Passive smoking.

One in three adults in the United States smokes. Smokers inhale one quarter of the smoke from cigarettes. But 75% of cigarette smoke is released into the environment. Nonsmokers are exposed to this environmental tobacco smoke and are at risk for disease. A growing body of literature supports the association of passive, involuntary, or secondhand smoking with human pathology. This discussion examines the makeup of environmental tobacco smoke and its role in causing human disease with a review of the literature relating environmental tobacco smoke to head and neck pathology.

Carotid artery sacrifice testing: assessment in patients with advanced head and neck cancer.

The otolaryngologist seeking a cure of the patient with advanced cancer of the head and neck removes all neck metastases along with the primary tumor. Tumor involvement of the carotid artery presents a special dilemma to the otolaryngologist because a complete resection would mean removal of the affected carotid artery, a procedure which has, historically, carried high morbidity and mortality rates. Today, the otolaryngologist will offer tumor resection with carotid artery sacrifice only after a patient passes a preoperative assessment of collateral circulation to the brain. Numerous methods have been devised to determine a patient's preoperative risk of neurologic compromise. Several tests are detailed and their usefulness discussed.

A review of odontogenic infections.

Odontogenic infections continue to affect a substantial portion of the population. These infections may be due to pulpal or periodontal involvement, and may occur after extraction of a tooth. Usually self-limiting and spatially confined, infection occasionally spreads due to a highly virulent organism leading to serious or potentially lethal conditions. Treatment priorities include establishing an airway if the airway is compromised, obtaining specimen for appropriate aerobic and anaerobic sensitivity, employing antibiotics empirically, and draining infection surgically. A discussion of the pathophysiology of odontogenic infection follows, along with a review of the anatomy basic to treatment of infection which may extend to the deep neck spaces.

Allostimulatory analysis of a newly-defined and widely-distributed Mls superantigen.

We previously noted that Mlsa,c C58/J responder cells proliferated unexpectedly to H-2k-compatible Mlsa or Mlsc prototypic stimulator cells in a primary mixed lymphocyte reaction. The present investigation was performed to evaluate whether the response of C58/J T cells to these H-2- and Mls-compatible stimulator cells could functionally identify a newly-defined member of the Mls superantigen family through its allostimulatory ability. We observed that C58/J responder cells also proliferated when cultured with H-2-compatible prototypic Mls(null), Mlsb (nonstimulatory), or Mlsa,c splenic stimulator cells. The widely distributed nature of the non-MHC ligand recognized by C58/J T cells is indicated by the finding that 11 of 12 H-2k inbred mouse strains clearly expressed this specificity. A gradient of stimulatory capacity from low to high across this newly-defined non-MHC difference was detected with splenocytes from these different inbred mouse strains. The Mls(a,c) genetic composition of C58/J was confirmed by the observation that crossing C58/J with parental B10.BR (responsive to both Mlsa and Mlsc determinants) generated F1 progeny that were unresponsive to H-2k-compatible Mlsa, Mlsc, or Mls(a,c) stimulator cells. Like prototypic Mlsa and Mlsc, the non-MHC specificity recognized by C58/J responder cells, termed Mlsf, was particularly sensitive to radiation (versus mitomycin C) treatment of the stimulator cells, was greatly augmented after anti-IgD activation of splenic stimulator cells, was blocked with anti-MHC class II antibody, and was effectively presented by phenotypically normal female but not B cell-defective xid+ male CBA/N F1 stimulator cells.

Genetic analysis of the presentation of minor lymphocyte-stimulating determinants. II. Differing non-MHC control of super-stimulatory and more poorly stimulatory Mls phenotypes.

Analysis of the capacity of splenocytes from non-prototypic Mlsa or Mlsc mouse strains to stimulate allogeneic H-2k-compatible T cells in a primary Mls-defined MLR provided interesting examples of exceptions to the usually stated characterization of Mlsa and Mlsc determinants as highly stimulatory of weakly stimulatory, respectively. Across the Mlsa barrier, MA/My stimulator cells had a significantly reduced capacity to elicit responder proliferation in comparison with prototypic AKR/J or less well studied C58/J, CE/J, or RF/J splenocytes. Across the Mlsc barrier, a gradient of stimulatory ability was observed with RF/J splenocytes being virtually nonstimulatory, prototypic C3H/HeJ splenocytes having an intermediate capacity, and CE/J and C58/J being highly stimulatory presenters of this non-MHC specificity. The differing capacity of each of these H-2k stimulator cells to elicit unprimed responder cell proliferation across an Mlsa or Mlsc difference correlated with the T cell growth factor activity that was secreted into the MLR supernatants. The super stimulatory form of Mlsc was expressed in an autosomal dominant fashion by (Mlsc poorly stimulatory x Mlsc super-stimulatory)F1 animals, (BALB.K x C58/J)F1 or (RF/J x CE/J)F1. The segregation of Mlsc stimulatory ability among first backcross and F2 animals derived from the former F1 was compatible with a single non-MHC gene controlling the expression and presentation of the super-stimulatory form of Mlsc. The regulatory nature of this gene was indicated by the observation that F1 animals generated from the Mlsc nonprototypic and poorly stimulatory BALB/c parental strain were self-tolerant to the super-stimulatory form of Mlsc. The existence of an Mls specificity other than a and c was suggested by positive non-MHC MLR responses in certain responder/stimulator cell combinations of Mls prototypic and nonprototypic mouse strains.