Biological Research For Nursing

Nurses caring for traumatic brain injury (TBI) patients with intracranial hypertension (ICH) recognize that patients whose intracranial adaptive capacity is reduced are susceptible to periods of disproportionate increase in intracranial pressure (DIICP) in response to a variety of stimuli. It is possible that DIICP signals potential secondary brain damage due to sustained or intermittent ICH. However, there are few clinically accessible intracranial pressure (ICP) measurement parameters that allow nurses and other critical care clinicians to identify patients at risk of DIICP. The purpose of this study was to investigate whether there are specific minute-to-minute trends in ICP variability during the first 48 hr of monitoring that might accurately predict DIICP in patients with severe TBI. A total of 38 patients with severe TBI were sampled from the data set of a randomized controlled trial testing bedside monitoring displays and cerebral perfusion pressure management in individuals with TBI or sub-arachnoid hemorrhage. The investigators retrospectively examined the rates of change (slope) in mean, standard deviation, and variance of ICP on a 1-min basis for 30 consecutive min prior to a specified DIICP event. There was a significantly increasing linear and quadratic slope in mean ICP prior to the development of DIICP, compared with the comparison data set (p < .05). It is feasible to display moving averages in modern bedside monitoring. Such an arrangement may be useful to provide visual displays that provide immediate clinically relevant information regarding the patients with decreased adaptive capacity and therefore increased risk of DIICP.

Traumatic brain injury (TBI) is a leading cause of morbidity and mortality. A cascade of events is initiated with TBI that leads to degradation of the membrane lipid bilayer of neurons and neuroglia. The purpose of this study was to (a) describe changes in the cerebrospinal fluid (CSF) phospholipid concentration over time for those who survived and those who died following TBI; and (b) determine whether there were differences in the CSF phospholipid concentration between those who survived and those who died following TBI. Thirty-nine CSF samples were obtained from 10 participants who sustained a TBI. Following extraction, phospholipids were separated and quantified by normal-phase high performance liquid chromatography with ultraviolet detector. For those who died, the highest median concentration was on Day 1 after TBI for lysophosphatidylcholine and on Day 4 after TBI for phosphatidylethanolamine, phosphatidylserine, phosphatidylcholine, and sphingomyelin. For those who survived, the highest median concentration was on Day 1 after TBI for phosphatidylcholine, on Day 3 after TBI for phosphatidylethanolamine and phosphatidylserine, on Day 4 after TBI for sphingomyelin, and on Day 5 after TBI for lysophosphatidylcholine. There were significant differences in the concentrations of phosphatidylethanolamine and phosphatidylserine on Days 1—2 and of phosphatidylethanolamine, phosphatidylcholine, and sphingomyelin on Days 3—4 after TBI between those who survived and died, with the highest concentrations in those who died. These findings provide preliminary evidence of greater disruption of central nervous system membrane phospholipids in participants who died after TBI.

In this study, an ethanol extract of Turnera ulmifolia L. (EETU) and chlorpromazine (CPZ) were tested for their antimicrobial activity alone or in combination with conventional antibiotics against two strains of Escherichia coli (E. coli). The growth of neither E. coli strain was inhibited by the extract. The minimal inhibitory concentration (MIC) and minimal bactericidal concentration values were ≥1 mg/ml for both the strains of E. coli. However, the extract did increase the antimicrobial effects of amikacin, neomycin, and tobramycin. A similar effect of CPZ on amikacin, kanamycin, and tobramycin indicated the involvement of an efflux system in the resistance to these aminoglycosides. Results suggest that extracts from T. ulmifolia could be used as a plant-derived natural product with resistance-modifying activity, constituting a new weapon against bacterial resistance to antibiotics.

Many chronic wounds fail to heal with conventional therapy, resulting in disability and impaired quality of life. New technologies using recombinant growth factors, autologous growth factors, or bioengineered skin—tissue substitutes have been shown to be effective, but these treatments are costly. An effective, low-cost treatment to improve healing of chronic wounds is needed. The molecular environment of chronic wounds, like many other chronic inflammatory diseases, contains abnormally high levels of proinflammatory cytokines (tumor necrosis factor [TNF]-α and interleukin [IL]-1β]) and matrix metalloproteinases (MMPs), which impair normal wound healing. In animal models and clinical studies of ulcerative diseases, doxycycline, an inexpensive and Food and Drug Administration (FDA)-approved antibiotic, appears to inhibit members of the MMP superfamily like MMPs and TNF-α-converting enzyme (TACE). This article provides an overview of the roles of MMPs and intrinsic tissue inhibitors of metalloproteinases (TIMPs) in wound healing and the damaging effects of chronically elevated levels of MMPSs in chronic wounds. It also explores the use of topical doxycycline, a synthetic MMP inhibitor (MMPI), to enhance healing of chronic wounds.

The study was conducted to test the aqueous extract of Brugmansia suaveolens (AEBs) flowers for their antinociceptive effects in mice. In the hot plate test, a significant increase in reaction time for two doses of AEBs at 60, 90, 120, and 150 min after treatment was noted. Pretreatment of animals with naloxone (5 mg/kg, intraperitoneally [IP]) left the antinociceptive effect of AEBs at a dose of 100 mg/kg unaffected at 60, 90, 120, and 150 min after treatment and at a dose of 300 mg/kg at 30 min but not at 90, 120, and 150 min. In the writhing test, the AEBs significantly inhibited acetic acid—induced abdominal constriction and was equally potent at both doses. Pretreatment with naloxone (5 mg/kg, IP) left the antinociceptive effect of both doses of AEBs unaffected. Pretreatment with N^G-nitro-L-arginine methyl ester (L-NAME; 20 mg/kg, IP) caused a significant change in the number of abdominal constrictions but did not change the antinociceptive effect of AEBs. Pretreatment of animals with methylene blue also did not change the effect of AEBs on the number of writhing movements in mice. Flumazenil (5 mg/kg, IP) antagonized the antinociceptive effects of diazepam and also reversed the antinociceptive effect of AEBs. AEBs showed a depressant effect on the central nervous system, and the treatment of mice with pentobarbital combined with AEBs increased the animals’ sleeping time in a dose-dependent manner. These results suggest that the antinociceptive activity of AEBs may be related in part to benzodiazepine receptors, although peripheral mechanisms cannot be excluded.

Prostate cancer is a leading malignancy in men, and prostatectomy is widely used for its treatment. Psychological distress and pain are commonly experienced in the perioperative period, and both can contribute to suppression of the immune response to cancer. This study evaluated perioperative pain, psychological distress, and immune function in men undergoing prostatectomy. Men were evaluated prior to surgery, 1 and 2 days postoperatively and 4—6 weeks postoperatively. Compared to cancer-free men, the prostatectomy group reported increased perceived stress, depression, confusion, and anxiety prior to surgery. During the 2 postoperative days, mood disturbance and anxiety persisted and were accompanied by mild elevations in pain and reduced vigor. At 4—6 weeks postoperative, mood, pain, and immune function were similar to those of the cancer-free group; however, the prostatectomy group continued to report significant elevations in anxiety. Natural killer cell activity (NKCA) was significantly reduced on Day 1 after prostatectomy, but by postoperative Day 2, NKCA returned to a level similar to that of the cancer-free group. The reduction in NKCA was not accompanied by changes in circulating immune cells, demonstrating that this reduction represented a functional change in NKCA. No correlations between immune variables and pain or psychological variables were found, suggesting that the postoperative reduction in NKCA was likely the result of the physical stress of the surgical experience. Suppression of immune defenses during the critical postoperative period can place cancer patients at risk for nascent tumor seeding. Additional interventions are needed to reduce this risk.

Purpose: The purpose of this experimental pilot study was to measure the effects of a mindfulness-based yoga intervention on sleep in pregnant women. Methods: Fifteen healthy, nulliparous women in their second or third trimesters with singleton pregnancies attended weekly mindfulness meditation and prenatal Hatha yoga classes in the community for 7 weeks. Sleep variables, as estimated by 72 hr of continuous wrist actigraphy and the General Sleep Disturbance Scale (GSDS), were recorded at baseline (Time 1) and postintervention (Time 2). Control data were obtained by evaluating sleep in the third-trimester group at Time 1. Due to small sample size, data were analyzed using parametric and nonparametric statistics. Results: Women who began the intervention in the second trimester had significantly fewer awakenings, less wake time during the night, and less perceived sleep disturbance at Time 2 than at baseline. Those who began during the third trimester had poorer sleep over time in spite of the intervention. Women who began the intervention in their second trimester had less awake time at Time 2 compared to third-trimester controls at Time 1. Conclusions: Mindful yoga shows promise for women in their second trimester of pregnancy to diminish total number of awakenings at night and improve sleep efficiency and merits further exploration. Results from this pilot study provide the data to estimate sample size and design and implement powered and more controlled studies in the future.

Preterm birth (PTB; spontaneous delivery prior to 37 weeks gestation) affects one out of eight infants born in the United States and is the most common cause of neonatal morbidity and mortality. Although the pathogenesis of PTB is multifactorial, a growing body of literature supports the hypothesis that one cause of PTB is inflammation in pregnancy. Investigators have implicated mediators of inflammation, most notably proinflammatory cytokines, as being associated with and perhaps a playing a causal role in the pathogenesis of preterm labor and adverse early fetal outcomes. Though researchers have pursued the association of cytokines with preterm labor and subsequent early adverse fetal outcomes as a line of research, there has been little integration of diverse findings across studies. This systematic review appraises the empirical evidence from human studies for the association of levels of cytokines in blood with preterm labor and adverse early fetal outcome to examine the current state of the science in this important area of biobehavioral research. The most consistent finding is that increased levels of proinflammatory cytokines, particularly interleukin (IL) 6, IL-β1, and tumor necrosis factor α (TNF-α), are associated with PTB as compared to levels found at term birth. However, there have been relatively few studies and results have not been consistent. Therefore, further research is needed to elucidate the association of these inflammatory mediators with adverse pregnancy outcomes.

A growing body of literature supports the relationship of maternal inflammation with preterm birth and adverse neonatal outcomes, including infection and central nervous system (CNS) dysfunction. Mediators of inflammation, most notably proinflammatory cytokines, have been implicated as having an association with and perhaps playing a causal role in the pathogenesis, leading to adverse neonatal outcomes. Even though the association of cytokines with early adverse neonatal outcomes has been actively pursued as a line of research, there has been little integration of diverse findings across studies. Therefore, the purpose of this systematic review was to appraise and classify empirical evidence from human studies for the association of cytokine levels in blood (serum, plasma, or cells; maternal, cord, or neonatal) with two adverse early outcomes in preterm infants: early infection and increased risk of neurologic damage. The review revealed that the proinflammatory cytokines most frequently linked with sepsis are in the interleukin (IL) 1 family as well as tumor necrosis factor α (TNF-α) and IL-6. The proinflammatory cytokines most frequently linked to neurologic insult in the reviewed studies were IL-1β, IL-6, and IL-8. In all cases where IL-1β was studied, the levels were increased when there was neurologic insult. A better understanding of the relationship of these inflammatory substances with these adverse conditions is needed for the future development of maternal and neonatal biobehavioral nursing research.

Fibromyalgia (FMS) is a chronic widespread pain (CWP) and fatigue syndrome that affects three to six million adults in the United States. Core symptoms of FMS include pain, fatigue, and mood and sleep disturbances. To date, consensus has not been reached among researchers regarding the pathogenesis of FMS nor the specific role of cytokine activation on the neuroendocrine—immune response patterns in persons with FMS. The purpose of this article is to describe and synthesize the results of research studies focused on the relationship between cytokines and FMS and among cytokines and core symptoms of FMS. There is some support in the literature for relationships among FMS symptoms and cytokines; however, there are discrepant findings related to whether proinflammatory and anti-inflammatory cytokines are elevated or reduced in persons with FMS and whether their levels correlate with the core symptoms of this disorder. Although the use of cytokine biomarkers must be considered exploratory at this time due to the lack of consistent empirical findings, biobehavioral research focused on understanding the relationship of FMS with cytokines may lead to a better understanding of this complex syndrome. This knowledge may ultimately contribute to the development of interventions for symptom management that address not only the symptom manifestation but also a biological mediator of symptoms.

The purpose of this study was to compare whole blood and plasma in terms of the subsequent accuracy of blood lactate, glucose, lactate dehydrogenase (LDH), creatine phosphokinase (CPK), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) measurement. Blood samples were drawn from 8 male Wistar-Kyoto rats. The rats were homologous, weighed 300— 380 g, were housed in the same environment, and were provided with food and water under the same conditions. Blood draws occurred in all rats at same time. The blood specimens were divided into two samples, one to be stored as whole blood (WBS) and one to be stored as plasma (PS). All the blood sample analyses were performed by trained and experienced personnel to ensure that differences in results were due to variation in form in which specimens were stored rather than to technique. The lactate concentration in the WBS group gradually increased over time, intraclass correlation coefficient (ICC) = 0.541, 95% confidence interval (CI; —0.197, 0.893), and was higher than that of the PS group, ICC = 0.897, 95% CI (0.733, 0.976). By contrast, glucose level gradually declined for the WBS group, ICC= —0.367, 95% CI (—2.563, 0.682). Whole blood storage increased measurement variation for lactate, glucose, LDH, and CPK. Plasma storage prolonged the stability of the biochemical components. This study demonstrates the importance of evaluating validity at each stage of developing and testing animal models.