Biomedical subjects
Publications and source records attributed to C Owens.
Recent applications of combined EXAFS/powder neutron and X-diffraction analysis are reviewed and provisional results for three additional compounds are presented. Criteria for successful refinements are suggested. The new results relate to the materials: CoAl2O4, La(6.4)Ca(1.6)Cu6Ni2O20 and Pr(0.5)Sr(0.5)FeO(2.75).
The aims of the UKW2 study were: (1) to further refine treatment for stage I and II favourable histology (FH) patients; (2) to consolidate the UKW1 results for stage III FH patients; (3) to improve the outlook for patients with inoperable primary tumours and those patients with stage IV and unfavourable histology disease. Treatment consisted of primary nephrectomy, wherever possible, followed by chemotherapy and radiotherapy, as dictated by stage and histology. Treatment was refined successfully for stage I and II FH patients. The 4-year event-free survival for these two groups was 94% and 91%, respectively. Stage III FH patients had a 4-year event free survival of 84%. The outlook for patients with clear cell sarcoma of the kidney is as good as for patients with favourable histology, whilst that for patients with anaplastic or rhabdoid variants remains poor. The outlook for the majority of children with Wilms' tumour is now excellent.
BACKGROUND: The endotracheal cardiac output monitor (ECOM) is a new device that uses an endotracheal tube with multiple electrodes to measure cardiac output (CO). It measures the changes in electrical impedance caused by pulsatile blood flow in the aorta. The system was tested for safety and efficacy in 10 swine. METHODS: Swine (60-80 kg) were chronically instrumented with a transit time flow probe on the ascending aorta and vascular occluders on the vena cava and pulmonary artery. After a minimum recovery of 4 days, the animals were anesthetized and intubated with an ECOM endotracheal tube. CO measurements from the ECOM system were compared to transit time flow probe measurements using linear regression and Bland-Altman analysis. Three different inotropic states were studied: (1) baseline; (2) increased (dobutamine); and (3) decreased (esmolol). CO was changed at each inotropic state by impeding left ventricular filling with the vena cava or pulmonary artery occluders. CO values between 0 and 15 l/min were studied. Pigs were studied for 24 h consecutively. RESULTS: There was no deterioration of the impedance signal with time and no tracheal injury from the ECOM electrodes. There is a linear relationship between the ECOM and transit time flow probe CO between 0 and 15 l/min (slope = 0.94; intercept = 0.15 l/min; R2= 0.77). The mean difference between the two measures (bias) is 0.15 l/min and the SD is 1.34 l/min. The limits of agreement are -2.53 to 2.82 l/min. CONCLUSION: Endotracheal CO monitor is a promising technology that needs further evaluation in clinical trials.
OBJECTIVE: Evaluation of the influence of emergency cranial computed tomography on the management of acute febrile encephalopathy in children. METHODS: A retrospective study in children with acute febrile encephalopathy who underwent emergency cranial computed tomography within 12 hours of admission to the paediatric intensive care unit. All scans were evaluated by two independent radiologists. RESULTS: Thirty nine children were included. Fourteen scans were abnormal and two had clinically insignificant incidental findings. Four children with focal neurological signs had scans demonstrating extra-axial collections. None required neurosurgical intervention. Clinically, raised intracranial pressure was present in 10 patients. Only five had cerebral oedema on computed tomography; these five children died. Emergency cranial computed tomography influenced subsequent management in no child without focal neurological signs and in only one child with focal neurology. CONCLUSION: Emergency cranial computed tomography in acute febrile encephalopathy in children without focal neurological signs has little influence on subsequent management. Where cranial computed tomography is thought to be necessary, it should be carried out when the child's clinical condition has been stabilised.
The perinephric space is a cone-shaped retroperitoneal compartment containing the kidney, adrenal gland, perinephric fat, fibrous bridging septa, and a rich network of perirenal vessel and lymphatics. Perinephric space pathology may originate from within or outside the confines of the perirenal fascia. Most intrinsic perinephric space disease arises from the kidney or adrenal gland, and secondarily involves the perinephric space. Disease originating outside the cone of renal fascia may spread to the perinephric space via lymphatics (i.e., metastatic spread) or by directly transgressing perirenal fascial planes (e.g., invasive tumor or infections). Additionally, infiltrating soft tissue or rapidly accumulating retroperitoneal fluid may travel into or out of the perinephric space via perinephric bridging septa and renal fascia. In this article, we review the normal anatomy of the perinephric space and renal fascia, emphasizing the significance of retroperitoneal interfascial planes and perinephric bridging septa as a potential conduit for retroperitoneal disease spread. This review of normal anatomy and pathways of disease spread serves as background for a discussion of a variety of specific pathologic conditions that may involve the perinephric space and retroperitoneal fascia, including pancreatitis, retroperitoneal hematoma, urinoma, metastatic disease, and perirenal varices.
BACKGROUND: The purpose of the present study was to examine the histological consequences of the endoluminal exclusion of blood flow effected with stent graft technology. METHODS AND RESULTS: In 25-kg mongrel dogs, patulous vein patch infrarenal aortoplasty with iliac vein produces a fusiform abdominal aortic dilation (AAD). All aortic tributaries were preserved. Endoluminal exclusion via transfemoral placement of a thin-wall Dacron graft occurred 4 +/- 2 months later (n = 23). Balloon-expandable stents anchored the ends of the graft to the aorta. Hematoxylin and eosin, elastin van Gieson's, and Masson's trichrome staining was performed 6 and 12 months later at death. In control nongrafted AADs, the arterial portion of the AAD was lined by elastin -and collagen-rich intimal hyperplasia, and the venous portion developed medial hyperplasia containing collagen but little elastin. After stent graft placement, the stent struts and the graft were completely incorporated into an elastin-poor, collagen-rich neointima. Fibrosis of the vein patch was observed at 1 year. laminated thrombus did not form in the AAD until immediately after stent graft placement; flow arrest occurred in the space between the graft and the AAD intima despite the patent tributaries. At 6 and 12 months, microscopic recanalization was seen in this thrombus, although macroscopic flow was not discernible by duplex imaging or angiography. No AAD growth was measured. CONCLUSIONS: Aortic dilation was not observed at 1 year after stent graft placement within AADs with patent side branches despite microscopic evidence of thrombus recanalization. A collagen-rich and elastin-poor neointima incorporated the entire stent graft.
We studied the impact of an endoluminally placed stented aortic graft on the geometry of a surgically created abdominal aortic dilation (AAD) in nonatherosclerotic mongrel dogs. Patulous iliac vein patch infrarenal aortoplasty produced a fusiform AAD, doubling the aorta diameter. Lumbar and mesenteric aortic tributaries were preserved and no mural thrombus formed. AADs created in 23 dogs were endoluminally excluded through transfemoral placement of a thin-wall Dacron graft 4 +/- 2 months later. Balloon-expandable stents were used to anchor each end of the graft to the aorta. The graft was crimped radially in its body and longitudinally at its ends to provide longitudinal and radial expandability in these respective zones. Serial color duplex, angiography, and direct caliper measurements were made. Before graft placement, a 19% +/- 11% diameter growth was observed. At graft placement, flow arrest immediately occurred in the space between the graft and the AAD intima in all cases. Although microscopic recanalization of the thrombus in this space was seen at sacrifice 6 and 12 months later, no macroscopic duplex flow was imaged. A 10% +/- 11% reduction in AAD diameter was measured at 6 months (p < 0.001), with no further reduction at 12 months. Graft dimensions remained stable. No anastomotic leaks developed. AAD growth stopped during the first year after effective endoluminal exclusion in normotensive dogs despite patent side branches (< 1.5 mm internal diameter) and no mural thrombus at the time of graft placement. Whether microscopic recanalization of the thrombus that forms outside the graft has an impact after 1 year remains to be seen.
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Imaging plays a significant role in the management of Wilms tumor. Appropriate imaging continually must undergo refinement related to improvements in therapy and imaging modalities. We must recognize the need to demonstrate effectiveness in all phases of patient management and address the contentious issue of maximizing yield and minimizing cost.
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Hepatic ultrasonography was performed on 70 patients with the hepatic glycogen storage diseases (GSDs) to assess parenchymal echogenicity. 27 patients had GSD-I, 24 had GSD-III and 19 had GSDs-VI/IX; ages varied from 0.6 to 35.7 years (median 11.7). 31 (44%) had normal or mild parenchymal changes, and 41% (11/27) of those with GSD-I, 25% (6/24) with GSD-III and 11% (2/19) with GSDs-VI/IX had marked changes. No relationships were found between the ultrasonographic appearances and other indices of metabolic control, including plasma triglycerides, total cholesterol or height standard deviation score. Seven adult patients (21-29 years) were found to have hepatic tumours: six with GSD-I and one with GSD-III. Those with GSD-I and tumours tended to have the more severe hepatic parenchymal changes. We conclude that ultrasonography may be useful in identifying patients with GSD-I at risk of hepatic tumour formation.
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1. The contribution of activity in spinothalamic tract (STT) neurons to the pain and neurogenic hyperalgesia produced by an intradermal injection of 100 micrograms of capsaicin was investigated. Electrophysiological responses of identified STT neurons recorded in anesthetized monkeys were compared with psychophysical measurements of pain and hyperalgesia obtained in humans using identical stimuli. 2. Magnitude estimates of pain in humans were obtained after an injection of capsaicin or the vehicle. Capsaicin produced immediate burning pain that was most intense within 15 s after injection and then declined over the next 10-30 min. The vehicle produced no pain. 3. Cutaneous hyperalgesia to gentle stroking (allodynia) and also hyperalgesia to punctate stimulation developed in a wide area surrounding the capsaicin injection. Within this area, magnitude estimates of pain produced by a punctate stimulus (von Frey type with force of 225 mN) increased over preinjection values by an average of sixfold at test sites, 1, 2, and 3 cm away from the injection site. At the capsaicin injection site, magnitude estimates of pain in response to punctate simulation typically remained the same or were decreased. 4. After capsaicin, but not vehicle, the mean heat pain thresholds were lowered from approximately 45 degrees C before injection to 34 degrees C after, but only in the immediate vicinity of the injection site. At a site located 2 cm away, the thresholds were not significantly altered. Similarly, magnitude estimates of pain produced by suprathreshold heat stimuli were increased after capsaicin only at the injection site. 5. STT neurons were classified as high-threshold (HT) or wide-dynamic-range (WDR) cells according to responses evoked by graded cutaneous mechanical stimulation. An intradermal injection of capsaicin excited 4 of 7 HT cells and 10 of 12 WDR cells. The discharge rates of STT neurons correlated in time course with the magnitude estimates of pain in humans. The correlation was considerably better for WDR than for HT neurons, suggesting a predominant contribution of WDR neurons to the pain from capsaicin. 6. Capsaicin significantly increased the responses of HT neurons (9-fold) and the responses of WDR neurons (2-fold) to stroking the skin within the receptive field. Similar increases in responses to a standard punctate stimulus were observed at test sites, 1, 2, and 3 cm away from the injection site. After injection of vehicle, the responses to punctate stimulation increased by a mean of only 1.2- and 1.4-fold for HT and WDR neurons, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)
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The effects of bergapten-containing preparations in sunlight-induced skin pigmentation were evaluated. Oil and lotion vehicles with bergapten/UV-B sunscreen or sunscreen alone were applied to the backs of subjects twice weekly for 4 weeks and the subjects were exposed to gradually increasing doses of midday sunlight. The degree of skin darkening was assessed by clinical examination, reflectometry, and light microscopy of skin biopsy specimens. At 5 weeks, 1 week after the last sunlight exposure, the sites treated with either the bergapten/UV-B sunscreen lotion or the lotion vehicle were significantly darker than the sites treated with the sunscreen lotions without bergapten. Oil preparations produced less clearcut results, possibly because of a less potent sunscreen or because the bergapten did not leave the vehicle and absorb into the epidermis. In type I skin, the bergapten/sunscreen and the oil vehicle alone produced the same amount of tanning; both yielded more tanning than the sunscreen in oil by clinical examination. The findings were not confirmed by reflectometry or by light microscopy. Thus, we conclude that bergapten added to a UV-B sunscreen lotion preparation can increase skin pigmentation over the sunscreen alone when one is exposed to sunlight. The bergapten/UV-B sunscreen combination is a potentially useful product since one can develop a psoralen and UV-A-induced tan while being protected from UV-B-induced sunburn by the UV-B sunscreen incorporated into the formulation.
An adolescent girl with idiopathic hypothalamic dysfunction and hypopituitarism was treated with human growth hormone between 1969 and 1979, dying of parainfluenza pneumonia 2 months after her last hormone treatment. Although she had no signs of progressive neurologic disease, reexamination of autopsy material revealed a focus of spongiform change and astrogliosis in the corpus striatum. Thus, this growth hormone recipient, who died of intercurrent infection, was unexpectedly found to be in an early, preclinical phase of Creutzfeldt-Jakob disease.
A patient is described who presented with visual loss due to infiltration of the optic chiasm by chronic lymphocytic leukaemia. This case demonstrates intracranial infiltration as a primary presentation of chronic lymphocytic leukaemia without lymphoreticular involvement and, to our knowledge, is the first report of a chiasmal syndrome due to this lymphoproliferative disorder.