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PubMed1986

Social skills and the stress-protective role of social support.

Cross-sectional analyses of data collected from a large sample of incoming college freshmen were used to determine whether the perceived availability of social support protects persons from stress-induced depressive affect; whether social competence, social anxiety, and self-disclosure are responsible for the stress-protective effect of perceived social support; and whether these social skill measures discriminate among persons for whom support will help, hinder, or be ineffective in the face of stress. Prospective analyses based on the original testing (beginning of school year) and 11- and 22-week follow-ups of a randomly selected subsample were used to determine how the same social skill factors influence the development and maintenance of support perceptions and of friendships. Evidence is provided for a stress-buffering role of the perceived availability of social support. The stress-buffering effect is unaffected by controls for the possible stress-protective influences of social anxiety, social competence, and self-disclosure. Although these social skill factors do not discriminate among persons for whom support will help, hinder, or be ineffective, they are prospectively predictive of the development of both social support and friendship formation. These prospective relations between social skills and the development of perceived availability of social support are only partly mediated by number of friends.

Adolescent↗
PubMed2005

Glucose and insulin influences on heart and brain in cardiac surgery.

The elective global ischemia of on-pump coronary artery bypass surgery contributes to the incidence of postoperative mortality, complications, and use of resources. In addition to cardiopulmonary bypass and techniques for myocardial protection such as aortic cross clamp, ventricular fibrillation, and cardioplegia, the administration of systemic glucose-insulin-potassium (GIK) in the perioperative period may act as both a metabolic modulator and potential inodilator. GIK may therefore serve to protect the myocardium and promote adequate cardiac and hemodynamic performance that would improve patient recovery. Cell, tissue, and animal experiments have determined a number of mechanisms of action by which this may be achieved, with increasing focus on insulin as the key component. The original concepts centered on GIK during or after ischemia switching metabolism away from that based on non-esterified fatty acids toward a more favorable glucose-based metabolism and thus improving the efficiency of adenosine triphosphate production and glycogen preservation. Insulin's ability to reduce intracellular fatty acid metabolism may also reduce cellular membrane damage. More recently other mechanisms have also been suggested, including osmotic, oxygen free radical scavenging, and antiapoptotic and anti-inflammatory effects. However, trials that have examined the role of GIK in cardiac surgery have been small, open label, and involved a wide variety of regimens. They have demonstrated improved glycogen preservation, reduced infarct size, reduced incidences of dysrhythmias, need for inotropic agents, and low cardiac output state, and overall reduced lengths of stay. The perceived need to achieve strict blood glucose control to reduce neurologic injury and improve overall mortality have conflicted with its practical difficulties, particularly during cold cardiopulmonary bypass, and the exact role of supplemental glucose administration and resulting hyperglycemia require re-examination.

Apoptosis↗
PubMed1992

[Coronary artery bypass grafting in patients with poor left ventricular function using retrograde continuous cold blood cardioplegia].

Patients with poor left ventricular function or those requiring urgent surgery may have more extensive ischemic myocardial injury if myocardial preservation is incomplete. We have performed coronary artery bypass grafting (CABG) aimed at complete revascularization in such cases using RC-CBCP, which is considered more effective on myocardial preservation during aortic cross-clamping in particular to protect ischemic area distal to severe coronary artery stenosis or obstruction. In the present study, in 25 patients with poor left ventricular function (left ventricular ejection fraction; LVEF less than or equal to 0.3) including 10 patients who required urgent surgery, the operative results were evaluated. All the distal and proximal anastomoses of grafts (average 2.5 grafts) were completed during one aortic cross-clamping using RC-CBCP, therefore graft flow was obtained immediately after release of the aortic clamping. Though this method required 142 minutes of a mean aortic cross-clamping time, myocardial protection was considered to be preferable judging from postoperative isoenzymatic evaluation and improved ventricular function. Fifteen patients with elective CABG were all alive and restored to NYHA class I to II. Among 10 patients requiring urgent CABG, 4 patients with acute myocardial infarction died but others were restored to NYHA class I to II. We conclude that it is important to aim at complete coronary revascularization in patients with poor left ventricular function and RC-CBCP achieves more effective myocardial protection during CABG in the patients.

Adult↗
PubMed1997

Ibuprofen protects alpha-crystallin against posttranslational modification by preventing protein cross-linking.

Posttranslational modification of bovine alpha-crystallin by D-erythrose-4-phosphate, fructose-6-phosphate, D-ribose-5-phosphate and carbamylation using potassium cyanate induced the loss of chaperone-like activity, as assessed by gamma-crystallin aggregation. The presence of high-molecular-weight aggregates indicated that erythrosylated, fructosylated and carbamylated alpha-crystallins were modified by non-reducible cross-linking. In contrast, ribosylation of alpha-crystallin induced the formation of reducible cross-links. Analysis of ribosylated, erythrosylated and carbamylated alpha-crystallin using non-denaturing acrylamide gels showed that the cross-linking did not sterically inhibit the normal aggregate formation or alter the oligomerisation of the aggregate. Co-incubation of ibuprofen in the presence of alpha-crystallin and the modifying agents protected the chaperone-like activity of alpha-crystallin, enabling the inhibition of gamma-crystallin aggregation. In addition, ibuprofen inhibited the formation of both reducible and non-reducible cross-linked high-molecular-weight alpha-crystallin aggregates. We show in this paper that ibuprofen can inhibit in vitro cross-linking events responsible for the loss of chaperone-like activity of alpha-crystallin and suggest that the protective effect of ibuprofen may be exerted by the binding of ibuprofen breakdown products to alpha-crystallin lysine groups, preventing posttranslational modification responsible for the loss of chaperone-like activity.

Animals↗
PubMed1982

Myocardial protection with cold blood potassium cardioplegia during prolonged aortic cross-clamping.

The efficacy of cold blood potassium cardioplegia during periods of aortic cross-clamping (greater than 100 minutes) was assessed in 127 patients undergoing a variety of open-heart surgical procedures at New York University Medical Center from january, 1978, to April, 1979. Ischemic intervals ranged from 100 to 267 minutes (mean, 128 minutes). Cardiac-related deaths occurred in only 3 patients (2.4%), and overall operative mortality was 8.7% (11 patients). The rate of perioperative infarction was 10%. Fourteen patients (11%) required vasopressor support or balloon counterpulsation after cardiopulmonary bypass despite the lengthy cross-clamp intervals. Multivariate analysis revealed no significant relationship between the length of cross-clamp time and operative mortality (p = 0.29), incidence of perioperative infarction (p = 0.54), or the occurrence of low-output syndrome postoperatively (p = 0.68). These findings suggest that cold blood potassium cardioplegia provides adequate myocardial protection when periods of arrest as long as 3 to 4 hours are required for complex cardiac surgical procedures.

Adult↗
PubMed2004

Induction of protective antibody response in rabbits against fascioliasis with Toxocara/Fasciola cross- reactive defined antigen.

A method of affinity chromatography purification of Toxocara vitulorum antigen cross- reacts with Fasciola gigantica antiserum is described. Characterization of the isolated cross- reactive fraction by SDS-polyacrylamide gel electrophoresis, isoelectric focusing and amino acid analysis resulted in a fraction consists of five polypeptides of 137.7KDa, 81KDa, 75KDa, 48KDa and 21.6KDa with isoelectric points of 8, 7.5, 7.2, 6.7 and 6.6. Seventeen amino acids were identified in the fraction with high proportions of only two of them (tyrosine and glutamic). Rabbits immunization with this identified T. vitulorum cross- reactive antigen in Freund's adjuvant followed by challenge with F. gigantica metacercariae resulted in 60% reduction in worm burden over control infected rabbits. Higher IgG level was detected in vaccinated rabbits four weeks post first immunization than control infected ones and remained high up to the end of the trial.

Animals↗
PubMed1996

Abdominal aortic aneurysectomy after kidney transplantation: case report and review of the literature.

Abdominal aortic aneurysms have been a rare finding in patients who have previously undergone renal transplantation. Previous operative strategies attempting to provide renal allograft protection during aortic cross-clamping have included extra-anatomic permanent as well as temporary bypass, heparin bonded shunts, in situ perfusion cooling of the allograft, and general hypothermia. These maneuvers, although generally successful, have recently been challenged by reports describing no specific protective measures. A case of a 5.0 cm but rapidly expanding abdominal aortic aneurysm in a patient who had undergone a prior successful kidney transplant is presented along with a literature review of 27 available cases on the subject.

Aortic Aneurysm, Abdominal↗
PubMed1984

Vaccination against Klebsiella aerogenes.

Klebsiella vaccine was prepared from strains of Klebsiella aerogenes with capsular types K1, K36, K44 and K Cross (a type which cross-reacts in vitro with sera from many klebsiella capsular types). The vaccine was extracted by dialysis and ultrafiltration from capsular material released during growth of the bacteria in a five-day batch culture. Mice given one dose of vaccine from K1a (1.0 microgram/mouse) survived lethal intraperitoneal challenge of 11/11 homologous klebsiella strains four days after vaccination; 14 days after vaccination protection against the same challenge strains had declined to 5/11 strains. Vaccines from K1a, b, c, K36, K44 and K Cross induced homologous protection and protected mice against different ranges of heterologous klebsiella capsular types. The protective response of the mice was greatly enhanced by administering three doses of the vaccines. Vaccines from K1, K36, K44 and K Cross protected mice against 14/20, 11/20, 10/20 and 9/20 homologous and heterologous klebsiella challenge strains respectively. None of the klebsiella vaccines was toxic for mice at the immunizing dose (1.0 microgram/mouse). Vaccine from K36 was the most lethal, killing mice at 10(3) immunizing doses. The least toxic vaccine was from K44, which killed mice at 10(4) immunizing doses.

Animals↗
PubMed1985

Cross-reactive cellular and humoral immunity to carcinogen-induced chicken fibrosarcomas. II. Effect of prior immunization with transplantable tumors on primary tumor incidence.

Primary carcinogen-induced (7,12-dimethyl-benz[a]anthracene; DMBA) tumor-bearing SC chickens (B2/B2) frequently showed antibodies in their sera which reacted with cells from their autochthonous tumors, chicken embryo fibroblasts (CEF), tumor cells from some transplantable tumor lines, and from approximately 10% of other primary tumors. Similar results were obtained by ELISA on glutaraldehyde-fixed cells and by immunofluorescence on viable cells. The serum antibody reactivity could be removed by absorption with CEF but not with non-cross-reacting primary tumor cells or a variety of normal tissues. Although sera from normal chickens never showed significant reactivity, a high percentage of sera from chickens that had been injected with DMBA but failed to develop detectable tumors showed antibody activity to a transplantable DMBA-induced tumor and to CEF. On the basis of previously established cross-reactivity patterns in protective immunity to transplantable carcinogen-induced fibrosarcomas, attempts were made to protect against chemical carcinogenesis by prior immunization with selected DMBA-induced transplantable tumors. Tumor-immune chickens showed a significant decrease in the development of tumors during the first 3 mo after injection of DMBA (p = 0.001) or methylcholanthrene (p = 0.033) when compared to controls. This resistance to tumor induction in immune chickens was correlated to the degree of tumor immunity to the immunizing tumor present 1 mo after carcinogen injection (p = 0.046). There was, however, no detectable difference in the incidence of tumors arising later than 3 mo after carcinogen injection. The reduction in tumor incidence in immune as compared to control chickens at 5 mo was therefore less striking than the reduction seen at 3 mo. Immunization with CEF and adjuvants or with adjuvants alone afforded no protection to tumor induction.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1985

The molecular morphology of bovine heart mitochondrial NADH-ubiquinone reductase. Cross-linking with dithiobis(succinimidyl propionate).

The molecular morphology of NADH-ubiquinone reductase (complex I) was investigated by cross-linking with the cleavable bifunctional reagent, dithiobis(succinimidyl propionate). Cross-linking inhibits the following activities of the complex--NADH----3-acetylpyridine adenine dinucleotide (oxidized), NADH----2,6-dichloroindophenol, NADH----ferricyanide, and NADH----menadione--to different degrees with the greatest inhibition occurring with either ferricyanide or 3-acetylpyridine adenine dinucleotide as electron acceptor. Addition of 150 microM NADH affords partial protection from inhibition. Cross-linking quenches the FMN fluorescence of complex I (288 nm excitation/515 nm emission), and addition of 150 microM NADH greatly reduces the quenching. Treatment of complex I (1 mg/ml) for 2 min with dithiobis(succinimidyl propionate) (0.2 mg/ml) at 4 degrees C revealed a cross-linked product consisting of the following seven subunits: 75-80, 53-57, 42, 33-35, 24-27, 17-18, and 12.5-15.5 kDa. Five minutes of treatment cross-linked the unidentified polypeptides of 69 and 51 kDa to six of the seven complex I subunits, but the 12.5-15.5-kDa subunit may be missing from this cross-linked product, while 15 min of treatment cross-linked additional unidentified polypeptides of 177, 107, 72, and 63 kDa. Since longer times of cross-linking result in a larger number of unidentifiable polypeptide spots, the shorter cross-linking time results are taken as a more accurate picture of the native enzyme conformation. This would indicate that within complex I the following subunits are within 12 A of each other at one or more points in space: 75-80, 53-57, 42-45, 33-35, 24-27, 17-18, and, perhaps, 12.5-15.5 kDa. These subunits represent portions of all three fractions of the enzyme, i.e. flavoprotein, iron-protein, and insoluble or hydrophobic fractions.

Animals↗
PubMed2002

Ischemic tolerance.

A brief period of cerebral ischemia confers transient tolerance to a subsequent ischemic challenge in the brain. This phenomenon of ischemic tolerance has been confirmed in various animal models of forebrain ischemia and focal cerebral ischemia. Since the ischemic tolerance afforded by preceding ischemia can bring about robust protection of the brain, the mechanism of tolerance induction has been extensively studied. It has been elucidated that ischemic tolerance protects neurons, and at the same time, it preserves brain function. Further experiments have shown that metabolic and physical stresses can also induce cross-tolerance to cerebral ischemia, but the protection by cross-tolerance is relatively modest. The underlying mechanism of ischemic tolerance still is not fully understood. Potential mechanisms may be divided into two categories: (1) A cellular defense function against ischemia may be enhanced by the mechanisms inherent to neurons. They may arise by posttranslational modification of proteins or by expression of new proteins via a signal transduction system to the nucleus. These cascades of events may strengthen the influence of survival factors or may inhibit apoptosis. (2) A cellular stress response and synthesis of stress proteins may lead to an increased capacity for health maintenance inside the cell. These proteins work as cellular "chaperones" by unfolding misfolded cellular proteins and helping the cell to dispose of unneeded denatured proteins. Recent experimental data have demonstrated the importance of the processing of unfolded proteins for cell survival and cell death. The brain may be protected from ischemia by using multiple mechanisms that are available for cellular survival. If tolerance induction can be manipulated and accelerated by a drug treatment that is safe and effective enough, it could greatly improve the treatment of stroke.

Adaptation, Physiological↗
PubMed1990

Non-A, non-B hepatitis and dentistry.

Non-A, non-B hepatitis (hepatitis C) is a viral infection(s) transmitted mainly by blood and blood products. Infection is usually asymptomatic, but typically followed by chronic infection, frequently with chronic liver disease. Although probably less than 1% of the UK population (and hence dental patients) are infected, groups at high risk for other blood-borne infections are also at risk for non-A, non-B hepatitis. Immunisation against hepatitis B cannot protect against non-A, non-B hepatitis; recommended cross-infection procedures must suffice to protect patients and staff.

Antibodies, Viral↗
PubMed2005

Glycoprotein D receptor-dependent, low-pH-independent endocytic entry of herpes simplex virus type 1.

Two herpes simplex virus type 1 (HSV-1) entry pathways have been described: direct fusion between the virion envelope and the plasma membrane, as seen on Vero cells, and low-pH-dependent endocytosis, as seen on CHO nectin-1 and HeLa cells. In this paper, we studied HSV entry into C10 murine melanoma cells and identified a third entry pathway for this virus. During entry into C10 cells, virion envelope glycoproteins rapidly became protected from the membrane-impermeable chemical cross-linker BS3 and from proteinase K. Protection was gD receptor dependent, and the time taken to detect protected protein was proportional to the rate of virus entry. Ultrastructural examination revealed that virions attached to the surface of C10 cells were localized to membrane invaginations, whereas those on the surface of receptor-negative B78 cells were peripherally attached. Virus entry into C10 cells was energy dependent, and intracellular enveloped virions were seen within membrane-bound vesicles consistent with endocytic entry. Entry was not inhibited by bafilomycin A1 or ammonium chloride, showing that passage of the virion through a low-pH environment was not required for infection. Resistance to similar reagents should therefore not be taken as proof of HSV entry by a nonendosomal pathway. These data define a novel gD receptor-dependent acid-independent endocytic entry pathway for HSV.

Adenosine Triphosphate↗