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We morphometrically evaluated 5-micron H&E-stained sections from 28 surgically resected high-grade pulmonary neuroendocrine neoplasms, including 16 small cell lung carcinomas (SCLCs) and 12 large cell neuroendocrine carcinomas (LCNECs). For each case, 200 tumor nuclei and 20 to 100 normal lymphocytes were measured. The frequency distributions of tumor cell/lymphocyte (TC/L) size ratios were plotted in bins ranging from 1 to 6, classified into 6 histogram types with TC/L size ratio peaks ranging from 2 to 6 (A-E) and a histogram with a wide distribution (F). SCLCs fit histograms A through E; LCNECs, A through F. Morphometry demonstrated considerable nuclear size overlap in high-grade neoplasms. Approximately one third of SCLCs exhibited considerable numbers of neoplastic cells that were larger than 3 normal lymphocytes, while 4 of 12 LCNECs had a predominant number of small cells. Ten tumors exhibited a B histogram with a "borderline" peak TC/L of 3. The rule that a TC/L size ratio larger than 3 helps distinguish "large" from "small" neoplastic cells was confirmed in only 9 of 28 cases. The use of more generic terminology such as "high-grade neuroendocrine carcinoma" or "grade III neuroendocrine carcinoma" for SCLC and LCNEC is discussed.

Abstract: Dendritic growth is the common mode of solidification encountered when metals and alloys freeze under low thermal gradients. The growth of dendrites in pure melts depends on the transport of latent heat from the moving crystal-melt interface and the influence of weaker effects like the interfacial energy. Experimental data for critical tests of dendritic growth theories remained limited because dendritic growth can be complicated by convection. The Isothermal Dendritic Growth Experiment (IDGE) was developed specifically to test dendritic growth theories by performing measurements with succinonitrile (SCN) in microgravity, thus eliminating buoyancy-induced convection. The first flight of the IDGE in 1994 operated for 9 days at a mean quasi-static acceleration of 0.7 10−6 g 0. The velocity and radius data show that at supercoolings above approximately 0.4 K, dendritic growth in SCN under microgravity conditions is diffusion limited. By contrast, under terrestrial conditions, dendritic growth of SCN is dominated by convection for supercoolings below 1.7 K. The theoretical and experimental Peclet numbers exhibit modest disagreement, indicating that transport theories of dendritic solidification required some modification. Finally, the kinetic selection role for dendritic growth, VR 2=constant, where V is the velocity of the tip and R is the radius of curvature at the tip, appears to be independent of the gravity environment, with a slight dependence on the supercooling.

Frequency-dependent pupillary dilations were evoked by electrical stimulation of the pre- or post-ganglionic cervical sympathetic nerve (sympatho-excitation) or the hypothalamus (parasympatho-inhibition) in sympathectomized anesthetized cats. Systemic administration of the selective histamine H3 receptor agonist (R)-a-methylhistamine (RaMeHA) produced a dose-dependent depression of mydriasis due to direct neural sympathetic activation but had no effect on responses elicited by parasympathetic withdrawal. The histamine H2 receptor agonist, dimaprit, was inactive. RaMeHA was much more effective in depressing sympathetic responses obtained at lower frequencies when compared to higher frequencies of stimulation.

Intravenous administration of epinephrine results in a dose-dependent inhibition of the peripherally evoked electrodermal response (EDR) in the cat. The magnitude of this depression of the EDR was greater when the responses were evoked by a single shock than by a train of shocks (10–12 Hz). The observation that this epinephrine-induced inhibition is antagonized by phentolamine suggests that an alpha-adrenergic mechanism is involved. It is unlikely that this effect is due primarily to the vascular actions of epinephrine because the inhibition of the EDR was much more prolonged than was the pressor action. Angiotensin was ineffective in inhibiting these responses.

Background & Aims: The gastroduodenal epithelium is protected from acid-peptic damage, in part, by its ability to secrete bicarbonate. Patients with duodenal ulcer disease have impaired proximal duodenal mucosal bicarbonate secretion. We have shown in vitro that histamine inhibits prostaglandin-stimulated bicarbonate secretion in rabbit duodenal mucosa via histamine H"2 receptors and enteric nerves. In this study we examined whether the proulcerogenic compounds aspirin or ethanol regulate duodenal bicarbonate secretion and the involvement of histamine. Methods: Bicarbonate secretion by rabbit proximal duodenal mucosa was examined in vitro in Ussing chambers. Results: Aspirin and ethanol decreased basal and prostaglandin-stimulated bicarbonate secretion; the latter effect was specific for prostaglandin. The inhibitory effects of the two ulcerogenic compounds were at least additive. Ranitidine and tetrodotoxin abolished the inhibitory effects on stimulated, but not basal, secretion. Aspirin and ethanol also induced release of duodenal histamine. Conclusions: Aspirin and ethanol act by two distinct pathways to impair duodenal bicarbonate secretion. Both agents inhibit basal secretion via a histamine-independent and neurally independent pathway while they inhibit prostaglandin E"2-stimulated secretion via histamine release, likely from mast cells, and actions on enteric nerves. Our findings may be of relevance to the understanding and potential treatment of nonsteroidal anti-inflammatory drug-associated mucosal injury. GASTROENTEROLOGY 1998;114:527-535

Summary The effect of varying oral doses of 11R, 16, 16-trimethyl prostaglandin E2 (TmPGE2) on meal-stimulated gastric acid secretion and serum gastrin concentrations was studied in 10 male subjects with asymptomatic duodenal ulcer disease. A liquid protein meal was infused intragastrically 0.5 h and 3.5 h after drug administration. TmPGE2 inhibited gastric acid secretion in a dose dependent manner during the first meal and no significant effect was observed during the second meal. Except for the highest dose, no TmPGE2 was detected in plasma 3 h after drug administration. The degree of inhibition of meal-stimulated gastric acid was positively correlated with the plasma level of TmPGE2, but it was not due to inhibition of postprandial gastrin release. The results indicate that oral TmPGE2 inhibits meal-stimulated gastric acid secretion but not gastrin release in humans with asymptomatic duodenal ulcer disease.

U.S. Navy recruits (n = 3,776) were surveyed for premilitary histories of adult sexual assault. They completed a survey designed to estimate rates for experiences as victims (women) and perpetrators (men) of attempted and completed rape since the age of 14. The results show that 45.5% of the women reported being the victim of attempted (9.4%) or completed rape (36.1%) before entering the Navy. Male recruits' self-reports indicated that 14.8% admitted perpetrating attempted (3.5%) or completed rape (11.3%) before entering the Navy. A high percentage of recruits in this study reported histories of sexual assault. Female victims of sexual assault are at high risk of incurring somatic and/or psychological problems that require treatment by health care professionals. Male perpetrators of sexual assault are at high risk of repeating their behavior. The results of this study suggest that it may be cost-effective to develop treatment education, and prevention programs for military recruits.

The present study was designed to assess the relative contribution of postjunctional alpha-1 and alpha-2 adrenoceptors in neurally evoked cutaneous vasoconstrictor responses in anesthetized cats. Preganglionic stimulation of the thoracic sympathetic nerve trunk produced an intensity-related decrease of digital skin blood flow as measured by laser-Doppler flowmetry. Sympathetic-cholinergic sudomotor (electrodermal) responses were recorded simultaneously as an additional index of neuronal activation. Vasoconstrictor responses were not altered by pretreatment with i.v. propranolol (1 mg/kg) or atropine (1 mg/kg) and were refractory to low doses (2 mg/kg) of hexamethonium. As expected, atropine abolished evoked skin potential responses which were also sensitive only to higher doses (20 mg/kg) of hexamethonium. Pretreatment with either phentolamine (1 mg/kg i.v.), yohimbine (0.5 mg/kg i.v.) or prazosin (0.3 mg/kg i.v.) produced significant reduction of sympathetic vasoconstriction with blockade by phentolamine and yohimbine being far greater than that seen with prazosin. In animals previously given prazosin (0.3 mg/kg), subsequent administration of yohimbine (0.5 mg/kg) almost totally blocked the remaining evoked cutaneous vasoconstriction. These results demonstrate that both alpha-1 and alpha-2 adrenoceptors are present in the cutaneous bed of the cat with the predominant effect mediated by innervated alpha-2 adrenoceptors.

Mechanisms in the superior cervical ganglion resulting in contraction of the nictitating membrane (NM) and dilation of the parasympathectimized pupil were studies in anesthetized cats. Frequency-response curves were obtained following pregangionic stimulation with NM and pupillary responses recorded simultaneously in the same preparations.