The dorsomedial hypothalamus mediates stress-induced hyperalgesia and is the source of the pronociceptive peptide cholecystokinin in the rostral ventromedial medulla.

While intense or highly arousing stressors have long been known to suppress pain, relatively mild or chronic stress can enhance pain. The mechanisms underlying stress-induced hyperalgesia (SIH) are only now being defined. The physiological and neuroendocrine effects of mild stress are mediated by the dorsomedial hypothalamus (DMH), which has documented connections with the rostral ventromedial medulla (RVM), a brainstem region capable of facilitating nociception. We hypothesized that stress engages both the DMH and the RVM to produce hyperalgesia. Direct pharmacological activation of the DMH increased sensitivity to mechanical stimulation in awake animals, confirming that the DMH can mediate behavioral hyperalgesia. A behavioral model of mild stress also produced mechanical hyperalgesia, which was blocked by inactivation of either the DMH or the RVM. The neuropeptide cholecystokinin (CCK) acts in the RVM to enhance nociception and is abundant in the DMH. Using a retrograde tracer and immunohistochemical labeling, we determined that CCK-expressing neurons in the DMH are the only significant supraspinal source of CCK in the RVM. However, not all neurons projecting from the DMH to the RVM contained CCK, and microinjection of the CCK2 receptor antagonist YM022 in the RVM did not interfere with SIH, suggesting that transmitters in addition to CCK play a significant role in this connection during acute stress. While the RVM has a well-established role in facilitation of nociception, the DMH, with its well-documented role in stress, may also be engaged in a number of chronic or abnormal pain states. Taken as a whole, these findings establish an anatomical and functional connection between the DMH and RVM by which stress can facilitate pain.

Reduction of copper(II) by iron(II).

Laboratory and field investigations have clearly demonstrated the important role of reduced iron (Fe(II)) in reductive transformations of first-row transition metal species. However, interactions of Fe(II) and copper (Cu) are not clearly understood. This study examined the reduction of Cu(II) by Fe(II) in stirred-batch experiments at pH 5.2 and 5.5 as influenced by chloride (Cl-) concentration (0.002-0.1 M), initial metal concentration (0.1-9.1 mM), and reaction time (1-60 min) under anoxic conditions. Reduction of Cu(II) to Cu(I) by dissolved Fe(II) was rapid under all experimental conditions and the stability of the products explains the driving force for the redox reaction. Under conditions of low [Cl-] and high initial metal concentration, >40% of total Cu and Fe were removed from solution after 1 min, which accompanied formation of a brownish-red precipitate. X-ray diffraction (XRD) patterns of the precipitates revealed the presence of cuprite (Cu2O), a Cu(I) mineral, based on d-spacings located at 0.248, 0.215, 0.151, and 0.129 nm. Fourier transform infrared (FTIR) spectroscopy corroborated XRD data for the presence of Cu2O, with features located at 518, 625, and 698 cm(-1). Increasing [Cl-] stabilized the dissolved Cu(I) product against Cu2O precipitation and resulted in more Fe precipitated from solution (relative to Cu) that appears to be present as poorly crystalline lepidocrocite (gamma-FeOOH). This process may be important in anoxic soil environments, where dissolved Fe(II) levels can accumulate.

Adjuvant, pulse total parenteral nutrition and tumor response to cycle-specific and cycle-nonspecific chemotherapy.

Previous work has demonstrated that substrate-induced alterations of tumor metabolism can be exploited to enhance tumor response to a cycle-specific chemotherapeutic agent (methotrexate). This study was designed to further investigate the biologic mechanism of this phenomenon by determination of tumor response to additional cycle-specific (Adriamycin) and cycle-nonspecific (Cytoxan) chemotherapeutic agents. Significant potentiation of tumor response during adjuvant total parenteral nutrition (TPN) was observed with methotrexate and Adriamycin but not with Cytoxan. This may imply that tumor sensitization by adjuvant TPN occurs by acceleration of the growth rate of proliferating tumor cells and not by recruitment of dormant tumor cells into the cell cycle.

Atypical cellular chorangioma of the placenta.

A rare and atypical type of chorangioma is presented. The tumor was unusual in three aspects: (a) clinically, it was delivered after the placenta and required lavage; (b) grossly, the lesion was quite large; and (c) most importantly, it exhibited histologic features suggestive of sarcoma. Immunochemical staining of the tumor for factor VIII antigen demonstrated its endothelial origin. However, the tumor lacked evidence of invasion or biological aggressiveness. We propose that peculiar lesions of this type be termed "atypical cellular chorangiomas." No documented case of chorangiosarcoma could be identified in the literature.

Thirteen primary adenocarcinomas of the ileum and appendix: a case report.

Adenocarcinomas of the ileum and appendix are uncommon. Multiple synchronous adenocarcinomas of the small bowel without carcinoid features are even more unusual, with only seven reported cases in the literature. The radiologic and pathologic findings are reported in a case with 13 separate, well-documented synchronous primary adenocarcinomas of the ileum and appendix. The value of the double-contrast small bowel enema is emphasized.