Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antiviral effects of selected combinations between acemannan (ACE-M), a long-chained, polydispersed, beta-(1,4)-acetylated mannan, were tested in combination with azidothymidine (AZT) and acyclovir (ACY) in vitro. The rationale for such combinations was based on the antiviral and immunomodulatory properties exhibited by ACE-M. In addition, the observed antiviral effects of ACE-M against human immunodeficiency virus type 1 (HIV-1) and other enveloped viruses appear to be related to modification of the glycosylation of viral glycoproteins. Therefore, the inhibitory effect of ACE-M does not overlap with that of AZT or ACY. The studies presented herein show that ACE-M combined with suboptimal noncytotoxic concentrations of AZT or ACY act synergistically to inhibit the replication of HIV-1 and herpes simplex virus type 1 (HSV-1), respectively. The median effect method was not applicable for analysis because the test compounds show mutually nonexclusive drug effects. For a meaningful evaluation and interpretation of the effects of drug combinations, the biological significance of combinations must be considered, that is, the protective effect of the combination, the noncytotoxicity of the combination, the mechanism(s) of action of the individual compounds comprising the combination, and so forth. With respect to effects on U1 cells latently infected with HIV-1, treatment with combinations of AZT and ACE-M does not potentiate virus replication.
 ...
PMID:In vitro evaluation of the synergistic antiviral effects of acemannan in combination with azidothymidine and acyclovir. 166 57

Acemannan (ACE-M), a beta-(1,4)-linked acetylated mannan, was evaluated for in vitro activity against human immunodeficiency virus type 1 (HIV-1). Castanospermine (CAS), deoxymannojirimycin (DMN), swainsonine (SWS), azidothymidine (AZT), and dideoxythymidine (DDC) were tested in parallel as control compounds. In vitro antiviral efficacy of ACE-M was evaluated in a variety of cell lines including human peripheral mononuclear, CEM-SS1 and MT-2(2) cells. The virus strain, number of infectious units per cell, and target cell line were important factors in determining the degree of inhibition of viral cytopathic effect in the presence of ACE-M and other control compounds tested. Maximum inhibitory effect was observed in CEM-SS cells infected with the RFII strain of HIV-1. This inhibitory effect was determined to be concentration-dependent. Assay design included primary screening to measure cell viabilities of infected target cells in the presence and absence of test compounds. When tested on HIV-1/RFII-infected CEM-SS cells, the 50% inhibitory effect of CAS (IC50 = 28), an inhibitor of alpha-glucosidase I, was determined to be similar to that observed for ACE-M (IC50 = 45). However, DMN and SWS, inhibitors of mannosidase I and II, tested in parallel to CAS and ACE-M, exhibited no IC50 values. Antiviral potential of ACE-M as an inhibitor of syncytia formation was also explored using CEM-SS cells. Suppression of syncytia formation was observed at an ACE-M concentration of 31.25 micrograms/ml, and complete inhibition was observed at 62.5 micrograms/ml. In addition, HIV-1 RNA levels were studied to establish the antiviral potential of ACE-M in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Inhibition of AIDS virus replication by acemannan in vitro. 176 65

There will always be birth defects and pregnancy complications due to factors beyond our control. However, we are rapidly discovering many interventions women can use to optimize their chances of having a healthy pregnancy and baby. Most of these, such as immunization and normalization of a diabetic woman's glycosylated hemoglobin level, are most effective when begun before conception. Since the discovery of the congenital rubella syndrome in 1941, there has been a steady accumulation of information on the prevention of birth defects through preconception health. In just the last few years, we have learned that folic acid can decrease neural tube defects, angiotensin converting enzyme inhibitors are teratogenic, and zidovudine can decrease the vertical transmission rate of human immunodeficiency virus. The Varivax vaccine released last year is expected to decrease the perinatal morbidity from varicella. By using the time before conception, we may be able to fully maximize the benefits of good nutrition, exercise, medical screening, and avoidance of environmental toxins.
 ...
PMID:Preconception health care for the primary care practitioner. 877 69

Nine pediatric symptomatic patients infected with human immunodeficiency virus with elevated pulmonary arterial pressure (MPA pressure) and ejection fraction (EF); and with fractional shortening, (FS) mean velocity of circumferential fiber shortening (MVCfc) and left ventricular peak systolic wall stress (PS) were prospectively evaluated using 2-dimensional and M-mode serial echocardiography and Doppler cardiography after administration of an ACE inhibitor (Inhibace 0.025 mg/kg/D orally) for 12 weeks. The MPA pressure was not decreased, however the MVCfc and PS improved significantly (p < 0.05). Further, long term evaluation is required to determine its effect in preventing dilated cardiomyopathy and elevated mean pulmonary pressure.
 ...
PMID:Ventricular functions in children with human immunodeficiency virus infection after ACE-inhibitors. 944 24

The amino acid, taurine, is an important nutrient found in very high concentration in excitable tissue. Cellular depletion of taurine has been linked to developmental defects, retinal damage, immunodeficiency, impaired cellular growth and the development of a cardiomyopathy. These findings have encouraged the use of taurine in infant formula, nutritional supplements and energy promoting drinks. Nonetheless, the use of taurine as a drug to treat specific diseases has been limited. One disease that responds favorably to taurine therapy is congestive heart failure. In this review, we discuss three mechanisms that might underlie the beneficial effect of taurine in heart failure. First, taurine promotes natriuresis and diuresis, presumably through its osmoregulatory activity in the kidney, its modulation of atrial natriuretic factor secretion and its putative regulation of vasopressin release. However, it remains to be determined whether taurine treatment promotes salt and water excretion in humans with heart failure. Second, taurine mediates a modest positive inotropic effect by regulating [Na+]i and Na+/Ca2+ exchanger flux. Although this effect of taurine has not been examined in human tissue, it is significant that it bypasses the major calcium transport defects found in the failing human heart. Third, taurine attenuates the actions of angiotensin II on Ca2+ transport, protein synthesis and angiotensin II signaling. Through this mechanism taurine would be expected to minimize many of the adverse actions of angiotensin II, including the induction of cardiac hypertrophy, volume overload and myocardial remodeling. Since the ACE inhibitors are the mainstay in the treatment of congestive heart failure, this action of taurine is probably very important.
 ...
PMID:Interaction between the actions of taurine and angiotensin II. 1094 14

HIV-associated nephropathy (HIVAN) is the most common cause of renal failure in patients infected with type 1 human immunodeficiency virus (HIV-1). The renal prognosis for HIVAN is poor and is typically associated with rapid progression to renal death. We report a patient with biopsy-proven HIVAN who was successfully treated with corticosteroids and review the currently available evidence supporting the specific treatments of this condition. A 34-year-old African-American male with a 2-year history of uncomplicated HIV disease developed progressive azotemia despite treatment with highly active antiretroviral therapy (HAART). He was treated with an uncomplicated 4-month course of prednisone, which improved his serum creatinine from 2.9 to 1.9 mg/dl and decreased his degree of proteinuria from 8 to 2.1 g/day. Two years post-steroid treatment his renal function remains stable. Increasing evidence supports that both ACE inhibitors and HAART are effective in preventing and in some cases of reversing HIVAN induced renal failure. In selected patients who progress despite these measures, a limited course of corticosteroid may achieve long-standing disease remissions. In general, with adequate supervision, corticosteroid therapy appears to be well tolerated and has an acceptable side effect profile. Although persuasive in view of the abysmal natural history of HIVAN, the currently available studies are subject to major methodological limitations. Appropriate randomized controlled trials are urgently required in order to further examine the efficacy, optimal timing, and potential side effects of these treatments.
 ...
PMID:Treatment of HIV-associated nephropathy. 1148 63

Human immunodeficiency virus-associated nephropathy (HIVAN) is a distinct clinico-pathological syndrome that occurs almost exclusively in black patients with an AIDS defining diagnosis. It is characterized by rapidly progressive renal failure with a severe nephrotic syndrome. The renal biopsy typically shows a collapsing glomerular sclerosis and variable tubulo-interstitial nephritis. The pathogenesis most likely involves infection of renal tubular and epithelial cells with HIV. The use of ACE-inhibitors and steroids may slow down the progression to end-stage renal failure. With the introduction of highly active anti-retroviral therapy, HIVAN may now be treated effectively although clinical data are so far limited to case-reports.
 ...
PMID:Diagnosis and treatment of HIV-associated nephropathy. 1158 26

Human immunodeficiency virus-associated nephropathy (HIVAN) is a clinicopathological entity characterised by proteinuria, rapidly developing azotemia and histologically by collapsig variant of focal and segmental glomerulosclerosis with acute tubular necrosis and mild interstitial inflammation. Untreated, it may result in end stage renal disease (ESRD) in as little as four months. The incidence of HIVAN continues to increase and is the single most common cause of chronic renal disease in HIV-1 seropositive patients. It affects predominantly black individuals. Exact pathogenesis is still not clear but a great deal of progress has been made in the recent past by studies on transgenic mouse model, renal cell cultures and from study of human biopsy material. Current considerations revolve around the role of HIV or protein in renal epithelium and the effects of cytokines, including transforming growth factor-beta and basic fibroblast growth factor on renal structures. Different modalities of treatment with corticosteroids, zidovudine or angiotensin converting enzyme inhibitors have been tried with modest success.
 ...
PMID:Human immunodeficiency virus-associated nephropathy. 1183 70

Initially described in 1984, human immunodeficiency virus-associated nephropathy (HIVAN) has now become a common disease within the HIV-seropositive population. It is a focal segmental glomerulosclerosis causing rapid deterioration of renal function. It is the most common cause of chronic renal disease in HIV patients and occurs almost exclusively in blacks. Through murine and human studies, it is now clear that HIVAN is caused by a direct effect of infection of renal cells by HIV-1 and that the virus actively replicates within renal cells. How the virus causes disease within cells is not yet understood, but there is evidence for factors within infected cells causing both proliferation and apoptosis. Steroids, angiotensin converting enzyme (ACE) inhibitors, and highly active antiretroviral therapy (HAART) have been used for the treatment of HIVAN, with HAART, in particular, showing a dramatic improvement in both the pathologic changes and clinical course of HIVAN.
 ...
PMID:HIV-associated nephropathy: Epidemiology, pathogenesis, and treatment. 1270 80

Collapsing glomerulopathy is a morphologic variant of focal segmental glomerulosclerosis (FSGS) characterized by segmental and global collapse of the glomerular capillaries, marked hypertrophy and hyperplasia of podocytes, and severe tubulointerstitial disease. The cause of this disorder is unknown, but nearly identical pathologic findings are present in idiopathic collapsing glomerulopathy and human immunodeficiency virus (HIV)-associated nephropathy, and collapsing glomerulopathy has been associated with parvovirus B19 infection and treatment with pamidronate. The pathogenesis of collapsing glomerulopathy involves visceral epithelial cell injury leading to cell cycle dysregulation and a proliferative phenotype. Clinically, collapsing glomerulopathy is characterized by black racial predominance, a high incidence of nephrotic syndrome, and rapidly progressive renal failure. Collapsing glomerulopathy also may recur after renal transplantation or present de novo, often leading to loss of the allograft. The optimal treatment for collapsing glomerulopathy is unknown. Treatments may include steroids or cyclosporine in addition to aggressive blood pressure control, angiotensin converting enzyme inhibitors and/or angiotensin II receptor blockers, and lipid lowering agents. The role of other immunosuppressive agents such as mycophenolate mofetil in the treatment of collapsing FSGS remains to be defined. Prospective clinical trials are needed to define optimal therapy of this aggressive form of FSGS.
 ...
PMID:Collapsing glomerulopathy. 1270 81


1 2 Next >>