Removal of superfluous ICD leads.
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Biomedical subjects
Publications and source records attributed to C Byrd.
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Elliptic flow from nuclear collisions is a hadronic observable sensitive to the early stages of system evolution. We report first results on elliptic flow of charged particles at midrapidity in Au+Au collisions at square root(S)NN = 130 GeV using the STAR Time Projection Chamber at the Relativistic Heavy Ion Collider. The elliptic flow signal, v2, averaged over transverse momentum, reaches values of about 6% for relatively peripheral collisions and decreases for the more central collisions. This can be interpreted as the observation of a higher degree of thermalization than at lower collision energies. Pseudorapidity and transverse momentum dependence of elliptic flow are also presented.
B7 costimulation is a required component of many type 2 immune responses, including allergy and protective immunity to many nematode parasites. This response includes elevations in Th2 cytokines and associated effector functions including elevations in serum IgG1 and IgE and parasite expulsion. In studies of mice infected with Trichuris muris, blocking B7 ligand interactions inhibited protective immunity, suppressed IL-4 production, and enhanced IFN-gamma production, but unexpectedly did not inhibit production of the Th2 cytokine, IL-13. Blocking both IFN-gamma and B7 restored protective immunity, which was IL-13 dependent, but did not restore IL-4 or associated IgE responses. Although IL-13 was required for worm expulsion in mice in which both IFN-gamma and B7 were blocked, IL-4 could mediate expulsion in the absence of both IL-13 and IFN-gamma. These studies demonstrate that 1) B7 costimulation is required to induce IL-4, but not IL-13 responses; 2) IL-13 is elevated in association with the IFN-gamma response that occurs following inhibition of B7 interactions, but can only mediate IL-4-independent protection when IFN-gamma is also inhibited; and 3) increased IL-13 production, in the absence of increased IL-4 production, is not associated with an IgE response, even in the absence of IFN-gamma.
Studies in mice infected with the gastrointestinal nematode parasite Nippostrongylus brasiliensis demonstrated that IL-4/IL-13 activation of Stat6 suppresses development of intestinal mastocytosis and does not contribute to IL-4/IL-13 production, but is still essential for parasite expulsion. Because expulsion of another gastrointestinal nematode, Trichinella spiralis, unlike N. brasiliensis expulsion, is mast cell dependent, these observations suggested that T. spiralis expulsion would be Stat6 independent. Instead, we find that Stat6 activation by IL-4/IL-13 is required in T. spiralis-infected mice for the mast cell responses that induce worm expulsion and for the cytokine responses that induce intestinal mastocytosis. Furthermore, although IL-4 induces N. brasiliensis expulsion in the absence of B cells, T cells, and mast cells, mast cells and T cells are required for IL-4 induction of T. spiralis expulsion. Thus, Stat6 signaling is required for host protection against N. brasiliensis and T. spiralis but contributes to expulsion of these two worms by different mechanisms. The induction of multiple effector mechanisms by Stat6 signaling provides a way for a cytokine response induced by most gastrointestinal nematode parasites to protect against most of these parasites, even though different effector mechanisms are required for protection against different nematodes.
In recent years, laparoscopic surgery has become a matter of growing interest. It has been shown that laparoscopic colectomy is well tolerated and safe for benign disease. However, there is some uncertainty about using this method for malignant disease when curative resection is the aim. These uncertainties mainly consist of spread of cancer to port site, long-term survival, and adequacy of resection. The majority of laparoscopic colectomies are technically assisted procedures in which anastomosis is performed outside the abdomen. However, some surgeons are now performing this surgery totally laparoscopically with the anastomosis performed inside the abdomen. Laparoscopic colectomy is currently practiced with great frequency by general surgeons. Its performance requires a steep learning curve and a large number of cases to obtain proficiency. The indications for laparoscopic colectomy are different from one institution to another. In some institutions all patients with colorectal disease are candidates for laparoscopic colectomy and in others it may be limited to benign disease only. The purpose of this review is to analyze all laparoscopic colectomies performed at our medical center since 1992. We conducted a retrospective chart review of both hospital and clinic charts of patients who underwent colectomies at our hospital. A total of 338 patient charts were reviewed. In a comparison of both laparoscopic (n = 285) and converted (n = 53) methods, the age and operative time were about the same. Age average and operating room time average were similar for both groups. With laparoscopy, there was a 3-day drop in length of hospital stay as well as a 1-day-earlier regaining of bowel function. Hospital cost dropped 5000 dollars average for the laparoscopic colectomy. The conversion rate at our center was 15 per cent. Complication rates were lower in the laparoscopic group. Recurrence of cancer at the port site (0.7%) was no higher than in the converted group (incisional recurrence, 1.8%). We conclude that laparoscopic colectomy does show an improvement in return of bowel function, hospital cost, and shorter hospital stay. Long-term follow-up will be necessary to determine the effectiveness of laparoscopic colon resection for colorectal cancer.
Ubiquitin-dependent proteolytic systems underlie many processes, including the cell cycle, cell differentiation and responses to stress. One such system is the N-end rule pathway, which targets proteins bearing destabilizing N-terminal residues. Here we report that Ubr1p, the main recognition component of this pathway, regulates peptide import in the yeast Saccharomyces cerevisiae through degradation of Cup9p, a 35 kDa homeodomain protein. Cup9p was identified using a screen for mutants that bypass the previously observed requirement for Ubr1p in peptide import. We show that Cup9p is a short-lived protein (t1/2 approximately 5 min) whose degradation requires Ubr1p. Cup9p acts as a repressor of PTR2, a gene encoding the transmembrane peptide transporter. In contrast to engineered N-end rule substrates, which are recognized by Ubr1p through their destabilizing N-terminal residues, Cup9p is targeted by Ubr1p through an internal degradation signal. The Ubr1p-Cup9p-Ptr2p circuit is the first example of a physiological process controlled by the N-end rule pathway. An earlier study identified Cup9p as a protein required for an aspect of resistance to copper toxicity in S.cerevisiae. Thus, one physiological substrate of the N-end rule pathway functions as both a repressor of peptide import and a regulator of copper homeostasis.
The voltage-dependent anion channel (VDAC) is a voltage-gated channel from the mitochondrial outer membrane. It has two gating processes: one at positive potentials and the other at negative potentials. The energetics of VDAC gating are quite different when measured in the presence or absence of an ion gradient. A positive potential on the high-salt side results in channel closure at lower transmembrane potentials. The midpoint potential (V0) shifted from 25 to 5.7 mV, with an activity gradient for KCl of 0.6 versus 0.06. The opposite occurred for negative potentials on the high-salt side (V0 shifted from -25 to -29 mV). Thus the salt gradient favored closure for one gating process and opening for the other. These results could be explained if part of the electrochemical potential of the gradients present were transferred to the gating mechanism. If the kinetic energy of the ion flow were coupled to the gating process, the effects of the gradient would depend on the mass and velocities of these ions. This was tested by using a series of different salts (KCl, NaCl, LiCl, KBr, K acetate, Na butyrate, and RbBr) under an identical activity gradient. The kinetic energy correlated very well with the measured shifts in free energy of the channel gating. This was true for both polarities. Thus the gating of VDAC is influenced by ion flow. These results are consistent in sign and direction with the voltage gating process in VDAC, which is believed to involve the movement of a positively charged portion of the wall of the channel out of the membrane.
Comparative Molecular Field Analysis (CoMFA) was applied to a comprehensive data set of heterogeneous nitroaromatics tested in Salmonella typhimurium TA98 and TA100 with and without S9 microsomal activation. The four CoMFA models developed agree with postulated mechanisms of mutagenicity, and explain over 70% of the corresponding mutagenic variance The standard deviation coefficient contours common in the four models included high electronic density regions equivalent to C4-C5 in the pyrene ring, and an electron deficient site equivalent to C6. These areas are associated with high mutagenicity. Electron deficient areas may be related with the nitroreductive bioactivation of nitroaromatics. Electron rich sites may be involved with oxidative mechanisms analogous to the bioactivation pathway of polycyclic aromatic hydrocarbons. The contribution of steric factors to mutagenicity follows the order TA98 + S9 > TA98 > TA100 + S9 > TA100. The models indicated that increasing bulk perpendicular to the aromatic plane would decrease mutagenicity, but increasing the aromatic ring system along a region corresponding to C6-C7 in 1-nitropyrene would increase mutagenicity.
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Fas receptor-induced apoptosis plays critical roles in immune homeostasis. However, most of the signal transduction events distal to Fas ligation have not been elucidated. Here, we show that Ras is activated following ligation of Fas on lymphoid lines. The activation of Ras is a critical component of this apoptotic pathway, since inhibition of Ras by neutralizing antibody or a dominant-negative Ras mutant interfered with Fas-induced apoptosis. Furthermore, ligation of Fas also resulted in stimulation of the sphingomyelin signalling pathway to produce ceramides, which, in turn, are capable of inducing both Ras activation and apoptosis. This suggests that ceramides acts as second messengers in Fas signaling via Ras. Thus, ligation of the Fas molecule on lymphocyte lines induces activation of Ras via the action of ceramide, and this activation is necessary, but not sufficient, for subsequent apoptosis.
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Neuroleptic malignant syndrome is a potentially fatal syndrome that can occur in patients taking neuroleptics or other psychotropic drugs. It is characterized by muscle rigidity, hyperthermia, altered mentation, autonomic dysfunction, increased CPK and leukocytosis. A primary factor in NMS may be a decrease in functioning of dopaminergic neurons. Treatment usually consists of discontinuation of the neuroleptic drug, drug therapy with bromocriptine and dantrolene and supportive measures. The key to successful medical and nursing management is aggressive supportive care with a focus on preventing complications. With the frequency of administration of neuroleptic drugs, neuroscience nurses should be aware of this potentially lethal complication of neuroleptic therapy.
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The E.coli Tus protein is an anti-helicase involved in the termination of chromosome replication. The binding site for this protein, ter, was cloned into derivatives of the broad host-range plasmid R1162. The ter site caused the orientation-specific termination of plasmid replication fork movement in cell extracts containing Tus. Plasmids were constructed so that two sites for initiation of R1162 replication flanked the iteron-containing domain of the origin. In these plasmids, the site next to the AT-rich region within the iteron-containing domain was more active. In addition, when ter was placed between the more active site and the iterons, initiation of replication from this site was specifically inhibited. The data support a model for entry of the essential, plasmid-encoded helicase at one side of the direct repeats, and for its movement primarily in one direction away from these repeats to activate the initiation sites for DNA replication.
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A 68-year-old white male underwent permanent pacemaker implantation with an atrial synchronous ventricular inhibited pulse generator (Medtronic model 2409) because of syncope and abnormal H-V interval of 70 ms. Paroxysmal bouts of pacemaker associated tachycardia were subsequently recorded on several occasions, initiated and terminated by spontaneous ventricular premature beats. The mechanism for the occurrence of the tachyarrhythmia is discussed in detail and the functional characteristics of the pulse generator are described. Replacement of the unit with a different pacer device prevented further occurrence of the arrhythmia.
We have observed abnormal echoes in the left ventricular outflow tract in 4 patients: 3 of the subjects had bacterial endocarditis and the fourth patient had myxomatous degeneration of the aortic valve (floppy aortic valve). A single diastolic echo with fine high frequency fluttering was seen in the patient with the floppy aortic valve, whereas the patients with endocarditis had associated infection of the mitral valve and an aneurysm of the anterior mitral leaflet, which was represented by dense systolic echoes on the proximal part of the mitral valve...