Given an abstract of a paper, generate a title for this paper such that conveys the key focus of the paper.

Q: Abstract: To test the hypothesis that occlusive apneas result from sleep-induced periodic breathing in association with some degree of upper airway compromise, periodic breathing was induced during non-rapid-eye-movement (NREM) sleep by administering hypoxic gas mixtures with and without applied external inspiratory resistance (9 cmH2O X l-1 X s) in five normal male volunteers. In addition to standard polysomnography for sleep staging and respiratory pattern monitoring, esophageal pressure, tidal volume (VT), and airflow were measured via an esophageal catheter and pneumotachograph, respectively, with the latter attached to a tight-fitting face mask, allowing calculation of total pulmonary system resistance (Rp). During stage I/II NREM sleep minimal period breathing was evident in two of the subjects; however, in four subjects during hypoxia and/or relief from hypoxia, with and without added resistance, pronounced periodic breathing developed with waxing and waning of VT, sometimes with apneic phases. Resistive loading without hypoxia did not cause periodicity. At the nadir of periodic changes in VT, Rp was usually at its highest and there was a significant linear relationship between Rp and 1/VT, indicating the development of obstructive hypopneas. In one subject without added resistance and in the same subject and in another during resistive loading, upper airway obstruction at the nadir of the periodic fluctuations in VT was observed. We conclude that periodic breathing resulting in periodic diminution of upper airway muscle activity is associated with increased upper airway resistance that predisposes upper airways to collapse.

A: Induction of periodic breathing during sleep causes upper airway obstruction in humans.
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Q: Abstract: One hundred patients who underwent carotid endarterectomy for transient ischemic attacks (TIAs) have been followed up for 3 to 10 years (mean, 5.5 years). Seven patients have been lost to follow-up but none is recorded as dead (National Registry of Deaths) at least 5 years after operation. Fifteen patients (16.5%) have died, four from cerebral and eight from cardiac causes. Three patients had cerebral infarction with permanent deficits, one occurring immediately after operation, one at 3 months, and one at 9 years. Four patients had minor strokes but a full clinical recovery, three patients postoperatively and one patient at 4 years. Fourteen patients had ipsilateral TIAs, four occurred postoperatively and 10 occurred from 1 to 8 years later. Ten patients had contralateral TIAs and five patients then had a contralateral carotid endarterectomy. Another nine patients also had bilateral operations, three for bilateral TIAs, five as prophylactic procedures on the basis of arteriographic findings, and one for a contralateral cerebral event that occurred after arteriography. Thus, at the mean follow-up time (5.5 years) and including the operative complications, four deaths (4%) of cerebral origin and seven serious cerebral problems (7%) have occurred--an annual morbidity and mortality rate of less than 2%. This compares favorably with the commonly predicted rate of stroke occurring after TIAs of 5% per year. These figures support the argument that carotid endarterectomy reduces the incidence of stroke occurring after TIA and stops TIAs caused by emboli from the carotid bifurcation.

A: The long-term results of carotid endarterectomy for transient ischemic attacks.
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Q: Abstract: In earlier studies, it was shown that the human plasma-spreading glycoprotein, epibolin (the 65 kD species of serum-spreading factor or vitronectin), requires a second plasma component, termed coepibolin, in order to support maximal dissociated epidermal cell spreading in tissue culture. Whereas epibolin alone in defined medium supports some cell spreading, the purified plasma coepibolin preparations do not effect spreading in the absence of epibolin. Although not yet entirely purified, coepibolin associates with some plasma fractions but not with others; it is certainly not a property of all proteins, e.g., while bovine serum albumin (BSA) has coepibolin activity, ovalbumin does not. The data presented here show that the phorbol ester, 12-tetra-decanoyl-1-phorbol-13-acetate (TPA) can act as a potent coepibolin and support maximal spreading over a concentration range of 10-100 ng/ml. In the absence of epibolin TPA does not stimulate the spreading of epidermal cells when given alone or in the presence of BSA or ovalbumin. Coepibolin activity appears to associate with tumor-promoting activity in that the phorbol derivative, phorbol-12,13-didecanoate, shows coepibolin activity, while its inactive non-tumor-promoting isomer, phorbol-4 alpha-phorbol-12,13-didecanoate, does not. These data suggest that the proteinaceous plasma-derived cofactor acts in a fashion similar to TPA and that this as yet unexplained mechanism of TPA action is important to the full expression of epibolin and to the early phase of epidermal cell spreading.

A:
Phorbol ester serves as a coepibolin in the spreading of primary guinea pig epidermal cells.
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