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We Are the Crisis Convergence Saga Book 2 Cadwell Turnbull, Blackstone Publishing (NOV 7) Hardcover $26.99 (312pp) 978-1-982603-75-5 What if monsters were real, and everyone knew it? The second book [...]

Gay Poems for Red States Willie Edward Taylor Carver Jr. University Press of Kentucky (JUN 6) Softcover $19.95 (120pp), 978-0-8131-9812-5 POETRY Willie Edward Taylor Carver Jr.'s poetry collection is a [...]

The Disappearance of Mr. Nobody Ahmed Taibaoui, Jonathan Wright (Translator), Hoopoe (JAN 3) Softcover $16.95 (152pp), 978-1-64903-214-O Ahmed Taibaoui's literary novel The Disappearance of Mr. Nobody is about the crime [...]

Translating Myself and Others Jhumpa Lahiri, Princeton University Press (MAY 17) Hardcover $21.95 (184pp) 978-0-691-23116-7 Translating Myself and Others is an academic collection of Jhumpa Lahiri's musings on language and [...]

A Sketch of Venetian History Sarah Pierroz (Author, Illustrator), Mosaic Press (OCT 21) Softcover $29.95 (170pp), 978-1-77161-584-6 A thorough history accompanied by intricate illustrations, Sarah Pierroz's A Sketch of Venetian [...]

* God of Mercy Okezie Nwoka, Astra House (NOV 2) Hardcover $23.99 (304pp), 978-1-66260-083-8 In Okezie Nwoka's dazzling and disquieting novel God of Mercy, battles between gods reignite a war [...]

No Gods, No Monsters Cadwell Turnbull, Blackstone Publishing (SEP 7) Hardcover $26.99 (330pp), 978-1-982603-72-4 A distinctive urban fantasy novel, Cadwell Turnbull's No Gods, No Monsters is an operatic story involving [...]

And Miles to Go Before I Sleep Jocelyne Saucier, Rhonda Mullins (Translator) Coach House Books (JUN 15) Softcover $17.95 (196pp), 978-1-55245-421-3 Jocelyne Saucier's novel And Miles to Go Before I [...]

Roundabout of Death Faysal Khartash, Max Weiss (Translator) New Vessel Press (MAY 18) Softcover $16.95 (176pp), 978-1-939931-92-4 A heartwrenching and shocking work of historical fiction, Faysal Khartash's Roundabout of Death [...]

THE ISLAND OF HAPPINESS Tales of Madame d'Aulnoy Baroness Madame d'Aulnoy Jack Zipes (Editor, Translator) Natalie Frank (Contributor, Illustrator) Princeton University Press (MAR 16) Hardcover $39.95 (240pp), 978-0-691-18024-3 LITERARY COLLECTIONS [...]

Revascularization of atherosclerotic renal artery stenosis may cure hypertension, but paradoxically, improvement in systemic blood pressure in response to successful revascularization may precipitate ischemia in other organs affected by previously silent atherosclerotic disease. We describe bowel ischemia secondary to preexisting celiac artery stenosis after revascularisation. Prior knowledge of multivessel disease facilitated prompt diagnosis and management of this condition.

This trial was conducted to determine the pharmacokinetics, dosimetry, dose-limiting toxicity, and the maximum tolerated dose of iodine-131 humanized MN-14 immunoglobulin G (131I-hMN-14 IgG), a humanized complementary-determining region—grafted anti—carcinoembryonic antigen monoclonal antibody, in metastatic gastrointestinal and colorectal cancer patients. Patients were divided into 2 groups: group A consisted of patients who had prior external beam radiation therapy (n = 8), and group B included patients who had received standard chemotherapy (n = 13). All patients received a diagnostic infusion of 131I-hMN-14 IgG (≈ 8.0 mCi, 15 mg/m2) to study the pharmacokinetics, biodistribution, and dosimetry. One week later, 17 of 21 patients received infusional therapy of escalating radioactive doses of 131I-hMN-14 IgG. Blood pharmacokinetics and quantitative imaging were performed again after the therapeutic dose. Radiation-absorbed doses to normal organs and tumors were determined by MIRDOSE-3 algorithms. The primary dose-limiting toxicity was hematologic toxicity at 40 mCi/m2. The blood half-life (n = 20) was identical for the diagnostic and therapy infusions. The mean red marrow dose was 2.2 ± 2.4 cGy/mCi. The mean tumor radiation dose (n = 8) was 24.2 ± 22.6 cGy/mCi. Tumor targeting was seen in most large metastatic lesions. No objective responses were seen in these heavily pretreated and mostly advanced patients. In conclusion, 131I-hMN-14 IgG has good targeting, good tumor to normal organs radiation absorbed ratios, and an acceptable toxicity profile in advanced metastatic gastrointestinal and colorectal cancer patients.

Monoclonal antibodies (MAbs) against carcinoembryonic antigen (CEA) have been recognized as targeting agents for medullary thyroid carcinoma (MTC). This Phase I/II study was initiated to determine the safety, maximum tolerated dose (MTD), and therapeutic potential of ¹³¹I-MN-14 F(ab)2 anti-CEA MAb for patients with metastatic MTC. Fifteen patients were enrolled in this study. Dose escalation was based on estimates of radiation dose to the bone marrow, and the radioactive dose given was determined by a pretherapy diagnostic study in which 8 mCi (0.6–20 mg) of ¹³¹I-MN-14 F(ab)2 was administered 1 week prior to therapy. Three patients received an initial dose of 140 centigray (cGy) to bone marrow, 11 received 180 cGy, and 1 received 220 cGy. Myelosuppression was the only significant treatment-related dose-limiting toxicity (DLT), and the MTD appeared to be 180 cGy to the bone marrow. Human antimouse antibodies (HAMA) developed in 8 patients 2–6 weeks after therapy. Seven patients had a median of 55% reduction of tumor markers. One patient showed a dramatic improvement in the mass effect on the airways caused by 3 tumor lesions in the neck, with a 45% reduction of overall tumor burden. The disease has continued to be radiologically stable in 11 of 12 assessable patients for periods ranging from 3+ to 26+ months. Therapy with ¹³¹I-MN-14 F(ab)2 is well tolerated and shows evidence of biochemical and radiologic antitumor activity. HAMA development suggests that humanized MAbs will be required in trials with repeated dose schedules. Further dose escalation, alone or in combination with other therapy modalities, is indicated for future trials, preferably with humanized anti-CEA MAbs. Cancer 1999;85:1828–42. © 1999 American Cancer Society.

Isometric contraction to direct supramaximal tetanic stimulation of the anterior tibialis (AT) muscle was measured in 50 New Zealand White rabbits after ischemia and reperfusion. Ischemia was produced unilaterally by collateral ligation and temporary inflow control until AT muscle function decreased to <5% of contralateral (control) AT muscle and the ischemic interval was recorded. Reperfusion was carried out in one of the following ways: group I (n = 20), release of vascular clamps (blood reperfusion [BR]); group II (n = 10), release of vascular clamps and simultaneous intraarterial administration of 50,000 units of urokinase (urokinase reperfusion [UR]); group III (n = 10), release of vascular clamps and simultaneous administration of 50,000 units of urokinase and 28 mg (5 units) of purified rabbit plasminogen (urokinase plasminogen reperfusion [UPR]); and group IV (n = 10), animals defibrinated to <50 mg/dl with ancrod prior to ischemia and received BR (ancrod blood reperfusion [ABR]). During reperfusion, function was recorded every 60 min for 2 hr. Recovery of experimental muscle function is expressed as the percentage of contralateral control limb function. The mean ischemic interval (means ± SEM), to achieve <5% of contralateral control limb function, was 206.7 ± 9.9, 209.5 ± 16.6, 221.7 ± 12.5, and 272.0 ± 14.2 min for animals in groups I-IV, respectively. The mean experimental muscle function (means ± SEM) following the ischemic interval was 3.2 ± 0.8, 4.5 ± 1.4, 4.4 ± 1.2, and 3.3 ± 1.0 for groups I-IV, respectively. The difference in the ischemia time to reach <5% of control function in between the control (group I) rabbits and the animals which received ancrod (group IV) is statistically significant (P < 0.01). After 2 hr of reperfusion, the mean muscle function was 25.5 ± 6.4 for controls (BR), 60.4 ± 18.6 for group II (UR), 72.7 ± 10.3 for group III (UPR), and 42.4 ± 9.7 for group IV (ABR). Both groups II (UR) and IlI (UPR) are statistically significant when compared to the unmodified blood reperfusion group (P < 0.05 and P < 0.01, respectively). We conclude that urokinase infusion during reperfusion improves the recovery of skeletal muscle function after ischemia. This effect is further enhanced by the addition of substrate (plasminogen), suggesting that fibrinolysis is responsible for this effect. Defibrination with ancrod increased the tolerance of skeletal muscle to ischemia but did not significantly improve its function compared to that of unmodified blood. These experiments suggest that manipulations of the fibrinogen/fibrin system may play an important role in the tolerance of skeletal muscle to ischemia and recovery of contractile function following reperfusion. Copyright 1994, 1999 Academic Press

Abstract: Intimal hyperplasia appears to result from the deposition of collagen and matrix by medial myofibroblasts, which are stimulated in response to vascular injury. We hypothesized that pharmacologic inhibitors of fibroblast proliferation would suppress the development of intimal hyperplasia. We evaluated the effect of two agents known to inhibit fibroblast proliferation in vitro: enalaprilat, an angiotensin-converting enzyme (ACE) inhibitor, and dimethyl sulfoxide (DMSO), an organic solvent. Thirty-five New Zealand white rabbits underwent standardized balloon catheter injury of the left common carotid artery. Experimental groups received daily intramuscular injections of the following: group I (n = 15), saline solution; group II (n = 10), 0.07 mg/kg enalaprilat; and group III (n = 10), 2 ml/kg of a 25% by weight DMSO solution. Injections were started 1 day prior to injury and continued 5 days a week for 8 weeks. Carotid arteries were perfusion-fixed at 12 weeks and cross-sectioned for measurement by planimetry. Intimal hyperplasia was measured as the ratio of the absolute area of intimal hyperplasia to the normalized area enclosed by the internal elastic lamina (IH/IEL) and was expressed as a percent. Mean values for IH/IEL were as follows: group I (control), 20.6 ± 2.3%; group II (enalaprilat), 9.5 ± 0.7%; and group III (DMSO), 17.6 ± 2.6%. Enalaprilat-treated animals demonstrated a statistically significant suppression of intimal hyperplasia compared with controls (p<0.01, ANOVA, Student's t test), whereas the DMSO-treated group did not. We conclude that enalaprilat is effective in suppressing the development of intimal hyperplasia in this model of arterial injury. These results support the theory that the smooth muscle cell mitogen angiotensin II plays an important role in the proliferation of medial myofibroblasts following vascular injury.

TO THE EDITOR:— Differences of opinion, theory, and method are to be expected in any complex new field of medical investigation. While these differences are well recognized by the few physicians working on a specific problem, they are not apparent to physicians engaged primarily in other pursuits. Therefore, when the data and conclusions of one group in a highly specialized field are published, such information may be generally interpreted as fact rather than as representative of one point of view. These considerations have prompted this belated comment on an article by Fletcher and asso associates which appeared on Feb. 27, 1960 in The Journal; this report seems seems to have promoted confusion among physicians regarding the status of fibrinolytic agents.The methods used by Fletcher and associates and their interpretation of data led them to express the opinion that one fibrinolytic agent of the activatorplasmin type (Actase) might not prove effective as a clot dissolvant in man. This