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At least 775 records · Page 43Linked to original sources
PubMed2003

ESCRS Binkhorst lecture 2002: Pseudophakic preservative maculopathy.

Many antiglaucoma eyedrops are reported to cause cystoid macular edema (CME) in aphakia and pseudophakia. We review 4 clinical and laboratory studies that compare the incidence of CME in early postoperative pseudophakia in eyes that received preserved latanoprost and timolol, nonpreserved timolol, and the preserved and nonpreserved vehicle for these drugs and looked at the morphological damage to cells and the changes in the indicators of cytokine and prostaglandin (PG) synthesis caused by latanoprost and timolol and the preservative benzalkonium chloride. Based on the findings of these studies, which indicate that the preservative causes increased synthesis of PGs and other substances and intensified postoperative inflammation, the term pseudophakic preservative maculopathy is proposed for CME caused by antiglaucoma eyedrops.

Aqueous Humor↗
PubMed1996

JSID Tanioku Memorial Lecture 1996. Genetic disorders of keratins and their associated proteins.

It has recently been demonstrated that genetic defects in keratin genes cause a number of different skin disorders, including epidermolysis bullosa simplex (EBS), epidermolytic hyperkeratosis (EH), the EH form of epidermal nevi, epidermolytic and non-epidermolytic forms of palmoplantar keratoderma (EPPK and PPK) and pachyonychia congenita (PC). In this review, I describe the research that led to this discovery.

Animals↗
PubMed2001

Hamao Umezawa Memorial Award Lecture: "An Odyssey in the Viral Chemotherapy Field".

In the search of effective and selective chemotherapeutic agents for the treatment of viral infections, my "Odyssey" brought me to explore a variety of approaches, encompassing interferon and interferon inducers, suramin and other polyanionic substances, S-adenosylhomocysteine hydrolase inhibitors, inosine 5'-monophosphate dehydrogenase inhibitors, 5-substituted 2'-deoxyuridines such as (E)-5-(2-bromovinyl)-2'-deoxyuridine, acyclovir (esters) and other acyclic guanosine analogues, 2',3'-dideoxynucleoside analogues, non-nucleoside reverse transcriptase inhibitors (NNRTIs), bicyclams, and acyclic nucleoside phosphonates. This had led to the identification of a number of compounds, efficacious against such important viral pathogens as human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV), herpes simplex virus (HSV), varicella-zoster virus (VZV), cytomegalovirus (CMV), and other herpesviruses, pox-, adeno-, polyoma-, and papillomaviruses, and hemorrhagic fever viruses.

Antiviral Agents↗
PubMed1996

Matas Lecture. Heparin--controversies and misconceptions.

The previous dogmas regarding heparin therapy are currently being challenged. It is apparent that the experimental work on which guidelines for heparin therapy are based do not necessarily have any relevance clinically. Once clotting has been initiated, there are multiple factors that result in a relative refractory response to heparin anticoagulation. In addition, it is now apparent that heparin's effect cannot be accurately monitored with current tests of anticoagulation. Most importantly, the risk of bleeding does not correlate with heparin levels but with clinical risk factors and to the presence or absence of functioning platelets. For this reason, sufficient heparin should be given initially to ensure that clotting is under control. If this is not done, all of the risk of heparin anticoagulation is assumed with none of the benefit. Life-threatening clotting conditions require high doses of heparin, equivalent to those required for cardiopulmonary bypass. Even though there is no good laboratory test available to ascertain the adequacy of anticoagulation, assessment of the clinical response is sufficient. When heparin levels are adequate, clinical improvement is evident as manifest by decreased pain and improvement in well-being, cardiac function, and/or collateral flow.

Anticoagulants↗