Care Coordination for Breast Cancer Survivors in Urban Underserved Communities: Will Treatment Summaries and Survivorship Care Plans Be Enough?

Background: Few studies have examined cancer care coordination at federally qualified health centers (FHQCs). The Commission on Cancer's (CoC) standard 3.3, i.

The importance of transdisciplinary collaborations for understanding and resolving health disparities.

Group disparities in health have been documented for several decades. Despite recent efforts to eliminate them, group differences persist and challenge the ability of scientists to address them using traditional research paradigms. Because the determinants of disparities occur at multiple levels, from the molecular to the societal, and interact with one another in ways not yet fully understood, they represent a challenge to researchers attempting to capture their complexity.

Targeting health disparities: a model linking upstream determinants to downstream interventions.

Certain social/environmental factors put some groups at extraordinary risk for adverse health outcomes, creating health disparities. We present a downward causal model, originating at the population level and ending at disease, with psychological and behavioral responses linking the two. This approach identifies how specific social environments "get under the skin" to cause disease, illustrated with the disparity in mortality from aggressive premenopausal breast cancer suffered by black women.

Salicylic acid injection before noise exposure reduces permanent threshold shift.

The permanent threshold shift (PTS) following exposure to intense noise may be due to the noise-induced excessive vibrations in the cochlea or to the generation of elevated levels of reactive oxygen species. Thus, it is possible that the resulting PTS may be reduced if the cochlear amplifier could be temporarily depressed beginningjust before the onset of the noise and continuing during the noise exposure or if antioxidant drugs were administered. These possibilities were assessed in mice by administering a single injection of salicylic acid (an antioxidant drug which also reversibly depresses the motor protein prestin of the cochlear amplifier) just before, and in other mice, just after, 3.

Early-life conditions and mechanisms of population health vulnerabilities.

The social status of groups is key to determining health vulnerability at the population level. The impact of material and psychological stresses imposed by social inequities and marginalization is felt most intensely during perinatal/early childhood and puberty/adolescent periods, when developmental genes are expressed and interact with social-physical environments. The influence of chronic psychosocial stresses on gene expression via neuroendocrine regulatory dysfunction is crucial to understanding the biological bases of adult health vulnerability.

Prior heat acclimation confers protection against noise-induced hearing loss.

Exposure to intense noise stress can cause a permanent noise-induced hearing loss which is thought to be due to elevation of reactive oxygen species in excess of the inherent antioxidant mechanisms of the cell. However, preconditioning to low levels of stress of one type can activate cellular mechanisms leading to the elevation of antioxidant levels so that the cell is then better able to tolerate subsequent severe stress of a different type. This has been called cross-tolerance.

Susceptibility of young adult and old rats to noise-induced hearing loss.

This study was designed to test whether old rats show signs of presbyacusis and whether they would be either similarly or more or less susceptible to noise-induced hearing loss than young adult rats. Old (24 months) and young adult (3-4 months) Wistar rats were exposed to a broad-band noise of 113 dB SPL for a duration of 1 h (producing temporary threshold shifts) or 3 days (12 h noise/12 h quiet; permanent shifts). Auditory brainstem response (ABR), distortion product otoacoustic emissions (DPOAEs) and transient evoked otoacoustic emissions (TEOAEs) were measured before and after exposure.

The effect of various durations of noise exposure on auditory brainstem response, distortion product otoacoustic emissions and transient evoked otoacoustic emissions in rats.

This study was designed to investigate the effect of various durations of noise exposure in animals on physiological responses from the cochlea which are also used clinically in humans: auditory brainstem response (ABR), transient evoked otoacoustic emissions (TEOAEs) and distortion product otoacoustic emissions (DPOAEs). Rats were exposed to 113 dB SPL broad-band noise (12 h on/12 h off) for durations of 3, 6, 9, 12, 15 and 21 days, and tested 24 h after cessation of the noise and again after a period of 6 weeks. ABR threshold to click stimuli and to a 2-kHz tone burst (TB), TEOAE energy content and DPOAE amplitude in the exposed rats were compared to those in a group of control rats not exposed to noise.

The effect of head orientation on the vestibular evoked potentials to linear acceleration impulses in rats.

Objective: To investigate the influence of linear acceleration impulses delivered when the head is held in different static head orientations, on the first wave of the short latency vestibular evoked potential (VsEP). The first wave is the compound action potential of the primary vestibular neurons synchronously activated.

Background: It has been shown previously that the VsEP elicited in response to linear acceleration is initiated mainly in the otolith organs.

Effect of long-term noise exposure on the developing and developed ear in the Rat.

There have been reports that the developing ear is more sensitive than the adult ear to noise-induced hearing loss. This was investigated by testing auditory function in rats, both electrophysiologically and histologically, following exposure to broad-band noise (12 h/day for 15 days) at different stages of auditory development (neonates and adults), and also in age-matched controls. An exposure of 90 dB SPL broad-band noise caused no long-term change in auditory function in either age group.

Effect of white noise "masking" on vestibular evoked potentials recorded using different stimulus modalities.

Short latency vestibular evoked potentials (VsEPs) to linear acceleration impulses (L-VsEPs) are initiated in the otolith organs (saccule and utricle). Some of the saccule afferents have been reported to respond not only to linear acceleration, but also to high intensity acoustic stimuli. If so, the L-VsEP recorded from the saccule (elicited with the stimulus orientated relative to the head so as to optimally activate the saccule, i.

Origins of the short latency vestibular evoked potentials (VsEPs) to linear acceleration impulses.

Objective: To verify the vestibular origin of the short latency (t < 12.5 msec) vestibular evoked potentials (VsEPs) in response to linear acceleration impulses (L-VsEPs) and to differentiate between the contributions of the otolith organs and the semi-circular canals (SCCs) to their initiation.

Design And Methods: L-VsEPs (stimulus intensity, 3 g; rise time, 1.

Differential effect of the loop diuretic furosemide on short latency auditory and vestibular-evoked potentials.

Objective: This study aimed to investigate the differential effect of the loop diuretic furosemide on the auditory and vestibular (otolith) end organs in the same animals simultaneously.

Design And Methods: Auditory nerve-brain stem-evoked responses (ABR-generated in the cochlea) and short latency vestibular-evoked responses to linear acceleration impulses (L-VsEP-generated in the otolith organs) were recorded from albino Sabra rats both before and at minute intervals after intravenous injections of the loop diuretic furosemide. In some animals, an equal volume of saline was injected to control for the effect of the injection itself.

Short latency vestibular evoked potentials (VsEPs) to linear acceleration impulses in rats.

In this study, short latency (t < 12.7 ms) vestibular evoked potentials (VsEPs) in response to linear acceleration impulses were recorded in 37 rats. A new technique (based on a solenoid) was used for generating linear force impulses that were delivered to the animal's head.

Contribution of the eighth nerve and cranial nerve nuclei to the short-latency vestibular evoked potentials in cats.

The object of this study was to assess the contributions of the vestibular nerve and various cranial nerve nuclei to the short-latency vestibular evoked potentials in cat. The following nuclei were investigated: vestibular nuclei and the third, sixth, and tenth cranial nerve nuclei. In unilateral labyrinthectomized cats, we performed suboccipital craniectomy and partial cerebellectomy to place bipolar electrodes into the neural structures under investigation.

Postnatal development of somatosensory evoked potential in jaundiced Gunn rats and effects of sulfadimethoxine administration.

Bilirubin encephalopathy results from the entry of bilirubin into the brain and is expressed by motor, sensory, and/or behavioral impairment. The jaundiced (jj) Gunn rat is a valuable animal model for studying the kinetics of bilirubin-induced neurotoxicity. This is often done by recording evoked potentials, which are also used as indices of brain damage in infants who develop neonatal jaundice, as is the case with the auditory nerve and brainstem evoked response (ABR).

Vertical plane short and middle latency vestibular evoked potentials in humans.

In order to determine whether short and middle latency vestibular evoked potentials (VsEPs) can be recorded in humans in response to angular acceleration stimuli in the vertical plane, a drum, head-holder, and stepper motor were designed to deliver upward acceleration impulses of 10,000 degrees/s2 (1.8 degrees displacement) to the human head. Forehead and mastoid electrodes recorded electrical activity that was filtered, differentially amplified, and averaged in short (12.

Visual evoked potential abnormalities in jaundiced Gunn rats treated with sulfadimethoxine.

The manifestations of bilirubin encephalopathy include disturbances in the visual pathway (visual gaze paralysis and distorted visual perception). In the young jaundiced Gunn rat (jj) model of hyperbilirubinemia, significant differences in visual evoked potential (VEP) patterns have been recorded during development. In the present study, the effects of sulfadimethoxine (SDM) on VEP and electroretinogram (ERG) were examined in 3-wk-old jj rats.

Peripheral generators of the vestibular evoked potentials in the cat.

Objectives: The contributions of each of the vertical semicircular canals (SCCs) and otoliths to the short-latency vestibular evoked potentials in response to angular acceleration impulses were studied in the cat.

Design: The experiments were conducted on unilateral labyrinthectomized cats. Vestibular activation was achieved by delivering angular acceleration impulses to the animal's head, held in the position presumed to be optimal for maximal stimulation of either the anterior or the posterior SCCs before and after obliteration of the SCC studied, and before and after obliteration of the other SCCs and ablation of the maculae.

The contribution of the lateral semicircular canal to the short latency vestibular evoked potentials in cat.

Short latency vestibular evoked potentials (VsEPs) to angular acceleration impulses (maximal intensity 20,000 degrees/sec2, rise time 1.5-3 msec) were recorded by skin electrodes in cats before and after various surgical procedures. Under general anesthesia, the animals underwent unilateral labyrinthectomy and the VsEPs in response to stimulation of the remaining inner ear in the plane of the lateral semicicular canal (SCC) with the head flexed 20 degrees-25 degrees were recorded as a baseline.

Influence of experimentally elevated blood viscosity on the auditory nerve-brainstem evoked response and threshold.

Blood viscosity, due to its effect on blood flow, is one of the determinants of oxygen delivery. Therefore the influence of elevated blood viscosity on hearing was studied in rats using the auditory brainstem response (ABR) threshold, wave 1 latency, brainstem transmission time (BTT) and wave 1/4 amplitude ratio. Whole blood viscosity (WBV) was elevated by 15-21% in two different ways: elevating the hematocrit (Polycythemia) by acclimation in a hypobaric chamber, or elevating the plasma viscosity by infusing a solution of Polyvinylpyrrolidone-360 (PVP).

A multicenter proficiency trial of gene amplification (PCR) for the detection of HIV-1.

The sensitivity and specificity of the polymerase chain reaction (PCR) for the detection of HIV-1 proviral DNA was determined in five laboratories with extensive experience in PCR testing. Five panels consisting of 105 HIV-1-seronegative specimens from regularly repeating blood donors with no risk factors for HIV infection and 99 HIV-1-seropositive and culture-positive specimens from a cohort of homosexual/bisexual men were sent under code to each laboratory. Amplification procedures and testing algorithms by which specimens were judged positive, negative, or indeterminate varied between laboratories.

Noise and hypoxia induced temporary threshold shifts in rats studied by ABR.

Rats were exposed for 2 h either to 115 dB SPL noise, to 5% oxygen in nitrogen (hypoxia) or to both hypoxia and noise. Auditory nerve-brainstem evoked responses (ABR) to 80 dB HL clicks and threshold were recorded prior to exposure, immediately (5-10 min) after the exposure, 2 h after and 2 weeks after the exposure. The findings in each experimental animal were compared to those in the control (non-exposed) group and to those in the other groups.

Detection of human immunodeficiency virus DNA using the polymerase chain reaction in a well-characterized group of homosexual and bisexual men.

The polymerase chain reaction (PCR) for human immunodeficiency virus type 1 (HIV-1) DNA was performed on specimens from 197 homosexual and bisexual men enrolled in studies of HIV-1 infection. Thirty cycles of amplification were conducted, followed by detection with probes corresponding to two gag primer pairs (SK 38/39 and SK 101/145). Of 107 men who were HIV-1 antibody-negative, 105 (98%) were PCR-negative.