PubMed Health⌕ Search

Biomedical subjects

L M Klein

Publications and source records attributed to L M Klein.

6 recordsLinked to original sources
PubMed1998

Thirty-month naturalistic follow-up study of early-onset dysthymic disorder: course, diagnostic stability, and prediction of outcome.

Dysthymic disorder (DD) is defined and distinguished from major depressive disorder (MDD) largely on the basis of its course. Surprisingly, however, there have been few prospective, longitudinal studies of the naturalistic course of DD. This article reports the major findings from a prospective, longitudinal 30-month follow-up study of 86 outpatients with early-onset DD (EOD) and 39 outpatients with episodic MDD. Follow-up assessments included the Longitudinal Interval Follow-Up Evaluation and Hamilton Rating Scale for Depression. Compared with patients with episodic MDD, patients with EOD exhibited less improvement from the baseline evaluation and were more symptomatic at follow-up. Only 39% of patients with EOD recovered from DD during the follow-up period. The diagnosis of DD was fairly stable, with 52% of the EOD group meeting full criteria for DD at follow-up. These data provide prospective confirmation of the chronic course of DD.

Adolescent↗
PubMed1997

Response of SCC-12F, a human squamous cell carcinoma cell line, to complement attack.

We studied the response of a human squamous cell carcinoma cell line, SCC-12F, to human complement attack and found that the cells were completely resistant to complement lysis. In the absence of lysis, there was significant C3 deposition and C5b-9 deposition on the cells. Removal of the lipid-linked complement regulatory proteins CD59 and decay-accelerating factor (DAF) by treatment of the cells with phosphatidylinositol-specific phospholipase C (PIPLC) resulted in increased C3b and C5b-9 deposition on the cells and a slight increase in cell death. Treatment of the cells with complement caused them to release membrane vesicles containing the terminal complement proteins. In addition, complement induced SCC-12F to produce significant amounts of prostaglandin F2alpha (PGF2alpha). We conclude that CD59 and DAF are important in the resistance of SCC-12F to complement and that these cells produce membrane vesicles and PGF2alpha in response to complement attack. These responses, in the absence of cell death, may be important in the pathogenesis of inflammatory skin disease in which complement is deposited.

Animals↗
PubMed1996

The economic impact of ALS.

ALS is a progressive degenerative neuromuscular disease for which there is no known cause, treatment, or cure. The steady disease progression of muscle weakness eventually causes paralysis, disabling the patient. Day-to-day patient care and management most frequently fall to family members. The resultant financial burden can be enormous. We review financial issues related to the diagnosis, management of disease progression, and issues of life support. Cost-effective solutions are discussed. It is believed the key to reduction of costs is education of the health care community, patients and families, and third-party payers.

Amyotrophic Lateral Sclerosis↗
PubMed1989

Degranulation of human mast cells induces an endothelial antigen central to leukocyte adhesion.

To understand better the role of mast cell secretory products in the genesis of inflammation, a system was developed for in vitro degranulation of human mast cells in skin organ cultures. Within 2 hr after morphine sulfate-induced degranulation, endothelial cells lining microvessels adjacent to affected mast cells expressed an activation antigen important for endothelial-leukocyte adhesion. Identical results were obtained when other mast cell secretagogues (anti-IgE, compound 48/80, and calcium ionophore A23187) were used. Induction of this antigen was abrogated by preincubation with cromolyn sodium, an inhibitor of mast cell secretion, and by antiserum to tumor necrosis factor alpha. These findings indicate that degranulation of mast cells activates dermal endothelium through tumor necrosis factor-dependent mechanisms. This event may be critical to the elicitation phase of cutaneous inflammation.

Adult↗