Axis II psychopathology in individuals with traumatic brain injury.

Primary Objectives: To determine the frequency and nature of post-TBI personality disorders (PDs) in a community-based sample of individuals with TBI.

Research Design: One hundred individuals with TBI were administered a structural clinical interview to determine Axis II psychopathology. METHODS OF PROCEDURES: The Structured Clinical Interview for DSM-IV Personality Disorders, Clinician Version (SCID II) was used to determine 12 Axis II personality disorders.

The Beck Depression Inventory: is it a suitable measure of depression for individuals with traumatic brain injury?

Objective: This study examined the relationship between Beck Depression Inventory (BDI) scores and current diagnosis of depression, based on The Structured Clinical Interview for DSM-IV Diagnosis (SCID).

Design: Correlation.

Setting: Community-based sample.

Axis I psychopathology in individuals with traumatic brain injury.

Objectives: To assess the incidence, comorbidity, and patterns of resolution of DSM-IV mood, anxiety, and substance use disorders in individuals with traumatic brain injury (TBI).

Design: The Structured Clinical Interview for DSM-IV Diagnoses (SCID) was utilized. Diagnoses were determined for three onset points relative to TBI onset: pre-TBI, post-TBI, and current diagnosis.

Increased numbers of mast cells in human middle ear cholesteatomas: implications for treatment.

Hypothesis: Because many of the biologic phenomena in which mast cells are involved also are observed in human cholesteatoma pathology, the authors hypothesized that mast cells may play a role in this disease. The first test of this hypothesis is to determine whether there are an increased number of mast cells associated with cholesteatomas.

Background: The molecular and cellular defects that result in the pathologic features observed in acquired and congenital cholesteatomas are unknown.

Expression of p53 protein in human middle ear cholesteatomas: pathogenetic implications.

Background: Cholesteatoma is a destructive lesion of the middle ear or mastoid process or both. The molecular and cellular defects that result in the clinical hallmarks of acquired and congenital cholesteatomas, namely invasion, migration, uncoordinated proliferation, altered differentiation, aggressiveness, and recidivism, are unknown. Determining the existence of defects in the normal biology, biochemistry, and genetic complement of the major cellular constituents comprising a cholesteatoma (i.

Expression of the mast cell growth factor interleukin-3 in melanocytic lesions correlates with an increased number of mast cells in the perilesional stroma: implications for melanoma progression.

The molecular events responsible for tumor progression in human cutaneous malignant melanoma remain unclear; however, critical to the process is the dysregulated proliferation of tumor cells and the development of new vascular channels which allow further growth and dissemination. Connective tissue mast cells (MC) have been implicated in tumor progression because they concentrate around tumors (including melanomas) prior to the formation of new blood vessels, and because they contain many chemical mediators, including basic fibroblast growth factor (bFGF), known to have mitogenic and angiogenic effects. Several MC chemotactic and mitogenic factors have been described including interleukin-3 (IL-3).

Differential expression of CD44 in malignant cutaneous epithelial neoplasms.

The CD44 antigen (ECMRIII, Hermes antigen) is a highly glycosylated cell-surface polypeptide involved in diverse cellular functions, including cell adhesion and lymphocyte-homing receptor activity. CD44 is also expressed in vivo by several tumors, including astrocytomas, meningiomas, and colonic adenocarcinomas. In addition, it has been shown that expression of CD44 appears to confer metastatic potential to cell lines derived from certain adenocarcinomas.

p53 expression is rare in cutaneous melanomas.

Alterations in the tumor-suppressor gene p53 are common in many types of human malignancies, but the potential role of p53 in the pathogenesis of cutaneous melanoma is controversial. The gene product, p53 protein, is normally present in very small amounts in noncancerous tissues. Missense mutations lead to accumulation of mutant p53 in the cells, which makes it detectable immunohistochemically in many cancers.

Loss of expression of the p16/cyclin-dependent kinase inhibitor 2 tumor suppressor gene in melanocytic lesions correlates with invasive stage of tumor progression.

Sporadic and familial malignant melanoma susceptibility has been linked to defects in the chromosomal region 9p21. Recently, a putative 9p21 tumor suppressor gene, the cyclin dependent kinase inhibitor 2 (CDKN2) or p16 gene, has been shown to be deleted, mutated, or rearranged in a high percentage of sporadic melanoma cell lines, as well as mutated in the germline of a proportion of familial melanoma patients. CDKN2 encodes a M(r) 16,000 protein (p16) that plays a key role in cell cycle control by binding to the cyclin-dependent kinase 4 enzyme and inhibiting its ability to phosphorylate critical substrates necessary for transition past the G1 phase of the cell cycle.