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At least 199 records · Page 11Linked to original sources
PubMed1992

Infertility: psychotherapeutic issues.

In supportive therapy with infertility patients, the clinician tries to relieve dysphoria and enhance self-esteem. Dynamically informed supportive interventions are designed to decrease guilt that may relate to past sexual activities, sexually related diseases, or abortions. These interventions should also be empathetic, promote optimism and reality testing, help with problem solving, allow catharsis and ventilation, decrease feelings of isolation and loneliness, educate and clarify, and praise and encourage where appropriate. Mental health clinicians have an important role to play in the treatment of these patients, provided they learn enough about the psychology of the experience of infertility and about the technology utilized in its treatment. As the number of people seeking treatment for infertility grows, the need for skilled therapists for this population will grow at a parallel rate.

Female↗
PubMed2001

Central CRH suppresses specific antibody responses: effects of beta-adrenoceptor antagonism and adrenalectomy.

Central corticotropin releasing hormone (CRH)-induced activation of the sympathetic nervous system and/or the pituitary-adrenal axis is hypothesized to mediate suppression of in vivo specific antibody responses. To test whether beta-adrenergic receptor activation is involved in the immunosuppressive effects of central CRH, rats were pretreated with propranolol or saline before intracerebroventricular infusion of CRH and immunization with keyhole limpet hemocyanin (KLH). KLH (3 microg/kg) immunization induced significant increases in circulating levels of antigen-specific IgM and IgG. Central infusion of CRH (200 pmol) suppressed both IgM and IgG responses. Pretreatment with propranolol (20 mg/kg IP) reversed CRH-induced suppression of IgG responses but had no effect on IgM levels. To test whether adrenal activation also plays a role in the effects of KLH on specific antibody responses, a separate group of animals underwent adrenalectomy prior to CRH infusion and immunization with KLH. As compared to nonadrenalectomized control rats, adrenalectomized rats showed a reduction of antibody responses, and CRH failed to induce a further suppression of IgM or IgG responses in adrenalectomized animals. Collectively, these data suggest that beta-adrenoceptors mediate the suppression of primary antibody responses induced by central CRH. Moreover, the adrenals may promote optimal primary antibody responses after exposure to physiological levels of antigen.

Adjuvants, Immunologic↗
PubMed2001

Involvement of GDNF in neuronal protection against 6-OHDA-induced parkinsonism following intracerebral transplantation of fetal kidney tissues in adult rats.

Exogenous application of transforming growth factors-beta (TGF beta) family proteins, including glial cell line-derived neurotrophic factor (GDNF), neurturin, activin, and bone morphogenetic proteins, has been shown to protect neurons in many models of neurological disorders. Finding a tissue source containing a variety of these proteins may promote optimal beneficial effects for treatment of neurodegenerative diseases. Because fetal kidneys express many TGF beta trophic factors, we transplanted these tissues directly into the substantia nigra after a unilateral 6-hydroxydopamine lesion. We found that animals that received fetal kidney tissue grafts exhibited (1) significantly reduced hemiparkinsonian asymmetrical behaviors, (2) a near normal tyrosine hydroxylase immunoreactivity in the lesioned nigra and striatum, (3) a preservation of K(+)-induced dopamine release in the lesioned striatum, and (4) high levels of GDNF protein within the grafts. In contrast, lesioned animals that received grafts of adult kidney tissues displayed significant behavioral deficits, dopaminergic depletion, reduced K(+)-mediated striatal dopamine release, and low levels of GDNF protein within the grafts. The present study suggests that fetal kidney tissue grafts can protect the nigrostriatal dopaminergic system against a neurotoxin-induced parkinsonism, possibly through the synergistic release of GDNF and several other neurotrophic factors.

Age Factors↗
PubMed1989

Familial resemblance of radial bone mass between premenopausal mothers and their college-age daughters.

The influences of heredity and environmental factors on radial bone mass were evaluated in 84 premenopausal mothers with their biological daughters (ages 18-22). Mid- and distal radial bone mineral content (BMC) and density (BMD) were assessed using single-photon absorptiometry. As a group, the daughters (mean age 18.6 years) had 5-10% less bone mass at both the distal and midradial sites than their mothers (mean age 44.2 years). Familial resemblance estimates showed significant relationships between mothers and daughters for mid- and distal BMC and BMD after considering the influence of body mass index (BMI). Daughters with a maternal family history of osteoporosis had 6-7% lower but nonsignificant values of mid- (P = 0.086) and distal BMC (P = 0.075) compared to values of women with a negative family history, whereas mothers with a positive family history had 3-4% lower (NS) values of distal and mid-BMC compared to those of mothers with a negative family history after adjustment for BMI. Multiple regression analyses showed BMI to be the most important determinant of the bone values of the mothers, and both BMI and dietary calcium intake were found to be significant for the daughters. The findings of this study suggest that hereditary contributions from the mothers play an overwhelmingly critical role in the accrual of bone mass by their daughters by ages 18-22, but that environmental influences on bone consolidation during the premenopausal decades may be more important in promoting optimal (peak) bone mass and thereby may help to delay the postmenopausal onset of osteoporotic fractures.

Adolescent↗
PubMed1996

Patient misunderstanding of dosing instructions.

OBJECTIVE: To compare outpatients' understanding of medication dosing instructions written in terms of daily frequency with patients' understanding of instructions specifying hourly intervals. DESIGN: Prospective cohort study involving patient interviews. SETTING: A university hospital outpatient pharmacy. PATIENTS: Five hundred patients presenting new and refill prescriptions to the hospital outpatient pharmacy. INTERVENTION: Patients were interviewed using a standardised questionnaire. MEASUREMENTS AND MAIN RESULTS: Of the 71 patients with prescriptions specifying dosing instructions in hourly intervals (e.g., q6h), 55 (77%) misinterpreted the recommended frequency of dosage compared with only 4 (0.99%) of the 429 patients with dosing instructions specifying daily frequency (e.g., qid) (relative risk 83; 95% confidence interval 31-200). This difference remained when patient subgroups were evaluated by education level, new versus refill prescriptions, and analgesic versus nonanalgesic medications. CONCLUSIONS: This study indicates that the intended dosing regimen is frequently misunderstood when the physician writes outpatient prescriptions in hourly intervals. To promote optimal patient compliance, the outpatient prescription label should state the number of times a day a medication is to be taken.

Adult↗
PubMed1995

Quantification of the interactions among fatty acid, lysophosphatidylcholine, calcium, dimyristoylphosphatidylcholine vesicles, and phospholipase A2.

The rate of hydrolysis of phosphatidylcholine bilayers by soluble phospholipase A2 (PLA2) is greatly enhanced by the presence in the bilayer of a threshold mole fraction of the reaction products: fatty acid and lysophosphatidylcholine (lyso-PC). The threshold requirement of these products appears to vary as a function of vesicle and calcium concentration. To further identify the roles of myristic acid, lyso-PC, and calcium in promoting optimal PLA2 activity, we have quantified the various interactions among these components and dimyristoylphosphatidylcholine large unilamellar vesicles. The bilayer/water partition coefficient for myristic acid was obtained by competition of vesicles for the binding of the fatty acid to an acrylodan conjugate of an intestinal fatty acid binding protein as monitored by the acrylodan fluorescence emission spectrum. The partition coefficient for lyso-PC was obtained by a similar procedure using the tryptophan emission spectrum of bovine serum albumin. The effect of calcium concentration on these interactions was also quantified. These results were incorporated into an empirical model to describe the threshold requirements for these products in the bilayer. This information is vital for elucidating the mechanism of activation of PLA2 by the hydrolysis products.

Calcium↗
PubMed1989

Chemical phosphorylation of proteins by zinc-ATP.

During an examination of in vitro phosphorylation of the adipocyte lipid-binding protein (ALBP) by the insulin receptor, we detected insulin receptor-independent, chemical phosphorylation of ALBP. This activity was present in ALBP purified to homogeneity from murine 3T3-L1 cells and in recombinant murine ALBP purified from expressing E. coli cultures. Phosphoamino acid analysis revealed that chemical phosphorylation of ALBP occurred primarily on Ser residues. The phosphorylation activity occurred in the alkaline pH range from 8 to 11 and exhibited a broad temperature dependence. The reaction rate was linearly dependent upon the ATP concentration and exhibited a biphasic kinetic profile. Eight of twelve other proteins tested also underwent chemical phosphorylation. Zn+2, Mg+2, or Mn+2 promoted optimal phosphorylation of different proteins. We conclude that many proteins are capable of undergoing chemical phosphorylation.

Adenosine Triphosphate↗
PubMed1987

NADPH- and linoleic acid hydroperoxide-induced lipid peroxidation and destruction of cytochrome P-450 in hepatic microsomes.

Temporal aspects of the effects of inhibitors on hepatic cytochrome P-450 destruction and lipid peroxidation induced by NADPH and linoleic acid hydroperoxide (LAHP) were compared. In the absence of added Fe2+, NADPH-induced lipid peroxidation in hepatic microsomes exhibited a slow phase followed by a fast phase. The addition of Fe2+ eliminated the slow phase, thus demonstrating that iron is a rate-limiting component in the reaction. EDTA, which complexes iron, and p-chloromercurobenzoate (pCMB), which inhibits NADPH-cytochrome P-450 reductase, inhibited both phases of the reaction. Catalase as well as scavengers of hydroxyl radical, inhibited NADPH-induced lipid peroxidation almost completely. GSH also inhibited the NADPH-dependent reaction but only when added at the beginning of the reaction. In contrast with NADPH-dependent lipid peroxidation, the autocatalytic reaction induced by LAHP was not biphasic, NADPH-dependent or iron-dependent, nor was it inhibited by hydroxyl radical scavengers, catalase or GSH. A synergistic effect on lipid peroxidation was observed when both NADPH and LAHP were added to microsomes. It is concluded that both the fast and slow phases of NADPH-dependent microsomal lipid peroxidation are catalyzed enzymatically and are dependent upon Fe2+, whereas LAHP-dependent lipid peroxidation is autocatalytic. Since the fast phase of enzymatic lipid peroxidation occurred during the fast phase of destruction of cytochrome P-450, it is postulated that iron made available from cytochrome P-450 is sufficient to promote optimal lipid peroxidation. Since catalase and hydroxyl radical scavengers inhibited NADPH-dependent but not LAHP-dependent lipid peroxidation, it is concluded that the hydroxyl radical derived from H2O2 is the initiating active-oxygen species in the enzymatic reaction but not in the autocatalytic reaction.

Animals↗
PubMed1987

Transforming growth factor type beta (TGF beta) inhibits G1 to S transition, but not activation of human B lymphocytes.

Type beta transforming growth factor (TGF beta) is a polypeptide that may influence the growth of a variety of cell types in a positive or negative fashion. In this study we show that TGF beta markedly inhibits DNA synthesis in normal and neoplastic human B lymphocytes stimulated to proliferate with anti-immunoglobulins and B-cell growth factor (BCGF). Although TGF beta was needed during the initial 12 h of the culture to promote optimal inhibition, we found that it had little or no effect on several early to intermediate parameters of cell activation [( Ca2+]i increase, c-myc mRNA increase, cellular enlargement, RNA increase, and the increase in the expression of the 4F2 activation antigen). In contrast, TGF beta almost completely blocked the induction of transferrin receptor expression, which normally occurs in the late G1 phase of the cell cycle. Therefore, we conclude that TGF beta treatment leads to arrest of the cells in the middle to late G1 phase, prior to transferrin receptor expression.

Antibodies, Anti-Idiotypic↗
PubMed1989

Does exposure to HLA alloantigens trigger immunoregulatory mechanisms operative in both pregnancy and AIDS?

The complex biological processes responsible for regulating the immune system are presently the subject of considerable interest and study. New insight into this process comes from a variety of observations and it is the purpose of this communication to develop the hypothesis that two seemingly quite disparate observations point to a common biological mechanism bearing on immunoregulation. The observations concern the unique immunologic relationship between mother and fetus and the immunoregulatory abnormalities encountered in HIV-induced acquired immunodeficiency syndrome (AIDS). Exposure to foreign (allo) major histocompatibility complex (MHC) antigens can potentially occur during pregnancy, the transfusion of blood or blood products, or anal insemination. The hypothesis, in its simplest form, states that such MHC alloantigenic exposure triggers a sequence of immunoregulatory mechanisms resulting in immunosuppression and that this response has evolved in placental mammals as a means of protecting the fetus from maternal immune rejection and promoting optimal fetal development.

Acquired Immunodeficiency Syndrome↗
PubMed1983

Three regions upstream from the cap site are required for efficient and accurate transcription of the rabbit beta-globin gene in mouse 3T6 cells.

Cloned rabbit beta-globin genes, modified in vitro by restructuring or site-directed mutagenesis, were introduced into mouse 3T6 cells, and the resulting transcripts were analyzed by nuclease S1 mapping. The first 109 bp preceding the cap site sufficed for maximal beta-globin transcription. This segment contained three functionally important regions of the ATA box region; the CCAAT box region; and the -100 region. The latter consists of an imperfect tandemly repeated sequence of 14 bp and 15 bp, both copies of which are required for optimal promoter function. Each of three regions contains two or more nucleotide positions where the introduction of point mutations reduces transcription by at least a factor of 2.

Animals↗
PubMed1993

Insulin resistance in Mexican Americans--a precursor to obesity and diabetes?

Mexican Americans appear to have a strong genetic predisposition to insulin resistance, android obesity, and type II diabetes, apparently as a function of Native American genetic heritage. Theoretical considerations suggest that insulin resistance may be a primary factor that plays a causative role in the induction of both obesity and diabetes. Measures which promote optimal insulin sensitivity--chromium picolinate, brewer's yeast, soluble fiber supplements, metformin, very-low-fat diet, exercise training--may have value for preventing, treating, or retarding the onset of obesity and diabetes, and merit clinical evaluation in this regard. Correction of insulin resistance may also lessen cardiovascular risk, in part by reducing LDL cholesterol and improving risk factors associated with Syndrome X. These comments are likely to be valid for other Native American groups at high risk for diabetes.

Animals↗
PubMed2006

Age-related differences in the management and outcome of patients with acute coronary syndromes.

BACKGROUND: Age-related differences in patients with an acute coronary syndrome (ACS) have not been well characterized in prior observational studies that often included only certain age groups or subjects with myocardial infarction (MI). METHODS: We stratified 4627 patients admitted with an ACS across 9 provinces between 1999 and 2001 enrolled in the Canadian ACS Registry into 3 age groups (< 65, 65-74, and > or = 75 years) to evaluate differences in clinical characteristics, management, and 1-year outcome. RESULTS: Older patients more frequently had previous angina, MI, or heart failure and were less likely to have positive cardiac markers, ST elevation, and Q-wave MI or to receive thrombolytics, beta-blockers, and cholesterol-lowering and antiplatelet agents in hospital, at discharge, and at 1 year. In multivariable analyses controlling for patient factors, every decade increase in age was independently associated with reduced use of coronary angiography (odds ratio [OR] 0.79, 95% CI 0.74-0.84, P < .001) and percutaneous coronary intervention (OR 0.88, 95% CI 0.81-0.95, P = .001). When adjusted for validated clinical prognosticators and differences in management, every decade of age increment independently predicted an increased risk of death at 1 year (OR 1.87, 95% CI 1.66-2.12, P < .001). CONCLUSIONS: Across the broad spectrum of ACS, elderly patients had more complex comorbidities and worse outcome, yet they were less likely to undergo revascularization or to receive acute and long-term evidence-based medications. Our findings emphasize the ongoing need to better define and promote optimal therapeutic regimens for elderly patients with ACS.

Age Factors↗
PubMed2005

Obesity and risk of nonfatal unintentional injuries.

BACKGROUND: Obesity is recognized as a risk factor for multiple chronic diseases. Yet, it is unclear whether obesity is also associated with an increased risk of nonfatal unintentional injury. METHODS: A population-based survey was conducted among adults aged > or = 18 years from January 1999 through October 2000. The relationship was investigated between body mass index (BMI), defined as weight in kilograms divided by the square of the height in meters (kg/m2), and risk of nonfatal unintentional injuries among 2575 respondents aged > or = 20 years by comparing percentage of adults between obese and nonobese respondents who had injuries. Multivariate logistic regression further examined this relationship by controlling for confounding demographics. RESULTS: A total of 370 respondents reported injuries in the previous year. We observed a linear dose-response trend among women. An estimated 7.0% of underweight individuals (BMI <18.5) reported injuries. In contrast, 26.0% of men and 21.7% of women with a BMI > or = 35.0 reported injuries. The odds ratio of injuries for individuals with a BMI > or = 35.0 was 2.00 (95% confidence interval=1.07-3.74, p<0.05) after controlling for gender, age, education level, marital status, family poverty status, and area of residence. CONCLUSIONS: A marginally significant association between extreme obesity and elevated risk of injuries was observed. Efforts to promote optimal body weight may reduce not only the risk of chronic diseases but also the risk of unintentional injury among overweight and obese individuals.

Adolescent↗
PubMed2004

Blood and marrow transplantation compensation: perspective in payer and provider relations.

The high cost per patient of hematopoietic cell transplantation (HCT) causes this therapy to be the focus of much controversy, given the competing societal demands to provide all possible therapy to preserve life while simultaneously limiting global health care expenditures. Treatment and eligibility decisions for HCT often are heavily scrutinized by both governmental and private payers and not simply determined by physicians, facility providers, and the patient. In an effort to control costs, payers have administrative infrastructure to review resource utilization by these patients. Additionally payers have developed payment methodologies, usually in the form of a case rate payment structure, that place facilities and physician providers of HCT at financial risk for adverse patient financial outcomes in an effort to promote optimal utilization and selection of patients for HCT. As providers enter into such financial risk arrangements with payers, the providers need to understand the true cost of care and be able to identify predictable and unpredictable outlier risks for the financial consequences of medical complications. HCT providers try to protect themselves from excessive financial risk by having different payment rates for different types of transplant, eg, autologous versus HLA or genotypically matched related versus HLA mismatched transplants. Because at certain times in the HCT process risk is more unpredictable, HCT providers require different payment system strategies for the different time periods of care such as evaluation, pre-transplant disease management, harvesting, and cell processing, as well as short- and long-term follow-up. Involvement by clinicians is essential for this process to be done well, especially given the rapid changes technological innovation brings to HCT. Constant dialogue and interaction between providers and payers on these difficult financial issues with HCT is essential to preserve patient access to this potentially lifesaving therapy.

Blood Transfusion↗
PubMed2003

Skin immune responses to peptide and protein antigen are TLR4 independent.

Little is known about the innate immune mechanisms regulating adaptive immune responses elicited through the skin. Tissue injury is postulated to liberate Toll like receptor 4 (TLR4) ligands. In this study, we determined whether TLR4 signaling modulates the response to epidermal injury induced by tape stripping (TS) and whether it alters humoral and cellular immune responses generated through epicutaneous immunization with peptide+cholera toxin (CT). The combined use of cholera toxin and TS with antigen promoted optimal antigen-specific CD4(+) and CD8(+) T cell proliferation in Balb/c and C57BL/6 mice, respectively. TLR4 mutant mice had similar T cell responses to wild type mice. Further, OVA-protein specific IgG, IgG(1), IgG(2a), and IgE titers were similar in wild type and TLR4 mutant mice. Thus, TLR4 signaling was not required for the generation of epicutaneous T cell or antibody mediated immune responses and did not alter the quality of the immune responses elicited.

Adoptive Transfer↗
PubMed2006

Activation impairment alters muscle torque-velocity in the knee extensors of persons with post-stroke hemiparesis.

OBJECTIVE: To elucidate mechanisms of impaired force production in post-stroke hemiparesis. METHODS: Knee extensor torque-velocity and activation-velocity relationships were examined in seventeen persons with post-stroke hemiparesis (age 57.5, +/-6.9) and thirteen non-disabled (age 63.0 +/-10.4) persons. RESULTS: Velocity-dependent concentric torque impairment was exaggerated in subjects with hemiparesis relative to control subjects (p<.001). Muscle power was also less in the group with hemiparesis (p<.001), and plateaued at velocities > or =90deg/s (p>.05). In the control group agonist EMG during concentric actions exhibited a positive linear relationship as velocity increased (R(2)=.93, p<.05). The group with hemiparesis produced 34-60% less agonist EMG than controls (p<.02) and modulation was absent (p>.05). Antagonist EMG was either greater in the control (biceps femoris, p<.006) or similar between groups (semimembranosus, p=.95). Under eccentric testing conditions, torque normalized to peak isometric torque (p=.44) and rectus femoris activation (p=.33) were similar between groups, indicating a relative preservation of eccentric torque producing capacity post-stroke. CONCLUSIONS: Certain clinical perspectives assert that weakness following central nervous system injury stems from spastic antagonist restraint. Instead, absence of an antagonist restraint strongly suggests that impaired agonist activation is the principal determinant of hemiparetic weakness. SIGNIFICANCE: These findings have important implications for promoting optimal recovery of motor function in neuro-rehabilitation.

Electromyography↗
PubMed2006

Pancreatic beta cells: responding to the matrix.

In a recent issue of Developmental Cell, Nikolova et al. (2006) make the unusual discovery that, unlike most epithelial cells, pancreatic beta cells do not produce a basement membrane of extracellular matrix. Rather, the matrix is provided to a subset of beta cells by local capillary endothelial cells, explaining in part how the endothelium helps promote optimal levels of insulin production.

Animals↗