Pars plana vitrectomy in the management of dislocated posterior chamber lenses.
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Biomedical subjects
Publications and source records attributed to T G Murray.
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We studied collagen shield heparin delivery to the rabbit eye utilizing radiolabeled heparin as well as a fibrin inhibition assay. Radiolabeled heparin studies revealed significant tritium delivery to the cornea, aqueous, and iris, with only trace levels detectable for the lens, vitreous, and sclera. An aqueous fibrin inhibition assay revealed that a single collagen shield soaked in heparin achieved anterior chamber anticoagulant levels that paralleled the time course of the radiolabeled heparin delivery and resulted in fibrin inhibition during the 6-hour study period. Subconjunctival heparin injection did not alter baseline aqueous anticoagulant activity. No complications related to collagen shield heparin delivery were encountered. These studies suggest that a heparin-hydrated collagen shield may prevent postoperative fibrin formation in eyes at risk for this complication, including eyes undergoing surgery for the complications of proliferative diabetic retinopathy proliferative vitreoretinopathy, and glaucoma filtration surgery.
We adapted a 27-gauge, 0.75-in needle for the placement of iris fixation sutures. The needle requires neither the formation of a paracentesis nor a sclerotomy site. Additionally, the self-sealing nature of the needle tract eliminates the need for closure of the entry site. We have found this instrument to be helpful in the rapid, atraumatic placement of iris fixation sutures.
In order to evaluate potential risk factors for the development of hospital-acquired acute renal failure, a case-control study was performed, comparing patients with hospital-acquired acute renal failure with control subjects matched on age, sex, hospital, service of admission, and baseline renal function. The same patients were then reanalyzed utilizing a cohort study design to investigate outcomes from this syndrome. The following elevated odds ratios (95 percent confidence interval) were found while simultaneously adjusting for possible confounding variables using logistic regression: volume depletion, 9.4 (2.1 to 42.8); aminoglycoside use, 5.6 (1.3 to 23.7); congestive heart failure 9.0 (2.1 to 38.9); radiocontrast exposure, 4.9 (1.2 to 19.7); and septic shock, approached infinity, p less than 0.0001. The effect of volume depletion was markedly accentuated in those with diabetes (odds ratio = 1.9) (p less than 0.05). The risk from aminoglycoside use markedly increased with increasing age (p less than 0.002). Finally, the development of hospital-acquired acute renal failure was associated with a marked increase in the risk of dying--the relative risk (95 percent confidence interval) was 6.2 (2.6 to 14.9)--and a marked increase in length of stay, from a median of 13 days in control subjects to a median of 23 days in case subjects (p = 0.005). In conclusion, hospital-acquired acute renal failure is a serious illness. Attempts to prevent it should focus on proved risk factors.
A 5-month-old infant with spondyloepiphyseal dysplasia congenita (SEDC) died after an anoxic episode. Ophthalmologic examination one month before death revealed marked myopia and a normal ophthalmoscopic examination, without evidence of retinal detachment, lattice degeneration, or vitreoretinal changes. On postmortem histopathologic and electron microscopic examination of the eyes, we found the vitreous to have central liquefaction, to be detached in multifocal areas, and exerting traction on the retina. The internal limiting membrane of the retina was thin throughout and displayed many areas of discontinuity. There were multiple areas of preretinal cellular proliferation and a few small areas of retinoschisis. Our observation of extensive vitreoretinal degeneration with traction of the retina indicates that eyes of patients with SEDC are at an increased risk for the development of retinal detachment.
We studied the molecular composition of the complement C5b-9 complex required for optimal killing of Escherichia coli strain J5. J5 cells were incubated in 3.3%, 6.6%, or 10.0% C8-deficient serum previously absorbed to remove specific antibody and lysozyme. This resulted in the stable deposition after washing of 310, 560, and 890 C5b67 molecules per colony-forming unit, respectively, as determined by binding of 125I-labeled C7. Organisms were then incubated with excess C8 and various amounts of 131I-labeled C9. Plots of the logarithm (base 10) of E. coli J5 cells killed (log kill) vs. C9 input were sigmoidal, confirming the multihit nature of the lethal process. When C9 was supplied in excess, 3300, 5700, and 9600 molecules of C9 were bound per organism for cells bearing 310, 560, and 890 C5b-8 complexes, respectively, leading to C9-to-C7 ratios of 11.0:1, 10.8:1, and 11.4:1 and to log kill values of 1.3, 2.1, and 3.9. However, at low inputs of C9 that lead to C9-to-C7 ratios of less than 3.3:1, no killing occurred, and this was independent of the number of C5b-9 complexes bound. Formation of multimeric C9 at C9-to-C7 ratios permissive for killing was confirmed by electron microscopy and by binding of 125I-labeled antibody with specificity for multimeric but not monomeric C9. These experiments are the first to demonstrate a biological function for C9 polymerization and suggest that multimeric C9 is necessary for optimal killing of E. coli J5 cells by C5b-9.
The histologic effects of various Neodymium:YAG laser energy levels were evaluated after iridotomy formation in cynomolgus monkey eyes. Scanning election microscopy of the corneal endothelium above the treated areas revealed no significant cell loss or pleomorphism when compared to the adjacent untreated areas. Light and phase contrast microscopy demonstrated closure of the iridotomies in most cases by a bridge of iris pigment epithelium. In several specimens, stromal tissue and pigment laden cells were present over the attenuated iris pigment epithelium. There were four lens opacities with rupture of the anterior lens capsule and anterior epithelial cell hyperplasia in one. No damage was apparent in the trabecular meshwork or retina with light microscopy or fluorescein angiography.
In a prospective study the Nd:YAG laser was used to create iridotomies in cynomolgus monkeys, using various levels of energy and pulse-trains of 1 to 9. Although no change occurred in the endothelial cell count of the cornea, opacities of the corneal endothelium and lens did occur. In addition, one eye showed rupture of the anterior lens capsule immediately behind the iridotomy. Most of the iridotomies in these animals closed within 3 to 4 weeks. Attenuated pigment epithelium bridged the gap within 9 days and in many sections it appeared that the iridotomies closed by fibrous contraction or early stromal regeneration. A prospective short-term clinical study evaluated argon and Q-Nd:YAG laser iridotomies in 42 eyes of 21 patients with primary chronic angle-closure glaucoma. In each patient one eye was randomly treated with an argon laser iridotomy and the fellow eye with a Nd:YAG laser iridotomy. In every case a patent iridotomy was created in one session. A mean of 12 +/- 11 and 0.033 +/- 0.025 Joules was required to complete an iridotomy with the argon and Nd:YAG lasers, respectively. Thirty percent of the argon iridotomies became sufficiently closed with pigment to require retreatment; whereas none of the Nd:YAG iridotomies closed. A postoperative rise in IOP greater than 10 mm Hg was seen in 38% argon- and 29% Nd:YAG-treated eyes. Although bleeding around the iridotomy occurred in 48% of eyes, in no case was this of significant consequence. No acute lens damage was observed in the Nd:YAG-treated human eyes, while 43% of lenses in the argon group had focal opacities. Thirty-three percent of Nd:YAG- and 24% of argon-treated eyes had focal, nonprogressive corneal opacities above the iridotomy. Specular microscopy showed a significant central corneal epithelial cell loss in argon laser eyes only. The potential of creating a laser iridotomy with a single burst of energy is extremely attractive and worthy of further investigation.
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A case-control study of the relationship between regular analgesic consumption and end-stage renal disease (ESRD) development was conducted and was made up of 527 patients with ESRD and 1,047 matched controls from southeastern Pennsylvania and southern New Jersey. The study was unable to demonstrate an increased risk of ESRD associated with use of analgesics either as single compounds or in combinations. In addition, no consistent dose or duration relationship was shown for users of specific analgesic combinations or for single compounds. We suggest that if there is an association between the use of analgesics and ESRD development, the risk is not large or at least not large in the geographic area where the study was carried out.
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Effects of renal insufficiency and age on oxazepam kinetics were assessed in 13 normal subjects (21 to 72 yr old), four patients with renal insufficiency, and eight patients on hemodialysis. Normal intact oxazepam results were: mean elimination half-life (t1/2), 10 hr; area under the curve (AUC), 6.0 microgram.hr/ml; unbound oxazepam fraction (fup), 3.2%; maximum concentration of unbound oxazepam (Cmax,u), 16 ng/ml; and intrinsic (unbound drug) clearance (Clint), 2.9 l/hr/kg. Less than 1% of the dose was excreted intact in urine. Age differences had no influence on results. In renal insufficiency patients, t1/2 was prolonged to 25 hr, fup increased to 7%, and Cmax,u and Clint were unchanged. Volume of distribution of unbound oxazepam (Vu) increased, thereby prolonging t1/2. In dialysis patients, t1/2 was prolonged to 33 hr, fup increased to 6.2%, and Cmax,u and Clint again were unchanged. Oxazepam was undialyzable; since unbound oxazepam disposition kinetics are not altered, no dosage adjustment for patients is necessary.
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An anephric patient undergoing hemodialysis experienced an increase in his hematocrit value (19 +/- 1 per cent to 31 +/- 1 per cent) as a result of increased erythropoiesis (reticulocyte count 1.8 per cent to 7.4 per cent). This increase occurred in concert with an elevation of the patient's liver enzyme levels and was maintained for four months. The hematocrit value returned to its base line only after the liver function tests showed improvement. During the period when the hematocrit value was increasing, the circulating level of erythropoietin was elavated to 71.0 mU/ml--a level higher than that seen in either anephric or nephric patients undergoing dialysis. When the hematocrit value and liver enzyme levels had returned to their base line values, the erythropoietin level was 4.3 mU/ml--a level in the range seen in anephric patients undergoing dialysis. The observations in this patient suggest that under certain circumstances, the liver can produce erythropoietin in the anephric patient; and, more importantly, that the bone marrow of at least some uremic patients is capable of responding to the endogenous erythropoietin.
Ticrynafen was given to 6 anephric patients undergoing maintenance hemodialysis. Ticrynafen was given daily for the 3 days between hemodialyses. Ticrynafen had no effect on the interdialysis rise in serum uric acid levels. Ticrynafen did not accumulate in serum, but levels of metabolites continued to rise over the 3 days. Hemodialysis (5 hr) reduced levels of ticrynafen by 38% but had less effect on metabolite levels. There was no effect on serum cholesterol or triglycerides.
The plasma and 24-hr urinary levels of cyclic adenosine 3':5'-monophosphate and of cyclic guanosine 3':5'-monophosphate (cGMP) were determined for 19 healthy normal patients, 54 patients with six types of nonneoplastic diseases (cholelithiasis, peptic ulcer, coronary heart disease, hypertension, regional ileitis, and cirrhosis), and 54 patients with five types of neoplastic disease (cancers of the lung, colon, and breast, acute myelocyte leukemia, and Hodgkin's disease). The cyclic adenosine 3':5'-monophosphate levels of urine and plasma in normal subjects, in noncancer subjects, and in cancer subjects did not differ significantly. The cGMP levels in the noncancer group were similarly unchanged from those in the normal group. However, mean cGMP levels in the urine and plasma of patients with neoplastic diseases were, respectively, 2- and 3-fold greater than the normal values (p less than 0.005 for urine and p less than 0.05 for plasma). Pharmacokinetic studies with [3H]cGMP in nine healthy controls and 15 patients with neoplasia showed that the mean production rate of this nucleotide in patients with metastatic cancer was elevated when compared to normal patients, but many values fell within the normal range. In acute leukemia, the production rate was seven times normal, with four of five patients having values clearly outside the normal range. The plasma clearance rate in patients with neoplasia was not decreased when compared to that in normal patients. It is proposed that an increased production rate, rather than any change in plasma clearance, accounts for the increased levels of cGMP in the plasma and urine of some patients with neoplastic disease.
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