Optical coherence tomography: its clinical use for the diagnosis, pathogenesis, and management of macular conditions.

BACKGROUND: Optical coherence tomography (OCT) is a noninvasive, noncontact transpupillary imaging technology that can image retinal structures in vive with a resolution of up to 10 microns. Anatomic layers within the retina can be differentiated and retinal thickness measured. The objective is to demonstrate clinical viability and useful interpretation of macular images derived from a commercially available OCT instrument. MEHODS: A Stratus OCT (Zeiss-Humphrey, Dublin, California) imaging system was used to evaluate several pathological presentations of the macula in selected patients. Conditions illustrated in this case series were macular holes, epiretinal membranes, macular edema, idiopathic central serous choroidopathy, detachments of pigment epithelium and sensory retina, choroidal neovascular membranes, and retinal vascular occlusions. CONCLUSIONS: Acquired OCT images achieved structural information regarding anatomical characteristics of the conditions scanned. A cross-sectional resolution of 10 microns was accomplished, which is 10 times greater than current ultrasound. OCT provides important information that may be critical in the diagnosis and management of some ocular conditions. Its high-resolution scans may contribute to the better understanding of disease pathogenesis, as well as assistance in or confirmation of a diagnosis. This imaging technology provides important information beyond what can be seen on clinical examination, and offers a useful adjunct to other diagnostic imaging tools such as fundus photography, fluorescein angiography, and indocyanine green angiography.     

The porous coated anatomic total hip replacement. A ten to fourteen-year follow-up study of a cementless total hip arthroplasty

BACKGROUND: We previously reported our two and five-year results of arthroplasty with the Porous Coated Anatomic total hip prosthesis. We now report on the performance of this prosthesis at ten to fourteen years. METHODS: The results of 311 total hip replacements in which a Porous Coated Anatomic prosthesis was inserted without cement in 279 patients were analyzed prospectively. The average age of the patients at the time of the replacement was sixty--one years (range, twenty to eighty-one years). Sixty-four patients (seventy-six hips) died postoperatively. Forty-five patients (forty-seven hips) were lost to follow-up, and four were excluded because of their medical condition. One hundred and sixty-eight patients (187 hips) were followed for ten to fourteen years (average, twelve years). Seventeen of those patients (seventeen hips) had a revision. RESULTS: The overall survival rate (with any revision as the end point) was 90.0% +/- 5.4% at fourteen years, with an average Harris hip score of 85 +/- 14 points. The prevalence of thigh pain was 36% (fifty-six of 157) in the late period (more than ten years postoperatively). Radiographs showed stable fixation, with bone ingrowth, of 83% (130) of the 156 acetabular components and 88% (137) of the 156 femoral components at the latest follow-up evaluation. Men had a significantly higher rate of femoral osteolysis than did women (p < 0.001). The rates of acetabular and femoral osteolysis associated with 32-mm femoral heads (49% [twenty-three] of forty-seven and 70% [thirty-three] of forty-seven, respectively) were significantly higher (p < 0.01) than those associated with 26-mm heads (26% [twenty-eight] of 109 and 30% [thirty-three] of 109, respectively). Despite this, revision (removal or exchange of components) was not directly related to head size; instead, it was related to polyethylene thickness. CONCLUSIONS: There have been persistent problems with the Porous Coated Anatomic hip system, including thigh pain and an increasing prevalence of osteolysis with time. Revision because of aseptic loosening was related more to the thickness of the polyethylene liner than to the size of the femoral head. Femoral heads with a 32-mm diameter did not increase the risk for revision provided that an adequate thickness of polyethylene had been used.     

Referred phantom sensations and cortical reorganization after spinal cord injury in humans

To test the hypothesis that cortical remapping supports phantom sensations, we examined referred phantom sensations and cortical activation in humans after spinal-cord injury (SCI) at the thoracic level (T3-T12). Of 12 SCI subjects, 9 reported phantom sensations, and 2 reported referred phantom sensations. In both of these subjects, referred phantom sensations were evoked by contact in reference zones (RZ) that were not adjacent in the periphery and were not predicted to be adjacent in the postcentral gyrus (PoCG), suggesting that representations separated by centimeters of cortical space were simultaneously engaged. This finding was supported by functional MRI (fMRI). In a subject with a T6-level complete SCI, contact in RZ on the left or right forearm projected referred phantom sensations to the ipsilateral chest. During fMRI, contact in either forearm RZ evoked activity in the central PoCG (the position of the forearm representation) and the medial PoCG (the position of the chest representation) with >/=1.6 cm of nonresponsive cortex intervening. In contrast, stimulation in non-RZ forearm and palm regions in this subject and in lesion-matched SCI subjects evoked central but not medial PoCG activation. Our findings support a relation between PoCG activation and the percept of referred phantom sensations. These results, however, present an alternative to somatotopic cortical reorganization, namely, cortical plasticity expressed in coactivation of nonadjacent representations. The observed pattern suggests that somatotopic subcortical remapping, projected to the cortex, can support perceptual and cortical reorganization after deafferentation in humans.     

Loss of tumor-promoting activity of unleaded gasoline in N- nitrosodiethylamine-initiated ovariectomized B6C3F1 mouse liver

Unleaded gasoline (UG) vapor (2056 ppm) increased the incidence of liver tumors in a chronic bioassay and exhibited tumor-promoting activity in N-nitrosodiethylamine (DEN)-initiated female mouse liver. Estrogen inhibited mouse liver tumor development and the hepatocarcinogenic and tumor-promoting dose of UG produced uterine changes suggestive of estrogen antagonism. To directly test the hypothesis that UG-induced tumor-promoting ability is secondary to its interaction with the mouse liver tumor inhibitor, estrogen, we compared the tumor-promoting ability of UG in ovariectomized (Ovex) mice with the hepatic tumor-promoting ability of UG in intact mice. Ovaries were surgically removed at 4 weeks of age. Exposure to wholly vaporized UG (2018 ppm) under bioassay and tumor-promoting conditions began at 8 weeks of age. After 4 months of exposure, UG increased relative liver weight and hepatic microsomal cytochrome P450 pentoxyresourfin-O- dealkylase and ethoxyresorufin-O-deethylase activity to a similar extent in intact and Ovex mice. Non-focal hepatocyte proliferation, as measured by the incorporation of bromo-deoxyuridine, was not changed by UG exposure and was similar in all treatment groups. After 4 months of exposure to DEN-initiated mice, UG significantly increased the volume fraction of liver occupied by foci (three-fold) as compared to control intact mice. As expected, volume of foci was elevated in DEN/Ovex/control mice as compared to DEN/intact/control mice. In DEN/Ovex mice UG did not significantly increase the focal volume fraction. Thus, the tumor promoting activity of UG, as demonstrated by increased volume fraction of liver occupied by hepatic foci in intact mice, is greatly attenuated in Ovex mice. The volume fraction data in Ovex mice support the hypothesis that the tumor promoting activity of UG is dependent upon the interaction of UG with ovarian hormones. These data also indicate that hepatic microsomal cytochrome P450 PROD and EROD induction, hepatomegaly and non-focal hepatic LI are not specific markers of hepatic tumor promoting activity of UG.      

Chemoprevention of spontaneous tumorigenesis in nullizygous p53- deficient mice by dehydroepiandrosterone and its analog 16alpha-fluoro- 5-androsten-17-one

Transgenic mice with both alleles of the p53 tumor suppressor gene product 'knocked out' by gene targeting are susceptible to early development of tumors, chiefly lymphomas and sarcomas. Compared with the control group, administration of dehydroepiandrosterone (DHEA) at 0.3% of the diet to male p53-deficient mice extended their lifespan by delaying death due to neoplasms (from 105 to 166 days on study, P = 0.002), primarily by suppressing lymphoblastic lymphoma (from 45 to 6% of neoplastic deaths, P = 0.010). Treatment with a synthetic DHEA analog, 16alpha-fluoro-5-androsten-17-one (compound 8354), at 0.15% of the diet also increased lifespan, to 140 days for mice that developed tumors (P = 0.037). The effects of these steroids on lifespan and tumor development did not appear to be strongly related to inhibition of food consumption and weight gain, in that a group pair-fed with control diet to the reduced food consumption of the DHEA-treated group developed and died of the same types of neoplasms at the same rate as the controls fed ad libitum. The chemopreventive effect of these steroids has been proposed to be due to suppression of DNA synthesis by inhibition of glucose 6-phosphate dehydrogenase, the rate-limiting enzyme of the pentose phosphate pathway. Although DHEA and its analog are strong non- competitive inhibitors of this enzyme in vitro, treatment with DHEA did not deplete cellular nucleotide pools in the liver, as would have been predicted. The chemopreventive effect of DHEA in this model may be due to steroid-induced thymic atrophy and suppression of T cell lymphoma, permitting these mice to survive long enough to develop tumors with longer latency.      

Mitomycin-C induced hemolytic uremic syndrome: a case report and literature review

Hemolytic uremic syndrome spontaneously arises in a few patients with advanced cancer, but it is more commonly related to the use of certain chemotherapeutic agents. Mitomycin-C is, etiologically, the most common causative agent inducing hemolytic uremic syndrome, in a dose dependent manner. We report this syndrome, attributable to mitomycin-C at a cumulative dose of 40 mg/m2, in a gastric cancer patient. A 42-year-old female with stage III gastric cancer underwent radical gastrectomy and was given mitomycin-C at 10 mg/m2 intravenously every four weeks as adjuvant therapy. Hemolytic uremic syndrome was diagnosed three months after the last dose of mitomycin-C administration. The most prominent symptoms included pallor, hypertension and anasarca, with laboratory evidence of microangiopathic hemolytic anemia, azotemia and hyperkalemia. Her disease was progressive, but fortunately stabilized after staphylococcus column A dialysis. Her disease remained in remission for 24 months from the time of diagnosis, and then relapsed in the form of peritoneal carcinomatosis with partial intestinal obstruction.