > 60 min for recovery. Fitness (i.e., as implied from VO2max) appears to allow greater diaphragmatic work for a similar degree of fatigue. Unloading the respiratory muscles (with helium/oxygen gas or using a pressure-assist device) during heavy exercise < 90-95% of VO2max does not appear to alter exercise time, VO2max, or minute ventilation, implying that respiratory muscle fatigue plays little role in altering human performance at these work intensities. However, unloading the respiratory system with helium at work intensities > 90-95% of VO2max has been shown to improve exercise time. This would imply that respiratory muscle fatigue may play a role in limiting human performance at the extremes of human performance or that other factors related to the respiratory system (i.e., alterations in the sensation of dyspnea or mechanical load) may play an important role.

Diaphragm↗
PubMed1996

Hypothyroidism alters diaphragm muscle development.

The impact of hypothyroidism (Hyp) on myosin heavy chain (MHC) isoform expression, maximum specific force (P0), fatigability, and maximum unloaded shortening velocity (V0) was determined in the rat diaphragm muscle (Dia) at 0, 7, 14, 21, and 28 days of age. Hyp was induced by treating pregnant rats with 6-n-propyl-2-thiouracil (0.05% in drinking water) beginning at gestational day 10 and was confirmed by reduced plasma levels of 3,5,3'-triiodothyronine and thyroxine. MHC isoforms were separated on sodium dodecyl sulfate-polyacrylamide gel electrophoresis gels and analyzed by densitometry. Isometric P0 and fatigue resistance of the Dia were measured in vitro at 26 degrees C, and V0 was determined at 15 degrees C with the slack test. Compared with control muscles, expression of MHC-slow was higher and expression of adult fast MHC isoforms was lower in Hyp Dia at all ages. The neonatal isoform of MHC continued to be expressed in the Hyp Dia until day 28. At each age, P0 and fatigability were reduced and V0 was slower in the Hyp Dia. We conclude that Hyp-induced alterations in MHC isoform expression do not fully predict the changes in Dia contractile properties.

Aging↗
PubMed1996

Aerobic fitness effects on exercise-induced low-frequency diaphragm fatigue.

We used bilateral phrenic nerve stimulation (BPNS; at 1, 10, and 20 Hz at functional residual capacity) to compare the amount of exercise-induced diaphragm fatigue between two groups of healthy subjects, a high-fit group [maximal O2 consumption (VO2max) = 69.0 +/- 1.8 ml.kg-1.min-1, n = 11] and a fit group (VO2max = 50.4 +/- 1.7 ml.kg-1.min-1, n = 13). Both groups exercised at 88-92% VO2max for about the same duration (15.2 +/- 1.7 and 17.9 +/- 2.6 min for high-fit and fit subjects, respectively, P > 0.05). The supramaximal BPNS test showed a significant reduction (P < 0.01) in the BPNS transdiaphragmatic pressure (Pdi) immediately after exercise of -23.1 +/- 3.1% for the high-fit group and -23.1 +/- 3.8% (P > 0.05) for the fit group. Recovery of the BPNS Pdi took 60 min in both groups. The high-fit group exercised at a higher absolute workload, which resulted in a higher CO2 production (+26%), a greater ventilatory demand (+16%) throughout the exercise, and an increased diaphragm force output (+28%) over the initial 60% of the exercise period. Thereafter, diaphragm force output declined, despite a rising minute ventilation, and it was not different between most of the high-fit and fit subjects. In summary, the high-fit subjects showed diaphragm fatigue as a result of heavy endurance exercise but were also partially protected from excessive fatigue, despite high ventilatory requirements, because their hyperventilatory response to endurance exercise was reduced, their diaphragm was utilized less in providing the total ventilatory response, and possibly their diaphragm aerobic capacity was greater.

Adult↗
PubMed1996

Further increase in oxygen uptake during early active recovery following maximal exercise in chronic heart failure.

STUDY OBJECTIVE: Some patients with chronic heart failure manifest a further increase in oxygen uptake (VO2) after maximal exercise whereas others do not. The purpose of this study was to determine the characteristics of chronic heart failure patients with further increase in VO2 in early active recovery following maximal exercise. DESIGN: Retrospective analysis of clinical and exercise testing characteristics in patients with or without a further increase in VO2 during early active recovery. PATIENTS: One hundred forty-two patients with a history of congestive heart failure and left ventricular ejection fraction of 45%, or less who performed a symptom-limited graded treadmill exercise test. MEASUREMENTS AND RESULTS: Expired gases were monitored breath by breath from rest throughout exercise and during 1 min of active recovery. Patients were defined as having a further increase in VO2 if the average VO2 during the initial 30 s of active recovery was greater than or equal to VO2 during the final 30 s of graded exercise and the instantaneous VO2 (from the breath-by-breath plot) at 30 s of active recovery was greater than or equal to the instantaneous VO2 at peak exercise. Thirty patients (21%) showed a further increase in VO2 following peak exercise (group 1), and 112 had decreased VO2 at 30 s after peak exercise (group 2). In group 1, treadmill time was significantly shorter, peak VO2 was significantly lower (16.6 +/- 3.6 vs 21.6 +/- 6.4 mL/kg/min), and peak ventilatory equivalent for carbon dioxide (VE/VCO2) was significantly higher than those in group 2. There was no difference in etiology of heart failure or functional class and medication status. CONCLUSION: A further increase in VO2 during early active recovery was associated with poorer exercise tolerance, lower peak VO2, and higher peak VE/VCO2 in chronic heart failure patients. This sign may be a new functional variable for assessment of chronic heart failure. Further investigations are warranted to clarify the mechanisms and clinical implications of this phenomenon.

Carbon Dioxide↗
PubMed1996

Short-term responses to periodontal therapy in insulin-dependent diabetic patients.

This investigation studied relative changes in periodontal conditions of 18 insulin-dependent diabetic patients. Measures of gingival inflammation, crevicular fluid aspartate aminotransferase (AST) levels, probing depth and attachment levels, the presence of three periodontal pathogens (Porphyromonas gingivalis, Bacteroides forsythus, and Actinobacillus actinomycetemcomitans) and serum antibody titers to these bacteria, and blood sugar levels (glycosylated hemoglobin, HbAlc) were studied before and 2 months after non-surgical debridement. Antibody titers to the same bacteria were also studied in sera from 18 sex- and age-matched periodontally healthy and non-diabetic subjects. Periodontal conditions showed significant improvement. The mean probing depth at 4 of the worst sites selected in each patient decreased from 5.7 mm to 4.8 mm (p < 0.0001). The mean full width probing depth changed from 2.9 mm (s.d. +/- 0.2) to 2.5 mm (s.d. +/- 0.3). A mean gain of 0.4 mm attachment level was recorded (P < 0.0001). The mean AST value decreased from 1009 microIU to 518 microIU (P < 0.006). Minimal differences in mean glycosylated hemoglobin values (HbAlc) were noticed before and after treatment. A. actinomycetemcomitans was never detected. P. gingivalis was present at 7% of the sites both before and after treatment. B. forsythus was found at 29% of sites (50% of patients) before and at 36% of sites (61% of patients) after treatment. Positive associations were found between the presence of B. forsythus and AST values, gingival index, probing depth, and attachment level (P < 0.05). Baseline serum IgG titers to P. gingivalis were significantly lower in the patients with diabetes (9.5 ELISA units vs. 28.5 ELISA units in the healthy controls). IgG titers to B. forsythus did not differ between diabetic and non-diabetic subjects. No changes in IgG titers occurred after treatment. Clinical improvements after mechanical non-surgical therapy in patients with insulin-dependent diabetes mellitus were modest after 2 months. Treatment did not eliminate B. forsythus and P. gingivalis and did not affect IgG titer responses. More intense therapy, and longer follow-up times, may be necessary to see more pronounced clinical and systemic effects.

Adult↗
PubMed1996

The graft-versus-leukemia effect of post-transplant donor leukocyte infusion.

Tumor relapse remains a major obstacle to the success of allogeneic bone marrow transplantation (BMT) as a treatment for leukemia. Due to limited treatment options, the outlook for most patients that relapse following allogeneic BMT has been poor. The infusion of normal immunocompetent leukocytes from the original marrow donor has become a promising new option for treating/preventing leukemia relapse in allogeneic BMT recipients. This form of treatment has often been referred to as donor leukocyte infusion (DLI) therapy. Our laboratory is using murine models of allogeneic BMT to address important unresolved issues regarding DLI therapy in an effort to make the treatment more effective. These include identification of the antileukemic effector cells, augmentation of the antileukemic effect, and understanding why graft-versus-host-disease (GVHD) is less severe than anticipated. This article reviews our work in murine models of DLI and introduces our current working hypotheses concerning DLI therapy.

Animals↗
PubMed1996

Distinct effects of mutations in transmembrane segment IVS6 on block of L-type calcium channels by structurally similar phenylalkylamines.

The phenylalkylamines (-)-D888, verapamil, and D600, cause voltage- and use-dependent block of L-type Ca2+ channels and differ from each other only in the number of methoxy groups on each of their two terminal phenyl rings. To study the effects of mutations in the phenylalkylamine receptor site on block by these drugs, wild-type and mutant Ca2+ channels were transiently expressed in the tsA-201 clone of human embryonic kidney 293 cells. The combined mutations Y1463A, A1467S, and I1470A (mutant YAI) in transmembrane segment S6 of domain IV of the alpha 1c subunit disrupted block by all three phenylalkylamines. Surprisingly, although this mutation reduced both resting block at -60 mV and depolarized block at +10 mV by (-)-D888, resting and depolarized block by verapamil and D600 were relatively unaffected. In contrast, for all three drugs, use-dependent block during repetitive stimulations was sharply reduced, and the rate of recovery from depolarized block was accelerated for YAI channels. Thus, the effects of the YAI mutation on apparent affinity were specific to (-)-D888, whereas effects on the kinetics of block were observed for all three drugs. Additional experiments with substitution of phenylalanine for Y1463 suggested that (-)-D888 affinity is specifically sensitive to removal of the hydroxyl group of Y1463, whereas effects on the kinetics of block by all three phenylalkylamines require larger molecular changes, perhaps related to residue size and hydrophobicity. Analysis of the data using a state-dependent model of drug block suggests that these kinetic differences are caused by both changes in drug access to the receptor site and affinity for binding to the inactivated state of the channel. The different effects of the YAI mutations on the actions of (-)-D888, verapamil, and D600 indicate that these residues interact differently with these closely related drugs.

Amino Acid Sequence↗
PubMed1995

Molecular determinants of high affinity phenylalkylamine block of L-type calcium channels.

The high affinity phenylalkylamine (-)D888 blocks ion currents through L-type Ca2+ channels containing the alpha 1C subunit with an apparent Kd of 50 nM, but N-type Ca2+ channels in the pheochromocytoma cell line PC12 are blocked with a 100-fold higher Kd value of 5 microM. L-type Ca2+ channels containing alpha 1C subunits with the site-directed mutations Y1463A, A1467S, or I1470A in the putative transmembrane segment S6 in domain IV (IVS6) were 6-12 times less sensitive to block by (-)D888 than control alpha 1C. Ca2+ channels containing paired combinations of these mutations were even less sensitive to block by (-)D888 than the single mutants, and channels containing all three mutations were > 100 times less sensitive to (-)D888 block, similar to N-type Ca2+ channels. In addition, the Y1463A mutant and all combination mutants including the Y1463A mutation had altered ion selectivity, suggesting that Tyr-1463 faces the pore and is involved in ion permeation. Since these three critical amino acid residues are aligned on the same face of the putative IVS6 alpha-helix, we propose that they contribute to a receptor site in the pore that confers a high affinity block of L-type channels by (-)D888.

Amino Acid Sequence↗
PubMed1995

Delayed infusion of immunocompetent donor cells after bone marrow transplantation breaks graft-host tolerance allows for persistent antileukemic reactivity without severe graft-versus-host disease.

The development of graft-host tolerance after bone marrow transplantation (BMT) is crucial to avoid the problems of graft-versus-host disease (GVHD) and graft rejection. GVHD can be eliminated by depleting mature donor T cells from the BM inoculum, thereby facilitating the development of graft-host tolerance. However, T-cell depletion often results in an increased incidence of graft rejection and an increased frequency of leukemia relapse. Thus, although graft-host tolerance is a desirable outcome, it can pose a significant threat to leukemia-bearing hosts. Using a major histocompatability complex (MHC)-matched allogeneic model of BMT (B10.BR into AKR), we found that irradiated recipients given donor BM alone displayed mixed T-cell chimerism and did not develop GVHD. Graft-host tolerance developed by 8 weeks after BMT in these chimeras, and they were susceptible to low-dose leukemia challenge. When sufficient numbers of donor spleen cells, as a source of T-cells, were added to the BM graft, AKR hosts developed severe and lethal GVHD. Antihost reactive donor T cells persisted in chimeras undergoing GVHD, indicating that graft-host tolerance did not develop. When administration of the spleen cells was delayed for 7 to 21 days after BMT, there was significantly less mortality because of GVHD. Day 21 was the optimal time for infusion of cells without development of GVHD. Graft-host tolerance was broken by the delayed infusion of donor cells, as indicated by the persistence of antihost-reactive donor T cells in these chimeras in T-cell receptor cross-linking and mixed lymphocyte reaction assays. Importantly, the persistence of antihost-reactive donor T cells correlated with along-term antileukemic effect that was still present at 100 days after transplant. Multiple infusions of immunocompetent donor cells could be administered without increasing the risk for GVHD if delayed until 21 days post-BMT. Delayed infusions of donor spleen cells also resulted in a long-term antileukemic effect in the absence of GVHD in an MHC-haplotype-mismatched model of BMT (SJL into [SJL x AKR]F1). Although delayed infusion of normal donor cells did not induce GVHD, spleen cells from donors previously sensitized to host alloantigens induced GVHD when infused 21 days after BMT. Thus, the ability of previously activated cells to induce GVHD was not inhibited in the same manner as naive cells. Results from limiting dilution analysis assays indicated that alloactivated interleukin-2-secreting CD4+ T cells were preferentially inhibited over cytolytic T cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

Effect of transition-state analogues on the redox properties of medium-chain acyl-CoA dehydrogenase.

The binding of substrate/product or transition-state intermediates modifies the properties of medium-chain fatty acyl-CoA dehydrogenase (MCAD) by causing the redox potential to shift positive and the oxygen reactivity to slow by 3000-fold. Two ligands, identified as being the most effective in slowing oxygen reactivity, were 2-azaoctanoyl-CoA and 3-thiaoctanoyl-CoA [Wang, R., & Thorpe, C. (1991) Biochemistry 30, 7895-7901]. We have measured the potential shifts caused by the binding of both ligands to determine which is most similar to the potential shift caused by substrate/product mixture, the assumption being that the best transition-state structural intermediate would give the potential shift most similar to that of substrate/product [Lenn, N.D., Stankovich, M.T., & Liu, H. (1990) Biochemistry 29, 10594-10602]. Both ligands shifted the potential positive, but the shift caused by 2-azaoctanoyl-CoA was 65% that of substrate/product, while 3-thiaoctanoyl-CoA was only 20% of that value. This positive shift is proposed to be caused by a resonance form stabilized by the interaction of the catalytically essential carbonyl of the acyl-CoA with two hydrogen bonds from the enzyme, which induces a partial negative charge on the carbonyl and a partial positive charge on carbon 2 of the ligand and carbon 3 of the substrate/product couple. The X-ray structure shows that carbons 2 and 3 of the substrate/product overlap the diazadiene portion of the flavin ring [Kim, J.-J. P., Wang, M., & Paschke, R. (1993) Proc. Natl. Acad. Sci. U.S.A. 90, 7523-7527].(ABSTRACT TRUNCATED AT 250 WORDS)

Acyl-CoA Dehydrogenase↗
PubMed1995

Use of anti-CD3 epsilon F(ab')2 fragments in vivo to modulate graft-versus-host disease without loss of graft-versus-leukemia reactivity after MHC-matched bone marrow transplantation.

The use of T cell-specific mAb in vivo for prevention and treatment of graft-vs-host disease (GVHD) and its impact on graft-vs-leukemia (GVL) reactivity was examined in a murine model of MHC-matched bone marrow transplantation (BMT). F(ab')2 fragments of a CD3 epsilon-specific mAb were administered to irradiated AKR (H-2k) hosts after transplantation of BM plus spleen cells from B10.BR donors (BMS chimeras). The effects on GVH and GVL reactivity were Ab dose- and schedule-dependent. A short course of mAb (qe2d, days 0 to 8) prevented clinical evidence of GVHD and mortality. Anti-CD3 F(ab')2 mAb reversed clinical symptoms of acute GVHD when delayed up to 18 days post-transplant. Anti-host (Mls-1a)-specific V beta 6+ cells were absent from the spleens of GVH-negative control mice, but persisted in Ab-treated BMS chimeras despite the absence of GVHD. Leukemic mice given 16.7 micrograms of Ab on days 0, 2, and 4 survived leukemia-free without developing severe GVHD. A longer course of Ab completely prevented GVHD, but led to leukemia relapse in tumor-bearing hosts, despite engraftment of donor T cells. The GVL effect was quantitatively stronger when Ab was used for GVH therapy as compared with GVH prevention. Some Ab-treated, GVH-free chimeras relapsed with lymphomas in unusual sites, suggesting that occult tumor cells may persist in nonlymphoid tissues. These experiments demonstrate that T cell-specific mAb can be used successfully in vivo to avoid severe GVHD, but that excessive or ill-timed administration of Ab may eliminate GVL reactivity.

Animals↗
PubMed1995

Synaptic connectivity of local circuit neurons in laminae III and IV of hamster spinal cord.

The present study was undertaken to examine the morphological bases of local synaptic interactions between dorsal horn interneurons. Seven interneurons responding to innocuous mechanical stimuli were intracellularly recorded in lamina III/IV of an isolated preparation of hamster spinal cord with partially intact innervation from an excised patch of hairy skin. Axonal arborizations were stained with horseradish peroxidase (HRP) and examined with an electron microscope. Five cells had extensive synaptic terminations (375-1,785 boutons/axon) with localized distributions (rostrocaudal distance, 425-1,251 microns) overlapping the dendritic trees. Two cells gave rise to deep stem axons that bifurcated into rostrocaudal daughter branches with collaterals ventral to the parent cell bodies (79-661 boutons/axon). Axons of local interneurons were thinly myelinated and formed terminal and en passant enlargements (mean [+/- S.D.] diameter = 0.88 +/- 0.24 microns, n = 157) containing clear, round vesicles 20-60 nm in diameter. Collateral branches of deep axon cells produced round, vesicle-containing boutons comparable in diameter (0.93 +/- 0.22 microns, n = 31) to local axon cells. Both types of interneurons formed asymmetric synaptic contacts with dendritic profiles, but not with cell bodies or axon terminals. Postsynaptic profiles contained sparse ribosomes and had a mean diameter of 1.0 +/- 0.5 microns (n = 49), significantly smaller than a population of identified proximal dendrites (2.3 +/- 0.9 microns, n = 47). HRP-labeled boutons were rarely (5/45 or 11%) in synaptic contact with more than one profile. We conclude that lamina III/IV interneurons make axodendritic synapses predominantly with distal dendrites. Thus, terminations of deep dorsal horn interneurons appear to have a postsynaptic distribution overlapping with axodendritic contacts formed by several functional classes of cutaneous sensory fibers signaling innocuous mechanical stimuli. Such overlap suggests that local spinal networks selectively and strongly influence afferent signals at initial stages of somatosensory integration.

Adaptation, Physiological↗
PubMed1995

Evolution of parental stress and coping processes: a framework for critical care practice.

Crisis theory, stress and coping theory, and research on parental stress and coping during pediatric critical care experiences are integrated into a conceptual framework for understanding, assessing, and ultimately intervening to reduce parental stress and bolster coping. Within this framework, cognitive appraisal of stress, coping and person and situation factors are discussed as important determinants of parents' adaptation to this stressful situation. The nurse's ability to respond to the evolving nature of parental stress and coping processes over the course of the experience enhances the use of the framework in designing coping interventions.

Adaptation, Psychological↗