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PubMed1994

Review of thrombolytic intervention for acute myocardial infarction--is it valuable?

Complete thrombolytic occlusion of a coronary artery has been thought to be the etiology of a acute myocardial infarction (MI) since 1912 and was proven by coronary angiography in 1980. Dissolution of the thrombus with the use of pharmacological agents has been proposed to decrease the morbidity and mortality associated with acute MI. This article reviews the historical development, pharmacology, efficacy, and complications associated with the four currently available thrombolytic agents. In 1912, James Herrick proposed that acute myocardial infarction (MI) was due to thrombotic occlusion of the coronary artery and was not inevitably associated with a fatal outcome. Although this view was revolutionary, it was virtually ignored for some 50 years. During the interim, the prevailing concept of the pathogenesis of acute MI revolved around gradual occlusion of a coronary artery by an atherosclerotic process with secondary thrombotic occlusion. Marcus DeWood settled the debate regarding the pathogenesis of acute MI in 1980 with a landmark publication which documented angiographically the presence of an intracoronary thrombus in patients with acute transmural myocardial infarction. He found that 87% of the patients who underwent cardiac catheterization within four hours of the onset of chest pain had thrombotic occlusion of the infarct-related artery. This percentage decreased to approximately 65% when the cardiac catheterization was performed within 12-24 hours after the onset of symptoms. Herrick's hypothesis, plus documentation that coronary thrombosis resulted in an acute MI presented investigators with the theory that thrombolytic agents could potentially prevent or limit the extent of myocardial damage. This discussion will focus on the historical development, pharmacology, and current knowledge regarding the efficacy of the available thrombolytic agents in the United States.

Cause of Death↗

PubMed2002

Adult respiratory distress syndrome: do selective anticoagulants help?

The adult respiratory distress syndrome (ARDS) is a form of acute lung injury that is characterized by florid extravascular fibrin deposition. Thrombosis in the pulmonary vasculature and disseminated intravascular coagulation have also been observed in association with ARDS. Fibrin deposition does not occur in the normal lung but is virtually universal in acute lung injury induced by disparate insults. A large body of basic and preclinical evidence further implicates abnormalities of pathways of fibrin turnover in the pathogenesis of acute inflammation and fibrotic repair. Coagulation is locally upregulated in the injured lung, while fibrinolytic activity is depressed. These abnormalities occur concurrently and favor alveolar fibrin deposition. The systemic derangements of fibrin turnover in sepsis are similar to those that occur in the injured lung. Recent clinical trials demonstrate that interventions using selective anticoagulation can provide a mortality advantage and that selective anticoagulants differ in their ability to provide clinical benefit. Preclinical trials in primates with sepsis-induced ARDS now indicate that anticoagulant interventions that block the extrinsic coagulation pathway can protect against the development of pulmonary fibrin deposition as well as lung dysfunction and acute inflammation. These observations provide proof of principle that key steps in the coagulation cascade are appropriate therapeutic targets to prevent the development of acute lung injury in ARDS. Ongoing studies and prior publications also support the hypothesis that reversal of the fibrinolytic defect in ARDS could protect against the development of acute lung injury. In all, these studies suggest that fibrin deposition in the injured lung as well as abnormalities of coagulation and fibrinolysis are integral to the pathogenesis of ARDS. The ability of selective anticoagulants to effectively and safely alter clinical outcome in ARDS remains to be determined.

Adult↗

PubMed1996

Histone H4 stimulates glucose uptake through the insulin receptor.

Histone H4 stimulates the uptake of glucose in rat adipocytes and muscle cells. However, the mechanism of this unusual activity is not known. Therefore, we have begun to investigate the mechanism by which histone H4 stimulates the glucose uptake in rat adipocytes. We report that histone H4 requires 15-20 min to achieve its maximum effect and its time course is virtually indistinguishable from the time course of insulin itself. Reduction of the concentration of insulin receptors on the surface of adipocytes, either by trypsin digestion of the receptor, or by insulin-induced down regulation of the receptor, reduced the histone H4 effect as well as the insulin effects. Also, quercetin, a bioflavenoid that inhibits the insulin receptor tyrosine kinase activity, inhibits the actions of both histone H4 and insulin. However, histone H4 activity is somewhat more resistant to these interventions than insulin activity. In contrast to the activity of insulin, histone H4 does not appear to be able to down regulate the insulin receptor, since the pretreatment of adipocytes with histone H4 did not affect the subsequent actions of either insulin or histone H4. Finally, Scatchard analysis of the binding of 125I-insulin in the presence and absence of histone H4 increases the specific binding of insulin in a concentration dependent fashion. Histone H2b, a histone that does not have insulin-like activity, does not affect insulin binding. Taken together, these data suggest that the greatest portion of the insulin-like activity of histone H4 is initiated at the insulin receptor. However, the interaction of histone H4 and the insulin receptor is more complex than a simple binding of H4 to the insulin binding site. These studies may provide additional insight into alternate mechanisms for activation of the insulin receptor.

Adipocytes↗

PubMed2005

AutoLink: automated sequential resonance assignment of biopolymers from NMR data by relative-hypothesis-prioritization-based simulated logic.

We have developed a new computer algorithm for determining the backbone resonance assignments for biopolymers. The approach we have taken, relative hypothesis prioritization, is implemented as a Lua program interfaced to the recently developed computer-aided resonance assignment (CARA) program. Our program can work with virtually any spectrum type, and is especially good with NOESY data. The results of the program are displayed in an easy-to-read, color-coded, graphic representation, allowing users to assess the quality of the results in minutes. Here we report the application of the program to two RNA recognition motifs of Apobec-1 Complementation Factor. The assignment of these domains demonstrates AutoLink's ability to deliver accurate resonance assignments from very minimal data and with minimal user intervention.

Algorithms↗

PubMed2004

Motor tele-rehabilitation in post-stroke patients.

PRIMARY OBJECTIVE: The advanced communication technology may allow rehabilitative interventions to patients living at home from a remote provider. We evaluated the effects of a tele-rehabilitation system for the therapy of arm motor impairments due to a stroke. RESEARCH DESIGN: Experimental observational study. METHODS AND PROCEDURES: We selected five patients suffering from mild/intermediate arm motor impairments due to a long-lasting ischaemic stroke. Two workstations were utilized, one in the patient's house and the other in the rehabilitation hospital, connected through the phone lines. A virtual reality based software allowed the patient to perform adequate motor tasks created by the physiotherapist. During performance, the patient could see not only their movement but also the correct trajectory that they had to accomplish. The feedback derived from the patient's action, its outcome, and feedback from the supervision of the physiotherapist may favour the acquisition of new motor abilities. MAIN OUTCOME MEASURES: The arm motor performance and the activities of daily living were evaluated using the Fugl-Meyer and Functional Independence Measure scale, together with the determination of the velocity and duration of 10 representative reaching movements. RESULTS: Subjects underwent the tele-rehabilitation programme for 4 weeks. The therapy significantly improved the Fugl-Meyer mean score, the mean duration and the velocity of the movements, but not the Functional Independence Measure scale score. CONCLUSIONS: These results indicated that this tele-rehabilitation system did not appear to adversely affect rehabilitation; rather it may improve arm motor deficits due to a stroke. If these evidences are further confirmed, tele-rehabilitation may represent a new home-based therapy to treat disabled people.

Activities of Daily Living↗

PubMed1992

Effective arterial elastance as index of arterial vascular load in humans.

BACKGROUND: This study tested whether the simple ratio of ventricular end-systolic pressure to stroke volume, known as the effective arterial elastance (Ea), provides a valid measure of arterial load in humans with normal and aged hypertensive vasculatures. METHODS AND RESULTS: Ventricular pressure-volume and invasive aortic pressure and flow were simultaneously determined in 10 subjects (four young normotensive and six older hypertensive). Measurements were obtained at rest, during mechanically reduced preload, and after pharmacological interventions. Two measures of arterial load were compared: One was derived from aortic input impedance and arterial compliance data using an algebraic expression based on a three-element Windkessel model of the arterial system [Ea(Z)], and the other was more simply measured as the ratio of ventricular end-systolic pressure to stroke volume [Ea(PV)]. Although derived from completely different data sources and despite the simplifying assumptions of Ea(PV), both Ea(Z) and Ea(PV) were virtually identical over a broad range of altered conditions: Ea(PV) = 0.97.Ea(Z) + 0.17; n = 33, r2 = 0.98, SEE = 0.09, p less than 0.0001. Whereas Ea(PV) also correlated with mean arterial resistance, it exceeded resistance by as much as 25% in older hypertensive subjects (because of reduced compliance and wave reflections), which better indexed the arterial load effects on the ventricle. Simple methods to estimate Ea (PV) from routine arterial pressures were tested and validated. CONCLUSIONS: Ea(PV) provides a convenient, useful method to assess arterial load and its impact on the human ventricle. These results highlight effects of increased pulsatile load caused by aging or hypertension on the pressure-volume loop and indicate that this load and its effects on cardiac performance are often underestimated by mean arterial resistance but are better accounted for by Ea.

Adult↗

PubMed1998

The use of a retinoid receptor antagonist in a new model to study vitamin A-dependent developmental events.

Multiple fetal anomalies occur in vitamin A deficient animals as well as in retinoic acid receptor gene 'knockout' mice, indicating that retinoic acid (an active metabolite of vitamin A) performs some essential functions in normal development. Additional approaches are needed to probe directly the stages and sites in the embryo where a presence of endogenous retinoic acid is indispensable. We have employed a new strategy for this purpose which involved an intervention in retinoic acid receptor (RAR)-dependent functions at specific developmental stages by means of a highly effective RAR antagonist, AGN 193109. We report that in an in vitro cell differentiation bioassay, AGN 193109 completely reversed the inhibitory action of a potent RAR agonist, AGN 190121. In pregnant mice, a single oral 1 mg/kg dose of the antagonist given on 8 day post coitum (dpc) produced a severe craniofacial anomaly (median cleft face or frontonasal dysplasia) and eye malformations in virtually all exposed fetuses. On the other hand, treatment on 11 dpc, a time in development when RARs are strategically expressed in the limb bud primordium, no limb anomalies could be induced by the antagonist. Even after a high dose of 100 mg/kg, limb development progressed normally in spite of the fact that measurable concentrations of the antagonist were present. Because retinoids are long known to influence skin morphology, we next monitored the effects of the antagonist on skin development. When given late in gestation, on 14 dpc, we found that the antagonist delayed differentiation and maturation of the fetal skin and hair follicles. We conclude that this model provides a convenient and pertinent system which enables us to seek and clarify true functions of retinoic acid and its cognate receptors in embryogenesis and in adult animals.

Animals↗

PubMed2005

Mechanisms of delivery of ubiquitylated proteins to the proteasome: new target for anti-cancer therapy?

The proteasome is the main proteolytic machinery of the cell. It is responsible for the basal turnover of many intracellular polypeptides, the elimination of abnormal proteins and the generation of the vast majority of peptides presented by class I major histocompatibility complex molecules. Proteasomal proteolysis is also involved in the control of virtually all cellular functions and major decisions through the spatially and timely regulated destruction of essential cell regulators. Therefore, the elucidation of its molecular mechanisms is crucial for the full understanding of the physiology of cells and whole organisms. Conversely, it is increasingly clear that proteasomal degradation is either altered in numerous pathological situations, including many cancers and diseases resulting from aberrant cell differentiation, or instrumental for the development of these pathologies. This, consequently, makes it an attractive target for therapeutical intervention. There is ample evidence that most cell proteins must be polyubiquitylated prior to proteasomal degradation. If the structure and the mode of functioning of the proteasome, as well as the enzymology of ubiquitylation, are relatively well understood, how substrates are delivered to and recognized by the proteolytic machine has remained mysterious till recently. The recent literature indicates that the mechanisms involved are multiple, complex and exquisitely regulated and provides new potential targets for anti-cancer pharmacological intervention.

Animals↗

PubMed2003

Mechanobiology and diseases of mechanotransduction.

The current focus of medicine on molecular genetics ignores the physical basis of disease even though many of the problems that lead to pain and morbidity, and bring patients to the doctor's office, result from changes in tissue structure or mechanics. The main goal of this article is therefore to help integrate mechanics into our understanding of the molecular basis of disease. This article first reviews the key roles that physical forces, extracellular matrix and cell structure play in the control of normal development, as well as in the maintenance of tissue form and function. Recent insights into cellular mechanotransduction--the molecular mechanism by which cells sense and respond to mechanical stress--also are described. Re-evaluation of human pathophysiology in this context reveals that a wide range of diseases included within virtually all fields of medicine and surgery share a common feature: their etiology or clinical presentation results from abnormal mechanotransduction. This process may be altered by changes in cell mechanics, variations in extracellular matrix structure, or by deregulation of the molecular mechanisms by which cells sense mechanical signals and convert them into a chemical or electrical response. Molecules that mediate mechanotransduction, including extracellular matrix molecules, transmembrane integrin receptors, cytoskeletal structures and associated signal transduction components, may therefore represent targets for therapeutic intervention in a variety of diseases. Insights into the mechanical basis of tissue regulation also may lead to development of improved medical devices, engineered tissues, and biologically-inspired materials for tissue repair and reconstruction.

Biology↗

PubMed1998

Resuscitation after hemorrhage using recombinant human hemoglobin (rHb1.1) in rats: effects on nitric oxide and prostanoid systems.

OBJECTIVES: Hemoglobin-based oxygen carriers are designed to replace blood volume and to increase oxygen delivery to tissues after blood loss. The goals of the present study were two-fold: a) to determine the systemic and regional vascular effects of resuscitation with recombinant human hemoglobin (rHb1.1) in rats during controlled hemorrhage; and b) to determine whether nitric oxide (NO) or prostaglandins were involved in the observed responses. DESIGN: Paralyzed, ventilated rats were hemorrhaged (18 mL blood/kg body weight) during halothane anesthesia and allowed to stabilize for 30 mins. Systemic and regional hemodynamics and oxygen delivery were monitored at three time points, using the radioactive microsphere method. Microspheres were first infused at the end of the hemorrhage stabilization period (t=0 min). rHb1.1 (1 g/kg body weight) or rHb1.1 diluent (phosphate buffered saline, 36 mL/kg body weight) were infused over 20 mins and microspheres were administered again, 30 mins later (t=50 mins). Saline (0.5 mL), indomethacin (5 mg/kg to inhibit cyclooxygenase), or NG-monomethyl-L-arginine (L-NMMA, 100 mg/kg, to inhibit NO synthase) were then infused in rHb1.1-treated rats and microspheres injected once more (t=80 mins). SETTING: Research laboratory. SUBJECTS: Male Wistar rats (n=37). INTERVENTIONS: Recombinant human hemoglobin (rHb1.1), rHb1.1 diluent (phosphate buffered saline) resuscitation of hemorrhaged rats. Saline, L-NMMA, or indomethacin treatment after resuscitation. MEASUREMENTS AND MAIN RESULTS: Resuscitation with rHb1.1 increased mean arterial pressure (MAP), cardiac output, and systemic oxygen delivery significantly when compared with diluent. After rHb1.1 resuscitation, regional blood flows were significantly increased in skin, kidney, spleen, and heart compared with diluent resuscitation. Compared with saline treatment after rHb1.1 resuscitation, L-NMMA increased MAP and regional resistances in virtually all tissues; indomethacin did not alter MAP, but increased resistance in the brain. CONCLUSIONS: These data indicate that rHb1.1 resuscitation was more effective than diluent in improving systemic and regional hemodynamics and oxygen delivery, suggesting that rHb1.1 may be of benefit in the treatment of acute blood loss. Increased resistance after L-NMMA in the presence of rHb1.1 indicated that rHb1.1 resuscitation did not eliminate NO dependent circulatory control. Increased resistance after indomethacin in brain indicated that vasodilator prostanoids were important in regulating vascular resistance in these tissues after rHb1.1 resuscitation.

Animals↗

PubMed1992

Transplant arteriosclerosis in a rat aortic model.

Transplant arteriosclerosis (TA) has emerged as an obstacle to the long-term survival of transplanted organs, especially cardiac transplants. The animal models that have been used to study TA have not been fully characterized with regard to features such as the time course of cell proliferation and the sequence of cell types arriving in the developing intimal lesion. We present a model of TA based on a transplanted segment of abdominal aorta that helps address these questions. Two strains of rats (PVG x DA) underwent orthotopic aortic transplantation without immunosuppression and were killed at 14, 20, 40, and 60 days after transplantation. The within-strain control group displayed minimal evidence of cellular rejection with minimal to absent intimal lesions. In contrast, the allograft group showed a linearly increasing intimal lesion, up through 60 days after transplantation. The mechanism of intimal thickening was by an increase in cell number at the earlier time points with the later deposition of extracellular matrix. The early intimal lesion consisted mostly of mononuclear inflammatory cells (45%) with gradually increasing presence of smooth muscle cells (SMC) in the intima between 20 and 60 days. Conversely, the media showed gradual infiltration by macrophage-type cells with virtual loss of all SMC from the media by 40 days. The proliferative index showed a peak of 6% and 8% at 20 days in both the intima and media, respectively, and was preceded by the presence of macrophages. In fact, most of the proliferating cells at the earlier time points were either monocytes/macrophages, or were immediately adjacent to monocyte-/macrophage-rich regions. This straight artery segment model of transplant arteriosclerosis provides an easily quantifiable system in which the effects of different interventions (e.g., immunosuppressive regimens) can be tested.

Animals↗

PubMed1992

Comparison of warfarin and external pneumatic compression in prevention of venous thrombosis after total hip replacement.

OBJECTIVE: To compare the effectiveness and safety of warfarin and external pneumatic compression (EPC) in prevention of venous thrombosis after total hip replacement. DESIGN: Prospective, randomized trial in consecutive patients, with blinded assessment of the primary end point. SETTING: University medical center and large community hospital. PATIENTS: Patients over age 18 years scheduled for elective primary total hip replacement were eligible. Of 254 patients interviewed, 232 were randomized, 220 patients had surgery and received prophylaxis, and 201 had venography. INTERVENTIONS: Patients were randomly assigned to prophylaxis with a device providing bilateral sequential EPC to both the calf and thigh or to receive warfarin in a low-intensity regimen beginning 10 to 14 days preoperatively. Prophylaxis was continued until venography. MAIN OUTCOME MEASURES: Venous thrombosis was diagnosed by venography between postoperative days 6 and 8. Bleeding was assessed by surgical blood loss, transfusion requirements, changes in hematocrit, and clinically identified bleeding complications. RESULTS: The total incidence of venous thrombosis was virtually the same in the warfarin and EPC groups (31% vs 27%), but the distribution of thrombi was different. Proximal thrombosis occurred in 12% of patients in the EPC group compared with only 3% in the warfarin group (P = .012, 95% confidence interval for difference, 2% to 18%). In contrast, calf vein thrombosis was more frequent in the warfarin group (21%) than in the EPC group (12%) (P = .021, 95% confidence interval for difference, 0% to 18%). Most proximal thrombi in EPC-treated patients were located within 15 cm of the femoral head and were not continuous with thrombi in deep calf veins. The high incidence of proximal thrombosis in the EPC group resulted in termination of the study by the safety monitoring committee. Blood loss and bleeding complications were similar in the two groups. CONCLUSION: Warfarin therapy is significantly more effective than EPC in preventing serious proximal vein thrombosis after total hip replacement. The greater effectiveness of warfarin therapy in preventing proximal vein thrombi and of EPC in preventing thrombosis in the calf suggests that there are differences in the pathogenesis of thrombosis in these two locations.

Aged↗

PubMed2005

Effects of 17beta-oestradiol plus different doses of drospirenone on adipose tissue, adiponectin and atherogenic metabolites in postmenopausal women.

OBJECTIVE: To investigate how variation in the dose of the progestogen influence the impact of 17beta-oestradiol plus drospirenone (DRSP) treatment on adipose tissue and its secretor function with direct implications for atherogenic metabolites. DESIGN: Randomized, double-blind, placebo-controlled trial. SETTING: Primary care, single study site. SUBJECTS: A total of 240 healthy postmenopausal women 53-65 years old, 178 completer. INTERVENTION: Daily treatment with 1 mg 17beta-oestradiol plus 1, 2, or 3 mg DRSP, or placebo for 2 years. MAIN OUTCOME MEASURES: Absolute changes in central (CFM) and peripheral fat mass (PFM; dual-energy X-ray absorptiometry, DEXA), adipokines [interleukin (IL)-6 and adiponectin], atherogenic metabolites [triglycerides, high-density lipoprotein cholesterol (HDL-C), glucose] and blood pressure. RESULTS: Oestradiol plus 1 mg DRSP evoked significant decreases in CFM and the CFM/PFM ratio from baseline. These benefits virtually decreased with increasing dose of DRSP confounded by dose-dependent increases in CFM and PFM in smokers (P-value for trends <0.001), in whom the increases in bioavailable oestradiol were half of that in nonsmokers (P < 0.001). Treatment with 3 mg DRSP induced decreases in serum adiponectin by month 6 (P < 0.05), which persisted in nonsmokers only and led to significant increases in glucose and triglycerides and decreases in HDL-C (P < 0.05). Adiponectin in smokers normalized by the end of the study parallel with the increases in body fat mass. CONCLUSIONS: Interactions of the sex steroids with adipose tissue and its secretor function are important determinants of the overall impact of hormone therapy on cardiovascular risk. A DRSP dose up to 2 mg does not seem to exert adverse effects when combined with 1 mg 17beta-oestradiol.

Absorptiometry, Photon↗

PubMedDate not supplied

Inpatient treatment of anorexia nervosa: review and recommendations.

Inpatient treatment of anorexia nervosa, difficult and at times complex, has been shown to promote enduring change. An integrated treatment approach that includes medical, psychological, nursing, and social interventions can restore patients to a healthy weight, improve abnormal eating behaviors, and ameliorate many of the central psychopathological attitudes and illness-driven behaviors characteristic of the disorder. This article reviews inpatient treatment of anorexia nervosa, evaluating empirical studies and providing a critique of their methodology and potential applicability, combining available published studies with clinical experience to suggest a comprehensive pragmatic treatment approach, and noting research needs for the future. More controlled double-blind studies are urgently needed to assess virtually every aspect of inpatient care, especially methods for promoting safe and rapid weight restoration. Comparative studies on the efficacy of behavioral, psychotherapeutic, and pharmacological approaches and determination of the optimum step-wise preparation for discharge into a weight-preoccupied society are also needed.

Anorexia Nervosa↗

PubMed1993

Beta-blockers after myocardial infarction: influence of first-year clinical course on long-term effectiveness.

OBJECTIVE: To develop a strategy for evaluating drug efficacy over time that accounts for heterogeneous clinical courses evolving after initiation of therapy and to demonstrate its use in assessing the long-term therapeutic benefit of propranolol after myocardial infarction. DESIGN: Analysis of data from the Beta-Blocker in Heart Attack Trial (BHAT), a randomized, double-blind, placebo-controlled trial that enrolled patients from 1978 to 1980 and followed participants for vital status to April 1982. SETTING: Thirty-one clinical centers in the United States and Canada. PATIENTS: Eligible patients included 3297 men and women 30 to 69 years of age who survived 1 year after trial entry. INTERVENTION: Patients were classified as being on treatment at 12 months after randomization if they were receiving beta-blocker therapy at the 12-month visit and off treatment if they were not receiving beta-blocker therapy at that time. OUTCOME MEASURE: Vital status evaluated at 720 days of follow-up. RESULTS: A total of 2914 patients (88%) was classified as being at lower risk (strata I and II). For these patients, survival curves by treatment at 12 months were virtually indistinguishable. Among the 383 patients categorized as being at high risk on the basis of recurrent ischemic events, arrhythmias, congestive heart failure, or severe comorbidity during the first 12 months, the use of beta-blockers was associated with a 43% proportional decline in the subsequent risk for death (P = 0.01 by log-rank test). CONCLUSIONS: In patients who survived to 1 year with low- to moderate-risk clinical courses, beta-blocker therapy did not have long-term beneficial effect. In contrast, among patients who had a high-risk clinical course during the first year, beta-blockers significantly reduced mortality in the follow-up period.

Adult↗

PubMed2004

[Interdisciplinary surgery and telemedicine].

Surgical therapy is becoming increasingly complex. Besides new surgical techniques, sophisticated diagnostic methods and innovative interventional procedures must be integrated into the therapeutic concept to increase the efficacy of surgery. Accurate application of these techniques requires close cooperation between surgeons, other medical specialists, and technicians. Consequently, there is a significant need for structures promoting efficient communication, organization, and interaction in surgical departments. New techniques developed from telecommunication and information technology enable the transferal of complex medical data at any time to any place and are therefore the basis for telemedical applications. Telemedicine and other new techniques such as virtual operation planning, simulation, and intraoperative navigation promise to increase the efficacy of surgical therapy in the future. This paper provides an overview of the applications of telesurgery and currently available techniques.

Computer Communication Networks↗

PubMed1991

AIDS in the transfusion recipient.

In summary, the HIV virus was transmitted to approximately 90% of recipients by infectious blood and blood products transfused prior to donor and product testing begun in March 1985. Self-elimination of at-risk donors several years prior to testing donor blood helped to reduce the number of infected donations. Virtually all contaminated donors are now eliminated. The multiply transfused patient developed a stimulated dysregulated immune system due to the numerous antigens and the iron in red cells and plasma. This dysregulated immune system has resulted in a variable response to the added exposure of the HIV virus. The incubation period and progression to disease have been prolonged and variable. Although a small number of patients have progressed as rapidly as other at-risk groups, many continue to do well without therapeutic intervention. Natural history of the disease needs continual monitoring to determine the ultimate outcome of these transfusion recipients.

Acquired Immunodeficiency Syndrome↗

PubMed1991

The private GP and leprosy: a study.

In urban and rural areas alike, people in India tend to prefer private medical care to the existing government health services. Nevertheless, the large private health care sector has hitherto been virtually alienated from activities of public health importance including priority disease control programmes. This study of 106 private general practitioners (GPs), practising in low socioeconomic areas of Bombay, shows a gross lack of knowledge and awareness among private doctors about leprosy and also about the National Leprosy Control Programme. The possible reasons are discussed. Effective involvement of GPs in the National Leprosy Control Programme should facilitate both integration and better implementation of leprosy control activities. The study also highlights some areas for future interventions at both primary and secondary health care levels and the need for a strategy, based on larger studies, to train and make private doctors participate in controlling diseases of major public health concern like leprosy.

Attitude of Health Personnel↗