Role of medical capsule and transverse metatarsal ligament in hallux valgus deformity

The role of the medial capsule and transverse metatarsal ligament in hallux valgus deformity including stability of the first metatarsophalangeal and adjacent joints was investigated in vitro. The three-dimensional positions of the proximal phalanx, first metatarsal, and second metatarsal before and after sectioning the medial capsule and metatarsal ligament were measured using a magnetic tracking system. Valgus deformity of the hallux increased with medial capsule sectioning an average of 22.3 degrees +/- 6 degrees. Valgus deformity of the hallux increased with medial capsule and metatarsal ligament sectioning an average of 27.4 degrees +/- 9.1 degrees. Valgus deformity of the hallux did not change significantly after sectioning the metatarsal ligament only. No significant changes were found in varus and eversion of the first metatarsal, in valgus of the second metatarsal, in the distance between first and second metatarsal heads after sectioning the medial capsule, or in the metatarsal ligament. This study shows the importance of the medial capsule in hallux valgus deformity. The transverse ligament did not contribute substantially to cause the deformity.     

Effect of phenylglyoxal-modified alpha2-antiplasmin on urokinase-induced fibrinolysis

1. In this study the mechanisms of the acute vasodilator action of bacterial lipopolysaccharide (LPS) were investigated in the rat Langendorff perfused heart. 2. Infusion of LPS (5 microg ml(-1)) caused a rapid and sustained fall in coronary perfusion pressure (PP) of 59 +/- 4 mmHg (n = 12) and a biphasic increase in NO levels determined in the coronary effluent by chemiluminescent detection. Both the fall in PP and the increase in NO release were completely abolished (n = 3) by pretreatment of hearts with the NO synthase inhibitor L-NAME (50 microM). 3. LPS-induced vasodilatation was markedly attenuated to 5 +/- 4 mmHg (n 3) by pretreatment of hearts with the B2 kinin receptor antagonist Hoe-140 (100 nM). 4. Vasodilator responses to LPS were also blocked by brief pretreatment with mepacrine (0.5 microM, n = 3) or nordihydroguaiaretic acid (0.1 microM, n = 4) and markedly attenuated by WEB 2086 (3 microM, n = 4). 5. Thirty minutes pretreatment of hearts with dexamethasone (1 nM), but not progesterone (1 microM), significantly modified responses to LPS. The action of dexamethasone was time-dependent, having no effect when applied either simultaneously with or pre-perfused for 5 min before the administration of LPS but inhibiting the response to LPS by 91 +/- 1% (n = 4) when pre-perfused for 15 min. The inhibition caused by dexamethasone was blocked by 15 min pretreatment with the glucocorticoid receptor antagonist RU-486 (100 nM) or by 2 min pre-perfusion of a 1:200 dilution of LCPS1, a selective antilipocortin 1 (LC1) neutralizing antibody. 6. Treatment with the protein synthesis inhibitor, cycloheximide (10 microM, for 15 min) selectively blunted LPS-induced vasodilatation, reducing the latter to 3 +/- 5 mmHg (n = 3), while having no effect on vasodilator responses to either bradykinin or sodium nitroprusside. 7. These results indicate that LPS-induced vasodilatation in the rat heart is dependent on activation of kinin B2 receptors and synthesis of NO. In addition, phospholipase A2 (PLA2) is activated by LPS resulting in the release of platelet-activating factor (PAF) and lipoxygenase but not cyclo-oxygenase products. These effects are dependent on de novo synthesis of an intermediate protein which remains to be identified.     

Sequence alterations of insulin-like growth factor binding protein 3 in neoplastic and normal gastrointestinal tissues

Insulin-like growth factor binding protein 3 (IGFBP-3) is an important regulator of normal and malignant cell growth. It modulates the mitogenic effects of insulin-like growth factors (IGFs) by inhibiting growth through mechanisms both dependent on and independent of IGF binding. IGF-I and IGF-II levels are regulated by binding to the IGF-II receptor, which is inactivated by mutation in human gastrointestinal (GI) tumors. We have previously demonstrated elevated IGF-II ligand expression in IGF-II receptor-mutant GI tumors, implicating the IGF signaling system in GI tumorigenesis. Therefore, to investigate the potential involvement of IGFBP-3 in human GI carcinogenesis, direct DNA sequencing of exons 1-4 and intron-exon boundaries of the IGFBP-3 gene was performed in 10 colorectal cancers, 10 gastric cancers, and 10 esophageal cancers. Four distinct sequence alterations were identified: (a) in one gastric and one esophageal tumor, an A to C transversion occurred at nucleotide 5795 (CAC-->CCC), leading to a His-->Pro substitution at codon 179; (b) a second esophageal tumor had a C to T transition at nucleotide 8291 (ACC-->ATC), leading to a Thr-->Ile substitution at codon 277 of IGFBP-3; (c) one alteration comprised a G to C transversion in exon 1 at nucleotide 2132 (GGG-->GCG), leading to a Gly-->Ala substitution at codon 32 in two gastric cancers, seven esophageal cancers, and nine colon cancers; and (d) a C to G transversion located 17 nucleotides from the 3' splice site in intron 1 was observed in three colon cancers and four esophageal cancers. All of these DNA sequence alterations were present in matched normal DNA from the same subjects, which suggests that some or all of them may represent polymorphisms. However, we cannot exclude the possibility that the germ-line nonconservative amino acid substitutions predicted to occur as a result of these alterations result in subtle changes to IGFBP-3 protein function and a predisposition to developing GI malignancy.     

Noncirrhotic portal hypertension and nodular regenerative hyperplasia of the liver in dogs with mucopolysaccharidosis type I

Seventy six consecutive patients with T2-4, N0-1, M0 primary breast cancer (BC) received a median of 3 cycles of CMF (cyclophosphamide, methotrexate, 5-fluorouracil) regimen. Tamoxifen was concomitantly administered in patients with estrogen receptor positive (ER+) BC. Ki67 antigen was evaluated immunohistochemically in tumor specimens obtained before chemotherapy and at mastectomy. At post chemotherapy evaluation, tumor shrinkage greater than 50% was obtained in 60 patients (78.9%), 21 of them being complete responders (27.6%). As a whole, primary chemotherapy significantly decreased the number of Ki67 positive cells. More than 50% decrease in Ki67 expression was observed in 78.9% of patients attaining a clinical complete response (CR), in 44.7% of patients with partial remission (PR) and in 50.0% of non-responders, while an increase (>25%) in Ki67 expression was found in 5.3%, 18.4% and 18.7% of patients with CR, PR and non-response, respectively. Both CR and PR rates were superimposable in patients with ER+ and ER- primary BC, while the reduction in Ki67 expression was mainly found in ER+ cases. Patients with increased Ki67 expression from baseline, at the end of primary chemotherapy, had a shorter disease-free interval (70 months) with respect to patients with no change (88+ months) or decrease (87+ months), p<0. 05. To conclude, the activity of CMF + tamoxifen in primary BC does not seem superior to that expected administering CMF alone. The reduction in Ki67 expression, as a whole, correlated with clinical CR, but some individual discrepancies between tumor shrinkage and Ki67 pattern have been observed. The Ki67 reduction mainly confined to the ER+ primary BC suggests that tumor response in this subset may be linked to the reduction in proliferation activity, whereas other mechanisms such as apoptosis might be responsible for the tumor shrinkage in ER- tumors. Since the increase in proliferation activity after primary chemotherapy was associated with a greater recurrence rate and lower disease free interval, irrespective of tumor response, changes in proliferation activity after primary chemotherapy may represent a potentially available parameter that, in addition to the tumor response, can discriminate patients who would benefit from the cytotoxic treatment from patients who would not.     

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.     

Retrograde coronary venous infusion of ethanol for ablation of canine ventricular myocardium

INTRODUCTION: Permanent cure of reentrant ventricular tachycardia (VT) associated with coronary artery disease is difficult to achieve. Retrograde coronary venous infusion of ethanol for ablation of ventricular myocardium associated with reentrant tachyarrhythmias has several potential advantages, including use of physiologic mapping techniques and production of deeper, wider necrotic zones. METHODS AND RESULTS: Nine anesthetized dogs had baseline hemodynamic measurement, left ventriculography, coronary arteriography, occlusive coronary venography, and programmed electrical stimulation of the right ventricular apex and outflow tract. A balloon-tipped infusion catheter was advanced into a distal coronary venous branch, the balloon slowly inflated, and pure ethanol infused at volumes of 1.5, 3, or 5 cc. Hemodynamic measurements, angiography, ventriculography, and programmed electrical stimulation were repeated immediately and 1 week following ablation. Formalin-perfused hearts were serially sectioned and lesion volumes determined. Histologic examination of ablation beds then was performed. No significant difference was found in any hemodynamic measurement before or after ablation. Coronary arteriograms and left ventriculograms were unchanged after ablation. Nonsustained VT occurred in eight dogs during ethanol infusion; however, VT was not inducible in any dog before or after ablation. Infusion volumes of 3 cc or more were required to produce transmural lesions. CONCLUSION: Retrograde coronary venous infusions of ethanol using a balloon-tipped infusion catheter were effective in ablating ventricular myocardium. Retrograde chemical ablation did not itself result in inducible VT or adversely affect hemodynamic measurements or coronary arteries. Transmural myocardial necrosis, necessary in the ablation of VT associated with coronary artery disease, can be produced by higher infusion volumes.     

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.     

Low-frequency vibrations in the treatment of patients with acute maxillary sinusitis and ethmoiditis. Non-specific resistance and immunity

Effect of sodium hypochlorite disinfection of impressions on the size and quality of plaster models is studied. Twenty-minute submerging of silicone impressions in 0.5% sodium hypochlorite solution did not change their size and did not deteriorate the quality of surface and hardness of plaster models. Stomalgin impressions cannot be disinfected by sodium hypochlorite solution because of expressed destructive effect of this disinfectant on the impressions.     

Analysis of three 2,3-dihydroxybiphenyl 1,2-dioxygenases found in Rhodococcus globerulus P6. Identification of a new family of extradiol dioxygenases

The polychlorobiphenyl-degrading bacterium Rhodococcus globerulus P6 contains three bphC genes encoding 2,3-dihydroxybiphenyl 1,2-dioxygenases. One of them, bphC1, is clustered with the bphB gene which encodes 2,3-dihydroxy-4-phenylhexa-4,6-diene dehydrogenase and constitutes part of the bph operon specifying the degradation of biphenyl. The nucleotide sequence of bphB and the three bphC genes has been determined. The protein products of the bphBC1 gene cluster were found to exhibit significant homology with the corresponding proteins of analogous degradative pathways in Gram-negative bacteria; the highest homology was in those of the toluene degradation pathway of Pseudomonas putida strain F1. No homology was found between bphC2 and bphC3 and any other sequence in the database. At least two of the three meta cleavage enzymes are inducible by biphenyl. 2,3-Dihydroxybiphenyl 1,2-dioxygenase II, encoded by the bphC2 gene, was purified to apparent homogeneity from a recombinant Escherichia coli strain. The enzyme differed from other extradiol dioxygenases in having a subunit molecular mass of 21 kDa and a hexameric structure. The enzyme contains one tightly bound iron per subunit. These characteristics demonstrate that the 2,3-dihydroxybiphenyl 1,2-dioxygenases encoded by bphC2 and bphC3 belong to a new class of extradiol dioxygenases.