The effect of prior leaning on human postural responses

This study examines how human postural responses are altered by leaning about the ankles to five different initial stance positions prior to anterior or posterior horizontal translations of the support surface. When subjects leaned in the same direction as the translation-induced sway, postural strategies changed to use of less ankle torque and more horizontal shear forces at the surface to return to equilibrium. This change in strategy was associated with reduced and delayed activation of the stretched ankle muscles and an increased activation of proximal muscles producing rapid hip flexions or extensions. The changes in ankle muscle activation strength and latencies cannot be predicted based on simple stretch or load reflexes, but match predictions from computational, biomechanical models of human stance co-ordination^1–4.     

Cytogenetic features of Hodgkin's disease suggest possible origin from a lymphocyte

Surface marker and gene rearrangement data have supported various hypotheses about the origin of the malignant cell in Hodgkin's disease. Cytogenetic data about this disorder, however, are very scanty. To determine if any chromosomal abnormalities that could add further information to this controversial point are present, we studied tumor samples from 49 patients. Abnormal metaphases were obtained in 18 cases. The most common breakpoints were in 11q23, 14q32, 6q11-21, and 8q22-24. These are common breakpoints in lymphoma and raise the possibility that the malignant cell in Hodgkin's disease may be derived from a lymphocyte. The 11q23 breakpoint is also seen in t(4;11) and t(9;11), which is typical of a type of childhood B-cell acute lymphoblastic leukemia characterized by the presence of aberrant myeloid and monocytic markers. Myeloid and monocytic markers are common in Reed-Sternberg cells.     

POLYMORPHISMS OF ANGIOTENSIN-CONVERTING ENZYME, ANGIOTENSINOGEN, ANGIOTENSIN II TYPE 1 AND TYPE 2 RECEPTORS AND ENDOTHELIAL NITRIC OXIDE SYNTHASE IN TURKISH RENAL TRANSPLANT RECIPIENTS: A PRELIMINARY STUDY

Immunosuppressive therapy for organ transplant recipients is complicated by high rates of malignant diseases, one of these being Kaposi's sarcoma (KS). We reviewed the records of 1075 patients who underwent kidney transplantation at our center between October 1985 and May 2002. A total of 52 malignant diseases were observed in 50 patients (4.7%), during the post-transplantation period. Kaposi's sarcoma was identified in 16 of these 50 individuals. Of the 16 recipients, six were male and 10 were female. The mean age in the group was 39±9 years (range: 10–62 years). At the time of the KS diagnosis, 14 of the recipients were taking triple-drug immunosuppressive therapy consisting of cyclosporine A, azathioprine, and prednisolone. The other two individuals were receiving azathioprine and prednisolone. The mean time from transplantation to diagnosis with KS was 24±15.2 months (range: 8–74 months). One recipient had concomitant lymphoma and KS. The lesions of seven patients were limited to the skin, five cases involved the skin and gastrointestinal tract, and four patients had disseminated disease. After KS was confirmed, the first-line of treatment was to withdraw cyclosporine A and azathioprine, and taper the prednisolone. The tumors were managed with appropriate surgical and/or medical therapy. At the time of writing, nine individuals were still alive: four had normal renal function and five had lost their grafts as a result of chronic rejection. We have found the combination of immunosuppressive drug withdrawal and chemotherapy to be very effective in patients with limited disease, but the results in cases of generalized disease have been poor.     

The use of Fogs' test to assess associated movements in Parkinsonism,dystonia, and controls

The Fogs' test elicits non‐homologous associated movements which reflect underlying pathology or immaturity of the CNS, but has not been thoroughly studied. We filmed participants performing a modified Fogs' test and developed a reliable scoring system for the associated movements. We assessed scores in healthy controls of all ages and compared scores in dystonia and parkinsonism to age similar controls. Associated movements were marked in children, lessened as they matured into adults, and then increased in old age. Associated movements were marked in dystonia but not in parkinsonism. Our scoring system showed robust inter‐ and intra‐rater reliability. The Fogs' test is a reliable addition to the clinical examination that can be used to screen for both normal and abnormal neurological status. We suggest a potential neural pathway via cervical‐lumbosacral connections within the spinal cord which are modulated by propriospinal and cerebral input. © 2010 Movement Disorder Society     

Dusart syndrome: a new concept of the relationship between fibrin clot architecture and fibrin clot degradability: hypofibrinolysis related to an abnormal clot structure

Fibrinogen Dusart is a congenital dysfibrinogenemia (A-alpha 554 Arginine-->Cysteine) associated with severe thrombotic disorder, high incidence of thrombotic embolism, and abnormal fibrin polymerization. This thrombotic disorder was attributed to an abnormal clot thrombolysis with reduced plasminogen binding to fibrin and defective plasminogen activation by tissue plasminogen activator. The purpose of this work was to assess whether clot architecture could be involved in the thromboresistance of the fibrin Dusart and the high incidence of embolism. An important change in Dusart fibrin clot structure was identified with dramatic decrease of gel porosity (Ks), fiber diameters (d), and fiber mass-length ratios (mu) derived from permeation analysis. In addition, rigidity of the Dusart clot was found to be greatly increased compared with normal fibrin. We provide evidence that both thrombolysis resistance and abnormal rigidity of the fibrin Dusart are related to this abnormal architecture, which impairs the access of fibrinolytic enzymes to the fibrin and which is responsible for a brittle clot that breaks easily, resulting in a high incidence of embolism. Indeed, when restoring a normal clot structure by adding dextran 40 (30 mg/mL) before coagulation, clot thrombolysis and clot rigidity recovered normal values. This effect was found to be dose- dependent. We conclude that clot architecture is crucial for the propensity of blood clot to be degraded and that abnormal clot structure can be highly thrombogenic in vivo. The alpha-C domains of fibrinogen are determinant in fibrin clot structure.     

多不饱和脂肪酸间相互作用与男性人群冠心病的危险性

进食多不饱和脂肪酸（polyunsaturated fatty acids）能降低冠心病的危险性,然而,6-位不饱和脂肪酸与3-位不饱和脂肪酸能在代谢上发生竞争,从而减弱其有益的作用。此外,来源于海洋食物的长链3-位不饱和脂肪酸可能改变植物来源的中链3-位不饱和脂肪酸的作用,然而,对这些多不饱和脂肪酸之间的相互作用与冠心病危险性的关系并没有足够了解。     

A multicenter study of viral hepatitis in a United States hemophilic population

Hemophilia A and B patients seen at nine US regional treatment centers were tested for serologic markers of hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis delta virus (HDV) during 1987 and 1988. Because human immunodeficiency virus (HIV) infection, a potentially confounding variable, was present in 53% of the group, the population was divided by HIV status for analysis purposes. In the HIV-positive group (N = 382), less than 1% had not been infected with HBV, HCV, or HDV, whereas 75% had evidence of infection with HBV and 98% with HCV. HBsAg, a marker of active HBV infection, was present in 12% of subjects; 96% of these were HCV positive. Anti-HDV was detected in 35 subjects (9.1%); all were anti-HBc positive. Ten of the 35 (29%) also were positive for IgM anti-HDV, indicating current infection. All 10 were HBsAg positive and 7 of the 9 tested were HDV RNA positive. Severe/moderate hemophilia B patients were more likely to have experienced an HBV infection and to be anti-HDV positive than were similar hemophilia A patients (22% v 8%, P < .05). In the HIV-negative group (N = 345), the subjects were younger and had less severe hemophilia than the HIV-positive patients. No evidence of HBV, HCV, or HDV infection was found in 18%, whereas 33% had experienced HBV infection and 79% were anti-HCV positive. Within this group, 4% were HBsAg positive. All 13 subjects with anti-HDV (4% of the HIV-negative group) also possessed anti-HBc. One (7.7%) was IgM anti-HDV positive and the serum from another contained HDV RNA. Both of these individuals were HBsAg positive. As in the HIV-positive group, severe/moderate hemophilia B patients were more likely to be HBV and HDV positive than were hemophilia A patients (9% v 3%, P < .05). A prevalence study of viral hepatitis in a large US hemophilic population showed that active infection with HCV is common, occurring in 89% of all study patients regardless of HIV status. Evidence of active HBV infection was found in 8%; 19% of these were actively infected with HDV. HDV was more common in hemophilia B patients after controlling for disease severity.     

Role of free protein S and C4b binding protein in regulating the coagulant response to Escherichia coli

Previous studies showed that infusion of C4b-binding protein with sublethal Escherichia coli (E. coli) in the primate produced a consumptive coagulopathy followed by microvascular thrombosis and renal failure. The first objective of this study was to characterize the pathophysiology and mechanism of this phenomena following infusion of both these agents with emphasis on defining the role of free protein S. The second objective was to examine the relevance of this model to the hemolytic uremic syndrome. Infusion of C4b-binding protein alone reduced free protein S and decreased platelet concentration to 20% of baseline, whereas infusion of the C4b-binding protein/protein S complex did not. There was no activation of other inflammatory or coagulant factors. Infusion of sublethal E coli alone produced a transient inflammatory response with no reduction of free protein S. However, coinfusion of C4b-binding protein with sublethal E coli reduced free protein S and produced a thrombocytopenia, anemia, and a microvascular thrombotic response, whereas infusion of the C4b-binding protein/protein S complex with sublethal E coli did not. Studies comparing the effects of neutralizing (S-163) and nonneutralizing (S- 145) antibodies with protein S coinfused with sublethal E coli produced similar contrasting results. Therefore, we concluded that neutralization of free protein S, and not some other property of C4b- binding protein influenced by protein S, accounted for this microvascular thrombotic response. This response is similar to the hemolytic uremic syndrome characterized by thrombocytopenia, anemia, shistocytosis, and renal glomerular thrombosis with uremia. Comparison of the respective renal histopathologic appearance supports this conclusion. This raises the possibility that inhibition of protein S activity (possibly by one of the forms of C4b-binding proteins) might be one of the factors contributing to microvascular thrombotic disorder, such as the hemolytic uremic syndrome.