Adjuvant perioperative hepatic arterial mitomycin C and floxuridine combined with surgical resection of metastatic colorectal cancer in the liver

Twenty patients with colon cancer metastatic to the liver underwent successful hepatic resection and adjuvant perioperative therapy that included hepatic arterial mitomycin C and floxuridine (FUDR). The median survival for all 20 patients was 51 months: 10 are still alive with a median postoperative follow-up of 49 months; 6 are disease-free with a median postoperative follow-up of 43 months. Among 10 patients in whom the surgical margins of the specimen contained tumor cells, the median survival was 52 months. This survival was comparable to that among 10 patients in whom the surgical margins were tumor free (P = 0.22). Neither the number of metastatic liver deposits nor the disease-free interval between the primary diagnosis of colorectal carcinoma and the development of liver metastases significantly affected survival. A transient chemical hepatitis which resolved before the next scheduled treatment was associated with 50% of arterial chemotherapy cycles (approximately 70% of the patients). Gastric or duodenal ulcerations occurred in 23% of the patients. Surgical complications were either pulmonary such as pleural effusion or atelectasis, or wound infections and subphrenic abscesses. Although these results compare favorably with the results in previously published series, this aggressive adjuvant chemotherapy appears to be particularly justified in patients with tumor positive surgical margins or those with multiple tumor masses and, therefore, are characterized by a poor prognosis.     

MR of the cerebral operculum: abnormal opercular formation in infants and children.

PURPOSETo evaluate abnormalities of the cerebral operculum in infants and children and to propose the embryogenic basis of abnormal opercular formation as determined from MR imaging findings.METHODSEighty-six infants and children who had abnormally wide interopercular distances and/or distorted opercular topography seen on MR images were studied retrospectively. Clinically, patients presented with tonal abnormalities, macrocephaly, microcephaly, seizures, developmental delay, cerebral palsy, or facial dysmorphism. The abnormal opercula were compared with developing opercula at different stages of gestation.RESULTSAmong the 86 infants and children, two categories of opercular abnormalities were identified: an underdeveloped operculum (n = 64) and a malformed operculum (n = 22). The malformed operculum was further classified into three subtypes: nonformation of the operculum with lissencephaly (n = 1, 1%), abnormal opercular formation with pachygyria (n = 11, 13%), and nonformation or abnormal formation of the operculum without pachygyria or lissencephaly (n = 10, 12%). Two subtypes of the underdeveloped operculum were identified: an open operculum without a normal insula (n = 6, 7%) and an open operculum with a normal insula (n = 58, 67%). The five subtypes of abnormal opercular configuration showed a range of maturity that was comparable to the developing operculum at different ages.CONCLUSIONOpercular anomalies appear to follow sequentially predetermined normal steps in development. Arrest in opercular development or malformation may occur after an initial insult. MR imaging is the method of choice by which to identify these abnormalities.     

ROBUST GUARANTEED COST CONTROL OF UNCERTAIN NON-LINEAR ROBOTIC SYSTEM USING MIXED MINIMUM TIME AND QUADRATIC PERFORMANCE INDEX

To provide better transient performance in controlling robots, a mixed minimum time and quadratic performance index is used. For known and uncertain revolute robot manipulators a conventional optimal control and a robust guaranteed cost control are proposed respectively. Asymptotic stability is also discussed based on the Lyapunov direct method. The proposed robust control is continuous and requires no knowledge of the uncertain system except for bounding functions.     

Inhibition of ligand binding to g protein-coupled receptors by arachidonic acid

Arachidonic acid (AA), released in response to muscarinic acetylcholine receptor (mAChR) stimulation, previously has been reported to function as a reversible feedback inhibitor of the mAChR. To determine if the effects of AA on binding to the mAChR are subtype specific and whether AA inhibits ligand binding to other G protein-coupled receptors (GPCRs), the effects of AA on ligand binding to the mAChR subtypes (M₁, M₂, M₃, M₄, and M₅) and to the μ-opioid receptor, β₂-adrenergic receptor (β₂-AR), 5-hydroxytryptamine receptor (5-HTR), and nicotinic receptors were examined. AA was found to inhibit ligand binding to all mAChR subtypes, to the β₂-AR, the 5-HTR, and to the μ-opioid receptor. However, AA does not inhibit ligand binding to the nicotinic receptor, even at high concentrations of AA. Thus, AA inhibits several types of GPCRs, with 50% inhibition occurring at 3–25 μM, whereas the nicotinic receptor, a non-GPCR, remains unaffected. Further research is needed to determine the mechanism by which AA inhibits GPCR function.     

双酚胺酸对小鼠和大鼠氯化镍解毒及分布的影响

AIM: To study the effect of catecholamic acid (CBMIDA) on detoxication of NiCl2. METHODS: Mice and rats were injected s.c. or i.m. CBMIDA immediately after i.p. NiCl2. Each mouse was injected i.p. CBMIDA after i.v. 63NiCl2 185 kBq, and radioactivities of various tissues were measured with liquid scintillation counter at 24 h. The localization of 63Ni was shown by the whole-body autoradiography. RESULTS: CBMIDA s.c. 0.5-1.5 g.kg-1 markedly reduced the mortality from acute poisoning of i.p. NiCl2 500 mg.kg-1. After i.p. NiCl2 in mice, the LD50 was 82.7 mg.kg-1. Mice were injected s.c. CBMIDA 1.5 or 2.5 g.kg-1 after Ni poisoning, the LD50 of NiCl2 were raised to 789 or 820 mg.kg-1, respectively. The LD50 of NiCl2 was 39 mg.kg-1 in rat. If CBMIDA was injected i.m. 0.5 g.kg-1 after i.p. NiCl2, the LD50 was 332 mg.kg-1. CBMIDA 1.5 g.kg-1 i.m. after i.v. 63NiCl2, decreased the contents of 63Ni in blood and lung of mice vs control mice at 24 h. The contents of 63Ni in brain, heart, spleen, and kidney were similar to those of the control mice. The content of 63Ni in bone was more than the control. The excretions of 63Ni through urine and feces were not increased by CBMIDA at 24 h. The whole-body autoradiography showed that the radioactivity was highly localized in the kidney, lung, and Harder's gland. There was a moderate level of 63Ni in the liver, bone, skin, and blood. A pronounced accumulation occurred in the bone. There was a marked reduction of 63Ni in the lung, skin, liver, and blood after i.p. CBMIDA. CONCLUSION: The CBMIDA markedly raised the survival rate of nickel-poisoned mice and rats, and decreased 63Ni levels in lung and blood.