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Previously explored as separate phenomena, this phenomenological-hermeneutic study integrated caring and presence with the experience of caring presence described within the context of a shared nurse practitioner-patient relationship. The results suggest that caring presence is (1) mutual trust and sharing; (2) transcending connectedness; and (3) experience. Research related to caring presence within the nurse practitioner-patient relationship in the context of a managed care outpatient system provides another basis from which to develop nursing knowledge that guides practice within the boundaries of and barriers to care in the technologic world of healthcare. [ABSTRACT FROM AUTHOR]

Interest in presence within a caring relationship has gained renewed attention in the past decade. For five decades, presence has been implicit and explicit in nursing theory. Recognizing caring presence as important to nursing, the 13th Annual Caring Research Conference in 1992 spotlighted the topic. Yet few publications appeared in nursing literature between the years 1980 to 1991. Since that time, interest in and literature about the topic has greatly increased. The elusive nature of the phenomenon, however, makes it difficult to define. This article presents a review of literature of presence and suggests a working definition that could be used as the basis for research. Placing presence within the context of caring provides a way for the holistic nurse to offer caring-healing ways of being and relating. [ABSTRACT FROM AUTHOR]

Previous research has demonstrated antidepressant-like effects in rodents upon intracerebral inhibition of histone deacetylases (HDACs). Such effects have been reported for local HDAC inhibition in the nucleus accumbens, hippocampus, and amygdala. However, the effect of HDAC inhibition within the medial prefrontal cortex, which is integral to depression-related symptoms and their treatment, remains unknown. Here we show that local infusion of the highly selective HDAC inhibitor, MS-275, into the medial prefrontal cortex exerts robust antidepressant-like effects in the chronic social defeat stress paradigm in mice. These findings provide further impetus for the assessment of HDAC inhibitors for the treatment of depression., (Copyright © 2015 IBRO. Published by Elsevier Ltd. All rights reserved.)

Repeated exposure to stress induces cross-sensitization to psychostimulants. The present study assessed functional neural activation during social defeat stress-induced sensitization to a subsequent amphetamine challenge. Social defeat stress was induced in intruder rats during short confrontations with an aggressive resident rat once every third day during the course of 10 days. Rats received d-amphetamine injections (1 mg/kg, i.p.) 17 or 70 days after the first social defeat stress exposure. Amphetamine administration induced a significantly higher frequency of locomotor activity in stressed animals than in handled control rats, which was still evident 2 months after the last social stress exposure. Immunohistochemistry for Fos-like proteins was used to detect activated neural profiles in the striatum, nucleus accumbens (NAc), prefrontal cortex, amygdala, and ventral tegmental area (VTA). Repeated social defeat stress significantly increased Fos-like immunoreactive (Fos-LI) labeling 17 days after the start of stress exposure in the prelimbic and infralimbic cortical regions, NAc shell and core, medial, central and basolateral amygdala, and VTA, which probably represented the expression of chronic Fos-related antigens. Amphetamine augmented stress-induced Fos-LI labeling 17 days after the first stress episode in the dorsal striatum, NAc core, and medial amygdala, reflecting a cross-sensitization of Fos response. Amphetamine challenge 70 days after social stress exposures revealed sensitized Fos-LI labeling in the VTA and the amygdala. These data suggest that episodes of repeated social stress induce a long-lasting neural change that leads to an augmented functional activation in the VTA and amygdala, which might represent a neurobiological substrate for long-lasting cross-sensitization of repeated social defeat stress with psychostimulant drugs.

Rationale: Repeated social stress experiences engender "behavioral sensitization" and may also increase the potential for abuse of psychomotor stimulants, particularly cocaine use during "binges.", Objective: Experimental protocols were designed to induce behavioral sensitization through exposures to social-defeat stress or injections of cocaine or morphine. The impact of stress, cocaine or morphine sensitization on cocaine self-administration was assessed using several protocols., Methods: Behavioral sensitization was induced in male Long-Evans rats by four social-defeat stress episodes, each separated by 72 h. Expression was assessed following a challenge of D-amphetamine (1.0 mg/kg) or cocaine (7.5 mg/kg or 10.0 mg/kg), 10-15 days after the last defeat. Sensitization to cocaine (15.0 mg/kg) or morphine (10.0 mg/kg) was induced via daily administrations for 10 days and later assessed by challenges with cocaine or morphine. Subsequently, i.v. self-administration of cocaine was analyzed for (i) rates of acquisition, (ii) sensitivity to various doses, (iii) "breaking points" during a progressive ratio schedule of cocaine reinforcement, and (iv) patterns of intake during a 24-h binge, in sensitized and control rats., Results: Social-defeat stress, cocaine or morphine administrations increased the locomotor response to stimulant challenges. During 24-h cocaine self-administration binges, sensitization to social-defeat stress or to cocaine prolonged responding, resulting in more cocaine intake. In addition, cocaine sensitization increased the rate of acquisition to cocaine self-administration and the breaking point during a progressive ratio schedule., Conclusion: The process of sensitization to social-defeat stress or cocaine intensifies cocaine intake during a binge, supporting the hypothesis that sensitization may facilitate the transition to compulsive drug taking.

Rationale: Repeated access to cocaine may engender behavioral sensitization, which emerges as an enhanced response to the effects of cocaine. Repeated exposure to prolonged self-administration sessions has been shown to produce an escalation in cocaine intake., Objective: The objective of the present study was to identify the consequence of repeated exposure to prolonged access to self-administered cocaine., Methods: Pairs of rats that were matched for training, housing, and surgery were treated as a single experimental unit, and these pairs were separated into groups for two separate experiments. In the first experiment, one animal of the pair acquired and maintained a stable rate for i.v. cocaine self-administration (0.5 mg/infusion), while the second rat was yoked such that it passively received saline infusions in the same pattern. After acquisition, the active self-administration rats were given free access to cocaine for 16 h (binge), while the yoked animal continued to receive infusions of saline. Twenty-four hours after the binge, both animals were exposed to tactile startle stimuli, and ultrasonic vocalizations (USVs) and startle reflexes were measured. The animals were exposed to three cocaine binges and 24 h post-binge startle tests with an interval of 10 days between binges, and then a fourth binge, with an interval of 24 h separating binges three and four. In the second experiment, pairs of rats were separated into three groups (A, B, and C). The active cocaine rats acquired self-administration and were allowed access to a 16-h cocaine binge while their yoked controls received saline. Twenty-four hours after the binge, all animals were tested for emission of USVs and startle reflexes with an identical protocol as that in experiment 1. Immediately after exposure to the startle stimuli, the self-administering animals were again allowed to self-administer cocaine for either 16 (group A), 12 (group B), or 8 h (group C)., Results: In experiment 1, the total amount of cocaine self-administered was significantly decreased when the cocaine binges were separated by 10 days, but total cocaine intake during the binge significantly increased when the drug-free interval was 24 h. The pattern of self-administration and the withdrawal response remained unchanged over consecutive binges. In experiment 2, rats that self-administered cocaine for either 16 or 12 h emitted significantly less USVs immediately after renewed access than they emitted 24 h after the first access period., Conclusion: It appeared that consecutive prolonged self-administration was insufficient to produce sensitization, as measured by cocaine intake and renewed access to self-administered cocaine was sufficient to reduce the large number of USVs that characterize withdrawal from a cocaine binge.

Many patients with psychiatric disorders struggle with poor skills in coping, communication, socialization, and self-expression that may result in dysfunctional behavioral, cognitive, and emotional responses. Therapeutic music offers a noninvasive approach to strengthen these skills and effect behavior change. At a regional inpatient psychiatric hospital in Colorado, a program of therapeutic music was developed using Rogers' theory of unitary human beings as the theoretical framework. This article describes the approach used to strengthen coping skills in communication, socialization, and self-expression. Suggestions are made for developing a program of music with similar patient populations.

1. Music, a universal language with many purposes, can be used in the health care setting to aid in stress reduction and anxiety. 2. When used in the psychiatric setting, music can elicit emotion and affect behavior change. 3. Nurses in the psychiatric setting can include music in a group session that evokes thoughts, feelings, and memories for the clients.

Elevated intraocular pressure secondary to rhegmatogenous retinal detachment was described by Ariah Schwartz in 1972, an entity commonly known as Schwartz's syndrome. Photoreceptor outer segments identified in the aqueous of patients with this syndrome are thought to play a role in the elevation of the intraocular pressure. We present two patients with open angles and elevated intraocular pressure associated with retinal detachment. Retinal reattachment surgery resulted in normalization of the intraocular pressure. Electron microscopic examination of aqueous specimens from our patients demonstrated a predominance of photoreceptor outer segments in varying stages of degeneration. In these specimens, inflammatory cells, fibrin, and pigment granules were rarely observed or were absent. We review the literature regarding the epidemiology, clinical characteristics, and pathogenesis of Schwartz's syndrome.

Ultrastructural localization of proteoglycans (PGs) in 1-week- to 2-year-old scar was determined by staining with cuprolinic blue dye (CBD) after specific enzymatic digestion of keratan sulfate (KS) glycosaminoglycans (GAGs) or chondroitin sulfate glycosaminoglycans (CSs). High critical electrolyte conditions were maintained for CBD-staining, specific for high-sulfated GAGs. Although KS was detected in the 1-week-old wound, no CBD-stained KS was seen in the anterior stroma adjacent to the wound. The CS was present throughout the 1-week-old wound and adjacent stroma, and PGs were biosynthetically 35SO4-labeled in normal stroma. Subsequently, radioactivity from labeled PGs in normal stroma adjacent to the wound moved into scar tissue during healing. Marked sensitivity of PGs to Chondroitinase ABC indicated an abundance of CS in 2-week-old scars. Punctate CBD-staining and immunohistochemical evidence suggested chemically altered KS is present in the 2-week-old anterior scar. The pattern of CBD-staining in 1- and 2-week scars, after chondroitinase treatment, suggested KS in the younger scar is similar to adult high-sulfated GAG, whereas KS in the 2-week scar contains primarily newly synthesized low-sulfated KS. The latter is consistent with previous immunochemical and biochemical analyses. Cytochemical and immunohistochemical evidence indicated that KS is not present in the 2-week-old posterior scar. By the week 8 of healing, CBD-stained KS was present throughout most of the scar, except along the posterior margin, consistent with earlier stages of healing. The CBD-stained structures in the first 8 weeks of healing were reminiscent of stained GAGs in normal developing cornea. This fetal-like CBD-staining pattern seen in scar, however, changed to that of the normal adult by the 2nd year of healing. The significance of these observations relate to our contention that healing adult cornea recapitulates some ontogenetic events of the normal cornea, and that the nonuniform distribution and chemical properties of GAGs in scar tissue are a function of the movement of existing proteoglycans and de novo synthesis of altered macromolecules.

We have localized type VI collagen in normal developing and corneal scar tissue. Indirect immunofluorescence showed that type VI collagen was distributed throughout the normal stroma and most of the scar. No fluorescence was detected along the posterior margin of the scar and in a retrocorneal membrane continuous with the scar. Since the corneal endothelium in rabbits contributes to the formation of scar tissue and retrocorneal membrane, our observations suggest that the endothelium does not synthesize type VI collagen. Indirect immunoelectron microscopy showed that type VI collagen was located abundantly between collagen fibrils as fine filamentous structures containing beads with a periodicity of 100 nm, consistent with published observations of other tissues. Because these filaments are more prominent when stained with ruthenium red, and predigestion of tissue with Chondroitinase ABC enhances binding of monoclonal antibody to type VI collagen, proteoglycans probably are associated with this collagen in the cornea. Ultrastructural observations supported by previous biochemical analyses show that the proportion of type VI collagen to fibrillar collagen is smaller in scar tissue compared with fetal cornea. The abundance of type VI collagen and its distribution and association with proteoglycans in rabbit corneal tissues suggest that this macromolecule plays a role in the tensile strength and transparency of the stroma.

Corneas of fetal and young albino rabbits were examined by light and transmission electron microscopy. In addition, DNA and hydroxyproline content were measured in developing stroma. The results were compared with similar data from healing corneas in adult rabbits and from developing corneas of other animal species. In the fetal rabbit, the prospective corneal stroma region contains an unorganized, sparse extracellular matrix until about the 13th day of gestation, when mesenchymal cells and capillaries from the hyaloid vessels move in to form the vascular pupillary membrane, endothelium, and stroma. Stromal growth is due to alteration in the density and morphology of the cell population early in development, along with a sequential thickening and thinning of the whole stroma. These events are similar to those reported in primates, but differ markedly from those reported in avian species. Normal developing cornea and healing adult cornea both involve migration of stomal fibroblasts and deposition of extracellular matrix. Stromal fibroblasts in the rabbit fetus are oriented with their long axis parallel to the corneal surface early in development compared with randomly oriented fibroblasts in the early healing wound of adult rabbit corneas. Although collagen and cell number progressively increase throughout the developmental periods studied, the ratio of cells to collagen is high initially but decreases with development. In contrast, the proportion of cells to collagen in the young scar tissue of adult cornea is low initially, indicating a marked deposition of collagen in comparison to that in the early normal developing stroma. The results suggest that the healing tissue differs from the normal fetal stroma in its coordination of cell population growth with collagen deposition and cellular organization.

Twenty biopsy specimens of the human conjunctival epithelial surface with its associated mucus from normal subjects and contact lens wearers with biomicroscopic evidence of excess mucus were studied by scanning electron microscopy. Mucus existed in strands, sheets, and granules; each morphologic type of mucus was observed in all samples. No qualitative difference in morphologic features of mucus was found between normal subjects and those with excess mucus. Mucous forms observed by scanning electron microscopy closely resembled structures previously shown by biomicroscopic and light microscopic techniques, providing evidence that careful scanning electron microscopic preparation of biopsy specimens containing mucus may not greatly alter in situ morphologic characteristics of mucus.

Whole neonate rabbit corneas and adult corneas containing 2-week-old scars were incubated in the presence of [14C] glycine. Radiolabeled collagen extracted from the corneas and scar tissue were analyzed by sodium dodecylsulfate/polyacrylamide gel electrophoresis and fluorography to determine the types and relative quantity of collagen polypeptides present and synthesized by these tissues. In addition to other collagen types, type III was found in both neonate cornea and scar tissue from adult cornea, albeit in relatively small quantities. Type III collagen in normal cornea was associated with the residue after pepsin digestion and formic acid extraction of the tissue, and the same type of collagen was extracted from scar tissue after similar treatment. Type III collagen-specific monoclonal antibody bound to developing normal corneas and healing adult tissue sections, as determined by immunofluorescence. Antibody binding was localized to the endothelium and growing Descemet's membrane in fetal and neonate corneas, and restricted to the most posterior region of the corneal scar tissue. Although monoclonal antibody to keratan sulfate, used as a marker for stromal fibroblasts, bound to most of the scar tissue, the antibody failed to bind to the posterior scar tissue positive for type III collagen. We conclude that endothelial cells from fetal and neonate rabbit cornea and endothelium-derived fibroblasts from healing wounds of adult cornea synthesize and deposit type III collagen. Moreover, this collagen appears to be incorporated into the growing Descemet's membrane of normal corneas and narrow posterior portion of the scar tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

We studied ultrastructurally the development of rabbit corneal endothelium from the 13th day of gestation to 3 days after birth. Precursor corneal endothelial cells, stromal cells, and a vascular network migrate in close association with each other between the developing corneal and lens epithelia. During development, newly deposited extracellular fibrous matrices separate the prospective endothelium from the capillaries and corneal stroma. The extracellular matrix between the apical endothelial surface and the vascular network loses its fibrous appearance early in development. Simultaneously, randomly organized fibrils are deposited on the basal endothelial surface facing the stroma. These fibrils, gradually obscured by the deposition of a nonfibrous component, eventually become part of Descemet's membrane. Early in development, prospective endothelial cells cannot be distinguished morphologically from the overlying corneal stromal cells. Morphologic differentiation of the endothelial cell is characterized by the formation of sinuous lateral borders that interdigitate with those of adjacent cells to form a continuous single-cell layer of tissue. The basal endothelial membrane forms a pitted surface, distinguishing it from the apical cell membrane. Intercellular junctions between lateral membranes, a cilium projecting into the anterior chamber, and deposition of Descemet's membrane on the basal endothelial surface contribute to the polarization of the endothelium. Throughout most of corneal development the vascular pupillary membrane maintains a close association with the apical surface of the differentiating endothelium. We conclude that fetal corneal endothelium develops within a complex extracellular matrix environment and in proximity to the underlying vascular network. These structures play an important role in the morphogenesis of corneal endothelium.

Tissues maintained in vitro often undergo changes in the pattern of protein synthesis that result in the deposition of macromolecules quantitatively or qualitatively unrelated to those normally synthesized. In these preliminary studies, we modified published techniques to maintain adult and neonate rabbit corneas in vitro for 24 to 48 h. Measurements of corneal wet weight, and histologic and ultrastructural analyses were made to determine the success of maintaining rabbit corneas in culture. The results show that rabbit corneas can maintain normal corneal hydration and tissue structure for at least 48 h when incubated in Coon's modification of Ham's F12, 5% fetal or newborn calf serum, 2 mM glutamine, and 2% chondroitin sulfate or 2% 50 kDa dextran sulfate at 37 degrees C in a 5% CO2/air atmosphere. In addition, we confirmed previous observations that corneal explants must have a 1 to 2 mm rim of limbal sclera, and the organ placed in the culture dish with the epithelial side down to guard against damage and insure endothelial functioning. Normal ultrastructure of neonate rabbit cornea is also maintained when organ-cultured with these procedures. Moreover, neonate corneas continue to synthesize collagen in culture.

Fibronectin is believed to be important in tissue morphogenesis. We examined the distribution of fibronectin in developing rabbit cornea by immunohistofluorescence. Cryostat sections of cornea from 13, 15, and 20-day-old fetuses, 3-day neonates, and adults were incubated with affinity-purified fluoresceinated guinea pig anti-rabbit fibronectin antiserum (aFN). aFN bound to components within the presumptive stromal region and along the basal surfaces of corneal and lens epithelia during early stages of mesenchymal invasion. At 15 days of gestation, fluorescence was associated with the stromal extracellular matrix of the cornea, the subepithelial zone, and the lens capsule. In the 20-day fetus an intense aFN fluorescence was present along the inner corneal stromal border coincident with the formation of Descemet's membrane. Fluorescence within the corneal stroma appeared as fine lines, restricted to the collagen lamellae, remaining through birth and disappearing in the adult. Although stromal fluorescence disappeared in the adult, Descemet's membrane continued to fluoresce, albeit to a lesser extent. The results of our studies indicate the presence of fibronectin in developing rabbit cornea. Because fibronectin is important to cell adhesion in vitro, and because intercellular and cell-extracellular matrix interactions, including adhesion, are necessary for tissue morphogenesis, our observation suggests that fibronectin plays an important role in corneal morphogenesis.

Biopsy specimens of the upper tarsal conjunctiva from 11 asymptomatic, biomicroscopically normal contact lens wearers (five hard and six soft) were studied by scanning electron microscopy. The conjunctiva in lens wearers showed areas of normal epithelial cell surfaces interspersed among areas of altered cells. The altered cell surfaces were characterized by centralized clumped microvilli and baring of that portion of plasma membrane around the cell periphery. The degree of centralization of microvilli varied widely, from a mild tendency to centralize accompanied by slight reduction in cell diameter, to an exteme centralization and dramatic diameter reduction. In some cells, the centralized microvillar structure had a unique mucuslike covering. Numerous altered cells were present in all 11 specimens from asymptomatic contact lens wearers. The number of these cells found by conjunctival biopsy of the hard contact lens wearers and the number in the soft contact lens wearers apparently did not differ. The upper tarsal conjunctiva in these asymptomatic contact lens wearers has an altered epithelial surface, different from that observed in normal subjects without contact lens-wearing experience and from subjects with contact lens-associated giant papillary conjunctivitis.

Corneal keratan sulfate proteoglycan (KSPG) from scar tissue of experimental penetrating corneal wounds in rabbits was analyzed 2-8 weeks after injury using three previously characterized antibodies. Keratan sulfate (KS) was identified in 2 week scars and normal corneal tissue by indirect immunofluorescence using a monoclonal antibody against sulfated KS epitopes. KSPG was measured in unfractionated extracts of scar and of normal corneal tissue using a "sandwich" enzyme-linked immunosorbent assay (ELISA). In extracts of 2 week scars, KSPG molecules reacting with two different anti-KS monoclonal antibodies were 55% and 82% as abundant as in normal tissue extracts. Ion exchange high performance liquid chromatography (HPLC) of tissue extracts found qualitatively similar elution profiles of KSPG antigens from both scar and normal tissues. Direct ELISA of the HPLC-purified KSPG showed identical quantitative binding of antibodies against core protein and KS from normal and scar tissue. KS in the HPLC-purified extracts was sensitive to digestion with endo-beta-galactosidase, whereas core protein antigens were not affected by this enzyme, as expected. Alteration of the antigenic characteristics of the KSPG of scars was detected with a competitive immunoassay using immobilized monoclonal antibodies against KS. KS in extracts from 2, 6, and 8 week scars competed only 5-11% as effectively as KS from normal cornea, although core protein antigens in the scar extracts competed 61-80% as well as those of normal cornea.(ABSTRACT TRUNCATED AT 250 WORDS)