Search PubMed⌕ Search

Biomedical subjects

G Siegel

Publications and source records attributed to G Siegel.

At least 19 recordsLinked to original sources
PubMed2006

Simulation of cerebral hemodynamics for preoperative risk assessment.

BACKGROUND: An important part of the medical treatment of many cerebrovascular diseases is the occlusion of brain supplying arteries. Until now, the risk of this intervention can only be estimated by invasive diagnostics including the risk of cerebrovascular accidents. METHODS AND RESULTS: As a supporting tool, a computer model of the circle of Willis was designed. The model is based upon linear differential equations describing electrotechnical circuits extended non-linearly. By these means, time continuous simulations of different states and the online observation of all calculated state variables such as blood pressure and blood flow in every modeled vessel became feasible. For individual simulations, model parameters were determined by MR-angiography and boundary values by simultaneous Duplex-measurements in both carotid and vertebral arteries. State variables generated by the model behaved physiologically and the reaction of individual cerebrovascular systems in critical situations could be investigated by special scenarios. Inaccuracies concerning the determination of model parameters and boundary values of the used differential equations are likely to be resolved in the near future through a more careful and technically improved determination of these values. CONCLUSIONS: Computer models of subjects were created taking in account the individual anatomical and non-linear physical properties of real vascular systems supplying the brain. Thereby information could be obtained concerning the hemodynamic effects of an iatrogenic vascular occlusion.

Brain↗
PubMed2006

Stable expression of the vesicular GABA transporter following photothrombotic infarct in rat brain.

Before exocytotic release of the inhibitory neurotransmitter GABA, this amino acid has to be stored in synaptic vesicles. Accumulation of GABA in vesicles is achieved by a specific membrane-integrated transporter termed vesicular GABA transporter. This vesicular protein is mainly located at presynaptic terminals of GABAergic interneurons. In the present study we investigated the effects of focal ischemia on the expression of the vesicular GABA transporter. Vesicular GABA transporter mRNA and protein expression was examined after photothrombosis in different cortical and hippocampal brain regions of Wistar rats. In situ hybridization and quantitative real-time RT-PCR were performed to analyze vesicular GABA transporter mRNA. Both vesicular GABA transporter mRNA-stained perikarya and mRNA expression levels remained unaffected. Vesicular GABA transporter protein-containing synaptic terminals and somata were visualized by immunohistochemistry. The pattern of vesicular GABA transporter immunoreactivity as well as the protein expression level revealed by semiquantitative image analysis and by Western blot remained stable after stroke. The steady expression of vesicular GABA transporter mRNA and protein after photothrombosis indicates that the exocytotic release mechanism of GABA is not affected by ischemia.

Animals↗
PubMed2005

Persistent anti-Dra in two pregnancies.

The Drori (Dr(a)) antigen is one of the ten high-prevalence antigens of the Cromer blood system, which are carried on decayaccelerating factor (DAF, CD55). The Dr(a-) phenotype was first described in a 48-year-old Jewish woman from Bukhara. Her serum contained an antibody to a high-prevalence antigen named anti-Dra. Most known individuals with the Dr(a-) phenotype are Jews from the geographic area of Bukhara, but individuals from Japan have also been described. Antibodies in the Cromer blood group system, including anti-Dra,have never been reported to cause HDN. In most of the cases with anti-Dra examined in Israel, the antibodies have been subtyped as IgG2 and IgG4. This report is of a woman with Dr(a-) phenotype and an anti-Dr(a) titer of 256 to 512 in her serum, observed during two successive pregnancies. At birth, the RBCs of the first- and second-born child were negative and positive in the DAT, respectively, and neither manifested clinical signs of HDN. The disappearance of Cromer system antibodies, including anti-Dra in midpregnancy, has been described in a previous study. In that study, it was theorized that the antibodies in the serum of the women were adsorbed onto placental DAF. The finding of a high anti-Dra titer in two successive pregnancies in this patient, with a positive DAT for the RBCs of one of the two babies at term, differs from published reports, suggesting that a different mechanism might be involved.

Adult↗
PubMed2004

The effect of garlic on arteriosclerotic nanoplaque formation and size.

OBJECTIVE: In an in vitro biosensor model (PCT/EP 97/05212), the interplay between different lipoproteins in arteriosclerotic nanoplaque formation, as well as aqueous garlic extract (0.2-5.0 g/l from LI 111 powder) as a possible candidate drug against arterio/atherosclerosis were tested within the frame of a high throughput screening. METHODS: The processes described below were studied by ellipsometric techniques quantifying the adsorbed amount (nanoplaque formation) and layer thickness (nanoplaque size). A thorough description of the experimental setup has been given previously. RESULTS: Proteoheparan sulfate (HS-PG) adsorption to hydrophobic silica was monoexponential and after approximately 30 min constant. The addition of 2.52 mmol/l Ca2+ led to a further increase in HS-PG adsorption because Ca2+ was bound to the polyanionic glycosaminoglycan (GAG) chains thus screening their negative fixed charges and turning the whole molecule more hydrophobic. Incubation with 0.2 g/l aqueous garlic extract (GE) for 30 min did not change the adsorption of HS-PG. However, the following addition of Ca2+ ions reduced the increase in adsorption by 50.8% within 40 min. The adsorption of a second Ca2+ step to 10.08 mmol/l was reduced by even 82.1% within the next 40 min. Having detected this inhibition of receptor calcification, it could be expected that the build-up of the ternary nanoplaque complex is also affected by garlic. The LDL plasma fraction (100 mg/dl) from a healthy probationer showed beginning arteriosclerotic nanoplaque formation already at a normal blood Ca2+ concentration, with a strong increase at higher Ca2+ concentrations. GE, preferably in a concentration of 1 g/l, applied acutely in the experiment, markedly slowed down this process of ternary aggregational nanoplaque complexation at all Ca2+ concentrations used. In a normal blood Ca2+ concentration of 2.52 mmol/l, the garlic induced reduction of nanoplaque formation and molecular size amounted to 14.8% and 3.9%, respectively, as compared to the controls. Furthermore, after ternary complex build-up, GE similar to HDL, was able to reduce nanoplaque formation and size. The incubation time for HDL and garlic was only 30 min each in these experiments. Nevertheless, after this short time the deposition of the ternary complex decreased by 6.2% resp. 16.5%, i.e. the complex aggregates were basically resolvable. CONCLUSIONS: These experiments clearly proved that garlic extract strongly inhibits Ca2+ binding to HS-PG. In consequence, the formation of the ternary HS-PG/LDL/Ca2+ complex, initially responsible for the 'nanoplaque' composition and ultimately for the arteriosclerotic plaque generation, is decisively blunted.

Arteriosclerosis↗
PubMed2003

Reduction of arteriosclerotic nanoplaque formation and size by fluvastatin in a receptor-based biosensor model.

Proteoheparan sulfate can be adsorbed onto a methylated silica surface in a monomolecular layer via its transmembrane hydrophobic protein core domain. Due to electrostatic repulsion, its anionic glycosaminoglycan side chains are stretched out into the blood substitute solution, thereby representing a receptor site for specific lipoprotein binding through basic amino acid-rich residues within their apolipoproteins. The binding process was studied by ellipsometric techniques suggesting that HDL has a high binding affinity and a protective effect on interfacial heparan sulfate proteoglycan layers with respect to LDL and Ca(2+) complexation. LDL was found to be deposited strongly at the proteoheparan sulfate-coated surface, particularly in the presence of Ca(2+), apparently through complex formation 'proteoglycan-low density lipoprotein-calcium'. This ternary complex build-up may be interpreted as arteriosclerotic nanoplaque formation on the molecular level responsible for the arteriosclerotic primary lesion. In a receptor-based biosensor application, this system was tested on its reliability to unveil possible acute pleiotropic effects of the lipid lowering drug fluvastatin. The VLDL/IDL/LDL and VLDL/IDL/LDL/HDL plasma fractions from a high risk patient with dyslipoproteinaemia and type 2 diabetes mellitus showed the start of arteriosclerotic nanoplaque formation at a normal blood Ca(2+) concentration, with a strong increase at higher Ca(2+) concentrations. Nanoplaque formation and size of the HDL-containing lipid fraction remained well below that of the LDL-containing lipid fraction. Fluvastatin, whether applied acutely to the patient (one single 80 mg slow release matrix tablet) or in a 2-month medication regimen, markedly slowed down this process of ternary aggregational nanoplaque build-up and substantially inhibited nanoplaque size development at all Ca(2+) concentrations used. The acute action gave no significant change in lipid concentrations of the patient. Furthermore, after nanoplaque generation, fluvastatin, similar to HDL, was able to reduce nanoplaque formation and size. These immediate effects of fluvastatin have to be taken into consideration when interpreting the clinical outcome of long-term studies.

Adsorption↗
PubMed2003

The effect of an HMG-CoA reductase inhibitor on arteriosclerotic nanoplaque formation and size in a biosensor model.

Proteoheparan sulfate can be adsorbed to a methylated silica surface in a monomolecular layer via its transmembrane hydrophobic protein core domain. Due to electrostatic repulsion, its anionic glycosaminoglycan side chains are stretched out into the blood substitute solution, thereby representing a receptor site for specific lipoprotein binding through basic amino acid-rich residues within their apolipoproteins. The binding process was studied by ellipsometric techniques. Low-density lipoprotein (LDL) was found to deposit strongly at the proteoheparan sulfate-coated surface, particularly in the presence of Ca(2+), apparently through complex formation 'proteoglycan-LDL-calcium'. This ternary complex build-up may be interpreted as arteriosclerotic nanoplaque formation on the molecular level responsible for the arteriosclerotic primary lesion. HDL bound to heparan sulfate proteoglycan protected against LDL deposition and completely suppressed calcification of the proteoglycan-lipoprotein complex. In addition, HDL was able to decelerate the ternary complex deposition and to disrupt newly formed nanoplaques. Therefore, HDL attached to its proteoglycan receptor sites is thought to raise a multidomain barrier, selection and control motif for transmembrane and paracellular lipoprotein uptake into the arterial wall. The molecular arteriosclerosis model was tested on its reliability in a biosensor application in order to unveil possible acute pleiotropic effects of the lipid lowering drug fluvastatin. The very low-density lipoprotein (VLDL)/intermediate-density lipoprotein (IDL)/LDL and VLDL/IDL/LDL/HDL plasma fractions from a high-risk patient with dyslipoproteinemia and type 2 diabetes mellitus showed beginning arteriosclerotic nanoplaque formation already at a normal blood Ca(2+) concentration, with a strong increase at higher Ca(2+) concentrations. Nanoplaque formation and size of the HDL-containing lipid fraction remained well below that of the LDL-containing lipid fraction. Fluvastatin, whether applied acutely to the patient (one single 80 mg slow release matrix tablet) or in a 2-months medication regimen, markedly slowed down this process of ternary aggregational nanoplaque build-up and substantially inhibited nanoplaque size development at all Ca(2+) concentrations used. The acute action resulted without any significant change in lipid concentrations of the patient. Furthermore, after nanoplaque generation, fluvastatin, similar to HDL, was able to reduce nanoplaque formation and size. These immediate effects of fluvastatin have to be taken into consideration while interpreting the clinical outcome of long-term studies.

Adsorption↗
PubMed2003

[Carcinomas of the esophago-gastric junction: surgical strategies].

There is increasing incidence of adenocarcinoma of the esophagastric junction (EGJ) especially in young white men (+35% in 30 years). The reasons for this are not yet well known, however one of the main causes is gastro-esophageal-reflux disease (GERD). The differentiation of a EGT carcinoma in three subtypes is important for therapy: adenocarcinoma of the distal esophagus (type I), cardia carcinoma (type II) and subcardial gastric carcinoma (type III). The most important risk-factor for type I-cancers is "barrett's metaplasia" resulting from GERD over years. The risks for the type II- and type III-carcinomas may be obesity and high caloric and fat intake. The role of Helicobacter pylori infection and adenocarcinoma of the subcardia is unproven. Preoperative tumor staging is difficult and tumor-stage is most often underestimated (esp. in the case of a high-grade dysplasia where in 43% carcinomas one already established). Therapy for all three types of EGJ tumors is surgical. Transhiatal (rarely transthoracic) esophagectomy with lymphadenectomy and proximal gastrectomy is performed for type-I-tumors, type-II and III-tumors are treated like a gastric cancer with total gastrectomy, lymphadenectomy and distal esophagectomy. Lymph-node metastases and advanced tumor-stage are bad prognostic factors, complete tumor resection (R0 resection) with extended lymphadenectomy will improve prognosis. The results of a preoperative combined-modality therapy are encouraging, but have not yet shown a definitive benefit. In case of distant metastases, radio-chemotherapy combined with gastroenterologic treatments (e.g. esophageal prostheses, PEG, etc.) will be used as a palliative treatment option.

Adenocarcinoma↗
PubMed2002

Polymorphism of the serotonin-2A receptor gene (HTR2A) associated with childhood attention deficit hyperactivity disorder (ADHD) in adult women with seasonal affective disorder.

INTRODUCTION: Several lines of research point to a possible overlap between seasonal affective disorder (SAD) and attention deficit hyperactivity disorder (ADHD), particularly in females. There is also emerging evidence that variation of the 5-HT2A receptor gene (HTR2A) contributes to both SAD and ADHD. The current study investigated whether variation in HTR2A was associated with symptoms of childhood ADHD in adult women with SAD. METHOD: Sixty-six women with SAD were administered the Wender-Utah Rating Scale (WURS), which retrospectively assesses childhood ADHD, as part of an ongoing genetic study of SAD. WURS scores were compared across the three genotypic groups defined by the T102C polymorphism of HT2RA. RESULTS: Analysis of variance indicated a significant difference in mean 25-item WURS scores across the three genotypic groups (p = 0.035). Post-hoc tests revealed that the C/C genotypic group had a significantly higher mean score than both the T/T group and T/C group. Based on previously established WURS criteria, 38% of subjects with the C/C genotype, and none with the T/T genotype, had scores consistent with childhood ADHD. LIMITATIONS: The current sample size is small, and childhood ADHD diagnoses were based on retrospective recall. CONCLUSION: These preliminary results suggest a possible association between variation in HTR2A, childhood ADHD, and the later development of SAD in women.

Adult↗
PubMed2002

Biosensing of arteriosclerotic nanoplaque formation and interaction with an HMG-CoA reductase inhibitor.

Proteoheparan sulphate can be adsorbed to a methylated silica surface in a monomolecular layer via its transmembrane hydrophobic protein core domain. As a result of electrostatic repulsion, its anionic glycosaminoglycan side chains are stretched out into the blood substitute solution, thereby representing one receptor site for specific lipoprotein binding through basic amino acid-rich residues within their apolipoproteins. The binding process was studied by ellipsometric techniques suggesting that high-density lipoprotein (HDL) has a high binding affinity and a protective effect on interfacial heparan sulphate proteoglycan layers with respect to low-density lipoprotein (LDL) and Ca2+ complexation. Low-density lipoprotein was found to deposit strongly at the proteoheparan sulphate-coated surface, particularly in the presence of Ca2+, apparently through complex formation 'proteoglycan-LDL-calcium'. This ternary complex build-up may be interpreted as arteriosclerotic nanoplaque formation on the molecular level responsible for the arteriosclerotic primary lesion. On the other hand, HDL bound to heparan sulphate proteoglycan protected against LDL deposition and completely suppressed calcification of the proteoglycan-lipoprotein complex. In addition, HDL was able to decelerate the ternary complex deposition. Therefore, HDL attached to its proteoglycan receptor sites is thought to raise a multidomain barrier, selection and control motif for transmembrane and paracellular lipoprotein uptake into the arterial wall. Although much remains unclear regarding the mechanism of lipoprotein depositions at proteoglycan-coated surfaces, it seems clear that the use of such systems offers possibilities for investigating lipoprotein deposition at a 'nanoscopic' level under close to physiological conditions. In particular, Ca2+-promoted LDL deposition and the protective effect of HDL even at high Ca2+ and LDL concentrations agree well with previous clinical observations regarding risk and beneficial factors for early stages of atherosclerosis. Considering this, the system was tested on its reliability in a biosensor application in order to unveil possible acute pleiotropic effects of the lipid lowering drug fluvastatin. The very low-density lipoprotein (VLDL)/intermediate-density lipoprotein (IDL)/LDL plasma fraction from a high risk patient with dyslipoproteinaemia and type 2 diabetes mellitus showed beginning arteriosclerotic nanoplaque formation already at a normal blood Ca2+ concentration, with a strong increase at higher Ca2+ concentrations. Fluvastatin, whether applied to the patient (one single 80 mg slow release matrix tablet) or acutely in the experiment (2.2 micromol L-1), markedly slowed down this process of ternary aggregational nanoplaque complexation at all Ca2+ concentrations used. This action resulted without any significant change in lipid concentrations of the patient. Furthermore, after ternary complex build-up, fluvastatin, similar to HDL, was able to reduce nanoplaque adsorption and size. These immediate effects of fluvastatin have to be taken into consideration while interpreting the clinical outcome of long-term studies.

Adsorption↗
PubMed2001

Arachidonic acid modulates the spatiotemporal characteristics of agonist-evoked Ca2+ waves in mouse pancreatic acinar cells.

In pancreatic acinar cells analysis of the propagation speed of secretagogue-evoked Ca2+ waves can be used to examine coupling of hormone receptors to intracellular signal cascades that cause activation of protein kinase C or production of arachidonic acid (AA). In the present study we have investigated the role of cytosolic phospholipase A2 (cPLA2) and AA in acetylcholine (ACh)- and bombesin-induced Ca2+ signaling. Inhibition of cPLA2 caused acceleration of ACh-induced Ca2+ waves, whereas bombesin-evoked Ca2+ waves were unaffected. When enzymatic metabolization of AA was prevented with the cyclooxygenase inhibitor indomethacin or the lipoxygenase inhibitor nordihydroguaiaretic acid, ACh-induced Ca2+ waves were slowed down. Agonist-induced activation of cPLA2 involves mitogen-activated protein kinase (MAPK) activation. An increase in phosphorylation of p38(MAPK) and p42/44(MAPK) within 10 s after stimulation could be demonstrated for ACh but was absent for bombesin. Rapid phosphorylation of p38(MAPK) and p42/44(MAPK) could also be observed in the presence of cholecystokinin (CCK), which also causes activation of cPLA2. ACh-and CCK-induced Ca2+ waves were slowed down when p38(MAPK) was inhibited with SB 203580, whereas inhibition of p42/44(MAPK) with PD 98059 caused acceleration of ACh- and CCK-induced Ca2+ waves. The spreading of bombesin-evoked Ca2+ waves was affected neither by PD 98059 nor by SB 203580. Our data indicate that in mouse pancreatic acinar cells both ACh and CCK receptors couple to the cPLA2 pathway. cPLA2 activation occurs within 1-2 s after hormone application and is promoted by p42/44(MAPK) and inhibited by p38(MAPK). Furthermore, the data demonstrate that secondary (Ca2+-induced) Ca2+ release, which supports Ca2+ wave spreading, is inhibited by AA itself and not by a metabolite of AA.

Acetylcholine↗
PubMed2001

A receptor-based biosensor for lipoprotein docking at the endothelial surface and vascular matrix.

Proteoheparan sulfate can be adsorbed to a methylated silica surface in a monomolecular layer via its transmembrane hydrophobic protein core domain. Due to electrostatic repulsion, its anionic glycosaminoglycan side chains are stretched out into the blood substitute solution, representing a receptor site for specific lipoprotein binding through basic amino acid-rich residues within their apolipoproteins. The binding process was studied by ellipsometric techniques showing that HDL has a high binding affinity to the receptor and a protective effect on interfacial heparan sulfate proteoglycan layers, with respect to LDL and Ca(2+) complexation. LDL was found to deposit strongly at the proteoheparan sulfate, particularly in the presence of Ca(2+), thus creating the complex formation "proteoglycan-low density lipoprotein-calcium". This ternary complex build-up may be interpreted as arteriosclerotic nanoplaque formation on the molecular level responsible for the arteriosclerotic primary lesion. On the other hand, HDL bound to heparan sulfate proteoglycan protected against LDL docking and completely suppressed calcification of the proteoglycan-lipoprotein complex. In addition, HDL and aqueous garlic extract were able to reduce the ternary complex deposition and to disintegrate HS-PG/LDL/Ca(2+) aggregates. Although much remains unclear regarding the mechanism of lipoprotein depositions at proteoglycan-coated surfaces, it seems clear that the use of such systems offers possibilities for investigating lipoprotein deposition at a "nanoscopic" level under close to physiological conditions. In particular, Ca(2+)-promoted LDL deposition and the protective effect of HDL, even at high Ca(2+) and LDL concentrations, agree well with previous clinical observations regarding risk and beneficial factors for early stages of atherosclerosis. Therefore, we believe that the system can be of some use in investigations, e.g. of the interplay between different lipoproteins in arteriosclerotic plaque formation, as well as in high throughput screening of candidate drugs to atherosclerosis in a biosensor application.

Arteriosclerosis↗
PubMed2000

Office-based laser assisted tympanic membrane fenestration in adults and children: pilot data to support an alternative to traditional approaches to otitis media.

OBJECTIVES: To determine the role of intermediate duration ( approximately 3 weeks) middle ear ventilation using office-based laser assisted tympanic membrane fenestration in resolving an episode of otitis media with effusion in adults and children who otherwise would have been treated with insertion of pressure equalization tubes. METHODS: A retrospective chart review of 92 patients (162 ears) was conducted to identify the utility and technical challenges associated with laser assisted tympanic membrane fenestration in an office setting. Clinical characteristics reviewed included: age, gender, duration of effusion, season performed, and hearing and health status of middle ear upon healing of the fenestration. RESULTS: 69% of all patients were effusion free upon closure of the fenestration; 68% of those <3 years; 70% of those 3-7 years; and 70% of those 25-80 years. Some episodes recurred and at final follow-up 64% had normal middle ear structure and function (range of follow-up =1-18 months, mean 2.5 months, median 2.0). Shorter duration of effusion pre-fenestration was more often associated with return to normal middle ear structure and function (P<0.01). Season performed, number of previous episodes of otitis media and pre-treatment tympanometry were not predictive of result. No significant complications were observed. CONCLUSIONS: The use of office-based laser assisted tympanic membrane fenestration is a reasonably safe and effective procedure for the treatment of otitis media in most adults and children. As a minimally invasive otologic procedure, laser assisted tympanic membrane fenestration has great potential to decrease the rates of both antibiotic usage and insertion of ear tubes.

Acoustic Impedance Tests↗
PubMed2000

Ellipsometry Studies of Lipoprotein Adsorption.

The adsorption of a number of lipoproteins, i.e., low-density lipoprotein (LDL), oxidized LDL (oxLDL), high-density lipoprotein (HDL), and lipoprotein (a), at silica and methylated silica as well as at the latter surface modified through adsorption of proteoheparan sulfate, was investigated with in situ ellipsometry at close to physiological conditions. It was found that LDL, oxLDL, HDL, and lipoprotein (a) all adsorbed more extensively at silica than at methylated silica. Upon exposure of the methylated silica surface to proteoheparan sulfate, this proteoglycan adsorbs through its hydrophobic moiety, thereby forming a layer similar to that in the biological system, with the polysaccharide chains forming brushes oriented toward the aqueous solution. Analogous to the biological system, both lipoprotein (a) and LDL were found to deposit at such surfaces, the latter particularly in the simultaneous presence of Ca(2+). After HDL pre-exposure, however, no LDL deposition was observed, even at high LDL and Ca(2+) concentrations. These findings correlate well with those obtained from clinical investigations on risk factors for atherosclerosis. Copyright 2000 Academic Press.

Journal Article↗
PubMed2000

Decreased prevalence of Alzheimer disease associated with 3-hydroxy-3-methyglutaryl coenzyme A reductase inhibitors.

CONTEXT: Increasing evidence suggests that cholesterol plays a role in the pathophysiology of Alzheimer disease (AD). For instance, an elevated serum cholesterol level has been shown to be a risk factor for AD. OBJECTIVE: To determine whether patients taking 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), which are a group of medicines that inhibit the synthesis of cholesterol, have a lower prevalence of probable AD. DESIGN: The experiment uses a cross-sectional analysis comparing the prevalence of probable AD in 3 groups of patients from hospital records: the entire population, patients receiving 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (hereafter referred to as the statins), and patients receiving medications used to treat hypertension or cardiovascular disease. PATIENTS: The subjects studied were those included in the computer databases of 3 different hospitals for the years October 1, 1996, through August 31, 1998. MAIN OUTCOME MEASURES: Diagnosis of probable AD. RESULTS: We find that the prevalence of probable AD in the cohort taking statins during the study interval is 60% to 73% (P < .001) lower than the total patient population or compared with patients taking other medications typically used in the treatment of hypertension or cardiovascular disease. CONCLUSIONS: There is a lower prevalence of diagnosed probable AD in patients taking 2 different 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors-lovastatin and pravastatin. While one cannot infer causative mechanisms based on these data, this study reveals an interesting association in the data, which warrants further study. Arch Neurol. 2000;57:1439-1443

Aged↗
PubMed2000

Development of a method to analyze orthopaedic practice expenses.

The purpose of the current investigation was to present a standard method by which an orthopaedic practice can analyze its practice expenses. To accomplish this, a five-step process was developed to analyze practice expenses using a modified version of activity-based costing. In this method, general ledger expenses were assigned to 17 activities that encompass all the tasks and processes typically performed in an orthopaedic practice. These 17 activities were identified in a practice expense study conducted for the American Academy of Orthopaedic Surgeons. To calculate the cost of each activity, financial data were used from a group of 19 orthopaedic surgeons in Houston, Texas. The activities that consumed the largest portion of the employee work force (person hours) were service patients in office (25.0% of all person hours), maintain medical records (13.6% of all person hours), and resolve collection disputes and rebill charges (12.3% of all person hours). The activities that comprised the largest portion of the total expenses were maintain facility (21.4%), service patients in office (16.0%), and sustain business by managing and coordinating practice (13.8%). The five-step process of analyzing practice expenses was relatively easy to perform and it may be used reliably by most orthopaedic practices.

Accounting↗
PubMed1999

Manage indirect practice expense the way you practice medicine: with information.

PURPOSE: Surgeons are increasingly faced with the pressures of maintaining the highest quality of patient care, while at the same time maintaining financial viability. The purpose of this project was to provide a framework for analyzing practice costs for colorectal surgeons using an activity-based cost accounting model. METHODS: A survey of 11 practices that were diverse in terms of geography, managed care penetration, academic vs. private practice style, and case distribution was performed. In activity-based costing the assignment of typical costs such as staff salaries are assigned to the appropriate business process. The business processes employed in this study were service patients in the office, perform in-office procedures, schedule cases in facilities, service patients in the hospital, insurance authorization, maintain medical records, billing, collections, resolve billing disputes, interaction with third parties, maintain professional education, sustain and manage the practice, maintain the facility, teaching and research, and performing drug studies. The final step is to assign the cost associated with all appropriate business processes to the appropriate cost object. The cost objects in this study were defined as a charge office visit, no-charge office visit, charge hospital visit, in-office procedures, in-facility procedures, and performing drug studies. The data were then analyzed to allow a comparison of four similar practices within the study group. RESULTS: The data demonstrated that the cost of seeing a charge office visit ranged from $55 to $105. Similarly, the cost of seeing a no-charge office visit during the global period ranged from $43 to $100. The study analyzed possible explanations for the wide variability in these costs. CONCLUSIONS: It is essential that physicians clearly understand the sources of expenses generated by the operation of their practices. A clear comprehension of costs will lead colorectal surgeons to make appropriate decisions regarding such important issues as office staffing ratios, office square footage, and instrumentation acquisitions.

Colorectal Surgery↗
PubMed1999

Oxygen-dependent regulation of membrane potential and vascular tone of human umbilical vein.

OBJECTIVE: We question the hypothesis that vascular tone of human umbilical vein is insensitive to oxygen pressure and minimal already at resting conditions. STUDY DESIGN: Isometric tension and intracellular membrane potential of native (n = 7) and endothelium-denuded (n = 7) human umbilical vein strips were recorded simultaneously at oxygen pressure values of 5 to 104 mm Hg. RESULTS: Increasing oxygen pressure from 5 to 104 mm Hg led to graded membrane depolarization from -58.2 +/- 1.3 mV (SEM) to -54.0 +/- 0.7 mV (P <.009) and increased isometric tension from 0.576 +/- 0.016 g to 0.790 +/- 0.032 g (P <.0001). The steepest increase in tension (Delta = 0.063 g) occurred within the physiologic intrauterine oxygen tension range (27-35 mm Hg). Isometric tension at hypoxia (partial oxygen pressure, 5 mm Hg) corresponded to 88% of resting tension. Tension and membrane potential were related linearly (r(2) = 0.99). Disruption of the endothelium reversed the effects of oxygen pressure. CONCLUSION: Human umbilical vein vascular tone was regulated by oxygen tension and showed a hypoxic vasodilator reserve. Oxygen-dependent effects were related to the membrane potential and required the endothelium.

Endothelium, Vascular↗