[Position of the genus Azygopterus (Stichaeidae, Perciformes) in the system of the suborder Zoarcoidei as inferred from sequence variation of mitochondrial and nuclear genes].

Analysis of sequence variation in the mitochondrial and nuclear genes in Azygopterus corallinus showed that this species was genetically close to the group uniting the representatives of the families Zoarcidae, Neozoarcidae, and Anarhichadidae. The considerable genetic differences between A. corallinus and the members of the family Stichaedae, to which it was assigned earlier, are consistent with the divergence estimates between the other families of the suborder Zoarcoidei (Zaproridae, Ptilichthyidae, Pholidae, Cryptacanthodidae, Bathymasteridae).

[Position of the genera Lycenchelys gill and Lycodapus gilbert in the family Zoarcidae (Perciformes: Zoarcoidei) inferred from molecular genetic analysis].

Sequence variation ofthe mitochondrial COI, cytochrome b, and 16S RNA genes, as well as nuclear RNF213 gene was examined in the genera Lycenchelys and Lycodapus with the purpose of determination of their positions in the system of the family Zoarcidae. It was demonstrated that the genus Lycodapus was considerably closer to the generic group of Lycogramminae (Lycogrammoides, Bothrocara, Allolepis, Bothrocarhichthys) than the genus Lycenchelys. However, on the phylogenetic trees both of these genera were located in the clade of the subfamily Lycodinae. Genetic heterogeneity of the genus Lycenchelys, represented by two species groups differing in distribution patterns (northeastern Pacific and Antarctic) and showing more profound differences than the genera of subfamily Lycodinae, was demonstrated.

[Relationships of eelpouts of genus Zoarces (Zoarcidae, Pisces) inferred from molecular genetic and morphological data].

Molecular genetic and morphological analysis of eelpouts of the genus Zoarces was carried out. Based on the mitochondrial DNA sequence variation, haplotypes of notched-fin eelpout, Z. elogatus, more closely related Fedorov eelpout, Z. fedorovi, and common eelpout, Z. viviparus, as well as of Andriyashev eelpout, Z. andriashevi, were grouped in one macrocluster. Haplotypes of American eelpout, Z. americanus, and blotched eelpout, Z. gillii, clustered separately from other species. The genetic differences between Z. gillii and the other eelpout species were very high for within-genus comparisons, constituting 7.62%. Species divergence in terms of morphological characters was generally consistent with molecular genetic data and confirmed distinct isolation of American eelpout, and especially of blotched eelpout.

[Nucleotide sequence variation of the mitochondrial COI gene in several eelpout species of the genus Zoarces (Zoarcidae, Pisces)].

The mitochondrial COI gene was for the first time sequenced in eelpout species of the genus Zoarces from the Taui Bay of the Sea of Okhotsk: notched-fin Z. elongatus Kner, 1868 and the new sympatric form Zoarces sp., differing in a large set of morphological traits. The two species were compared with European eelpout Z. viviparus Linnaeus, 1758 from the Finnish Bay of the Baltic Sea. Divergence and phylogenetic analyses demonstrated a greater genetic similarity between Zoarces sp. and Z. viviparus than between sympatric Zoarces sp. and Z. elongatus.

[Microvascular denudation of the femoral artery of the mouse as a model for restenosis]. / Mikrovaskuläre Denudation der Arteria femoralis der Maus--ein Restenosemodell für die Experimentelle Radiologie.

OBJECTIVE: To present technique and results of a microvascular denudation of the common femoral artery of the mouse as a model for inducing intimal hyperplasia in interventional radiology. MATERIALS AND METHODS: Under general anesthesia introduced by intraperitoneal injection, 14 B6129F1 hybrid mice (7 females and 7 males) at a mean age of 12.1 +/- 1.8 weeks and a mean weight of 28 +/- 2.8 grams had a groin incision of the vascular bundle directly distal to the inguinal ligament in preparation of placing a vascular clamp. Thereafter, the femoral artery was dissected distal to the origin of the epigastric artery and a loop prepared for a ligation proximal to the planned arteriotomy. Through an arteriotomy performed free-hand with a pair of micro scissors, a 0.010" (= 0.25 mm) guidewire was introduced into the vessel and advanced to the aortic bifurcation. The guide-wire was moved back and forth three times. The same procedure was performed on the other side as sham-operation, i.e., without introduction and passage of a guidewire. The resulting changes of the vessel wall were evaluated by histology and morphometry. RESULTS: Four weeks after intervention, the mean intima-to-media-ratio (IMR) was 1.80 +/- 0.28. A significant difference was observed between the sexes, with an IMR of 1.41 +/- 0.29 in females and an IMR of 2.24 +/- 0.45 in males (p = 0.0173). The neointima led to an overall luminal loss of 50.2% +/- 8.3% without significant sex difference (p = 0.09), but the average luminal loss was still more severe in females, amounting to 43.9% in comparison to 56.1% in males. This technique induces a significant neointima formation in a reproducible manner. The internal elastic membrane was preserved in all vessels. CONCLUSION: This technique is an excellent model to examine the differences between genetically modified mice to clarify the role of putative key molecules in the pathophysiology of restenosis.

Esophageal cancer as second primary tumor after breast cancer radiotherapy.

BACKGROUND: An increased risk of esophageal cancer has been reported in survivors of breast cancer treated with radiotherapy. This study further characterizes this association. METHODS: Through hospital databases, 118 patients (109 men, 9 women) treated for esophageal cancer between 1985 and 1993 were identified, of whom 37 had 60 synchronous or metachronous cancers. 5 women had primary esophageal cancer after having breast cancer, and are the subjects of this case-control study. RESULTS: All 5 women had been treated with radical mastectomy and adjuvant radiotherapy; none received chemotherapy. Their ages at the time of breast cancer ranged from 36 to 82 years; at esophageal cancer, 61 to 95 years. Time between radiotherapy and esophageal cancer varied from 13 to 31 years. All esophageal cancers were squamous cell carcinomas. Mean survival after esophageal cancer was 14.2 months. CONCLUSIONS: Radio-induced esophageal cancer can occur as a second primary cancer in women who survive at least 1 decade after mastectomy and adjuvant radiotherapy.

Analgesic synergy between topical lidocaine and topical opioids.

Topical drugs avoid many of the problematic side effects of systemic agents. Immersion of the tail of a mouse into a solution of dimethyl sulfoxide (DMSO)-containing morphine produces a dose-dependent, naloxone-sensitive, analgesia (ED(50) 6.1 mM; CL 4.3, 8.4) limited to the portion of the tail exposed to the drug. DMSO alone in this paradigm had no analgesic activity. Like morphine, the opioids levorphanol (ED(50) 5.0 mM; CL 3.8, 7.8) and buprenorphine (ED(50) 1. 1 mM; CL 0.7, 1.5) were effective topical analgesics. Lidocaine also was active in the tail-flick assay (ED(50) 2.5 mM; CL 2.0, 3.4), with a potency greater than morphine. As expected, the free base of lidocaine was more potent than its salt. Combinations of a low dose of lidocaine with a low dose of an opioid yielded significantly greater than additive effects for all opioids tested. Isobolographic analysis confirmed the presence of synergy between lidocaine and morphine, levorphanol and buprenorphine. These studies demonstrate a potent interaction peripherally between opioids and a local anesthetic and offer potential advantages in the clinical management of pain.

Acute decrease in cerebral nitric oxide levels after subarachnoid hemorrhage.

Disturbances in the nitric oxide (NO) vasodilatory pathway have been implicated in acute vasoconstriction and ischemia after subarachnoid hemorrhage (SAH). The authors hypothesize that blood released during SAH leads to vasoconstriction by scavenging NO and limiting its availability. This was tested by measuring the major NO metabolites nitrite and nitrate in five different brain regions before and after experimental SAH. The basal NO metabolites levels were as follows (mean +/- SD, micromol/mg wet weight): brain stem, 0.14 +/- 0.07; cerebellum, 0.12 +/- 0.08; ventral convexity cortex, 0.22 +/- 0.15; dorsal convexity cortex, 0.16 +/- 0.11; and hippocampus, 0.26 +/- 0.17. In sham-operated animals, no effect of the nitric oxide synthase (NOS) inhibitor L(G)-nitro-L-arginine-methyl-ester (30 mg/kg) was found on NO metabolites 40 minutes after administration, but a significant decrease was seen after 120 minutes. The NO metabolites decreased significantly 10 minutes after SAH in all brain regions except for hippocampus, and recovered to control levels in cerebellum at 60 minutes and in brain stem and dorsal cerebral cortex 180 minutes after SAH, while remaining low in ventral convexity cortex. Nitrite recovered completely in all brain regions at 180 minutes after SAH, whereas nitrate remained decreased in brain stem and ventral convexity cortex. Our results indicate that SAH causes acute decreases in cerebral NO levels by a mechanism other than NOS inhibition and provide further support for the hypothesis that alterations in the NO vasodilatory pathway contribute directly to the ischemic insult after SAH.

Effects of S-nitrosoglutathione on acute vasoconstriction and glutamate release after subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Subarachnoid hemorrhage (SAH) causes acute vasoconstriction that contributes to ischemic brain injury shortly after the initial bleed. It has been theorized that decreased availability of nitric oxide (NO) may contribute to acute vasoconstriction. Therefore we examined the effect of the NO donor N-nitroso glutathione (GSNO) on acute vasoconstriction and early ischemic glutamate release after experimental SAH. METHODS: SAH was induced by the endovascular suture method in anesthetized rats. GSNO (1 micromol/L/kg, n=31) or saline (n=21) was injected 5 minutes after SAH. Sham-operated rats received GSNO (1 micromol/L/kg, n=5) 5 minutes after sham surgery. Arterial and intracranial pressures, cerebral blood flow (CBF), and extracellular glutamate release were measured serially for 60 minutes after SAH. SAH size was determined, and vascular measurements were made histologically. RESULTS: GSNO had no effect on resting blood pressure, intracranial pressure, cerebral perfusion pressure, or CBF in sham-operated animals. However, administration of GSNO after SAH was associated with significantly increased CBF (161.6+/-26.6% versus saline 37.1+/-5.5%, 60 minutes after SAH, P<0.05), increased blood vessel diameter (internal carotid artery [ICA] 285.0+/-16.5 microm versus saline 149.2+/-14.1 microm, P<0.01), decreased vessel wall thickness (ICA12.9+/-0.7 microm versus saline 25.1+/-1.6 microm, P<0.01), and decreased extracellular glutamate levels (3315.6+/-1048.3% versus saline469. 7+/-134.3%, P<0.05). Blood pressure decreased transiently, whereas intracranial pressure, cerebral perfusion pressure, and SAH size were not affected. CONCLUSIONS: These results suggest that GSNO can reverse acute vasoconstriction and prevent ischemic brain injury after SAH. This further implies that acute vasoconstriction contributes significantly to ischemic brain injury after SAH and is mediated in part by decreased availability of NO.