The report of a clinical study of 104 electrical accidents which befell 85 men is divided into two parts.Part I enumerates the different types of accidents as flash burn, Joule burn, arc eye, "held on" shock and "not held" shock, physical shock, and death. These are related to the different voltages involved ranging from 240/415 (medium) voltage to 33 kilovolts. There appeared to be no association between voltage and type of injury and no evidence to suggest that any of the voltages are free from hazard. There were 53 cases of flash burn, affecting mostly the face and extensor surface of the hands and arms. The 16 cases of arc eye caused no serious concern. Of the 15 Joule burns all except one occurred at medium voltages in "held on" accidents, the other being associated with an electric shock at 33 kilovolts. The majority of Joule burns affected the flexor surfaces.Part II of the paper deals with the 43 cases of electric shock (passage of current through the body). Thirty of these cases were "held on" to the circuit by the current. It was found that the longer a victim was held on to the circuit the greater appeared to be his chances of developing heart and chest symptoms suggestive of impending asphyxia, and of losing consciousness. Although about half of these men were released by an external agmncy and others struggled off, a number suddenly became free from the circuit without, they claimed, losing consciousness. This is difficult to explain. Artificial respiration was administered in two cases, one of whom was "held on" and was being asphyxiated. The other case received flash burns only and did not in fact receive an electric shock. PART I: GENERAL REVIEW AND NON-SHOCK CASESElectrical accidents receive little attention in British medical literature. In fact, in the electricity supply industry they account for only 1 % of the total number of accidents but they are the commonest cause of accidental death (Hughes and Corney, 1956). In factories, electrical accidents account for less than 0-5 % of all accidents, but more than 5% of these electrical accidents prove fatal (Emerson, 1961). This paper reports a clinical investigation into a series of electrical accidents; detailed consideration of the cases of electric shock (passage of current through the body) is given in Part II of this paper. MethodThe names of all men in an electricity supply undertaking who had sustained an electrical accident during the preceding three years were obtained. Of the total of 114, 107 were still employed by the undertaking. One man was killed; the remainder were contacted and 84 attended for interview. (The majority of those who were not seen worked in one small area and there is no reason to suppose that the nature of their accidents was any different from the whole.) They were all seen by one investigator and were questioned about the electrical and physical circumstances of the accident, about symptoms, and about subsequent medical history.

The levels of regulatory T cells (Treg cells)

Neurotensin, a neuropeptide growth factor, and its two specific neurotensin receptors, NTSR1 and NTSR2, were shown to be expressed by human B cell lines. Another NTSR, sortilin, which is common to neurotensin and neurotrophins, was also detected as we have previously described. Neurotensin was functional in B cell lines; it induced their proliferation and inhibited apoptosis induced by serum deprivation or Fas activation. Quantitative study of gene expression in two malignant B cell diseases showed that NTSR2 was overexpressed, NTSR1 decreased, and neurotensin was unexpressed in B cell leukemia patient’s cells, as compared with healthy B cells. However, these expressions did not significantly change in large diffuse B cell lymphoma lymph nodes compared with benign ones. This study points out that neurotensin and its two specific receptors are expressed in human B lymphocytes. Such expressions were not described, and their relationship in B cell diseases, especially in chronic B cell leukemia, needs to be considered further in regard to these findings.

BackgroundDiffuse large B-cell lymphoma (DLBCL) is a common and often fatal malignancy. Immunochemotherapy, a combination of rituximab to standard chemotherapy, has resulted in improved survival. However a substantial proportion of patients still fail to reach sustained remission. We have previously demonstrated that autocrine brain-derived neurotrophic factor (BDNF) production plays a function in human B cell survival, at least partly via sortilin expression. As neurotrophin receptor (Trks) signaling involved activation of survival pathways that are inhibited by rituximab, we speculated that neurotrophins may provide additional support for tumour cell survival and therapeutic resistance in DLBCL.Methodology/Principal FindingsIn the present study, we used two DLBCL cell lines, SUDHL4 and SUDHL6, known to be respectively less and more sensitive to rituximab. We found by RT-PCR, western blotting, cytometry and confocal microscopy that both cell lines expressed, in normal culture conditions, BDNF and to a lesser extent NGF, as well as truncated TrkB and p75NTR/sortilin death neurotrophin receptors. Furthermore, BDNF secretion was detected in cell supernatants. NGF and BDNF production and Trk receptor expression, including TrkA, are regulated by apoptotic conditions (serum deprivation or rituximab exposure). Indeed, we show for the first time that rituximab exposure of DLBCL cell lines induces NGF secretion and that differences in rituximab sensitivity are associated with differential expression patterns of neurotrophins and their receptors (TrkA). Finally, these cells are sensitive to the Trk-inhibitor, K252a, as shown by the induction of apoptosis. Furthermore, K252a exhibits additive cytotoxic effects with rituximab.Conclusions/SignificanceCollectively, these data strongly suggest that a neurotrophin axis, such NGF/TrkA pathway, may contribute to malignant cell survival and rituximab resistance in DLBCL.

BackgroundNeurotrophins (NTs) are able to activate lymphocytes and fibroblasts; they can modulate angiogenesis and sympathic vascular function. Thus, they can be implicated in the three pathogenic processes of systemic sclerosis (SSc). The aims of this study are to determine blood levels of Nerve Growth Factor (NGF), Brain-Derived Neurotrophic Factor (BDNF) and Neurotrophin-3 (NT-3) in SSc and to correlate them with clinical and biological data.MethodsSerum samples were obtained from 55 SSc patients and 32 control subjects to measure NTs levels by ELISA and to determine their relationships with SSc profiles.FindingsSerum NGF levels were higher in SSc patients (288.26±170.34 pg/mL) than in control subjects (170.34±50.8 pg/mL, p<0.001) and correlated with gammaglobulins levels and the presence of both anti-cardiolipin and anti-Scl-70 antibodies (p<0.05). In contrast, BDNF levels were lower in SSc patients than in controls (1121.9±158.1 vs 1372.9±190.9 pg/mL, p<0.0001), especially in pulmonary arterial hypertension and diffuse SSc as compared to limited forms (all p<0.05). NT-3 levels were similar in SSc and in the control group (2657.2±2296 vs 2959.3±2555 pg/mL, NS). BDNF levels correlated negatively with increased NGF levels in the SSc group (and not in controls).ConclusionLow BDNF serum levels were not previously documented in SSc, particularly in the diffuse SSc subset and in patients with pulmonary hypertension or anti-Scl-70 antibodies. The negative correlation between NGF and BDNF levels observed in SSc and not in healthy controls could be implicated in sympathic vascular dysfunction in SSc.