Accessory extensor pollicis longus.

Phylogenetically the accessory extensor pollicis longus in man seems to find its origin in the deep extensor layer, and this has largely been described in primates. I describe a case and present a comprehensive review of other publications on the subject.     

Long-term results of treatment for articular calcaneus fractures with Westhues method]

In this paper the authors evaluate the long-term results of treatment for articular calcaneus fractures with Westhues method. This evaluation is performed with regard to triple measurement of B?hler's angle value and to subjective criteria. The clinical material from years 1985-2002 consists of 47 patients aged between 24 and 56 years (mean age 32 years) with articular calcaneus fractures--namely, 41 male patients (87.2%) and 6 female patients (12.8%). The follow-up examination was performed in 24 patients (51% of all patients), namely, in 23 male patients (48.8%) and in one female patient (2.2%). Minimum follow-up time was 12 months and maximum was 9 years. Acquired results suggest that Westhues method restores normal B?hler's angle value only in tongue-type calcaneous fractures.     

Impaired responses to toll-like receptor 4 and toll-like receptor 3 ligands in human cord blood

Toll-like receptor (TLR)-4 signaling pathway plays an essential role in host defense against gram-negative bacteria while TLR-3-mediated signaling is critically involved in anti-viral immunity. To gain insight into the defects responsible for impaired Th1 responses in human newborns, we investigated the responses of human cord blood cells to lipopolysaccharide, LPS, and to polyinosinic-polycytidylic acid, Poly (I:C), ligands of TLR-4 and TLR-3, respectively. Measurement of cytokine levels revealed a profound defect in IL-12 (p70) synthesis and an increased release of IL-10 in cord blood exposed to LPS or Poly (I:C), as compared to adult blood. Moreover, Poly (I:C)-induced IFN-alpha production was found to be significantly impaired in cord blood. Phenotypic maturation of myeloid DC in response to LPS or Poly (I:C) was next compared in cord and adult blood. We observed that neonatal myeloid DC displayed decreased upregulation of CD40, CD80 whereas CD86 and HLA-DR upregulation did not differ significantly between adults and neonates. Taken together, these findings might be relevant to the increased vulnerability of human newborns to intracellular pathogens and to their inability to develop efficient Th1-type responses.     

Swimming exercise training prior to acute myocardial infarction attenuates left ventricular remodeling and improves left ventricular function in rats

The effect of exercise training prior to acute myocardial infarction (AMI) on left ventricular (LV) remodeling is poorly understood. This study investigated the protective effect of 3 weeks of swimming exercise training prior to AMI on cardiac morphology and function. Male Sprague-Dawley rats (n = 35) were randomly assigned to 3 groups: swimming training (n = 14, 90 min, 5 days/wk, 3 wk), sedentary (n =14), and controls (n = 7, no exercise, no MI). At the end of the training/sedentary period, rats were subjected to AMI (ExMI and SedMI) induced by surgical ligation of the left coronary artery. Thereafter, the rats remained sedentary for a 4-wk recovery period. Trans-thoracic echocardiography was performed in each group at the end of the exercise/sedentary period (pre-AMI), 24 hr after AMI, and following recovery (4 wk after AMI). No differences were observed in LV dimensions and function pre-AMI among the 3 groups; however, LV-end systolic diameter (LVESD) and LV-end systolic area (LVES-area) were significantly lower in the prior trained rats, 24 hr post-AMI with no additional change 4 wk post-AMI, during remodeling. Both LV-shortening fraction (SF%) and fractional area change (FAC%) were higher in the trained animals 4 wk post-AMI (39+/-12% vs 23+/-8%; p 0.002, and 48+/-14% vs. 38+/-9%; p 0.07, respectively). In conclusion, 3 wk of swimming exercise training prior to AMI significantly attenuated LV remodeling and improved LV function, despite no changes in LV dimensions or systolic function at the end of the exercise session. The data suggest that even a short-term training period is sufficient to induce cardiac protection.     

Interference with CD28, CD80, CD86 or CD152 in collagen-induced arthritis. Limited role of IFN-gamma in anti-B7-mediated suppression of disease

We have investigated interference with co-stimulation by administering mAbs towards CD28, CD80, CD86, and CD152 in mice immunized for the development of collagen-induced arthritis (CIA). Anti-CD80 and anti-CD86 treatment inhibited disease score and incidence, whereas anti-CD28 treatment led only to a delayed disease onset. Administration of anti-CD152 had no effect. The CII-specific Ab-response was suppressed by the co-stimulatory blockade, with a stronger effect on IgG1 than on IgG2a. The CII-driven T cell proliferation, on the other hand, was not affected. Furthermore, T cells primed in the presence of either anti-B7 or anti-CD28 produced markedly increased amounts of IFN-gamma in response to CII. To investigate whether this increase in IFN-gamma was related to disease suppression, IFN-gamma-deficient mice were immunized with CII, treated with anti-B7 and followed for the development of arthritis. As in the wild-type mice, administration of anti-B7 to IFN-gamma-deficient mice led to a reduced disease incidence and severity as well as reduced anti-CII IgG titers. Collectively, these data stress the importance of co-stimulation for the delivery of B cell help rather than for production of Th1 cytokines. We also demonstrate that the enhanced production of IFN-gamma observed after B7-blockade is not accountable for the anti-B7 mediated inhibition of CIA.     

Transcription Factor PU.1 Promotes Conventional Dendritic Cell Identity and Function via Induction of Transcriptional Regulator DC-SCRIPT

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Peripheral neovascularization of the retina in diabetic retinopathy: fluorescein angiography classification and results of panretinal laser treatment

The prospective study reported here was based on 105 diabetic eyes with "new vessels elsewhere" (NVE), treated exclusively by panretinal laser application and followed up for 2.5 to 4 years. Fundus angiography was performed before treatment. The eyes were then classified in four categories according to the extent and location of capillary nonperfusion responsible for the NVE, namely 1) generalized ischemia (Type A); 2) extensive midperipheral ischemia (Type B); 3) moderate midperipheral ischemia (Type C); and 4) peripheral ischemia (Type D). Analysis of the neovascularization distribution pattern showed that NVE alone existed only in Type D, whereas in the other three types the neovascularization was present either only in the retina or in both the retina and the optic disk. This mixed vascularization was 100% in Type A, 71% in Type B, 31% in Type C, and nonexistent in Type D. Statistical analysis revealed a significant correlation between the type of ischemia and the location of the new vessels. The therapeutic results 3-4 months, 1 year, and 2.5-4 years after intervention showed a significant trend toward an increase in the number of eyes with recurrences when moving from Type D to Type A. This means that the prognosis of NVE after panretinal laser coagulation depends mainly on the type of retinal ischemia. The poorest prognosis is that for generalized ischemia (Type A), followed in descending order by Types B, C, and D. The critical period for increased recurrence in cases which initially responded positively to treatment is primarily in the first 3-4 months following the intervention.     

Immunological markers of disease activity in the course of 2-CDA treatment of multiple sclerosis

52 clinically definite multiple sclerosis (MS) patients were treated with subcutaneous injection of 5 mg 2-CDA in 5 consecutive days. The injection courses were repeated 6 times in one month interval. The MRI pattern and immunological markers were studied in serum and CSF before and after 6 months of treatment. The obtained results suggest that treatment with 2-CDA has not any significant effect on humoral immunological events in multiple sclerosis, what is in contrast to some normalization of cellular immunopathological processes.