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Forty-nine (5%) of 956 women referred for follow-up imaging after breast cancer treatment had a malignancy in both breasts. The mammograms and ultrasonograms or US reports, and histologic slides or pathologic reports of 31 of these patients were reviewed. Mammography was more sensitive than clinical examination or US in detecting contralateral breast cancer, the sensitivity of mammography being 81%. Thirty-nine percent of the contralateral cancers were nonpalpable, and all were first detected at mammography. No cancers were depicted by US alone. US provided complementary information about palpable masses in 50% of the cases in which the mammographic finding was difficult to interpret. The mammographic appearance and the difficulties in detecting a contralateral cancer were similar to those known to be characteristic for first primaries. Distinguishing a new primary from a metastasis from the first breast cancer was not always possible by means of mammography or US.

The main aim of the present study was to adapt an instrument measuring patients' adjustment to life with an ostomy to Swedish conditions and to test reliability and validity of the adapted instrument. The Ostomy Adjustment Scale (OAS), which is focused on three domains: physical function, psychologic state, and social interaction, was selected as suitable. After translation into Swedish, equivalence and internal consistency of the scale were calculated. Subjects with various types of urine or faeces diversions were recruited for self-rating with the OAS and a visual analogue scale estimating total quality of life (QOL). The instruments were tested in 48 patients with five different diagnoses, 36 with and 12 without ostomy, and re-tests were carried out in 25 of the patients. Reliability (Cronbach's alpha) was 0.95. A positive correlation was found between the OAS and QOL (r = 0.67), indicating that the instrument has some validity.

The body weights of male albino rats were reduced gradually to 80% of normal body weight by resricting food intake (dieting), and then the rats were given lateral hypothalamic (LH) lesions. Compared with rats of normal body weight sustaining similar brain lesions, the dieted group displayed a shorter period of postoperative aphagia and less gastric pathology. In a second experiment, a group of rats was reduced to 80% of normal body weight by withholding all food (fasting) and then given LH lesions. Compared with dieted rats sustaining similar brain damage, the fasted group displayed a longer period of post operative aphagia and greater gastric pathology. Since the duration of aphagia could be shortened or lengthened by simple manipulations of preoperative body weight, the adequacy of sensorimotor or motivational hypotheses to account for aphagia is questioned. The results are more consistent with the suggestion that gastric abnormalities produced by LH lesions inhibit eating.

In experiments on rats four types of ileal reservoirs were constructed and left to expand in situ. After 3 months the volumes and tissue weights of the various reservoirs were compared. The reservoir types were: two loops, isoperistaltic (type I), two loops, antiperistaltic (type II), three loops, S-shaped (type III) and "four loops', double-folded U loop (Kock pouch) (type IV). There was a considerable volume increase in all types of reservoir as well as a marked increase in their tissue weight. The expansion of the reservoirs in groups III and IV was significantly greater than that in groups I and II. The difference in expansion could possibly be explained by the greater radius in three- and four-loop reservoirs compared with two-loop reservoirs if Laplace's law is applied to this process. According to this law the tension in the wall of a tube increases with increasing radius.

Lacey and Lacey hypothesize the presence of cortical inhibitory influences which result from the cardiac events which initiate baroreceptor discharge. The current study provides evidence of cardiac-related cortical inhibitory influences when normal humans are required to attend to environmental input and respond to the information they perceive (fixed foreperiod reaction time task). Averaged EEG waveforms time locked to pulse transit time (PTT) were comprised of slower frequencies than averaged EEG waveforms randomly selected from the same cardiac cycles, and pre-PTT EEG was comprised of slower frequencies than post-PTT EEG in the averaged waveforms. Results of this experiment raise the speculation that cardiovascular events may modulate brain activity with variations in baroreceptor discharge setting constraints on cortical excitability on a beat-to-beat basis.

Subjects performed in a tone discrimination task at two levels of difficulty, and a reaction time response was required on half of the trials. Four prominent components of the event-related potential waveform (N1, P2, N2, and P3) were analyzed. The results suggested that P2 represents the beginning of a central process responsible for stimulus identification and the initiation of decision making, while N2 and possibly P3 represent the end of this process. The notion that the P3 component is an unusually important sign of central processing is questioned, and the notion that P3 represents a central process of memorial update is also questioned. It seems more likely that N2 or p3 represent the end of a central process started at the time of P2.

Rats made aphagic and adipsic by damage to the lateral hypothalamus develop gastric lesions and lose body weight excessively over a four day period. Control observations indicate that these effects cannot be accounted for by food and water deprivation or by operative trauma. The possibility that gastric lesions may contribute to aphagia or anorexia is discussed.

Neural control and modulation of gastric secretion is well established. The role of the parasympathetic vagal system as a final motor pathway in gastric acid secretion is clearer than the involvement of the sympathetic nervous system. Both portions of the autonomic nervous system, however, appear to play an important role in the pathogenesis of at least experimentally induced gastric erosions. With respect to higher neural control there are numerous reports of hypothalamic effects on gastric secretion, motility, and morphology, yet the results of many of these reports appear equivocal. This ambiguity can be attributed in part to species differences, time course of observations, and differences in stimulation and lesion parameters. However, a mcal description of the sites of central lesions and stimulation. Implications of several of the studies concerning hypothalamic involvement in gastric functions are reviewed and recent methodological advances including neural fiber transection, relatively specific neural cell damage with neurotoxins (e.g., 6-OHDA, kainic acid), histochemistry and intracerebral infusions of gut hormones are suggested as alternative approaches to studying brain-gut relationships.

Previous studies have shown that lateral hypothalamic (LH) damage produces aphagia, gastric pathology, hyperthermia, and sensorimotor dysfunctions. Furthermore, preoperative dieting has been reported to shorten the period of aphagia, reduce the incidence of gastric pathology, attenuate the hyperthermia, and facilitate recovery of certain sensorimotor dysfunctions following LH lesions in rats. The present study compared the effects of dieting and two additional restricted feeding regimens (meal feeding alone or in combination with a high-carbohydrate supplement) which produced different body weight functions on several disorders induced by LH lesions. Restricted feeding (i.e., dieting and meal feeding), which resulted in approximately at 5% to 25% drop in body weight prior to LH lesions, similarly shortened the period of postoperative aphagia, reduced the incidence of gastric pathology, prevented the hyperthermia, and facilitated recovery of responsivity to tactile stimulation; however, other sensorimotor dysfunctions were relatively unaffected. Because the initial reinstatement of eating occurred at different body weight levels and in the presence of obvious sensorimotor abnormalities, it is unlikely that either body or sensorimotor dysfunctions per se are critical factors in determining the period of aphagia. The results are more consistent with the view that metabolic disorders that are attenuated by restricted feeding significantly contribute to the ingestive deficits of LH-damaged rats.

Heart rate, heart rate variability, and skin conductance responses were continuously recorded from six naive males during learning of a simulated aircraft carrier landing task. There were 30 learning trials spanning more than 1 h. Over trials, heart rate decreased while flight performance increased, indicating that heart rate is sensitive to practice effects. Independent of practice, heart rate and skin conductance amplitude always increased during the last minute of final approach to landing. The results supported the following conclusions: (a) heart rate and skin conductance amplitude are reliable indicators of short-term workload increases as typified by final approach; (b) heart rate is a reliable indicator of longer term workload decreases resulting from practice and increased mastery of the task. Results are discussed within the framework of autonomic activation theory.

Twenty-nine consecutive patients with stress urinary incontinence were investigated by bead chain urethrocystography (UCG) and single cough urethrocystometry before operation and 8-12 months after a Burch colposuspension producing clinical improvement. The operation significantly elevated the bladder neck and reduced its mobility during acute stress. The urethral inclination angle and the posterior urethrovesical angle also became smaller at rest and on straining. A significant negative correlation was found between the postoperative mobility of the bladder neck and the post-operative pressure transmission ratio (PTR), indicating that correction of the urethrovesical anatomical disorder eliminates the functional disorder in this disease and restores continence.

Koriath and Lindholm (Int. J. Psychophysiol., 1986; 4: 183-195) reported cardiac-related cortical inhibition and speculated that cardiovascular events could modulate electrocortical activity by setting constraints on cortical excitability during diastole based on levels of blood pressure during systole. One dimension of this proposal could be supported if the extent of cardiac-related cortical activity (CRCA) varies with changes in heart rate and blood pressure. The current study investigated this dimension of cardio-cortical relationship by having each subject perform a fixed-foreperiod reaction time task while pedalling a bicycle ergometer under three conditions of workload: No Pedal (0 kpm/min), Lo Pedal (150 kpm/min), and Hi Pedal (450 kpm/min). Mean HR increased significantly from No Pedal to Lo Pedal to Hi Pedal. Results confirmed the presence of CRCA during variations in mean HR and indicated that the extent of CRCA increases with increases in mean HR. This investigation reinforces the importance of the extrahomeostatic effects of cardiovascular afferent fibers and supports the importance of psychophysiological measures which integrate the activity of cardiovascular, autonomic, and central nervous systems.

The aim of the present study was to explore the possible involvement of thromboxane A2(TxA2) in the development of cardiopulmonary dysfunction in experimental septic shock. Sepsis was induced in anesthetized cats by intravenous (i.v.) infusion of live Escherichia coli. One series (No. = 12) was pretreated with a specific TxA2 synthetase inhibitor, dazmegrel; another (No. = 8) served as a septic control series. In both series a systemic arterial hypotension developed after 2 hr; no differences in cardiac function were detected. After 2 hr bacteremia cardiac preload was increased by a rapid infusion of dextran. This showed that cardiac function was significantly more preserved in dazmegrel-pretreated cats compared with septic controls. Pretreatment with dazmegrel totally prevented the pulmonary vascular response to bacterial infusion. The pulmonary compliance decreased to 40% in controls but to only 75% in the dazmegrel series, and airway resistance increased to 300% and 140%, respectively. The ventilation-perfusion ratio was less impaired in the pretreated series. Pretreatment with dazmegrel abolished the increase in thromboxane B2 (TxB2), the stable metabolite of TxA2, seen in the untreated series. The rise in 6-keto-prostaglandin F1a (6-keto-PGF1a), the stable metabolite of prostaglandin I2PGI2, was evident in both series. We concluded that TxA2 is important for the impaired cardiac performance in septic shock. Furthermore, TxA2 is involved, but not as the only factor, in the development of pulmonary dysfunction.