ABSTRACT
Glass micromachining is a basic technology to achieve microfluidic networks for lab-on-a-chip applications. Among several methods to microstructure glass, the simplest and most widely applied is wet chemical etching (WE). However, accurate control of the reaction conditions to perform reproducible, fast and safe glass etching is not straightforward. Herein, microwave-assisted WE is demonstrated to intensify the glass etching action under safe working and finely monitored operative conditions and to produce smooth deep channels in short processing times with reduced underetching effects.
Subject(s)
Glass/chemistry , Microfluidic Analytical Techniques/instrumentation , Microtechnology/methods , MicrowavesABSTRACT
We report on a transition in random lasers that is induced by the geometrical confinement of the emitting material. Different dye doped paper devices with controlled geometry are fabricated by soft lithography and show two distinguished behaviors in the stimulated emission: in the absence of boundary constraints, the energy threshold decreases for larger laser volumes showing the typical trend of diffusive nonresonant random lasers, while when the same material is lithographed into channels, the walls act as cavity and the resonant behavior typical of standard lasers is observed. The experimental results are consistent with the general theories of random and standard lasers and a clear phase diagram of the transition is reported.
Subject(s)
Lasers , Optical Phenomena , Imaging, Three-Dimensional , Microscopy, Confocal , Scattering, RadiationABSTRACT
INTRODUCTION: The personal identification of living subjects through video filmed images can occasionally be necessary, particularly in the following circumstances: (1) the need to identify unknown subjects by comparing two-dimensional images of someone of known identity with the subject. (2) The need to identify subjects taken in photographs or recorded on video camera by using a comparison with individuals of known identity. METHODS AND APPARATUS: The final aim of our research was that of analysing a video clip of a bank robbery and to determine whether one of the subjects was identifiable with one of the suspects. Following the correct methodology for personal identification, the original videotape was first analysed, relating to the robbery carried out in the bank so as to study the characteristics of the criminal action and to pinpoint the best scenes for an antropomorphometrical analysis. The scene of the crime was therefore reconstructed by bringing the suspect back to the bank where the robbery took place, who was then filmed with the same closed circuit video cameras and made to assume positions as close as possible to those of the bank robber to be identified. RESULTS AND CONCLUSIONS: Taking frame no. 17, points of comparable similarity were identified on the face and right ear of the perpetrator of the crime and the same points of similarity identified on the face of the suspect: right and left eyebrows, right and left eyes, "glabella", nose, mouth, chin, fold between nose and upper lip, right ear, elix, tragus,"fossetta", "conca" and lobule. After careful comparative morphometric computer analysis, it was concluded that none of the 17 points of similarity showed the same anthropomorphology (points of negative similarity). It is reasonable to sustain that 17 points of negative similarity (or non coincidental points) is sufficient to exclude the identity of the person compared with the other.
Subject(s)
Anthropometry/methods , Forensic Medicine/methods , Image Processing, Computer-Assisted , Ear/anatomy & histology , Face/anatomy & histology , Humans , Video RecordingABSTRACT
BACKGROUND: Human tissue kallikrein (HK) releases kinins from kininogen. We investigated whether adenovirus-mediated HK gene delivery is angiogenic in the context of ischemia. METHODS AND RESULTS: Hindlimb ischemia, caused by femoral artery excision, increased muscular capillary density (P:<0.001) and induced the expression of kinin B(1) receptor gene (P:<0.05). Pharmacological blockade of B(1) receptors blunted ischemia-induced angiogenesis (P:<0.01), whereas kinin B(2) receptor antagonism was ineffective. Intramuscular delivery of adenovirus containing the HK gene (Ad. CMV-cHK) enhanced the increase in capillary density caused by ischemia (969+/-32 versus 541+/-18 capillaries/mm(2) for control, P:<0.001), accelerated blood flow recovery (P:<0.01), and preserved energetic charge of ischemic muscle (P:<0.01). Chronic blockade of kinin B(1) or B(2) receptors prevented HK-induced angiogenesis. CONCLUSIONS: HK gene delivery enhances the native angiogenic response to ischemia. Angiogenesis gene therapy with HK might be applicable to peripheral occlusive vascular disease.
Subject(s)
Genetic Therapy/methods , Hindlimb/blood supply , Ischemia/therapy , Neovascularization, Physiologic/drug effects , Tissue Kallikreins/administration & dosage , Adenoviridae/genetics , Animals , Bradykinin Receptor Antagonists , Capillaries/cytology , Capillaries/drug effects , Capillaries/metabolism , Disease Models, Animal , Gene Expression , Hindlimb/drug effects , Humans , Immunohistochemistry , Injections, Intramuscular , Ischemia/genetics , Ischemia/pathology , Male , Mice , Muscle, Skeletal/blood supply , Muscle, Skeletal/drug effects , Muscle, Skeletal/metabolism , Muscle, Skeletal/pathology , Neovascularization, Physiologic/genetics , Peripheral Vascular Diseases/therapy , Receptor, Bradykinin B1 , Receptor, Bradykinin B2 , Receptors, Bradykinin/metabolism , Regional Blood Flow/drug effects , Regional Blood Flow/genetics , Reverse Transcriptase Polymerase Chain Reaction , Tissue Kallikreins/genetics , Transgenes/geneticsABSTRACT
We investigated whether local delivery of the tissue kallikrein gene induces angiogenesis in normoperfused mouse hindlimb muscles. Intramuscular injection of adenovirus containing the human tissue kallikrein gene under the control of a cytomegalovirus enhancer/promoter sequence resulted in local production and release of recombinant human tissue kallikrein, whereas transgene expression was absent in muscles of the contralateral hindlimb. Angiogenesis in infected muscles was documented by histological evidence of increased capillary density. In contrast, no angiogenic effect was seen either in the ipsilateral gastrocnemius or contralateral hindlimb muscles. Neovascularization was associated with a transient increase in muscular blood flow as determined by laser Doppler flowmetry. We also investigated the mechanisms of kallikrein-induced angiogenesis. We found that the angiogenic response to kallikrein was abolished by chronic blockade of the kinin B(1) or B(2) receptor or by inhibition of nitric oxide synthase. In addition, inhibition of cyclooxygenase-2 by nimesulide significantly reduced kallikrein-induced effects. These results indicate that (1) human tissue kallikrein acts as an angiogenic factor in normoperfused skeletal muscle and (2) nitric oxide and prostacyclin are essential mediators of kallikrein-induced angiogenesis. Our findings provide new insights into the role of the tissue kallikrein-kinin system in vascular biology.
Subject(s)
Adenoviridae/genetics , Kallikreins/administration & dosage , Kallikreins/genetics , Muscle, Skeletal/physiology , Neovascularization, Physiologic/genetics , Perfusion , Animals , Cytomegalovirus/genetics , Gene Expression Regulation/physiology , Genetic Vectors/genetics , Hindlimb/blood supply , Hindlimb/enzymology , Hindlimb/physiology , Humans , Injections, Intramuscular , Kallikreins/physiology , Male , Mice , Mice, Inbred Strains , Mice, Knockout , Muscle, Skeletal/blood supply , Muscle, Skeletal/enzymologyABSTRACT
BACKGROUND: Administration of angiogenic factors stimulates neovascularization in ischemic tissues. However, there is no evidence that angiogenesis can be induced in normoperfused skeletal muscles. We tested the hypothesis that adenovirus-mediated intramuscular (IM) gene transfer of the 121-amino-acid form of vascular endothelial growth factor (AdCMV.VEGF(121)) could stimulate neovascularization in nonischemic skeletal muscle and consequently attenuate the hemodynamic deficit secondary to surgically induced ischemia. METHODS AND RESULTS: Rabbits and rats received IM injections of AdCMV.VEGF(121), AdCMV.Null, or saline in the thigh, 4 weeks (rabbits) or 2 weeks (rats) before femoral artery removal in the injected limb. In unoperated rats, at the site of injection of AdCMV.VEGF(121), we found 96% and 29% increases in length density of arterioles and capillaries, respectively. Increased tissue perfusion (TP) to the ischemic limb in the AdCMV.VEGF(121) group was documented, as early as day 1 after surgery, by improved blood flow to the ischemic gastrocnemius muscle measured by radioactive microspheres (AdCMV.VEGF(121)=5.69+/-0.40, AdCMV.Null=2.97+/-0.50, and saline=2.78+/-0.43 mL x min(-1) x 100 g(-1), P<0.001), more angiographically recognizable collateral vessels (angioscore) (AdCMV. VEGF(121)=50.58+/-1.48, AdCMV.Null=29.08+/-4.22, saline=11.83+/-1.90, P<0.0001), and improvement of the bioenergetic reserve of the gastrocnemius muscle as assessed by (31)P NMR spectroscopy. Follow-up studies showed that superior TP to the ischemic limb in the AdCMV.VEGF(121) group persisted until it was equalized by spontaneous collateral vessel development in untreated animals. CONCLUSIONS: IM administration of AdCMV.VEGF(121) stimulates angiogenesis in normoperfused skeletal muscles, and the newly formed vessels preserve TP after induction of ischemia.
