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At least 271 records · Page 15Linked to original sources
PubMed1994

Effect of adjuvant therapy on development of diabetes in mouse and man.

Freund's complete adjuvant (CFA) and BCG vaccine modulate the development of type 1 diabetes in animal models. In non-obese diabetic mice, CFA and BCG significantly reduced the proportion developing diabetes compared with controls. Histological examination showed that autoimmune disease still developed but had been diverted to become nondestructive. In a preliminary trial in 17 newly diagnosed, type 1 diabetic patients, intracutaneous administration of 0.1 mL of BCG 1 mg/mL led to clinical remission in 11 (65%)--by week 4 in 6. Remission has been sustained in 3 for 6-10 months. No side-effects were reported. A double-blind trial of BCG is warranted.

Adolescent↗
PubMed2001

Melanocyte-Directed enzyme prodrug therapy (MDEPT): development of second generation prodrugs for targeted treatment of malignant melanoma.

Evaluation of second generation prodrugs for MDEPT, by oximetry, has highlighted structural properties that are advantageous and disadvantageous for efficient oxidation using mushroom tyrosinase. In particular, a sterically undemanding prodrug bis-(2-chloroethyl)amino-4-hydroxyphenylaminomethanone 28 was synthesised and found to be oxidised by mushroom tyrosinase at a superior rate to tyrosine methyl ester, the carboxylic acid of which is the natural substrate for tyrosinase. The more sterically demanding phenyl mustard prodrugs 9 and 10 were oxidised by mushroom tyrosinase at a similar rate to tyrosine methyl ester. In contrast, tyramine chain elongation via heteroatom insertion was detrimental and the rate of mushroom tyrosinase oxidation of phenyl mustard prodrugs 21 and 22 decreased by 10 nanomol/min.

Agaricales↗
PubMed1999

Melanocyte-directed enzyme prodrug therapy (MDEPT): development of a targeted treatment for malignant melanoma.

A novel prodrug rationally designed to function as a tyrosinase substrate has been synthesised to allow targeted treatment of malignant melanoma. This agent has been evaluated for tyrosinase-mediated drug release, and has been shown to act in the desired manner. Furthermore, differential cytotoxicity has been demonstrated in cell lines which express tyrosinase and those which do not.

Animals↗
PubMed2003

Exogenous surfactant therapy: newer developments.

There are numerous pulmonary conditions in which qualitative or quantitative anomalies of the surfactant system have been demonstrated. In premature newborns with immature lungs, a functional deficit in surfactant is the main physiopathologic mechanism of the neonatal respiratory distress syndrome (RDS). Since the landmark pilot study of Fujiwara, published more than 20 years ago, the efficacy of exogenous surfactant for the treatment of neonatal RDS has been established by numerous controlled studies and meta-analyses. Promising results have also been reported in infants suffering from other lung disorders in which endogenous surfactant function is compromised. Enlightened by a growing insight into both the structure and function of the different surfactant components, a new generation of synthetic surfactants has been developed. Various complementary approaches have confirmed the fundamental role of the two hydrophobic proteins, SP-B and SP-C, in the surfactant system, thus opening the way to the design of analogues, either by chemical synthesis or expression in a prokaryotic system. These peptide-containing synthetic surfactant preparations are presently undergoing clinical trials, and may eventually replace the animal-derived surfactants currently used for the treatment of RDS.

Clinical Trials as Topic↗
PubMed2003

Cystatin C and cysteine proteinases during the development and therapy of Lewis lung adenocarcinoma in mice.

We measured plasma cystatin C concentration and activity of cathepsins B and L in tumor tissue as possible markers for the efficiency of antitumor therapy and prognostic criteria for Lewis lung adenocarcinoma in mice. Plasma cystatin C concentration markedly decreased in mice with tumors. During successive therapy the increase in plasma cystatin C concentration correlated with the degree of inhibition of tumor growth. Activities of cathepsins B and L in the liver increased in animals with tumors. In mice receiving successive antitumor therapy activities of cathepsins B and L increased in tumor tissue, but decreased in the liver (compared to untreated animals).

Animals↗
PubMed2002

Effect of acid suppression therapy on development of gastric erosions after cure of Helicobacter pylori infection.

BACKGROUND: Helicobacter pylori eradication markedly improves histological inflammation and decreases peptic ulcer recurrence, but little is known about the subsequent development of gastric mucosal injury. AIM: To investigate whether acid suppression treatment after eradication influences the development of gastric erosions. METHODS: Eighty-one patients (gastritis or peptic ulcer) after successful H. pylori eradication were divided into two groups: 40 received an H2-blocker for 6 months (H2-blocker-positive) and 41 received no treatment (H2-blocker-negative). Endoscopy was performed before, and at 3 and 6 months after completion of eradication. RESULTS: Cumulative prevalence of gastric erosions in the H2-blocker-positive group was significantly lower than in the H2-blocker-negative group, 25% vs. 42%, respectively. In the H2-blocker-negative group but not the H2-blocker-positive group, the cumulative prevalence of gastric erosions after eradication was higher in patients with less severe corpus atrophy or more severe corpus gastritis. CONCLUSIONS: Development of gastric erosions after H. pylori eradication may be controlled by acid suppression treatment. Less severe atrophy or more severe gastritis in oxyntic glands before eradication may be involved in the development of gastric erosions. These results support the idea that recovery of acid secretion may be one of factors for development of gastric mucosal erosions after successful eradication.

Biopsy↗
PubMed2000

[New developments in therapy of chronic hepatitis B. When are nucleoside analogs indicated?].

Nucleoside analogues are promising agents for the treatment of chronic hepatitis B infection (HBV-DNA-positive by hybridization assay). The drug being studied most intensively is Lamivudine (Zeffix) which has recently been approved in Germany. When given orally once daily (100 mg) Lamivudine is well-tolerated and suppresses HBV-DNA to undetectable levels in the majority of patients. Since relapse is frequent when medication is stopped long-term treatment (at least until seroconversion of HBeAg) is warranted. Indications for lamivudine monotherapy are patients with chronic hepatitis B in which interferon (IFN) is contraindicated or patients who did not respond to a previous course of interferon. Further indications are the HBV-DNA-positive cirrhosis prior to liver transplantation (OLT) and the HBV-reinfection after OLT. The main problem of long-term monotherapy with lamivudine is viral resistance. The clinical impact of the resistant mutants is often not clear. Withdrawal or even continuation of the medication may be acceptable approaches. Other nucleoside analogues like Entecavir or Adefovir are currently being tested in clinical studies. Famciclovir was investigated preferably in patients with decompensated liver disease or HBV-reinfection after OLT. Because of conflicting results the drug should only be used under study conditions. In IFN-naive patients with chronic hepatitis B (and compensated liver disease) alpha-interferon is still the first-line therapy. With a standard course of interferon 30-40% of the patients become seronegative for HBeAg as compared with 16-17% when treated with lamivudine for twelve months. Combination of lamivudine and interferon is not more effective than IFN alone. In the future combined antiviral treatment is likely to replace monotherapy.

Adenine↗
PubMed1994

Newer developments in therapy for endemic mycoses.

In the 1960s and 1970s, amphotericin B was the only effective therapy for serious systemic endemic fungal infections due to Histoplasma capsulatum, Blastomyces dermatitidis, and Sporothrix schenckii. In the 1980s, ketoconazole was introduced as therapy for endemic mycoses; after this antifungal agent was introduced, some of these infections could be treated orally in an outpatient setting rather than intravenously in an inpatient setting. The 1990s have become the triazole era. It is now standard practice to treat nonmeningeal, non-life-threatening histoplasmosis and blastomycosis orally on an outpatient basis; the drug of choice for this treatment is itraconazole. Itraconazole also has proved useful as treatment for histoplasmosis in patients infected with human immunodeficiency virus. Although itraconazole has not yet been approved for the treatment of sporotrichosis, in preliminary studies it has been shown to be effective therapy not only for cutaneous and lymphocutaneous sporotrichosis but also for disseminated infection with S. schenckii.

Antifungal Agents↗