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Thomas V Bilfinger

Publications and source records attributed to Thomas V Bilfinger.

15 recordsLinked to original sources
PubMed2006

Growing PET positive nodule in a patient with histoplasmosis: case report.

BACKGROUND: Pulmonary histoplasmosis is a mycotic infection that often resembles pulmonary malignancy and continues to complicate the evaluation of pulmonary nodules. CASE PRESENTATION: We report a case of an immunocompetent patient who, despite adequate treatment for known histoplasmosis lung infection, presented with radiological and F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) findings mimicking primary lung malignancy which eventually required surgical resection. CONCLUSION: Histoplasmosis infection may radiologically resemble pulmonary malignancy, often causing a diagnostic dilemma. PET imaging is currently used for and considered accurate in the evaluation of pulmonary nodules. However, overlap in PET standardized uptake value (SUV) between granulomatous and malignant lesions decreases the accuracy of PET as a diagnostic modality. Future advances in PET imaging are needed to improve its accuracy in the evaluation of pulmonary nodules in areas where histoplasmosis is endemic.

Diagnosis, Differential↗
PubMed2006

Invited commentary.

Explore the source record for details and available documents.

Cardiopulmonary Bypass↗
PubMed2006

Alcohol-, nicotine-, and cocaine-evoked release of morphine from invertebrate ganglia: model system for screening drugs of abuse.

BACKGROUND: Invertebrates express regulatory receptors, transporters, and channels responsive to established drugs of abuse, many of which mediate their effects through catecholamine pathways. We hypothesized that invertebrate neural systems may serve as models by which to evaluate the interactive pharmacological effects of these agents. MATERIAL AND METHODS: Ex vivo pharmacological trials determined the effects of saturating levels of ethanol on morphine levels in pooled Mytilus edulis ganglia via HPLC coupled to electrochemical detection and/or HPLC/RIA analyses. Additional trials evaluated the ability of ethanol, nicotine, and cocaine, to promote evoked release of 125I-labeled morphine from neural tissues, because intrinsically low levels of morphine did not allow direct quantification of its release. RESULTS: Incubation of pooled M. edulis pedal ganglia with 200 mM ethanol (approximately 1% ethanol v/v) resulted in a two-fold increase in morphine concentration at 15 min, return to baseline at 30 min, and a 50% decrease in morphine concentration at 60 min. Separate incubations of pooled M. edulis pedal ganglia and H. americanus nerve cord with ethanol, cocaine, and nicotine resulted in a statistically significant enhancement of 125I-trace labeled morphine release. CONCLUSIONS: The stimulatory effects of ethanol, nicotine, and cocaine on cellular expression and release of endogenous morphine suggest convergent mechanisms underlying the reinforcing and addictive properties for a variety of drugs of abuse. The evolutionary conservation of L-tyrosine as a common precursor to catecholamine and opiate/opioid signaling systems may define a functional triad involving endogenous morphine, dopamine, and other classes of addictive drugs.

Animals↗
PubMed2005

The impact of positron emission tomography on clinical decision making in a university-based multidisciplinary lung cancer practice.

INTRODUCTION: Positron emission tomography (PET) scanning has gained increasing application as a diagnostic and staging tool in the evaluation of lung cancer. Although PET scanning has been demonstrated to be a cost-effective adjunct to lung cancer diagnosis, its global impact on clinical decision making has not been assessed. STUDY OBJECTIVES: To evaluate the impact of the systematic use of PET scanning on clinical decision making. DESIGN: Retrospective study. SETTING: A university-based multidisciplinary lung cancer practice. PATIENTS: All patients undergoing diagnostic or staging PET scans from December 31, 2000, to December 31, 2002. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: One hundred ninety-eight patients underwent PET for diagnosis (161 patients) or staging (37 patients). PET scan results and clinical outcomes were retrospectively reviewed to determine the frequency with which PET scan findings (1) upstaged patients, (2) downstaged patients, (3) changed the diagnostic workup, (4) altered therapy, (5) resulted in a significant additional diagnosis, and (6) triggered evaluations that ultimately proved fruitless. PET upstaged 32 of 198 patients (16.2%) and downstaged 12 patients (6.1%), facilitating curative resection in 4 patients. Overall, PET scan findings changed the stage in 44 patients (22.2%). PET scan findings changed diagnostic management in 105 of 198 patients (53%), among whom biopsy was deferred in 65 patients (61.9%) and was triggered or guided in 40 patients (38.1%). PET scan findings altered treatment decisions in 38 patients (19.2%), leading to neoadjuvant therapy in 6 patients and resection in 5 patients, and forestalling noncurative thoracotomy in 6 patients. PET scan findings prompted or redirected chemotherapy or radiotherapy in the remainder of the patients. Overall, PET scan findings changed management in 143 patients (72.2%). PET scan findings triggered additional diagnostic testing in 32 patients (16.2%), resulting in no new diagnosis in 16 patients (50%) and a critical change in management in 7 patients (21.9%). PET scan findings were solely responsible for a significant non-lung cancer diagnosis in eight patients (4%). CONCLUSIONS: Systematically applied PET scanning has a significant impact on patient management, altering diagnostic or therapeutic interventions in 72.2% of patients, changing staging in 22.2% of patients, and identifying serious unsuspected diagnoses in 4.0% of patients, with potentially life-saving consequences in 2.0%. Key Words: diagnosis; lung neoplasms; positron emission tomography.

Decision Support Techniques↗
PubMed2005

Increased standardized uptake value in the primary lesion predicts nodal or distant metastases at presentation in lung cancer.

Standardized uptake value (SUV) has been linked to tumor aggressiveness and long-term prognosis. Based on the hypothesis that positron emission tomography (PET) SUV serves as a surrogate for biologic aggression, we investigated whether SUV in the primary lesion, independent of size, correlates with the presence of nodal or distant metastases at the time of presentation. We retrospectively reviewed computed tomography (CT) scan, PET scan, and histologic findings of consecutive patients in our lung cancer referral population evaluated between December 15, 2000 and April 15, 2004. Only patients with primary non-small-cell lung cancer and pathologic confirmation of nodal status or conventionally accepted non-PET proof of distant metastases were included for analysis. One hundred thirty-nine patients had complete results, including CT, PET, and independent confirmation of nodal or distant disease. The stage distribution was as follows: 33 IA, 24 IB, 5 IIA, 9 IIB, 21 IIIA, 8 IIIB, and 39 IV. Simple logistic regression analysis demonstrated a highly significant correlation between SUV of the primary lesion and the presence of nodal or distant metastases at the time of presentation (P = 0.0036). When odds ratios were calculated, a 13% increase in the likelihood of nodal/distant disease was found for every unit increase in SUV. We conclude that PET SUV, independent of size, is a marker of biologic aggression. Elevated SUV in the primary lesion at presentation should prompt high suspicion and mandates meticulous search for nodal or distant disease.

Adult↗
PubMed2004

Differential expression of the human mu opiate receptor from different primary vascular endothelial cells.

BACKGROUND: Studies from our laboratory have identified a novel mu opiate receptor, mu3, which is expressed in several tissues, such as human vascular endothelial cells, leukocytes and invertebrate neural tissues. This novel mu receptor has been shown to be selective for opiate alkaloids, insensitive to opioid peptides, and also is coupled to constitutive nitric oxide release. MATERIAL/METHODS: In this study, we compare the mu3 receptor gene expression from three different vascular endothelial primary cell lines at the molecular level using a Taqman probe for the mu opiate receptor. RESULTS: Results from this study demonstrate that human umbilical vein endothelial cells (2.0, relative gene expression) and human pulmonary artery endothelial cells (1.1, relative gene expression) expressed more of the mu opiate receptor as compared to human arteriole endothelial cells (0.82, relative gene expression). CONCLUSIONS: The individual variations in mu receptor expression in these vascular tissues may explain the large variance in graft survival using saphenous veins for coronary artery bypass surgery.

Base Sequence↗
PubMed2004

Surgical aspects in the treatment of lung cancer.

PURPOSE OF REVIEW: The treatment of lung cancer has been most successful when surgery is involved. This review is a succinct overview of lung cancer treatment from the thoracic surgeon's perspective over the past 2 years. RECENT FINDINGS: Starting with the evidence-based guidelines developed by the American College of Chest Physicians, the main themes in the literature are a multimodality approach and the miniaturization of surgical approaches. Palliative procedures, staging, and extension of surgery to patients previously thought inoperable are other subjects covered. SUMMARY: We are standing on the verge of having a definitive answer to the 20-year-old question whether adjuvant or neoadjuvant chemotherapy benefits patients with early-stage non-small cell lung cancer. Sufficient data will be available shortly to determine whether minimally invasive surgical approaches yield similar long-term outcomes as traditional approaches.

Carcinoma, Non-Small-Cell Lung↗
PubMed2004

Presence of morphine in rat amygdala: evidence for the mu3 opiate receptor subtype via nitric oxide release in limbic structures.

BACKGROUND: We have identified a novel mu opiate receptor, p3, which is expressed in several human tissues, is selective for opiate alkaloids, insensitive to opioid peptides, and also is coupled to constitutive nitric oxide release. We, and others, have also demonstrated the presence of opiate alkaloids as endogenous substances in various nerve tissues taken from mammals, man and invertebrates. MATERIAL/METHODS: Morphine isolation and identification was achieved by high pressure liquid chromatography coupled to electrochemical detection. This material was finally identified by nano-electrospray ionization quadruple time-of-flight tandem mass spectrometry (Q-TOF MS/MS). Morphine's ability to release nitric oxide from limbic tissues was determined in real-time via an amperometric probe. RESULTS: We demonstrate the presence of morphine in rat brain amygdala at 12.7 +/- 5.4 ng/g wet tissue. Morphine was able to stimulate the release of nitric oxide from hippocampus and amygdalar tissues in a naloxone and L-NAME sensitive manner. Furthermore, rat chow, incubation medium etc, did not contain morphine, eliminating the possibility of contamination. CONCLUSION: This finding provides evidence that morphine biosynthesis occurs in mammalian neural tissues. It also demonstrates that morphine releases nitric oxide in limbic tissues. Given the limbic system involvement in modulating emotion, including experiences related to pain perception, it appears that morphine is involved with this activity.

Amygdala↗
PubMed2003

Presence of reticuline in rat brain: a pathway for morphine biosynthesis.

We demonstrate the presence of reticuline, an isoquinoline alkaloid that was purified and identified in the rat brain. This was achieved by high-performance liquid chromatography coupled with electrochemical detection. This material was finally identified by nano-electrospray ionization quadrupole time-of-flight tandem mass spectrometry. The expression of this tetrahydroisoquinoline alkaloid in rat brain is at 12.7+/-5.4 ng/g wet tissue. Furthermore, rat chow, rat small and large intestine and bacteria cultured from these tissues did not contain either morphine or reticuline, eliminating the possibility of contamination or an exogenous source of these compounds. This finding adds information which suggests that morphine biosynthesis may occur in rat neural tissues, and that its biosynthesis pathway may be similar to that reported in the poppy plant.

Alkaloids↗
PubMed2003

Modeling stroke risk after coronary artery bypass and combined coronary artery bypass and carotid endarterectomy.

BACKGROUND AND PURPOSE: The goals of this study were to compare the ability of statewide and institutional models of stroke risk after coronary artery bypass (CAB) to predict institution-specific results and to examine the potential additive stroke risk of combined CAB and carotid endarterectomy (CEA) with these predictive models. METHODS: An institution-specific model of stroke risk after CAB was developed from 1975 consecutive patients who underwent nonemergent CAB from 1994 to 1999 in whom severe carotid stenosis was excluded by preoperative duplex screening. Variables recorded in the New York State Cardiac Surgery Program database were analyzed. This model (model I) was compared with a published model (model II) derived from analysis of the same variables using New York statewide data from 1995. Predicted and observed stroke risks were compared. These formulas were applied to 154 consecutive combined CAB/CEA patients operated on between 1994 and 1999 to determine the predicted stroke risk from CAB alone and thereby deduce the maximal added risk imputed to CEA. RESULTS: Risk factors common to both models included age, peripheral vascular disease, cardiopulmonary bypass time, and calcified aorta. Additional risk factors in model I also included left ventricular hypertrophy and hypertension. Risk factors exclusive to model II included diabetes, renal failure, smoking, and prior cerebrovascular disease. Our observed stroke rate for isolated CAB was 1.7% compared with a rate predicted with model II (statewide data) of 1.56%. The observed stroke rate for combined CEA/CAB was 3.9%. When the Stony Brook model (model I) based on patients without carotid stenosis was used, the predicted stroke rate was 2.8%. When the statewide model (model II), which included some patients with extracranial vascular disease, was used, the predicted stroke rate was 3.4%. The differences between observed and predicted stroke rates were not statistically significant. CONCLUSIONS: Estimation of stroke risk after CAB was similar whether statewide data or institution-specific data were used. The statewide model was applicable to institution-specific data collected over several years. Common risk factors included age, aortic calcification, and peripheral vascular disease. The observed differences in the predicted stroke rates between models I and II may be due to the fact that carotid stenosis was specifically excluded by duplex ultrasound from the patient population used to develop model I. Modeling stroke risk after CAB is possible. When these models were applied to patients undergoing combined CAB/CEA, no additional stroke risk could be ascribed to the addition of CEA. Such models may be used to identify groups at increased risk for stroke after both CAB and combined CAB/CEA. The ultimate place for CEA in patients undergoing CAB will be defined by prospective randomized trials.

Adult↗
PubMed2003

Surgical viewpoints for the definitive treatment of lung cancer.

Surgery remains a central pillar in the treatment of lung cancer. To optimize surgical interventions, careful preoperative assessment is necessary. Pulmonary status and cardiac status are the main risks to be considered. After operability has been established, resectability is assessed by staging the lung cancer. Surgery offers a variety of tools to accomplish complete staging before resection. Successful resection is defined as the complete removal of the cancer. To accomplish this goal, a multidisciplinary approach is evolving rapidly. For patients with nonoperable cancer, surgical techniques have been developed to manage airway obstructions and to drain effusions.

Humans↗
PubMed2002

Direct assessment and diminished production of morphine stimulated NO by diabetic endothelium from saphenous vein.

AIM: To directly measure in real time basal and stimulated levels of NO released from human saphenous vein endothelium and to quantify the expression of the mu opiate receptor, which has been linked with NO release. METHODS: Saphenous vein segments from patients with type 2 diabetes (n=12) and patients without diabetes (n=8) were obtained. The release of NO was measured directly from the endothelium using a NO-specific amperometric probe. N(Omega)-nitro-L-arginine methyl ester (L-NAME, 0.1 mmol/L), a NO synthase (NOS) inhibitor, or morphine (1 mumol/L), a stimulant, was administered and the measurements were repeated. Values were reported relative to the mean initial measurement of NO release from diabetic endothelium, which was defined as the relative zero level of NO release. A RT-PCR was then performed on the endothelium to measure mu opiate receptor expression. RESULTS: Diabetic patients (n=12) showed a relative and significantly diminished basal level of released NO, (0.049+/-0.012) nmol/L, compared with non diabetic patients (n=8), (0.42+/-0.12) nmol/L (P<0.05). Application of L-NAME to nonstimulated tissues resulted in no change in NO release from the diabetic group and a decrease in NO release of (0.21+/-0.09) nmol/L from the non diabetic group (P<0.05). Morphine stimulation of the diabetic endothelium resulted in a lower peak and shorter duration of NO release compared to the non-diabetic tissue, (21+/-6) nmol/L vs (38+/-4) nmol/L and (7.3+/-1.4) min vs (12.2+/-2.2) min, respectively (P<0.01). Lastly, evaluation of the mu opiate receptor expression was found to be diminished in the diabetics by 59.1 %. CONCLUSION: Maturity-onset diabetes attenuates both the constitutive basal and morphine stimulated NO release from human saphenous vein endothelium. In this study, after NOS inhibition, the actual basal NO release in diabetes was negligible. One explanation for the impaired capacity of diabetic endothelium to release NO was the diminished mu opiate receptor that was seen in diabetic endothelium.

Aged↗
PubMed2002

A hormonal role for endogenous opiate alkaloids: vascular tissues.

The distribution of morphine-containing cells in the central nervous system, adrenal gland, and its presence in blood may serve to demonstrate that this signal molecule can act as a hormone besides its role in cell-to-cell signaling within the brain. This speculative review is the result of a literature evaluation with an emphasis on studies from our laboratory. Opioid peptides and opiate alkaloids have been found to influence cardiac and vascular function. They have also been reported to promote ischemic preconditioning protection in the heart. Given the presence of morphine and the novel mu(3) opiate receptor on vascular endothelial cells, including cardiac and vascular endothelial cells in the median eminence, it would appear that endogenous opiate alkaloids are involved in modulating cardiac function, possible at the hormonal level. This peripheral target tissue, via nitric oxide coupling to mu opiate receptors, may serve to down regulate the excitability of this tissue given the heart's high performance state as compared to that of the saphenous vein, a passive resistance conduit. With this in mind, morphine and other endogenous opiate alkaloids may function as a hormone.

Alkaloids↗
PubMed2002

Morphine down regulates human vascular tissue estrogen receptor expression determined by real-time RT-PCR.

UNLABELLED: Human vascular endothelial cells express the estrogen receptor-beta (ER-beta), which can be modulated by the opiate alkaloid morphine. OBJECTIVES: To determine if morphine is capable of down regulating the ER-beta receptor in a similar fashion as the mu opiate receptor since they are both coupled to constitutive nitric oxide synthase derived nitric oxide release. METHODS AND RESULTS: Endothelial cells obtain from human vascular tissues (saphenous vein, atria and primary saphenous vein cells) were treated with 1 uM morphine plus or minus the mu opiate receptor antagonist naloxone or CTOP (10 uM) for 24 h at 37 degrees C. Total RNA was isolated from treated and untreated primary endothelial cells, and specific primers and a probe were used to determine the ER-beta gene expression by real-time RT-PCR. Cells treated with morphine exhibited a down-regulation of ER-beta, whereas naloxone and CTOP were able to partially block the morphine effect. In addition, the 266 bp fragment generated by RT-PCR using the same primers as in the real-time PCR was sequenced and revealed a 100% sequence identity as the authentic ER-beta gene sequence. CONCLUSIONS: These results indicate that ER-beta is expressed in human vascular endothelial cells, and morphine appears to regulate this receptor in a similar fashion as the mu opiate receptor.

Adult↗