Transnasal transesophageal echocardiography: a modified application mode for cardiac examination in ventilated patients

In 42 endotracheally intubated patients, we examined the utility of a miniaturized monoplane probe for transnasal transesophageal echocardiography (TEE). Transnasal TEE was prospectively evaluated in 26 deeply and 16 mildly sedated patients receiving topical anesthesia with lidocaine jelly 2%. The patients with deep sedation were additionally examined with transoral monoplane and multiplane TEE. Transnasal esophageal insertion of the TEE probe was successfully performed in 90% of patients. Endotracheal malpositioning was corrected in two patients. Nasal bleeding required treatment in another patient. Topical anesthesia was adequate in 82% of mildly sedated patients. Left ventricular short- and four-chamber long-axis views of good quality were obtained with transnasal (transoral) monoplane TEE in 76% (81%) and 92% (96%) of patients (differences not significant). Compared with conventional multiplane TEE, transnasal monoplane TEE missed diagnoses in 19% of patients. The relative error (mean +/- SEM) of quantification with transnasal TEE was <9% +/- 2% for ventricular diameters and <7% +/- 2% for cross-sectional area measurements, with a bias of 0.5 +/- 3.8 cm2 and 0.1 +/- 2.4 cm2 (mean +/- 2 SD) for left ventricular end-diastolic and end-systolic short-axis areas. The relative error in measuring intracardiac flow velocities was >40%, but systolic to diastolic peak velocity ratios at the valvular site were determined with an error <4% +/- 3%. Transnasal monoplane TEE can be performed even in mildly sedated patients with an endotracheal tube without further need for analgesia or sedation. The technique is as useful as conventional transoral TEE to image standard tomographic planes for quantification, but it is less suited for comprehensive echocardiographic diagnosing. Implications: Transnasal insertion of a miniaturized monoplane transesophageal echocardiography (TEE) probe was studied in endotracheally intubated patients. Nasal passage was well tolerated even by patients with only mild sedation. Imaging quality was similar to conventional transoral monoplane TEE with larger transducers, but technical restraints cause a deficit in complete cardiac diagnosing obtained with multiplane TEE.     

Anti-TGF-beta treatment promotes rapid healing of Leishmania major infection in mice by enhancing in vivo nitric oxide production

CB6F1 mice display intermediate susceptibility to Leishmania major infection compared with the highly susceptible BALB/c and resistant C57BL/6 parental strains. During early weeks of infection, these mice develop dominant Th2 type responses to L. major, although they eventually exhibit a Th2 to Th1 switch and spontaneously resolve their infections. In this study, we have examined the effects of either IL-12 or anti-TGF-beta therapy on the immune response and course of disease in chronically infected CB6F1 mice. Local treatment with IL-12 inoculated into the parasitized lesion at 4 wk of infection induced a marked increase in IFN-gamma production but did not result in a significant reduction in numbers of parasite or promote more rapid healing. However, local treatment with an Ab to TGF-beta led to both a decrease in parasite numbers and more rapid healing, despite the fact that such treatment did not significantly alter the pattern of IL-4 and IFN-gamma production. Immunohistochemical studies showed that anti-TGF-beta treatment resulted in increased nitric oxide production within parasitized lesions. Our results suggest that TGF-beta may play an important regulatory role during chronic stages of a L. major infection by suppressing macrophage production of nitric oxide and that, in the absence of TGF-beta, even the relatively low levels of IFN-gamma observed in mice with dominant Th2-type responses are sufficient to activate macrophages to destroy amastigotes within parasitized lesions.     

Evaluation of the MOS SF-36 Physical Functioning Scale (PF-10): II. Comparison of relative precision using Likert and Rasch scoring methods

Inhibition of NO synthesis represents a new therapeutical approach in the treatment of inflammation. Clinical use of NOS inhibitors will necessitate the design of drugs selective for iNOS, because inhibition of constitutive endothelial NOS may cause adverse cardiovascular side effects. This study examines the effect of ibuprofen and its stereoeisomeric components on the activation of iNOS and cNOS as well as on the NO production by human umbilical vein endothelial cells. At therapeutic concentrations Ibuprofen activated iNOS and inhibited NOS. In endothelial cell culture experiments activation of NO production was seen especially at supratherapeutic ibuprofen concentrations. Both stereoisomeric components of ibuprofen showed comparable effects. This drug can therefore not be used for the selective inhibition of iNOS.     

An association between air pollution and mortality in six U.S. cities

BACKGROUND: Recent studies have reported associations between particulate air pollution and daily mortality rates. Population-based, cross-sectional studies of metropolitan areas in the United States have also found associations between particulate air pollution and annual mortality rates, but these studies have been criticized, in part because they did not directly control for cigarette smoking and other health risks. METHODS: In this prospective cohort study, we estimated the effects of air pollution on mortality, while controlling for individual risk factors. Survival analysis, including Cox proportional-hazards regression modeling, was conducted with data from a 14-to-16-year mortality follow-up of 8111 adults in six U.S. cities. RESULTS: Mortality rates were most strongly associated with cigarette smoking. After adjusting for smoking and other risk factors, we observed statistically significant and robust associations between air pollution and mortality. The adjusted mortality-rate ratio for the most polluted of the cities as compared with the least polluted was 1.26 (95 percent confidence interval, 1.08 to 1.47). Air pollution was positively associated with death from lung cancer and cardiopulmonary disease but not with death from other causes considered together. Mortality was most strongly associated with air pollution with fine particulates, including sulfates. CONCLUSIONS: Although the effects of other, unmeasured risk factors cannot be excluded with certainty, these results suggest that fine-particulate air pollution, or a more complex pollution mixture associated with fine particulate matter, contributes to excess mortality in certain U.S. cities.     

Cell-seeding and in vitro biocompatibility evaluation of polymeric matrices of PEO/PBT copolymers and PLLA

Higher lipid content in gall bladder bile of sheep and goats as compared with monogastric species was due to higher proportion of glycerides. The volume of bile per gall bladder was higher in sheep than in goats. Bile from sheep and goats has a higher content of proteins and lower contents of dry matter, cholesterol and phospholipids compared with monogastric species. Biliary proteins partially purified by the ammonium sulfate precipitation method were characterized and quantified by polyacrylamide gel electrophoresis (PAGE), fast protein liquid chromatography (FPLC) and immunodiffusion. FPLC and PAGE profiles indicate that biliary proteins of sheep and goats are mainly of low mol. wt. of upto 65 KDa. Proportions of immunoglobulin (Ig) like molecules in biliary proteins precipitated by ammonium sulfate of different degrees of saturation, were 10.4 to 26.7 and 21.9 to 30.7 per cent of total proteins in bile of goats and sheep. IgG and IgA like molecules were the predominant Ig and lacked carbohydrates. On immunodiffusion such Ig like molecules did not show cross reactivity with humoral Ig. It was concluded that sheep and goats appear to secrete Ig into bile after deglycosylation and partial degradation. The proteins of smaller molecular weight may be secretory fragments or degradation products of Ig.     

An incidental finding of extreme self-limited thrombocytosis of unknown cause

This report describes an 11-year-old male who presented to his pediatrician at the Bowman Gray School of Medicine in Winston-Salem, N.C., because of long standing enuresis. During evaluation and the following two-week period, this patient was found to have extreme thrombocytosis ranging from 2,175 x 10(9)/L to 3,700 x 10(9)/L. In the absence of any apparent reactive cause, a presumptive diagnosis of essential thrombocythemia was made. Although chemotherapy was considered, the patient was temporarily lost to follow-up before there was a final decision about therapy. One year later, this patient's platelet count had spontaneously decreased to normal (273 x 10(9)/L), and has remained normal during a follow-up period of seven years, although only sporadic platelet counts have been obtained. His most recent physical examination revealed no abnormalities. The case is presented as further evidence that extremely high platelet counts are not necessarily dangerous and do not all require therapy.     

Fast tracking in cardiac surgery: implications for practice

Even though economic incentives might have been the impetus for its revival, fast tracking offers numerous other benefits, not the least of which is improved patient care. However, its benefits can be realized only through specific perioperative management, including preoperative assessment, identification and selection of appropriate candidates, optimal intra- and postoperative management and interdisciplinary discharge planning. Through interdisciplinary collaboration, the maximum benefits of fast tracking can be reaped by both the patient and the healthcare team.     

Effect of a coffee lipid (cafestol) on cholesterol metabolism in human skin fibroblasts

The receptor (R) for epidermal growth factor (EGF) is expressed at high levels on human breast cancer cells and associates with ErbB2, ErbB3, and Src proto-oncogene family protein tyrosine kinases (PTKs) to form membrane-associated PTK complexes with pivotal signaling functions. Recombinant human EGF was conjugated to the soybean-derived PTK inhibitor genistein (Gen) to construct an EGF-R-directed cytotoxic agent with PTK inhibitory activity. The EGF-Gen conjugate was capable of binding to and entering EGF-R-positive MDA-MB-231 and BT-20 breast cancer cells (but not EGF-R-negative NALM-6 or HL-60 leukemia cells) via its EGF moiety, and it effectively competed with unconjugated EGF for target EGF-R molecules in ligand binding assays. EGF-Gen inhibited the EGF-R tyrosine kinase in breast cancer cells at nanomolar concentrations, whereas the IC50 for unconjugated Gen was >10 microM. Notably, EGF-Gen triggered a rapid apoptotic cell death in MDA-MB-231 as well as BT-20 breast cancer cells at nanomolar concentrations. The EGF-Gen-induced apoptosis was EGF-R-specific because cells treated with the control granulocyte-colony stimulating factor-Gen conjugate did not become apoptotic. Apoptosis was dependent both on the PTK inhibitory function of Gen and the targeting function of EGF, because cells treated with unconjugated Gen plus unconjugated EGF did not undergo apoptosis. The IC50s of EGF-Gen versus unconjugated Gen against MDA-MB-231 and BT-20 cells in clonogenic assays were 30 +/- 3 nM versus 120 +/- 18 microM (P < 0.001) and 30 +/- 10 nM versus 112 +/- 17 microM (P < 0.001), respectively. Thus, the EGF-Gen conjugate is a >100-fold more potent inhibitor of EGF-R tyrosine kinase activity in intact breast cancer cells than unconjugated Gen and a >100-fold more potent cytotoxic agent against EGF-R+ human breast cancer cells than unconjugated Gen. Taken together, these results indicate that the EGF-R-associated PTK complexes have vital antiapoptotic functions in human breast cancer cells and may therefore be used as therapeutic targets.     

Repeatability of the Petrifilm HEC test and agreement with a hydrophobic grid membrane filtration method for the enumeration of Escherichia coli O157:H7 on beef carcasses

The review highlights recent advances in our understanding of basic mechanisms of reperfusion injury after warm hepatic ischemia. Kupffer cells play a central role as the initial cytotoxic cell type and as a source of many proinflammatory mediators. Subsequently, neutrophils are activated and recruited into the liver. Factors and conditions are outlined that determine whether neutrophils undergo apoptosis without causing damage or migrate out of the sinusoids and attack parenchymal cells. In addition to the inevitable inflammatory response during reperfusion, microcirculatory perfusion failure, due to an imbalance between the actions of vasodilators and vasoconstrictors, also has a serious impact on reperfusion injury. A better understanding of the basic pathophysiology will reveal potential targets for therapeutic interventions and will show us how to avoid risk factors that may aggravate reperfusion injury.