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Imaging properties of polydioxanone and titanium ligating clips following para-aortic lymphadenectomy for testicular cancer.

Stainless steel ligating clips produce serious artefacts on CT scans. Polydioxanone (PDS) and titanium ligating clips were used in 15 patients during para-aortic lymphadenectomy for residual metastatic testicular teratoma following chemotherapy, and follow-up CT images were compared with those following the use of stainless steel ligating clips. PDS ligating clips did not produce any artefacts and were progressively absorbed. Titanium ligating clips produced artefacts similar to but less intense than those of stainless steel. PDS ligating clips should be used when follow-up CT scanning is important.

Constriction↗

Efficacy of endoscopic clipping for bleeding gastroduodenal ulcer: comparison with topical ethanol injection.

OBJECTIVE: Although endoscopic clipping is used widely for the treatment of bleeding gastroduodenal ulcers, clinical trials on its efficacy are scarce. The aim of this study is to assess the efficacy and safety of endoscopic clipping for hemostasis from bleeding gastroduodenal ulcers. METHODS: The present study was designed as a retrospective study using historical controls. One hundred consecutive patients with bleeding gastroduodenal ulcers were treated by endoscopic clipping. The preceding 91 consecutive patients treated by endoscopic pure ethanol injection were regarded as controls. Forty-nine of the clipping group and 41 of the ethanol group had lesions at sites difficult to perform endoscopic manipulation. Hemostatic rates, rebleeding rates, amounts of blood transfusion, and durations of hospital stay were analyzed. RESULTS: The hemostatic rate was 96% in both clipping and ethanol groups, whereas the rebleeding rate was lower (15% vs 29%, p = 0.023) in the former than the latter. In technically difficult cases, the hemostatic rate was comparable (96 vs 90%). CONCLUSION: In patients with bleeding gastroduodenal ulcers, endoscopic clipping may be a choice of therapy because of a low rebleeding rate compared with pure ethanol injection.

Ethanol↗

LIS1, CLIP-170's key to the dynein/dynactin pathway.

CLIP-170 is a plus-end tracking protein which may act as an anticatastrophe factor. It has been proposed to mediate the association of dynein/dynactin to microtubule (MT) plus ends, and it also binds to kinetochores in a dynein/dynactin-dependent fashion, both via its C-terminal domain. This domain contains two zinc finger motifs (proximal and distal), which are hypothesized to mediate protein-protein interactions. LIS1, a protein implicated in brain development, acts in several processes mediated by the dynein/dynactin pathway by interacting with dynein and other proteins. Here we demonstrate colocalization and direct interaction between CLIP-170 and LIS1. In mammalian cells, LIS1 recruitment to kinetochores is dynein/dynactin dependent, and recruitment there of CLIP-170 is dependent on its site of binding to LIS1, located in the distal zinc finger motif. Overexpression of CLIP-170 results in a zinc finger-dependent localization of a phospho-LIS1 isoform and dynactin to MT bundles, raising the possibility that CLIP-170 and LIS1 regulate dynein/dynactin binding to MTs. This work suggests that LIS1 is a regulated adapter between CLIP-170 and cytoplasmic dynein at sites involved in cargo-MT loading, and/or in the control of MT dynamics.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗

Placement of a ferromagnetic intracerebral aneurysm clip in a magnetic field with a fatal outcome.

Magnetic resonance (MR) imaging may be contraindicated in patients with biomedical devices, among the most dangerous of which are intracranial aneurysm clips, owing to the possibility of torque and dislodgement. A case is presented in which a patient with a reportedly nonferromagnetic clip was placed in a magnetic field. The patient developed an acute intracerebral hemorrhage in the MR unit, with a fatal outcome. Imaging studies strongly suggested a torqued clip as the cause. Autopsy revealed a torn middle cerebral artery from clip movement, and the clip was identified as a ferromagnetic type. This is the first reported case, to the authors' knowledge, of a fatal outcome due to an intracranial aneurysm clip placed in a magnetic field.

Acute Disease↗

Spetzler titanium aneurysm clips: compatibility at MR imaging.

To evaluate the compatibility of a commercially pure titanium aneurysm clip associated with magnetic resonance (MR) imaging at 1.5 T. Artifacts of the Spetzler titanium aneurysm clip were compared with those produced by six different nonferromagnetic aneurysm clips. With the titanium clip, no magnetic attraction was present, heating was minor, and the artifacts involved a small signal void. With the six other aneurysm clips, artifacts were larger. The presence of Spetzler titanium aneurysm clips is safe at MR imaging at 1.5 T or less.

Artifacts↗

Yasargil aneurysm clips: evaluation of interactions with a 1.5-T MR system.

PURPOSE: To evaluate the magnetic field interactions with Yasargil aneurysm clips exposed to a 1.5-T MR system. MATERIALS AND METHODS: Sixteen Yasargil aneurysm clips made with Phynox (10 clips returned to the manufacturer due to suspected magnetic field interactions and six clips obtained from the manufacturer in sterile packages) were tested for magnetic field interaction at 1.5 T by using techniques to assess magnetic field-induced translational (deflection angle test) and torque (changes in alignment or rotation) forces. RESULTS: None of the aneurysm clips demonstrated magnetic field interactions; that is, deflection angles were zero and there were no changes in alignment or evidence of rotational forces present. CONCLUSION: It is safe to perform MR procedures at 1.5 T or less in patients with Yasargil aneurysm clips made with nonferromagnetic material.

Alloys↗

Different levels of hypertension induce opposite diuretic behaviors from the nonclipped kidney in the rat two-kidney, one-clip model.

This study was carried out on conscious two-kidney, one-clip (2K1C) rats to establish whether different levels of hypertension induced opposite diuretic behaviors from the nonclipped kidney. Mildly hypertensive rats and severely hypertensive rats were produced by, respectively, constricting their right renal arteries with 0.3-mm and 0.15-mm clips. On the 11th day of the study, the systolic blood pressure (SBP) of the 0.3-mm clip rats was 150 +/- 2 mm Hg, the water intake was 24 +/- 1 ml, and the urine output was 7 +/- 1 ml. The SBP of the 0.15-mm clip rats was 231 +/- 10 mm Hg, the water intake was 46 +/- 4 ml, and the urine output was 27 +/- 6 ml. The data from the two groups are significantly different. On the 19th day half of the mildly hypertensive (0.3-mm clip) rats that received cilazapril from day 15 had, with respect to their water-treated counterparts, a SBP of 140 +/- 8 as compared with 159 +/- 7 mm Hg, the water intake was 37 +/- 5 as compared with 26 +/- 4 ml, and the urine output was 18 +/- 4 as compared with 12 +/- 1 ml. In contrast, half of the severely hypertensive (0.15-mm clip) rats that received cilazapril had, with respect to their water-treated counterparts, a SBP of 143 +/- 4 as compared with 227 +/- 10 mm Hg, the water intake was 30 +/- 2 as compared with 51 +/- 9 ml, and the urine output was 8 +/- 2 as compared with 29 +/- 4 ml. All changes induced by cilazapril are significant in both groups. The data of this study suggest that different levels of hypertension in the rat 2K1C model induce opposite water elimination modes from the nonclipped kidney. This conclusion is supported by the different shift in the water intake and urine output among the cilazapril-treated rats of the two groups. This contrast in the response to cilazapril seems to be dependent on the magnitude of the resulting hypotension. Thus, it seems that in this model, when the hypertension is mild, the antidiuretic effect of angiotension II on the nonclipped kidney is exhibited, whereas, when the hypertension is severe, the diuretic influence of the blood pressure is evident. Irrespective of these different characteristics of the submodels of 2K1C, angiotensin I converting enzyme inhibitors, such as cilazapril, are effective in normalizing the blood pressure.

Angiotensin II↗

Body fluid volume and angiotensin II in maintenance of one-kidney, one clip hypertension.

To investigate the possible role of body fluid volume or the renin-angiotensin system in the maintenance of high blood pressure in chronic one-kidney, one clip (1K1C) hypertension, we studied whether blood pressure remained high after removal of the clip while the body fluid volume was kept constant or when angiotensin II (Ang II) was infused in conscious 1K1C rats. Blood pressure fell 58 +/- 13 mm Hg in 1K1C rats after removal of the clip. When body fluid volume was kept at the same level as before "unclipping," blood pressure fell only 9 +/- 2 mm Hg after removal of the clip; if body fluid volume was then allowed to decrease, blood pressure fell an additional 55 +/- 8 mm Hg. When Ang II was infused after removal of the clip, blood pressure fell 26 +/- 7 mm Hg despite the fact that plasma Ang II increased to nonphysiological concentrations (1,161 +/- 353 pg/ml). After Ang II infusion was stopped, blood pressure fell an additional 44 +/- 13 mm Hg. When Ang II was infused and body fluid volume kept constant, blood pressure still did not change after removal of the clip, although plasma Ang II concentrations increased to nonphysiological levels (618 +/- 98 pg/ml). After the Ang II infusion was discontinued and the body fluid volume was no longer kept constant, blood pressure fell 78 +/- 9 mm Hg. These data further support the hypothesis that a volume factor, not the renin-angiotensin system, is important in the maintenance of high blood pressure in 1K1C hypertension.

Angiotensin II↗

Impaired renorenal reflexes in two-kidney, one clip hypertensive rats.

In normotensive rats, stimulation of renal mechanoreceptors by an increase in ureteral pressure results in a contralateral inhibitory renorenal reflex response with contralateral natriuresis. Similar effects are produced by stimulation of renal chemoreceptors by renal pelvic perfusion with 0.9 M NaCl. However, in spontaneously hypertensive rats the renorenal reflex responses to renal mechanoreceptor and chemoreceptor stimulation are impaired. The present study was performed to examine whether the renorenal reflexes were altered in two-kidney, one clip hypertensive rats, a model of hypertension in which it has been suggested that the afferent renal nerves contribute to the enhanced peripheral sympathetic nervous activity. A 0.2 mm silver clip was placed around one renal artery 4 weeks before the study. At the time of study, mean arterial pressure was 156 +/- 4 mm Hg. Renal mechanoreceptor and chemoreceptor stimulation of either the nonclipped or clipped kidney failed to affect ipsilateral afferent renal nerve activity, contralateral efferent renal nerve activity, and contralateral urine flow rate and urinary sodium excretion. Renal denervation of the nonclipped kidney increased ipsilateral urinary sodium excretion from 0.65 +/- 0.13 to 1.50 +/- 0.42 mumol/min/g and decreased contralateral urinary sodium excretion from 0.18 +/- 0.03 to 0.13 +/- 0.03 mumol/min/g (p less than 0.05). Thus, denervation of the nonclipped kidney resulted in a similar contralateral excitatory renorenal reflex response as in normotensive rats. However, denervation of the clipped kidney increased both ipsilateral and contralateral urinary sodium excretion, from 0.14 +/- 0.04 to 0.27 +/- 0.5 mumol/min/g and from 1.29 +/- 0.33 to 2.09 +/- 0.59 mumol/min/g (p less than 0.01), respectively. Taken together these data suggest that the lack of inhibitory renorenal reflexes from the clipped kidney may enhance efferent sympathetic nervous activity and thereby contribute to the hypertension in two-kidney, one clip hypertensive rats.

Animals↗

Increased vascular formation of angiotensin II in one-kidney, one clip hypertension.

To assess the role of the vascular angiotensin II-generating system in one-kidney, one clip hypertension, we determined the angiotensin converting enzyme activity in plasma and vascular tissues and examined the pressor response to angiotensin II, angiotensin I, and tetradecapeptide renin substrate in isolated mesenteric arteries from one-kidney, one clip hypertensive rats 7 and 30 days after clipping the renal artery and in mesenteric arteries from age-matched normotensive rats. Angiotensin converting enzyme activity, determined in aortic and mesenteric tissues, was significantly augmented in the hypertensive (30 days after clipping) group, whereas plasma activity was normal. The vasoconstrictor responses elicited by angiotensin I and tetradecapeptide in arteries from hypertensive rats were found to be significantly potentiated 30 days after clipping, whereas the angiotensin II responses were basically unchanged. Saralasin completely blocked the vasoconstrictor responses, whereas captopril blocked only the responses to angiotensin I without affecting the responses elicited by angiotensin II and tetradecapeptide. Enalapril, an angiotensin converting enzyme inhibitor given intravenously to unanesthetized rats, significantly lowered the blood pressure of hypertensive rats. The pressor responses elicited by angiotensin II, angiotensin I, and tetradecapeptide were completely inhibited by saralasin, whereas enalapril blocked only the responses of angiotensin I but not those elicited by angiotensin II and tetradecapeptide. These results indicate that local formation of angiotensin II is increased in arteries of one-kidney, one clip hypertensive rats. The data obtained with tetradecapeptide renin substrate suggest an important role for nonrenin proteases in vascular angiotensin II formation.

Angiotensin I↗

Angiotensin and angiotensin converting enzyme tissue levels in two-kidney, one clip hypertensive rats.

Renal tissue angiotensin I (Ang I) and II (Ang II) content and angiotensin converting enzyme activity were assessed in both kidneys during initial (7 days) and maintenance (25 days) phases of two-kidney, one clip hypertension in rats. At 7 and 25 days, systolic arterial pressure was 146 +/- 2 and 170 +/- 7 mm Hg, respectively. After 7 days, Ang I content of clipped kidneys was 64% and 70% higher (p < 0.001) than in nonclipped and sham-operated kidneys, respectively, when compared with levels in kidneys from sham-operated rats. In kidneys harvested 25 days after clipping one renal artery, Ang I and Ang II contents in clipped kidneys were increased 102% and 24% (p < 0.01), respectively. Ang II content was also 32% higher in nonclipped kidneys. Angiotensin converting enzyme activity in nonclipped kidneys was greater (p < 0.05) than that in either clipped (46% higher) or sham-operated kidneys (57% higher). Plasma Ang I and Ang II levels were elevated at 7 days but were not different at 25 days in clipped rats. These results demonstrate a dissociation between intrarenal and circulating levels of Ang I and Ang II and suggest that qualitatively different mechanisms may be responsible for the elevated intrarenal Ang II levels during the initial and maintenance phases of renal hypertension.

Angiotensin I↗

Influence of nitric oxide in the chronic phase of two-kidney, one clip renovascular hypertension.

Chronic two-kidney, one clip (2K1C) renovascular hypertension is characterized by a largely angiotensin-independent elevated blood pressure (BP). We hypothesized that the long-term effect of hypertension would compromise endothelium-derived nitric oxide (NO) and diminish its influence in controlling renal perfusion. We determined the influence of endothelium-derived NO on renal hemodynamics and the angiotensin-NO interaction regulation of renal perfusion in rats with chronic 2K1C hypertension. Renal blood flow (RBF) was measured by radioactive microspheres in rats with either early-phase (4 weeks after clipping, n=7) or chronic-phase (13 to 16 weeks after clipping, n=7) 2K1C hypertension. The systemic and renal response to NO synthesis inhibition was determined with 10 mg/kg body wt N omega-nitro-L-arginine methyl ester (L-NAME). In rats with early-phase 2K1C hypertension, BP was 149+/-3 mm Hg, which increased by 42+/-3 mm Hg with L-NAME (P<.001). L-NAME decreased RBF by 20% (P<.02) and 17% (P<.005) and increased renal vascular resistance (RVR) by 58% (P<.005) and 62% (P<.02) in the nonclipped and clipped kidneys, respectively. In rats with chronic 2K1C hypertension, BP was 166+/-3 mm Hg, and L-NAME increased this by 35+/-6 mm Hg (P<.001). In the nonclipped and clipped kidneys of chronic 2K1C hypertensive rats, L-NAME decreased RBF by 20% (P<.01) and 17% (P<.01) and increased RVR by 51% (P<.005) and 60% (P<.02), respectively. There were no differences in L-NAME-induced changes between early- and chronic-phase 2K1C hypertensive rats. Next, we treated seven chronic-phase 2K1C hypertensive rats with 10 mg/kg body wt losartan, which reduced BP by only 7.7% (P<.005). After losartan, L-NAME increased BP by 41+/-3 mm Hg (P<.001), decreased RBF to the nonclipped kidney by 44% (P<.05), and increased RVR by 110% (P<.005); the decrease in RBF was significantly greater compared with untreated chronic-phase controls (P<.05). In the clipped kidney, L-NAME decreased RBF by 26% (P<.05) and increased RVR by 76% (P <.05). Thus, angiotensin blockade did not attenuate the systemic or renal vasoconstriction to L-NAME. Our results suggest that in both early and chronic phases of 2K1C hypertension, NO contributes significant dilator tone to buffer the hypertension and maintains perfusion of both kidneys by counterbalancing angiotensin-independent vasoconstriction.

Animals↗

Regional vascular capacitance in rabbit one-kidney, one clip hypertension.

One-kidney Goldblatt hypertensive rabbits (New Zealand White) were studied after durations of renal artery clipping that varied from 6 to 17 days. Measurements included arterial pressure (ABP), iliac venous pressure (IVP), left atrial pressure (LAP), cardiac output (CO) (by thermodilution), blood volume (BV), cardiopulmonary volume (CPV), and hindleg thermodilution volume (HLV). These were determined at steady-state as well as during acute blood volume expansion. In sham-clipped animals, ABP was 74 +/- 1 mm Hg. This increased to 92 +/- 3 mm Hg by 6 to 9 days post-clipping, to 96 +/- 3 mm Hg by 10 to 13 days, to 89 +/- 4 mm Hg by 14 to 17 days. CO remained near 150 ml/min . kg until Day 13 and fell to 127 +/- 8 ml/min . kg at 14 to 17 days because of a fall in heart rate. Blood volume and stroke volume did not change significantly from 62 +/- 1 ml/kg and 0.60 +/- 0.04 ml/kg, respectively. The development of hypertension was due entirely to changes in peripheral resistance. CPV was 8.5 ml/kg initially and increased significantly as hypertension developed. HLV did not change significantly from about 10 ml/kg. During acute blood volume expansion, hypertensive animals showed smaller transient increases in CO than did sham-clipped normotensives, but the associated blood pressure rise was greater. This reduced vasodilator capacity was accompanied by reduced distensibility of the cardiopulmonary bed. In sham-clipped animals, the cardiopulmonary pressure/volume slope was between 0.05 and 0.07 mm Hg per ml/kg. This increased to 0.44 mm Hg per ml/kg by 14--17 days of clipping. The corresponding value for the hindleg region did not change significantly from 0.2 mm Hg per ml/kg. Cardiac output and stroke volume were directly correlated with cardiopulmonary volume. The slope of this correlation decreased significantly during hypertension. The data suggest that decreased cardiopulmonary compliance in hypertension minimizes transient changes in cardiac output. This is especially important for arterial blood pressure control in view of the impaired vasodilator capacity of the hypertensive circulation.

Animals↗

Hodgkin and Reed-Sternberg cell-associated autoantigen CLIP-170/restin is a marker for dendritic cells and is involved in the trafficking of macropinosomes to the cytoskeleton, supporting a function-based concept of Hodgkin and Reed-Sternberg cells.

Little is known about the distribution in normal cells of CLIP-170, a linkage mediator between endocytic vesicles and microtubules, and restin, a splice variant encoded by the same gene and marker for Hodgkin and Reed-Sternberg (HRS) cells of Hodgkin disease. Although only trace amounts of CLIP-170/restin are present in peripheral blood mononuclear cell subpopulations, monocyte-derived dendritic cells (DCs) and interleukin-4 (IL-4) + CD40L-activated B cells express high levels of CLIP-170/restin. CLIP-170/restin colocalizes preferentially with membranes of intermediate macropinocytic vesicles, suggesting a new function of CLIP-170/restin in the trafficking of macropinosomes to the cytoskeleton, which is a crucial step in antigen presentation. The strong expression of CLIP-170/restin in HRS cells, DCs, and activated B cells underscores their functional similarities supporting a function-based concept of HRS cells as professional antigen-presenting cells.

Antigen-Presenting Cells↗

Newly designed bayonet clips for complicated aneurysms: technical note.

Three newly designed bayonet clips (crankshaft clips) are presented. They were designed to occlude aneurysms with irregular necks by using the angle and shank portion of a bayonet clip (shank clipping). The new clips have shorter distal blades and longer shanks (proximal blades), and the angle portions are bent to an angle of smaller degree. These clips are useful particularly for aneurysms located in a wider space.

Constriction↗

New tumor clips for the removal of large or deep-seated tumors: technical note.

We describe newly developed tumor-holding clips, which have been applied in more than 50 patients with large or deep-seated tumors. We devised various kinds of standard tumor clips by modifying Sugita aneurysm clips. Our new tumor clips permit gentle, steady, and easy retraction of the tumor in any direction without disturbance of the operative field. With the use of these clips, a surgeon can operate with both hands. From our experience of removing more than 50 tumors, we confirm that our tumor clips are useful for the removal of large or deep-seated tumors.

Brain Neoplasms↗

Arterial reconstruction by direct surgical clipping of a basilar artery dissecting aneurysm after failed vertebral artery occlusion: technical case report and literature review.

OBJECTIVE AND IMPORTANCE: Dissecting aneurysms of the basilar artery are rare lesions with significant morbidity and mortality. Their management is controversial and often difficult. Although the rebleeding rate is high, clip reconstruction carries prohibitive risk because of the damage to the parent vessel induced by the dissection and the lack of tissue to gather. An enlarging pseudoaneurysm in the chronic phase, however, may have sufficient tissue for clip reconstruction. We present a case in which this strategy was used successfully. CLINICAL PRESENTATION: A 45-year-old woman presented 3 months after an initial presentation with a subarachnoid hemorrhage from a dissecting aneurysm of the basilar trunk at an outside institution. The aneurysm had grown compared with previous angiograms. INTERVENTION: The dominant vertebral artery was sacrificed. Despite this, the aneurysm continued to enlarge. Given the progressive enlargement of the aneurysm, the decision was made to proceed with arterial reconstruction by direct surgical clipping of the saccular component of the dissecting aneurysm. The patient made an excellent recovery with a durable result. CONCLUSION: Although clipping an intracranial pseudoaneurysm in the acute phase may carry a prohibitive risk, clipping such an aneurysm in the chronic phase may occasionally be warranted. To our knowledge, this is the first case reported in the literature in which direct surgical clipping was used as the primary mode of treatment for a basilar artery dissecting aneurysm that enlarged despite occlusion of the dominant vertebral artery. We review the literature on this rare pathological entity and discuss our management strategy.

Aortic Dissection↗

Surgical clipping of complex basilar apex aneurysms: a strategy for successful outcome using the pretemporal transzygomatic transcavernous approach.

OBJECTIVE: Complex basilar apex aneurysms (large size, wide and complex neck, tortuous parent vessels) continue to pose a challenge in treatment. Endovascular treatment has a high risk of recanalization, and surgical treatment is limited by the space and time necessary to achieve safe clipping. To overcome these obstacles, a modification of previously reported approaches was developed. The pretemporal transzygomatic transcavernous approach and a clipping strategy were used in the treatment of 21 high-complexity basilar apex aneurysms. METHODS: By use of the pretemporal route, the zygomatic notch was widened, the anterior clinoid was removed, the cavernous sinus was partially exposed, and the oculomotor nerve was mobilized. The depth of the field was widened by further cavernous exposure and the removal of the posterior clinoid. Temporary clips were applied to the basilar trunk perforator-free zone to preserve visualization of the aneurysm neck and perforators and to maintain collateral flow to the brainstem. RESULTS: Twenty-one high-complexity basilar apex aneurysms, 11 of which caused subarachnoid hemorrhage, were treated. Twenty (95%) were successfully clipped (Glasgow Outcome Scale scores, 4 or 5 in 90.5% at discharge; Rankin Disability Score, 1 in 90.5% at 1-yr follow-up). Complications were transient oculomotor palsy in all patients, small thalamic infarct in one patient, and cerebrospinal fluid leak in another. There was no surgical mortality. Delayed follow-up angiography in 19 of the 21 patients showed no residual aneurysm. CONCLUSION: We report the largest series of a unique, challenging group of complex basilar apex aneurysms treated with the pretemporal transzygomatic transcavernous approach, which provided improved safety of clipping by 1) increased visualization of the basilar apex and perforator arteries, 2) improved maneuverability of clip application, 3) a safer perforator-free location, and 4) preservation of brainstem collateral flow.

Basilar Artery↗