Drugs online research references
Vestn Oftalmol. 2002 Mar-Apr;118(2):17-9.
[Actipol in treating stromal herpetic keratitis]
[Article in Russian]
Akberova SI.
Actipol (0.007% paraaminobenzoic acid--PABA) is a new interferon (IFN) inductor. It was recently introduced into ophthalmological practice. Its efficiency in surface herpetic keratitis is proven. We studied the therapeutic efficiency of actipol in the treatment of stromal herpetic keratitis and compared the results with combined therapy with acyclovir (ACV) and leukocytic IFN. The main group (141 patients) were treated with actipol and the reference group (40 patients) with ACV ointment and leukocytic IFN. Local injections of actipol in combination with its instillations into the conjunctival sac led to cure of 67.3% patients with stromal herpetic keratitis; this treatment was more effective than combined local ACV + leukocytic IFN therapy (clinical cure in 45% cases). Epithelialization in the actipol group was observed 2 days sooner, infiltration resorption and clinical cure 4 days sooner than in the reference group. Relatively high visual acuity in the actipol group was presumably due to the reparogenic effect on the corneal stroma and antithrombotic, fibrinolytic, and antioxidant activity of PABA. Hence, actipol is an effective drug for the treatment of stromal herpetic keratitis, exerting virtually no side effects.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12096527&dopt=Abstract
ualberta.ca
Pharmacological cyclin-dependent kinase (cdk) inhibitors (PCIs) block replication of several viruses, including herpes simplex virus type 1 (HSV-1) and human immunodeficiency virus type 1 (HIV-1). Yet, these antiviral effects could result from inhibition of either cellular cdks or viral enzymes. For example, in addition to cellular cdks, PCIs could inhibit any of the herpesvirus-encoded kinases, DNA replication proteins, or proteins involved in nucleotide metabolism. To address this issue, we asked whether purine-derived PCIs (P-PCIs) inhibit HSV and HIV-1 replication by targeting cellular or viral proteins. P-PCIs inhibited replication of HSV-1 and -2 and HIV-1, which require cellular cdks to replicate, but not vaccinia virus or lymphocytic choriomeningitis virus, which are not known to require cdks to replicate. P-PCIs also inhibited strains of HSV-1 and HIV-1 that are resistant to conventional antiviral drugs, which target viral proteins. In addition, the anti-HSV effects of P-PCIs and a conventional antiherpesvirus drug, acyclovir, were additive, demonstrating that the two drugs act by distinct mechanisms. Lastly, the spectrum of proteins that bound to P-PCIs in extracts of mock- and HSV-infected cells was the same. Based on these observations, we conclude that P-PCIs inhibit virus replication by targeting cellular, not viral, proteins.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12097601&dopt=Abstract
Emerg Med J. 2002 Jul;19(4):326-7.
Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. Bell's palsy and acyclovir.
Yuen MC, Crawford I.
Kwong Wah Hospital, Hong Kong.
A short cut review was carried out to establish whether acyclovir improves functional recovery in Bell's palsy. Altogether 49 papers were found using the reported search, of which two presented the best evidence to answer the clinical question. The author, date and country of publication, patient group studied, study type, relevant outcomes, results and study weaknesses of these papers are tabulated. A clinical bottom line is stated.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12101147&dopt=Abstract
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