Rotatory dorsal subluxation of the navicular: a complication of clubfoot surgery

PURPOSE: We studied serum ELAM-1 levels in colon cancer patients. METHODS AND RESULTS: Serum ELAM-1 levels were significantly higher in 52 patients with colon cancer (mean +/- standard deviation, 69.3 +/- 28.6 U/ml) compared with 32 healthy volunteers (36.5 +/- 11.9 U/ml; P < 0.001). The mean serum ELAM-1 level in patients with metastatic tumors was significantly greater than that of patients with nonmetastatic tumors. Sensitivity and specificity of serum ELAM-1 elevation in detecting metastasis was 75 and 87.5 percent, respectively. Those of carcinoembryonic antigen and carbohydrate antigen 19-9 elevations were 71.4 and 62.5 percent and 35.7 and 91.7 percent, respectively. Twenty-five (89.3 percent) of 28 metastatic tumors showed either serum ELAM-1 or carcinoembryonic antigen elevation. There were weak but significant correlations found between serum ELAM-1 and carcinoembryonic antigen or carbohydrate antigen 19-9 levels. Moreover, serum ELAM-1 increased before detecting the recurrence by imaging in five of seven recurrent colon cancer patients. CONCLUSION: These findings suggest that serum ELAM-1 could be a useful tumor marker for colon cancer, especially in synchronous and metaclonous metastasis.     

Trends in rates of occupational fatal injuries in the United States (1983-92)

Recent advancements in laparoscopic surgery have made laparoscopic splenectomy possible. We retrospectively compared the outcomes of laparoscopic versus open splenectomy in patients with idiopathic thrombocytopenic purpura (ITP) or beta-thalassemia. From July 1993 to July 1997, 52 patients (ITP, 43 cases; beta-thalassemia, 9 cases) underwent either laparoscopic (30 patients, 9 men, 21 women; average age, 36.9 years) or conventional open splenectomy (22 patients, 5 men, 17 women; average age, 34.3 years). The two groups were similar in terms of sex, age, diagnosis, duration of disease, preoperative platelet count, and spleen size. The mean surgical time, estimated amount of blood loss, duration of postoperative recovery, analgesic usage, and complications were compared between the two groups. Laparoscopic splenectomy was successful in 29 (97%) of the 30 patients. The mean surgical time in the laparoscopy group was longer than in the open splenectomy group (190.6 vs 113.9 minutes, p < 0.01). The laparoscopy group had earlier postoperative oral intake (15.2 vs 52.6 hours, p < 0.01), less usage of analgesics (meperidine 50 mg/unit, 1.1 vs 2.8 units, p < 0.01) and a shorter postoperative hospital stay (4.1 vs 6.8 days, p < 0.01). The estimated blood loss, incidence of accessory spleen, surgical complication rate, and recurrence rate of thrombocytopenia were similar in the two groups. Our findings show that laparoscopic splenectomy in patients with ITP or beta-thalassemia is as safe as the open approach. While laparoscopy required a longer surgical time, the recovery period was shorter, analgesic use was less, and physical discomfort was less severe.     

Ischemia of the anterior vestibular artery (Lindsay-Hemenway syndrome). Review and comments

INTRODUCTION: The Lindsay and Hemenway syndrome is produced by ischemia in the territory of the anterior vestibular artery and is characterized by an initial episode of acute vertigo followed by benign paroxysmal positional vertigo and decreased or abolished caloric response. OBJECTIVE: To determine the incidence of anterior vestibular artery syndrome in patients with benign paroxysmal positional vertigo. DESIGN: A 3-year retrospective study (January 1994 to December 1996). SETTING: Patients with benign paroxysmal positional vertigo of the Zamora and Salamanca (Spain) health districts seen in two outpatients clinics. STUDY SUBJECTS: Ninety-eight patients with benign paroxysmal positional vertigo. RESULTS: Sixteen patients diagnosed as anterior vestibular artery syndrome were revised (16.3%). CONCLUSIONS: Although the literature is scarce, the incidence of Lindsay-Hemenway syndrome seems to be underestimated.     

Iodide suppression of major histocompatibility class I gene expression in thyroid cells involves enhancer A and the transcription factor NF-kappa B

A sexual dimorphism more marked than in living humans has been claimed for European Middle Pleistocene humans, Neandertals and prehistoric modern humans. In this paper, body size and cranial capacity variation are studied in the Sima de los Huesos Middle Pleistocene sample. This is the largest sample of non-modern humans found to date from one single site, and with all skeletal elements represented. Since the techniques available to estimate the degree of sexual dimorphism in small palaeontological samples are all unsatisfactory, we have used the bootstraping method to asses the magnitude of the variation in the Sima de los Huesos sample compared to modern human intrapopulational variation. We analyze size variation without attempting to sex the specimens a priori. Anatomical regions investigated are scapular glenoid fossa; acetabulum; humeral proximal and distal epiphyses; ulnar proximal epiphysis; radial neck; proximal femur; humeral, femoral, ulnar and tibial shaft; lumbosacral joint; patella; calcaneum; and talar trochlea. In the Sima de los Huesos sample only the humeral midshaft perimeter shows an unusual high variation (only when it is expressed by the maximum ratio, not by the coefficient of variation). In spite of that the cranial capacity range at Sima de los Huesos almost spans the rest of the European and African Middle Pleistocene range. The maximum ratio is in the central part of the distribution of modern human samples. Thus, the hypothesis of a greater sexual dimorphism in Middle Pleistocene populations than in modern populations is not supported by either cranial or postcranial evidence from Sima de los Huesos.     

Analysis of neurological sequelae from radiosurgery of arteriovenous malformations: how location affects outcome

The present study evaluated the clinical significance of hepatocyte growth factor (HGF) in patients with pulmonary fibrosis. Twenty-one patients with a diagnosis of pulmonary fibrosis [14 with idiopathic pulmonary fibrosis (IPF) and seven with pulmonary fibrosis associated with a collagen vascular disorder (PF-CVD]) and 21 normal subjects as control were studied. HGF levels in sera of patients with pulmonary fibrosis (0.34 +/- 0.02 ng ml-1) were elevated significantly as compared with normal subjects (0.21 +/- 0.01 ng ml-1) (P < 0.0001). HGF/albumin levels in broncho-alveolar lavage fluid (BALF) of patients with pulmonary fibrosis (72 +/- 17 ng g-1 albumin) were also significantly elevated as compared with normal subjects (under the detection limit) (P < 0.01). HGF levels in sera correlated significantly with elastase levels in sera and C-reactive protein, and correlated negatively with PaO2. HGF levels in sera were significantly higher in smokers with pulmonary fibrosis (0.42 +/- 0.03 ng ml-1) as compared with non-smokers with pulmonary fibrosis (0.29 +/- 0.03 ng ml-1) (P < 0.005). HGF/albumin levels in BALF correlated significantly with elastase/albumin levels in BALF, lactate dehydrogenase/albumin in BALF, Immunoglobulin A/albumin in BALF, total cell count/albumin in BALF, total number of alveolar macrophage/albumin in BALF, total number of neutrophil/albumin in BALF, CEA/albumin in BALF, CA19-9/albumin in BALF, and SCC/albumin in BALF. These results suggest that following lung injury, HGF may be a mediator involved in the repair which leads to pulmonary fibrosis.     

Monocytes from Wiskott-Aldrich patients display reduced chemotaxis and lack of cell polarization in response to monocyte chemoattractant protein-1 and formyl-methionyl-leucyl-phenylalanine

Wiskott-Aldrich syndrome (WAS) is an X-linked disorder characterized by trombocytopenia, eczema, and progressive decline of the immune function. In addition, lymphocytes and platelets from WAS patients have morphologic abnormalities. Since chemokines may induce morphologic changes and migration of leukocytes, we investigated the monocyte response to chemoattractants in cells from WAS patients with an identified mutation in the WAS protein gene. Here, we report that monocytes derived from four patients with molecularly defined typical WAS have a severely impaired migration in response to FMLP and to the chemokines monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1alpha compared with normal donors. Conversely, neither MCP-1 binding to monocytes nor induction of the respiratory burst by MCP-1 and FMLP is significantly different between WAS patients and normal donors. Within a few minutes of stimulation, monocytes respond to chemokines with increased expression of adhesion molecules and with morphologic changes such as cell polarization. Although up-regulation of CD11b/CD18 expression following stimulation with FMLP or MCP-1 is preserved in WAS patients, cell polarization is dramatically decreased. Staining of F-actin by FITC-phalloidin in monocytes stimulated with chemoattractants shows F-actin to have a rounded shape in WAS patients, as opposed to the polymorphic distribution of F-actin in the polarized monocytes from healthy donors. These results suggest that WAS protein is involved in the monocyte response to the chemokines MCP-1 and macrophage inflammatory protein-1alpha.     

Characterization of the effect of 2-deoxy-D-glucose(2-DG) on the immune system

This study was designed to characterize the effects of the metabolic stress of administration of 2-deoxy-d-glucose (2-DG, 500 mg/kg) on immune function. Male Lewis rats were exposed to one or five injections (one every 48 h) of 2-DG. Control rats received saline injections. Administration of 2-DG induced a reduction of total leukocytes in the spleen, thymus, and blood. The reduction was most prominent in animals that received five injections of 2-DG. The ratio of CD4(+)/CD8(+) in the spleen was decreased due to a significant increase of CD8(+) T-cell subpopulation. Additionally, 2-DG induced a suppression of mitogenic responsiveness and IFN-gamma production in both whole blood and spleen lymphocytes. The production of IL-1 and IL-2 was significantly reduced in the blood, but not in the spleen. Conversely, there was a significant increase in nitric oxide production in cultures of Con A-, PHA-, and LPS-stimulated splenocytes from 2-DG-injected animals compared with saline-injected controls. In blood cultures stimulated with Con A and PHA, the nitric oxide production of the group that received five injections of 2-DG was significantly higher than in the group that received one injection of 2-DG or saline. These results demonstrated that the metabolic stress 2-DG induced a downregulation of Th 1 cellular immune function in a manner similar to physical and psychological stressors. Additionally, the use of 2-DG in rats provided an important model with which to study metabolic stress.