Total knee arthroplasty in patients with substantial deformities using primary knee components.

PURPOSE: Although advocated for severe varus and valgus deformities, constrained implant designs are associated with a number of disadvantages in total knee arthroplasty (TKA). Combining a minimally invasive surgical approach with an interchangeable posterior stabilized (PS) implant design may allow adequate soft tissue balancing with a minimal amount of constraint and without residual instability. METHODS: Retrospectively 51 patients operated with the minimally invasive far medial subvastus approach for severe varus or valgus deformity, who underwent primary TKA with a fully interchangeable PS implant (Vanguard, Biomet Inc., Warsaw IN, USA) between 2009 and 2013 were examined. Soft tissue releases was performed using a piecrust needling technique. Preoperative alignment and surgical parameters were collected for all patients. All patients underwent preoperative and follow-up radiographic assessment and completed a battery of clinical assessments. RESULTS: All procedures were performed successfully, with alignment improving from a preoperative mean (SD) varus deformity of 165° (3°) and a mean (SD) valgus deformity of 196° (4.5°) to an overall mean (SD) postoperative mechanical alignment of 179.5° (3.0°). Nine patients had postoperative varus, while three patients had a postoperative valgus deviation from neutral alignment >3°. The mean change in joint line position in extension was -0.0 ± 0.6 mm. Clinical scores at final follow-up were excellent for both groups. CONCLUSIONS: Good TKA outcomes can be achieved in patients with substantial varus or valgus deformities using a combination of a minimally invasive far medial subvastus approach, interchangeable PS implants and soft tissue releases with a piecrust needling technique. LEVEL OF EVIDENCE: III

Cardiovascular prevention in general practice : development and validation of an algorithm

General practice visits are a unique opportunity to identify and treat individuals with a high cardiovascular (CV) risk. However, a case-finding strategy suited to the daily general practice is not provided in the CV prevention guidelines. We wanted to create, validate and test an algorithm for global CV risk assessment and management

Gestational diabetes mellitus and fetal death in Mozambique: an incident case-referent study

Background. Third trimester fetal death is a common problem in Mozambique, occurring in approximately 5% of parturient women. Objective. To elucidate the magnitude of the gestational diabetes mellitus problem, and to estimate its prevalence in a group of women with unexplained late fetal deaths and in women with live fetuses (referents). Methods. An incident case-referent study of 109 pregnant Mozambican women with fetal deaths and 110 women delivering liveborns, regarding fasting B-glucose, oral glucose tolerance test and glycosylated hemoglobin. Result. The difference in gestational diabetes mellitus prevalence in the two groups is not significant. The prevalence of gestational diabetes mellitus was high in both groups: 11% and 7%, respectively

Adenylate Cyclases of Trypanosoma brucei Inhibit the Innate Immune Response of the Host

The parasite Trypanosoma brucei possesses a large family of transmembrane receptor–like adenylate cyclases. Activation of these enzymes requires the dimerization of the catalytic domain and typically occurs under stress. Using a dominant-negative strategy, we found that reducing adenylate cyclase activity by ~50% allowed trypanosome growth but reduced the parasite's ability to control the early innate immune defense of the host. Specifically, activation of trypanosome adenylate cyclase resulting from parasite phagocytosis by liver myeloid cells inhibited the synthesis of the trypanosome-controlling cytokine tumor necrosis factor–α through activation of protein kinase A in these cells. Thus, adenylate cyclase activity of lyzed trypanosomes favors early host colonization by live parasites. The role of adenylate cyclases at the host-parasite interface could explain the expansion and polymorphism of this gene family.info:eu-repo/semantics/publishe

A Trypanosoma brucei kinesin heavy chain promotes parasite growth by triggering host arginase activity.

In order to promote infection, the blood-borne parasite Trypanosoma brucei releases factors that upregulate arginase expression and activity in myeloid cells.Journal ArticleResearch Support, Non-U.S. Gov'tSCOPUS: ar.jinfo:eu-repo/semantics/publishe

SIGN-R1 receptor contribution to myeloid cell activation and liver injury.

<p>(<b>A,B</b>) Effects of rTbKHC1 on myeloid cells from non-infected control (Ctrl) or <i>SIGN-R1</i> KO mice (<b>A</b>: relative expression of <i>Arg1</i>, <i>Arg2</i>, <i>Il10</i> and <i>iNOS</i> genes; <b>B</b>: arginase activity in presence of indicated antibodies or sugars). Data are means ± SEM of 3 individual mice of one representative from 3 independent experiments. * p<0.05 compared to non-stimulated (-) cells. (<b>C</b>) Effects of rTbKHC1 on liver injury: microscopic analysis (hematoxylin-eosin staining, magnification 20×) of sections from WT- and <i>TbKHC1</i> KO-infected mice at day 30 p.i. Anoxic infarcts (ai), periportal (>>) and lobular (>) mononuclear cell infiltrates were representative of 8 animals tested in 2 independent experiments. (<b>D</b>) Spontaneous NO and IL-10 secretions in spleen myeloid cell supernatants from WT- and <i>TbKHC1</i> KO-infected mice treated with D-NAME or L-NAME (day 30 p.i.). (<b>E</b>) Idem as <b>D</b> in <i>SIGN-R1</i> KO and control (Ctrl) mice. Data are means ± SEM of 3–4 individual mice of one representative from 3 independent experiments. ∇ p<0.05 comparing WT or <i>TbKHC1</i> KO- infected mice to non-infected mice; £ p<0.05 comparing L-NAME and D-NAME treatment in WT- or <i>TbKHC1</i> KO-infected mice; # p<0.05 comparing WT- and <i>TbKHC1</i> KO-infected mice.</p

Mechanism of arginase activity induction by <i>T. brucei</i> PRF and rTbKHC1.

<p>Myeloid cells from non-infected WT (<b>A-D,F, G</b>) or IL-4Rα KO (<b>E</b>) mice were incubated with PRF or rTbKHC1. (<b>A</b>) IL-10 production induced by PRF. (<b>B</b>) Arginase activity induced by PRF incubated with indicated antibodies or sugars. (<b>C</b>) Arginase activity and IL-10 secretion induced by rTbKHC1 incubated with indicated antibodies or sugars. (<b>D–G</b>) Relative expression level of M2 genes after incubation with rTbKHC1. In <b>F</b>, M2 IL-10-dependent genes are indicated, and in <b>G</b>, rTbKHC1 was incubated with the indicated antibodies. Data are means ± SEM of 3 individual mice of one representative from 3 independent experiments. * p<0.05 compared to non-stimulated (-) cells.</p

Effects of TbKHC1 on <i>T. brucei</i> parasitaemia.

<p>WT and <i>TbKHC1</i> KO parasitaemias were monitored in various mice and conditions: (<b>A</b>) WT mice treated with L-NAME or D-NAME; (<b>B</b>) <i>iNOS</i> KO and WT mice; (<b>C,D</b>) myeloid cell <i>Arg1</i> KO mice (KO1 = <i>LysM</i>^cre<i>Arg1</i>^-/lox; KO2 = <i>Tie2</i>^cre<i>Arg1</i>^-/lox) and controls (<i>Arg1</i>^lox/lox); (<b>E,F</b>) WT mice treated with L-ornithine, D-mannose or D-galactose; (<b>G</b>) <i>MMR</i> KO and WT mice; (<b>H</b>) <i>SIGN-R1</i> KO and control (Ctrl) mice. Data are means ± SEM of 4 individual mice of one representative from 3 independent experiments. * p<0.05 comparing D-NAME and L-NAME treated mice (A) or WT and <i>iNOS</i> KO mice (B) infected with WT parasites; ∇ p<0.05 comparing <i>Arg1</i>^lox/lox and <i>LysM</i>^cre<i>Arg1</i>^-/lox or <i>Tie2</i>^cre<i>Arg1</i>^-/lox mice infected with WT parasites; # p<0.05 comparing L-ornithine treated and non treated mice infected with <i>TbKHC1</i> KO parasites; ¥ p<0.05 comparing D-mannose and D-galactose-treated mice infected with WT parasites; £ p<0.05 comparing <i>SIGN-R1</i> KO and control mice infected with WT parasites.</p