Preliminary investigations using Recover Latent Fingerprint Technology on unfired ammunition and fired cartridge cases.

Previous studies have identified the potential benefit of the disulfur dinitride (S2N2) process to operationally relevant substrates. However, the majority of this work was conducted on prototype equipment that had substantial differences to the commercialised system (Recover Latent Fingerprint Technology (LFT)) in terms of design and chemical delivery. This paper evaluates the performance of Recover LFT on a problematic exhibit encountered within a fingerprint enhancement laboratory: unfired and fired ammunition. Three pseudo-operational experiments involving non-groomed, naturally handled fingermarks were conducted on the most commonly encountered types of ammunition used in crime in the United Kingdom (UK). In addition, Recover LFT was compared against Superglue Fuming followed by Basic Yellow 40 (BY40) Fluorescent Dye Staining (a commonly used alternative) to ascertain if the process provides added benefit to fingermark recovery rates. The results show that fingermark visualisation on small calibre cartridge cases remains difficult with few marks achieving enough ridge detail for comparison. However, this paper also shows that the novel Recover LFT process, which is still in its infancy and requiring optimisation, is no worse than currently implemented visualisation processes and is therefore worth further investigation.

Sequelae and survivorship in patients treated with (131)I-MIBG therapy.

BACKGROUND: (131)I-meta-iodobenzylguanidine ((131)I-MIBG) has been in therapeutic use since 1980s. Newer treatment modalities are emerging for neuroendocrine tumours (NETs) and chromaffin cell tumours (CCTs), but many of these do not yet have adequate long-term follow-up to determine their longer term efficacy and sequelae. METHODS: Fifty-eight patients with metastatic NETs and CCTs who had received (131)I-MIBG therapy between 2000 and 2011 were analysed. Survival and any long-term haematological or renal sequelae were investigated. RESULTS: In the NET group, the overall median survival and median survival following the diagnosis of metastatic disease was 124 months. The median survival following the commencement of (131)I-MIBG was 66 months. For the CCT group, median survival had not been reached. The 5-year survival from diagnosis and following the diagnosis of metastatic disease was 67% and 67.5% for NETs and CCTs, respectively. The 5-year survival following the commencement of (131)I-MIBG therapy was 68%. Thirty-two patients had long-term haematological sequelae: 5 of these 32 patients developed haematological malignancies. Two patients developed a mild deterioration in renal function. CONCLUSION: Long follow up of (131)I-MIBG therapy reveals a noteable rate of bone marrow toxicities and malignancy and long term review of all patients receiving radionuclide therapies is recommended.

Postural change in ventilation and perfusion secondary to a thoracic scoliosis with complete resolution after surgery.

We present the case of a child with a thoracic scoliosis causing respiratory impairment in whom pre-surgical ventilation-perfusion lung scintigraphy in different postures was able to predict improvement in ventilation and perfusion after surgery.

The radiological management of bomb blast injury.

A need to understand the nature and patterns of bomb blast injury, particularly in confined spaces, has come to the fore with the current worldwide threat from terrorism. The purpose of this review article is to familiarize the radiologist with the imaging they might expect to see in a mass casualty terrorist event, illustrated by examples from two of the main institutions receiving patients from the London Underground tube blasts of 7 July 2005. We present examples of injuries that are typical in blast victims, as well as highlighting some blast sequelae that might also be found in other causes of multiple trauma. This should enable the radiologist to seek out typical injuries, including those that may not be initially clinically apparent. Terror-related injuries are often more severe than those seen in other trauma cases, and multi-system trauma at distant anatomical sites should be anticipated. We highlight the value of using a standardized imaging protocol to find clinically undetected traumatic effects and include a discussion on management of multiple human and non-human flying fragments. This review also discusses the role of radiology in the management and planning for a mass casualty terrorist incident and the optimal deployment of radiographic services during such an event.

Novel modalities of somatostatin actions.

The first part of this contribution reviews the current knowledge about endocrine and neuromodulatory actions of somatostatin. These biological actions are exerted according to endocrine, paracrine and autocrine modes of action and involve five distinct types of membrane receptors belonging to the 'super-family' of G-protein-coupled receptors. A new concept concerning a juxtacrine mode of action has recently been introduced to refer to the intervention of cytokines and growth factors in direct, cell-to-cell communication. The evidence in favor of juxtacrine actions of somatostatin will be presented in the second part of this review and illustrated by our own results on macrophage-lymphocyte T interactions in the immune system and spermatogonia-Sertoli cell interactions in mammalian testis. Another phenomenon such as ligand-induced somatostatin receptor homo- and hetero-dimerization resulting in 'poly'-receptors (with characteristics different from those of each of the two receptors forming the complex) is also at the origin of a novel mode of somatostatin action. The latter will be illustrated by the data obtained on human pituitary adenomas with somatostatin analogs specific for either 'poly'-receptor or relevant individual receptors. The arguments in favor of the analogous mode of actions among different families of chemical messengers such as peptides, cytokines and growth factors are discussed in the concluding section. The emerging unifying concepts on such functional analogies might provide a useful basis for the development of synthetic analogs not only for bioactive peptides but also for other types of chemical messengers.

Somatostatin inhibits stem cell factor messenger RNA expression by Sertoli cells and stem cell factor-induced DNA synthesis in isolated seminiferous tubules.

Immature porcine Sertoli cells have been reported to be targets for the regulatory peptide somatostatin (SRIF), which inhibits the basal and FSH-induced proliferation of Sertoli cells through a decrease of cAMP production. In the present study, we show that SRIF inhibits both basal and FSH-stimulated expression of the stem cell factor (SCF), a Sertoli cell-specific gene. The SRIF-mediated inhibition of forskolin-triggered, but not of 8-bromoadenosine-cAMP-triggered, SCF mRNA expression demonstrates the involvement of adenylyl cyclase in underlying peptide actions. Moreover, these effects require functional coupling of specific plasma membrane receptors to adenylyl cyclase via inhibitory G proteins, because pertussis toxin prevents SRIF-mediated inhibition of SCF mRNA expression. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blot assays suggest the involvement of sst2 receptors in SRIF actions on Sertoli cells. The biological relevance of these data is supported by an SRIF-mediated decrease in SCF-induced incorporation of [(3)H]thymidine in isolated seminiferous tubules. In situ hybridization and confocal microscopy show that, in seminiferous tubules only, spermatogonia display both c-kit and sst2 receptors. Taken together, these results suggest that SCF-stimulated DNA synthesis can be inhibited by SRIF in spermatogonia, but not in Sertoli and peritubular cells. Combined RT-PCR and immunohistochemical approaches point toward spermatogonia and Leydig cells as the source of testicular SRIF. These data argue in favor of paracrine/autocrine SRIF actions in testis.

Leukemia inhibitory factor antagonizes gonadotropin induced-testosterone synthesis in cultured porcine leydig cells: sites of action.

In the present report, the action of leukemia inhibitory factor (LIF) on testicular steroid hormone formation was studied. For this purpose, the direct effects of LIF were evaluated on basal and human (h)CG-stimulated testosterone synthesis by cultured, purified Leydig cells isolated from porcine testes. LIF reduced (more than 60%) hCG-stimulated testosterone synthesis. This inhibitory effect was exerted in a dose- and time-dependent manner. The maximal and half-maximal effects were obtained with, respectively, 10 ng/ml (0.5 nM ) and 2.5 ng/ml (0.125 nM ) of LIF after a 48-h treatment of the Leydig cells. Such an effect of the cytokine was not a cytotoxic effect, because it was reversible and Leydig cells recovered most of their steroidogenic activity after the removal of LIF. Considering the sites of action of LIF in inhibiting gonadotropin-stimulated testosterone formation, it was shown that LIF significantly (P < 0.002) reduced, in a comparable range (about 60% decrease), testosterone synthesis stimulated with LH/hCG or with pharmacological agents that enhance cAMP levels (cholera toxin, forskolin, and PG E2), and testosterone synthesis stimulated with 8-bromo-cAMP. Such an observation indicates that the antigonadotropic action of the cytokine is exerted in a predominant manner at a step (or steps) located beyond cAMP formation. Furthermore, incubation of Leydig cells with 22R-hydroxycholesterol (5 microg/ml, 2 h), a cholesterol substrate derivative that does not need an assisted process to be delivered to the inner mitochondrial membrane, reversed most of the inhibitory effect of LIF on the steroid hormone formation. Such results indicate that LIF acts by reducing cholesterol substrate availability in the mitochondria. Consequently, LIF action was tested on steroidogenic acute regulatory protein and PBR (peripheral benzodiazepine receptor) shown to be potentially involved in such a cholesterol transfer. LIF reduced, in a dose- and time-dependent manner, LH/hCG-induced steroidogenic acute regulatory protein messenger RNA levels. The maximal inhibitory effect was obtained with 6.6 ng/ml of LIF after 48 h of treatment. In contrast, LIF had no effect on PBR messenger RNA expression or PBR binding. This inhibitory effect of LIF on Leydig cell steroidogenesis is probably exerted via an auto/paracrine action of the cytokine. Indeed, by immunohistochemistry, LIF and LIF receptor proteins were identified in Leydig and Sertoli cells but not in other testicular cell types, except for LIF receptor in spermatogonia. Furthermore, the presence of LIF and its receptor in Leydig cells at the neonatal and adult periods suggests that the inhibitory effect of LIF on androgen formation reported here probably occurs in both the fetal and the adult Leydig cell populations during testicular development.

Transforming growth factor-beta receptor types I and II in cultured porcine leydig cells: expression and hormonal regulation.

The steroidogenic activity of testicular Leydig cells is controlled both by the pituitary hormone (LH) and by growth factors such as transforming growth factor-beta peptides (TGFbeta1, -2, and -3; inhibin/activin; and anti-Mullerian hormone). By using primary cultures of porcine Leydig cells as a model, the aim of the study was to identify and characterize the TGFbeta receptors and to study their regulation by LH/hCG. TGFbeta receptors have been identified and characterized through three different approaches, including cross-linking experiments and Western and Northern blotting analyses. In cross-linking experiments, labeled TGFbeta was shown to bind to three different molecular species of 300, 80, and 53 kDa, which may correspond to the protein betaglycan (also known as TGFbeta type III receptor) and TGFbeta type II and I receptors (TGFbetaRII and TGFbetaRI), respectively. The presence of TGFbetaRI and -RII was further demonstrated by Western blotting analysis using specific polyclonal antibodies. Finally, the expression of betaglycan, TGFbetaRII, and TGFbetaRI messenger RNAs, was confirmed by Northern blotting analysis, as shown by the presence of 6.4-, 4.6-, and 5.8-kb messenger RNAs, respectively. By using a RT-PCR approach, the mediators of the TGFbeta signal, Smads 1-7, were also detected in cultured Leydig cells. TGFbetaRI and TGFbetaRII protein levels were enhanced by hCG/LH in a dose-dependent (maximal effect with 0.3 ng/ml hCG) and time-dependent (maximal effect observed after 48 h of hCG treatment) manner. Furthermore, to determine whether the stimulatory effect of LH/hCG was mediated by testosterone, use was made of aminogluthetimide, an inhibitor of cytochrome P450scc. The inhibition oftestosterone formation did not affect the stimulatory effect of LH/hCG on TGFbetaRI and -RII levels, suggesting that the gonadotropin action is not mediated by the steroid hormone. Together, the present findings demonstrate that the TGFbeta receptors are expressed and are under hormonal (gonadotropin) control in cultured porcine Leydig cells.

Transforming growth factor beta receptor expression in cultured porcine granulosa cells.

By using primary cultures of porcine granulosa cells as a model, TGF beta receptors have been identified and characterized through three different approaches including cross-linking experiments, Western- and Northern-blotting analysis. In cross-linking experiments, labeled TGF beta was shown to bind to four different molecular species of 300, 168, 72 and 58 kDa. The 300-kDa species may correspond to beta-glycan, while the 72- and 58-kDa correspond to TGF beta type II and I receptors, respectively. The presence of these receptors was further demonstrated by Western-blotting analysis using specific polyclonal antibodies. Finally, both the expression of beta-glycan, type II and type I mRNA, was confirmed through Northern-blotting analysis as shown by the presence of 6.4, 4.6 and 5.8 kb mRNA, respectively. Additionally, we detected another TGF beta binding protein of 168 kDa which remains to be identified. Together, our present data indicate that the regulatory action of TGF beta on cultured granulosa cells previously reported in several laboratories may be mediated through the receptors identified here.

Expression of mRNAs for transforming growth factor-beta receptors in the rat testis.

In this study, we examined by means of northern blots, the mRNA expression of the three transforming growth factor-beta receptors (TGF-beta receptors) during rat testicular development and their cellular localization using fractionated testicular cells. Transcripts for receptors I and II were essentially detected in the immature testis, whereas receptor III mRNAs were present throughout testicular development. Somatic cells contained mRNAs for the three receptor types. In germ cells, transcripts for types I and II were in low abundance compared to type III mRNAs. In addition germ cells expressed three transcripts for the type III. Among the three transcripts, two were expressed exclusively in germ cells. TGF-beta being produced locally, our results are consistent with TGF-beta acting in testis via autocrine and/or paracrine mechanisms.

[TGF beta (transforming growth factor beta) and its related peptides in the local control of the testicle]. / TGF beta (transforming growth factor beta) et ses peptides apparentés dans le contrôle local du testicule.

Recent data on TGF beta (and related peptides) expression and action in the testis are briefly reviewed. At least, three isoforms of TGF beta are expressed during the male gonadal development. TGF betas are expressed in somatic and germ cells. The expression of the different isoforms varies during gonadal development and is cell specific. Both types I, II and III TGF beta receptors have been localized in somatic cells. TGF beta inhibits gonadotropin action both in Sertoli cells and Leydig cells as well as proliferation of germ cells and Leydig cells. Inhibins and activins (in terms of mRNA and proteins) are expressed in somatic cells and germ cells. Inhibin production in Sertoli cells is under the control of FSH, local factors (ex: EGF, insulin, opiods) and probably of germ cells. Activins and inhibins regulate Leydig and Sertoli cells activities and germ cells development. The existence of activin receptors in somatic and germ cells has been suggested by the presence of type II receptor mRNA (ActRII and ActRIIB).

Plasma exchange as a treatment for endogenous glycosaminoglycan anticoagulant induced haemorrhage in a patient with myeloma kidney.

A 57-year-old man with end-stage renal failure secondary to myeloma kidney developed haemorrhagic complications due to endogenous glycosaminoglycan anticoagulant production. Glycosaminoglycan levels and anticoagulant effect were reduced by plasma exchange and this contributed to control of the haemorrhagic manifestations.