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Idaho Institutional Development Award (IDeA) Network for Biomedical Research Excellence (INBRE) aims to build biomedical research capacity and enhance the scientific and technology knowledge of the Idaho workforce. A key INBRE Program at The College of Idaho, a primarily undergraduate institution of 1,100 students, is a 10-wk summer fellows research experience. This report documents outcomes from 2005 to present, including demographic trends, faculty and student research productivity, self-reported gains, educational attainment, and career outcomes. Of 103 participants, 83.7% were from Idaho, 26.7% from rural areas, and 23.9% first-generation college students. Faculty and student research productivity (conference presentations and peer-reviewed publications) increased threefold. We found that 91.4% of fellows entered a scientific- or healthcare-related career and that 70.7% completed or are currently enrolled in postgraduate training (51.7% doctoral and 19.0% master's level). Anonymous surveys were uniformly positive, with gains in self-confidence and independent laboratory work. Open-ended responses indicated students valued mentoring efforts and improved awareness of scientific opportunities and competitive preparation for postgraduate training. Lastly, we observed that student research involvement increased college-wide during the award period. These data suggest that the summer fellows program is successfully meeting National Institutes of Health IDeA goals and serving as a pipeline to future health research careers and a scientifically trained Idaho workforce.

Glioblastoma (GBM) is a lethal astrocyte-derived tumor that is currently treated with a multi-modal approach of surgical resection, radiotherapy, and temozolomide-based chemotherapy. Alternatives to current therapies are urgently needed as its prognosis remains poor. Anthracyclines are a class of compounds that show great potential as GBM chemotherapeutic agents and are widely used to treat solid tumors outside the central nervous system. Here we investigate the cytotoxic effects of doxorubicin and other anthracyclines on GL261 glioma tumor cells in anticipation of novel anthracycline-based CNS therapies. Three methods were used to quantify dose-dependent effects of anthracyclines on adherent GL261 tumor cells, a murine cell-based model of GBM. MTT assays quantified anthracycline effects on cell viability, comet assays examined doxorubicin genotoxicity, and flow cytometry with Annexin V/PI staining characterized doxorubicin-induced apoptosis and necrosis. Dose-dependent reductions in GL261 cell viability were found in cells treated with doxorubicin (EC 50  = 4.9 μM), epirubicin (EC 50  = 5.9 μM), and idarubicin (EC 50  = 4.4 μM). Comet assays showed DNA damage following doxorubicin treatments, peaking at concentrations of 1.0 μM and declining after 25 μM. Lastly, flow cytometric analysis of doxorubicin-treated cells showed dose-dependent induction of apoptosis (EC 50  = 5.2 μM). Together, these results characterized the cytotoxic effects of anthracyclines on GL261 glioma cells. We found dose-dependent apoptotic induction; however at high concentrations we find that cell death is likely necrotic. Our results support the continued exploration of anthracyclines as compounds with significant potential for improved GBM treatments.

Glioblastoma (GBM) is an aggressive brain cancer with an average survival rate of 15 months. The composition of the GBM tumor microenvironment-its pH, the presence of growth and immune factors, neurotransmitters, and gliotransmitters-plays an important role in GBM pathophysiology and facilitates tumor survival and growth. In particular, GBM tumor cells produce glutamate, which is toxic to healthy tissue and is associated with increased tumor invasion into adjacent brain regions. The conditions that lead to this excitotoxic release of glutamate are not completely understood. Previous studies have demonstrated that extracellular ATP is present at high levels in the tumor microenvironment, and that ATP stimulates the release of glutamate from astrocytes in culture. Here we examine the functional effects of extracellular ATP on the GL261 cell line, a model system for high-grade astrocytomas such as GBM. We show that treatment with ATP leads to an immediate, dose-dependent influx of calcium into the cell that is partially inhibited by an antagonist (o-ATP) of the ionotropic ATP receptor P2X7. In addition, GL261 cells respond to extracellular ATP with a dose-dependent release of glutamate. Consistent with other reports, we find that ATP is toxic to GL261 cells at high concentrations. Together, these results provide insight into the mechanisms responsible for glutamate production by tumor cells and inform future studies that will identify how the GBM tumor microenvironment facilitates tumor invasion into healthy areas of the brain.

Background: The tumor-derived GL261 cell line is used as a model for studying glioblastoma and other high-grade gliomas, and can be cultured adherently or as free-floating aggregates known as neurospheres. These different culture conditions give rise to distinct phenotypes, with increased tumorigenicity displayed by neurosphere-cultured cells. An important technique for understanding GL261 pathobiology is live cell fluorescent imaging of intracellular calcium. However, live cell imaging of GL261 neurospheres presents a technical challenge, as experimental manipulations where drugs are added to the extracellular media cause the cells to move during analysis. Here we present a method to immobilize GL261 neurospheres with low melting point agarose for calcium imaging using the fluorescent calcium sensor fura-2., Methods: GL261 cells were obtained from the NCI-Frederick Cancer Research Tumor Repository and cultured as adherent cells or induced to form neurospheres by placing freshly trypsinized cells into serum-free media containing fibroblast growth factor 2, epidermal growth factor, and B-27 supplement. Prior to experiments, adherent cells were loaded with fura-2 and cultured on 8-well chamber slides. Non-adherent neurospheres were first loaded with fura-2, placed in droplets onto an 8-well chamber slide, and finally covered with a thin layer of low melting point agarose to immobilize the cells. Ratiometric pseudocolored images were obtained during treatment with ATP, capsaicin, or vehicle control. Cells were marked as responsive if fluorescence levels increased more than 30% above baseline. Differences between treatment groups were tested using Student's t-tests and one-way ANOVA., Results: We found that cellular responses to pharmacological treatments differ based on cellular phenotype. Adherent cells and neurospheres both responded to ATP with a rise in intracellular calcium. Notably, capsaicin treatment led to robust responses in GL261 neurospheres but not adherent cells., Conclusions: We demonstrate the use of low melting point agarose for immobilizing GL261 cells, a method that is broadly applicable to any cell type cultured in suspension, including acutely trypsinized cells and primary tumor cells. Our results indicate that it is important to consider GL261 phenotype (adherent or neurosphere) when interpreting data regarding physiological responses to experimental compounds.

Mycobacteriophages--viruses of mycobacterial hosts--are genetically diverse but morphologically are all classified in the Caudovirales with double-stranded DNA and tails. We describe here a group of five closely related mycobacteriophages--Corndog, Catdawg, Dylan, Firecracker, and YungJamal--designated as Cluster O with long flexible tails but with unusual prolate capsids. Proteomic analysis of phage Corndog particles, Catdawg particles, and Corndog-infected cells confirms expression of half of the predicted gene products and indicates a non-canonical mechanism for translation of the Corndog tape measure protein. Bioinformatic analysis identifies 8-9 strongly predicted SigA promoters and all five Cluster O genomes contain more than 30 copies of a 17 bp repeat sequence with dyad symmetry located throughout the genomes. Comparison of the Cluster O phages provides insights into phage genome evolution including the processes of gene flux by horizontal genetic exchange.

TRPM8 (Transient Receptor Potential Melastatin-8) is a cold- and menthol-gated ion channel necessary for the detection of cold temperatures in the mammalian peripheral nervous system. Functioning TRPM8 channels are required for behavioral responses to innocuous cool, noxious cold, injury-evoked cold hypersensitivity, cooling-mediated analgesia, and thermoregulation. Because of these various roles, the ability to pharmacologically manipulate TRPM8 function to alter the excitability of cold-sensing neurons may have broad impact clinically. Here we examined a novel compound, PBMC (1-phenylethyl-4-(benzyloxy)-3-methoxybenzyl(2-aminoethyl)carbamate) which robustly and selectively inhibited TRPM8 channels in vitro with sub-nanomolar affinity, as determined by calcium microfluorimetry and electrophysiology. The actions of PBMC were selective for TRPM8, with no functional effects observed for the sensory ion channels TRPV1 and TRPA1. PBMC altered TRPM8 gating by shifting the voltage-dependence of menthol-evoked currents towards positive membrane potentials. When administered systemically to mice, PBMC treatment produced a dose-dependent hypothermia in wildtype animals while TRPM8-knockout mice remained unaffected. This hypothermic response was reduced at lower doses, whereas responses to evaporative cooling were still significantly attenuated. Lastly, systemic PBMC also diminished cold hypersensitivity in inflammatory and nerve-injury pain models, but was ineffective against oxaliplatin-induced neuropathic cold hypersensitivity, despite our findings that TRPM8 is required for the cold-related symptoms of this pathology. Thus PBMC is an attractive compound that serves as a template for the formulation of highly specific and potent TRPM8 antagonists that will have utility both in vitro and in vivo.

Behavioral assays in the undergraduate neuroscience laboratory are useful for illustrating a variety of physiological concepts. An example is homeostatic temperature regulation (thermoregulation). Many model organisms, from flies to mice, regulate internal temperatures in part by moving to suitable climates (thermotaxis). A particularly reliable method of quantifying temperature-dependent thermotactic behaviors is the two-temperature preference behavioral assay. In this preparation, an organism is free to move between two temperature-controlled surfaces, thus revealing its preferred thermal environment. Here we present the design and construction of a two-temperature preference assay chamber. The device uses Peltier-based thermoelectric modules (TECs) for heating and cooling, and is capable of precision control of temperatures from -5ºC to 60ºC. Our approach can be easily adapted for use in a variety of physiological and behavioral assays that require precise temperature control over a wide range of temperatures.

Numerous cases of urate nephrolithiasis in managed collections of common bottlenose dolphins (Tursiops truncatus) have been reported, but nephrolithiasis is believed to be uncommon in wild dolphins. Risk factors for urate nephrolithiasis in humans include low urinary pH and hypocitraturia. Urine samples from 94 dolphins were collected during April 2006 through June 2009 from 4 wild populations (n = 62) and 4 managed collections (n = 32). In addition, urine uric acid and pH were tested in a subset of these animals. Our null hypothesis was that wild and managed collection dolphins would have no significant differences in urinary creatinine, citrate, and uric acid concentrations and pH. Among urine samples from all 94 dolphins, the urinary levels (mean +/- SEM) for creatinine, citrate, uric acid, and pH were 139 +/- 7.6 mg/dL, 100 +/- 20 mg citrate/g creatinine, 305 +/- 32 mg uric acid/g creatinine, and 6.2 +/- 0.05, respectively. Of the 4 urinary variables, only citrate concentration varied significantly between the 2 primary study groups; compared with wild dolphins, managed collection dolphins were more likely to have undetectable levels of citrate in the urine (21.0% and 81.3%, respectively). Mean urinary citrate concentrations for managed collection and wild dolphin populations were 2 and 150 mg citrate/g creatinine, respectively. We conclude that some managed collections of dolphins, like humans, may be predisposed to urate nephrolithiasis due to the presence of hypocitraturia. Subsequent investigations can include associations between metabolic syndrome, hypocitraturia, and urate nephrolithiasis in humans and dolphins; and the impact of varying levels of seawater ingestion on citrate excretion.

The occurrence of trace levels of prescription and over-the-counter pharmaceuticals in the environment began to receive concerted attention nearly two decades ago. The public's growing awareness and concern over the presence of these chemicals, especially in drinking water, has served to catalyze considerable discussion and debate regarding the best practices for disposal of unused or unwanted medications. In the United States, the first federal guidance for consumers was issued in 2007. It recommends discarding unused pharmaceuticals to household trash, after taking precautions to mix the pharmaceuticals with an inert substance and conceal the contents from view. Providing the consumer with additional options for conscientious disposal are various community, city, and state collection events, ongoing programs, and government-funded pilot projects. These strategies include the opportunity to mail or bring unused medications to various collection points, such as pharmacies, for eventual destruction. All of these approaches to medication disposal play roles in reducing the introduction of pharmaceuticals to the environment.

Cold temperatures robustly activate a small cohort of somatosensory nerves, yet during a prolonged cold stimulus their activity will decrease, or adapt, over time. This process allows for the discrimination of subtle changes in temperature. At the molecular level, cold is detected by transient receptor potential melastatin 8 (TRPM8), a nonselective cation channel expressed on a subset of peripheral afferent fibers. We and others have reported that TRPM8 channels also adapt in a calcium-dependent manner when activated by the cooling compound menthol. Additionally, TRPM8 activity is sensitive to the phospholipid phosphoinositol 4,5-bisphosphate (PIP2), a substrate for the enzyme phospholipase C (PLC). These results suggest an adaptation model whereby TRPM8-mediated Ca2+ influx activates PLC, thereby decreasing PIP2 levels and resulting in reduced TRPM8 activity. Here we tested this model using pharmacological activation of PLC and by manipulating PIP2 levels independent of both PLC and Ca2+. PLC activation leads to adaptation-like reductions in cold- or menthol-evoked TRPM8 currents in both heterologous and native cells. Moreover, PLC-independent reductions in PIP2 had a similar effect on cold- and menthol-evoked currents. Mechanistically, either form of adaptation does not alter temperature sensitivity of TRPM8 but does lead to a change in channel gating. Our results show that adaptation is a shift in voltage dependence toward more positive potentials, reversing the trend toward negative potentials caused by agonist. These data suggest that PLC activity not only mediates adaptation to thermal stimuli, but likely underlies a more general mechanism that establishes the temperature sensitivity of somatosensory neurons.

Sensory nerves detect an extensive array of somatosensory stimuli, including environmental temperatures. Despite activating only a small cohort of sensory neurons, cold temperatures generate a variety of distinct sensations that range from pleasantly cool to painfully aching, prickling, and burning. Psychophysical and functional data show that cold responses are mediated by both C- and A delta-fibers with separate peripheral receptive zones, each of which likely provides one or more of these distinct cold sensations. With this diversity in the neural basis for cold, it is remarkable that the majority of cold responses in vivo are dependent on the cold and menthol receptor transient receptor potential melastatin 8 (TRPM8). TRPM8-null mice are deficient in temperature discrimination, detection of noxious cold temperatures, injury-evoked hypersensitivity to cold, and nocifensive responses to cooling compounds. To determine how TRPM8 plays such a critical yet diverse role in cold signaling, we generated mice expressing a genetically encoded axonal tracer in TRPM8 neurons. Based on tracer expression, we show that TRPM8 neurons bear the neurochemical hallmarks of both C- and A delta-fibers, and presumptive nociceptors and non-nociceptors. More strikingly, TRPM8 axons diffusely innervate the skin and oral cavity, terminating in peripheral zones that contain nerve endings mediating distinct perceptions of innocuous cool, noxious cold, and first- and second-cold pain. These results further demonstrate that the peripheral neural circuitry of cold sensing is cellularly and anatomically complex, yet suggests that cold fibers, caused by the diverse neuronal context of TRPM8 expression, use a single molecular sensor to convey a wide range of cold sensations.

Detection of innocuous temperatures allows an organism to select an appropriate environmental climate, while the ability to recognize noxious temperature extremes warns of impending tissue damage. For temperatures considered cold, the menthol receptor TRPM8 is activated when temperatures drop below approximately 26 degrees C, thus making it an intriguing candidate as the molecular mediator of cold perception. However, confirmation of this hypothesis in vivo has eluded researchers until recently. Three independent research groups have reported that mice lacking this single gene are severely impaired in their ability to detect cold temperatures. Remarkably, these animals are deficient in many diverse aspects of cold signaling, including cool and noxious cold perception, injury-evoked sensitization to cold, and cooling-induced analgesia. These animals provide a great deal of insight into the molecular signaling pathways that participate in the detection of cold and painful stimuli.

Soybean oil with an iodine value of 136 was hydrogenated to have iodine values of 126 and 117. The soybean oils with iodine values of 136, 126, and 117 were randomly interesterified using sodium methoxide. The oxidative stabilities of the hydrogenated and/or interesterified soybean oils were evaluated by measuring the headspace oxygen content by gas chromatography, and the induction time was measured using Rancimat. The melting points of the oils were evaluated by differential scanning calorimetry. Duncan's multiple range test of the headspace oxygen and induction time showed that hydrogenation increased the headspace oxygen content and induction time at alpha = 0.05. Interesterification decreased the headspace oxygen and the induction time for the soybean oils with iodine values of 136, 126, and 117 at alpha = 0.05. Hydrogenation increased the melting points as the iodine value decreased from 136 and 126 to 117 at alpha = 0.05. The random interesterification increased the melting points of soybean oils with iodine values of 136, 126, and 117 at alpha = 0.05. The combined effects of hydrogenation and interesterification increased the oxidative stability of soybean oil at alpha = 0.05 and the melting point at alpha = 0.01. The optimum combination of hydrogenation and random interesterification can improve the oxidative stability and increase the melting point to expand the application of soybean oil in foods.

Objectives: To determine the incidence of middle ear abnormalities in patients with bilateral otosclerosis, which could potentially affect successful stapedectomy, and the rates of success in these patients, including the chance of overclosure in the second ear., Study Design: Retrospective case review of operative and audiologic records., Setting: Private otology practice., Patients: One thousand eight hundred patients underwent 3,600 primary stapedectomies for bilateral otosclerosis., Intervention: Analysis of perioperative and follow-up audiograms with associated operative findings, including obliterative otosclerosis and solid footplates, dehiscent or overhanging facial nerve, narrow oval window niche, promontory overhang, and ossicular fixation or malformation., Main Outcome Measures: Audiologic stapedectomy success was determined as overclosure or closure of preoperative air-bone gap to less than 10 dB at 1 year or more of follow-up., Results: The rate of finding any abnormality was 25%. Abnormalities present bilaterally were found in 135 patients (7%), with otosclerosis requiring an oval window drillout as the most common finding (41%), followed by dehiscent or overhanging facial nerves (25%). Success in patients with abnormalities was 78% overall, with bilateral overclosure in 40%., Conclusions: Abnormal middle ear findings during stapedectomy occur in a significant percentage of patients. Reasonable rates of success and overclosure can still be expected, but this is somewhat finding-specific. The predictive value of these findings, the associated rates of success with potential impact on surgical counseling, and planning for the "other ear" are discussed.

Objective: It is hypothesized that transcriptional regulation plays an important role for neurofibromatosis type 2 (NF2) expression in Schwann cells and other cell types. The objective of this study is the isolation and characterization of the transcriptional regulatory elements of the NF2 gene., Study Design and Setting: A bacterial artificial chromosome library and a partial genomic DNA library were used to isolate the human NF2 gene; NF2 promoter-luciferase constructs were generated, and promoter activities were assayed. This study was carried out in a molecular biology laboratory., Results: A bacterial artificial chromosome clone with an approximately 100-kilobase insert containing nearly the entire human NF2 gene has been isolated. An additional 5' NF2 sequence has also been cloned. Transient transfection experiments demonstrate strong promoter activity from the NF2 5' flanking DNA., Conclusions: The NF2 gene is approximately 100 kilobases long. Both positive and negative regulatory elements are present in NF2 5' flanking regions., Significance: Better understanding of the NF2 gene and its regulation will improve molecular diagnostics and ultimately treatment of patients with NF2.

Objective: Evaluation of the ability of screening high-resolution, nonenhanced, fast spin echo (FSE) T2-weighted magnetic resonance imaging (MRI) of the internal auditory canal (IAC) and cerebellopontine angle (CPA) to detect nonacoustic schwannoma causes of unilateral sensorineural hearing loss (SNHL). FSE-MRI is equally sensitive in detecting acoustic (vestibular) schwannoma as gadolinium-enhanced MRI, but sensitivity to other causes of hearing loss is unknown., Study Design: Retrospective review of screening FSE-MRI studies., Setting: Academic otology/neurotology and neuroradiology practices., Patients: There were 1,070 patients with unilateral SNHL who underwent radiologic screening for retrocochlear pathology., Results: Normal findings were found in 944 cases. Typical (acoustic) vestibular schwannoma were found in 56 patients. Seventy additional lesions were identified: 27 CPA lesions, 29 inner ear lesions, and 12 intraaxial lesions including 9 infarctions, 1 multiple sclerosis case, 1 mesial temporal lobe sclerosis, and 1 colloid cyst., Conclusions: High-resolution T2 FSE-MRI of the IAC and CPA is a highly sensitive screening tool for unilateral SNHL, which can detect a variety of lesions in addition to vestibular schwannomas. To our knowledge in 2 years of follow-up in these patients screened for IAC/CPA lesions, no other lesions causing SNHL have been found. High-resolution FSE screening technique, used in conjunction with appropriate clinical prescreening and referral, can provide an equally sensitive method of evaluating unilateral SNHL compared to gadolinium-enhanced T1 MRI while reducing costs and providing distinct advantages in evaluating nonacoustic schwannoma causes of SNHL.

The financial burden for the evaluation of patients for acoustic neuroma in an otolaryngology practice is substantial. Patients with sudden sensorineural hearing loss represent a portion of that population seen with unilateral, asymmetric auditory symptoms who require investigation for acoustic neuroma. For these patients, gadolinium-enhanced magnetic resonance imaging is the diagnostic gold standard. Auditory brain stem response testing has been used in the past as a screening test for acoustic neuroma, but its apparent sensitivity has fallen as the ability to image smaller acoustic neuromas has improved. Fast spin echo magnetic resonance imaging techniques without gadolinium have been shown to be as effective in the detection of acoustic neuroma as contrast-enhanced magnetic resonance imaging. Limited nonenhanced fast spin echo magnetic resonance imaging now provides an inexpensive alternative for high-resolution imaging of the internal auditory canal and cerebellopontine angle. Fast spin echo magnetic resonance imaging can now be done at a cost approximating auditory brain stem response testing while providing the anatomic information of contrast-enhanced magnetic resonance imaging. Cost analysis was done in the cases of 58 patients with sudden sensorineural hearing loss by comparing the costs for routine workup and screening of acoustic neuroma with the cost of fast spin echo magnetic resonance imaging with the use of screening protocols based on literature review. The potential cost savings of evaluating patients with sudden sensorineural hearing loss with fast spin echo magnetic resonance imaging for acoustic neuroma was substantial, with a 54% reduction in screening costs. In an era of medical economic scrutiny, fast spin echo magnetic resonance imaging has become the most cost-effective method to screen suspected cases of acoustic tumors at our institution by improving existing technology while reducing the cost of providing that technology and eliminating charges for impedance audiometry, auditory brain stem response testing, and contrast-enhanced magnetic resonance imaging.

Hemangiopericytomas are rare tumors of the head and neck. The benign presentation of this tumor belies its high local recurrence rate, local aggressiveness, and malignant potential. In view of these characteristics, workup to provide a diagnosis preoperatively is of significant importance. Diagnostic imaging is helpful in planning operative management, detecting metastases, and narrowing the list of differential diagnoses. However, because of the variety and lack of specificity of radiologic findings, it is generally difficult to provide a diagnosis. A history of a painless, slowly growing, otherwise asymptomatic mass, together with the radiologic findings of a vascular neoplasm, should enhance the suspicion of an HPC as a diagnosis. Hemangiopericytoma should be included in the differential diagnosis of any vascular soft tissue lesion presenting in the head and neck, and plans for surgical intervention should include the possibility of aggressive, wide local resection in order to adequately treat such a lesion should it be encountered.

Neurotropic viruses have been postulated to play a role in the development of Menière's disease (MD). The purpose of this study was to evaluate the endolymphatic sacs of patients undergoing surgery for MD in a single-blind study for evidence of herpes simplex virus (HSV), varicella zoster (VZ), or cytomegalovirus (CMV) DNA. Polymerase chain reaction (PCR) was used as the method of detection because of its sensitivity, specificity, and applicability to fresh, as well as fixed tissues. Twenty-two patients with MD and 11 control patients with vestibular schwannomas had a portion of the endolymphatic sac removed at the time of surgery. The specimens were then evaluated for herpes simplex type and 2, varicella zoster, and cytomegalovirus DNA. Herpes simplex virus DNA was detected in 2 of the 22 extracts from the endolymphatic sacs obtained from patients with MD. There was no evidence of a positive signal obtained with any of the other viral DNA probes when PCR was performed on the control tissue extracts or the other MD tissue extracts. These results do not demonstrate a significant difference and do not statistically support the postulate that ongoing viral infection in the endolymphatic sac is a frequent factor in the development of Menière's disease.

The changes in the cell surface carbohydrates of the eustachian tube (ET) and middle ear subsequent to the intranasal (i.n.) inoculation of Streptococcus pneumoniae (Spn) type 6A were studied in the chinchilla model of otitis media (OM) using a lectin histochemical technique with six different lectins (SNA, WGA, Succ WGA, BSL II, PNA, ECL). The labeling pattern revealed not only the removal of the terminal sialic acid, but also exposure of N-acetylglucosamine (GlcNAc), a component of the trisaccharide receptor for Spn previously identified on human pharyngeal cells. The removal of sialic acid residues progressed from the nasopharyngeal to the tympanic orifice and was most pronounced in those animals from which Spn could be isolated from the middle ear. Our data indicate an alteration of the normal lectin labeling pattern and exposure of GlcNAc restricted mainly to the roof and neck portion, along the course of the eustachian tube. Exposure of part or all of a Spn adherence receptor structure by the pneumococcal enzymes, may facilitate colonization, invasion of the middle ear, and induction of OM.

The incidence of pulmonary atelectasis following head and neck surgery is not well reported. This study retrospectively evaluated the incidence of pulmonary atelectasis in 161 head and neck cancer patients, with 152 being evaluable. There were 90 patients evaluated following pectoralis musculocutaneous flap reconstruction with their effective flap size and 71 nonflap patients as a control group. Clinical findings were correlated to radiographic scores. Of pectoralis musculocutaneous flap patients screened for preexisting pulmonary disease (PEPD), nine of 45 (20%) demonstrated pulmonary atelectasis in the first 24 hours compared with 10 of 39 or 25.6% nonflap controls. Major pulmonary atelectasis was not found in the pectoralis musculocutaneous flap patients by scoring criteria, and in only one of 39 (2.6%) nonflap patients. In flaps larger than 40 cm2, the incidence was eight of 37 (21.6%), with no major pulmonary atelectasis noted. Only one of nine (11.1%) patients with radiographic pulmonary atelectasis exhibited clinical symptoms (three of 10 or 30% control). In patients with PEPD and pectoralis musculocutaneous flaps, 22 of 45 (48.9%) had evidence of pulmonary atelectasis in contrast to 13 of 32 or 40.6% controls. There were two of 45 (4.4%) who had major pulmonary atelectasis with zero of 32 in the nonflap group. For flaps larger than 40 cm2, the incidence was 19 of 39 (48.7%) with two of 39 (5.1%) scored as major pulmonary atelectasis. The clinical correlation for this group and the major pulmonary atelectasis group was each approximately 50% compared to 15.4% for nonflap patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Previous studies have shown that viral upper respiratory tract (URT) infection predisposes to the development of bacterial otitis media (OM). The mechanisms underlying this phenomenon have been well defined for influenza A virus in the chinchilla model of experimental OM but have not been for adenovirus because of the heretofore lack of an appropriate model. In this study, chinchillas were inoculated intranasally or transbullarly with type 1 adenovirus to assess whether or not the chinchilla could serve as a suitable model for future investigation of adenovirus predisposition to bacterial OM. Data indicated that the chinchilla readily supported an active infection by and responded serologically to this agent and that route of inoculation markedly influenced otoscopic findings, elicitation of middle ear fluids, onset and location of histopathology, and progression of disease. The time course of disease onset and recovery and an assessment of the effect of this virus isolate on the mucosal epithelial integrity and on both the ciliary activity and transport function of the eustachian tube epithelium for both routes of inoculation are presented.