The significance of HAI should be not only whether it is better t

The significance of HAI should be not only whether it is better than systemic, but also that it can be used with systemic therapy. When using drugs such as FUDR there is no systemic toxicity because there is a 95% extraction rate, so almost full doses of systemic therapy can be combined with the HAI therapy,

allowing for more drug to actually be seen by the tumor. Inhibitors,research,lifescience,medical This allows for a higher response rate, which could possibly translate into a higher resection rate for Crenolanib 670220-88-9 patients with unresectable disease. In an MSKCC study on patients with unresectable liver metastases, 57% of chemo naive patients and 43% of previously treated patients were able to go on to liver resection after HAI and systemic therapy (16). How do we move forward? One of the problems of funding studies looking at HAI therapy is that drugs

such Inhibitors,research,lifescience,medical as 5-FU and FUDR are no longer made by drug companies; therefore, there is no support for testing them. The port and catheter companies don’t seem to be interested in funding studies to show that hepatic arterial therapy may be better than systemic therapy and less expensive. There needs to be studies funded by governmental agencies to compare effective treatments, but also include cost analysis. If HAI therapies produce better Inhibitors,research,lifescience,medical results and are less costly, they certainly can be part of our therapeutic armamentarium to take care of colorectal patients in the future. Acknowledgements Disclosure: The author declares no conflict of interest. Notes Submitted Inhibitors,research,lifescience,medical Feb 21 2013. Accepted for publication Mar 15, 2013
Although liver is one of the extranodal organs commonly involved in both Hodgkin and non-Hodgkin lymphoma, Primary Hepatic Lymphoma (PHL) is rare. In non-immunocompromised patients, primary hepatic malignant non-hodgkin’s lymphoma is a rare disease, with less than 100 cases reported (1). Anaplastic large-cell lymphomas (ALCL) Inhibitors,research,lifescience,medical were first described by Stein et al. in 1985 (2) as large-cell neoplasms with a pleomorphic appearance, subtotal effacement of the lymph node structure

and expression of the lymphoid activation antigen CD-30 (ki-1). ALCL frequently involves both lymph nodes and extranodal sites (3). The most common Entinostat extra-nodal sites affected by ALCL include skin, bone, soft tissue, lung, and liver. However, is extremely rare for ALCL to present as a liver primary lymphoma, and only eight cases have been reported. ALCL accounts for approximately 3% of adult non-Hodgkin lymphomas. The neoplastic cells selleck consistently express CD30 molecule in all variants. Most cases of ALCL are associated with the characteristic chromosomal translocation t[2;5], which results in up regulation of anaplastic lymphoma kinase (ALK) protein. We report a case of a primary hepatic anaplastic large T-cell ki-1 non-Hodgkin lymphoma in a 55-year-old patient with celiac disease.

The latter energetic hypothesis is supported by the


The latter energetic hypothesis is supported by the

notion that GAA activity normally “returns” to the cytoplasm the end product of lysosomal glycogen digestion, glucose. It is also telling that in muscle from patients with the infantile form of GSD II most glycogen is free in the cytoplasm, probably released by “burst Inhibitors,research,lifescience,medical lysosomes” (13). A more compelling scenario for the selleck bio pathogenesis of GSD II, as well as other lysosomal storage disorders (16), involves a disruption of the vital autophagic process, with accumulation of autophagosomes resulting from defective autophagosome-lysosome fusion (16, 17). In fact, Nishino Inhibitors,research,lifescience,medical and colleagues went as far as stating that “Pompe disease can no longer be viewed simply as a glycogen storage disease,” but rather as a problem in handling excessive numbers of autophagosomes (13). A unique feature of GSD II is the availability of a generally effective – and now widely utilized – enzyme replacement therapy (ERT) with recombinant human GAA (rhGAA). There is already Inhibitors,research,lifescience,medical a vast literature on the subject (10), and a few problems have emerged, such as the immune reaction to rhGAA in infants with null mutations and no GAA protein (i.e. no cross-reactive immunological material, CRIM) (18). Assumption of rhGAA

into lysosomes is probably hindered by the more general autophagic

dysfunction mentioned above and Inhibitors,research,lifescience,medical several stratagems have been proposed to improve uptake, including conjugation of rhGAA with a synthetic oligosaccharide harboring mannose-6-phosphate (19), combining ERT with chaperones (20), and inhibition of glycogen synthesis (21, 22). One final clinical note: besides skeletal muscle, smooth muscle must also be affected in kinase inhibitor Pacritinib late-onset GSD II because there have been a few reports of cerebral arteriopathies, Inhibitors,research,lifescience,medical often affecting the basilar artery (23, 24). GSD III (debrancher enzyme deficiency; Cori-Forbes disease) The debrancher is a “double duty” enzyme, with two AV-951 catalytic functions, oligo-1,4-1,4-glucantransferase and amylo-1,6-glucosidase. Once phosphorylase has shortened the peripheral chains of glycogen to about four glucosyl units (this partially digested glycogen is called phosphorylase-limit dextrin, PLD), the debrancher enzyme removes the residual stumps in two steps. First, a maltotriosyl unit is transferred from a donor to an acceptor chain (transferase activity), leaving behind a single glucosyl unit, which is then hydrolyzed by the amylo-1- ,6-glucosidase, at which point the branch is off. A singlecopy gene, AGL, encodes the debrancher enzyme.

A free-breathing CT scan with 4-D respiratory correlation was als

A free-breathing CT scan with 4-D respiratory correlation was also obtained to characterize target motion during quiet respiration. If target motion was >5 mm, respiratory gating using the Varian Respiratory Management System™ (Stanford), Cyberknife™ respiratory tracking (Stanford), or the Elekta Active Breathing Coordinator System™ (Hopkins) was utilized during treatment delivery. When available (12 of 18 patients), FDG-PET/CT

scans were fused with simulation scans. SBRT treatment plans were developed using Eclipse™ (Varian, Palo Alto, CA), Multi-Plan™ (Accuray, Sunnyvale, CA), or Pinnacle™ (Philips, Amsterdam, Netherlands). The gross tumor volume (GTV) was contoured Inhibitors,research,lifescience,medical by a radiation oncologist using the simulation scan. An internal target Inhibitors,research,lifescience,medical volume (ITV) was then defined after review of diagnostic imaging, respiratory-correlated

4D-CT, pancreas-protocol CT, and FDG-PET/CT scans. Final planning target volume (PTV) was obtained by an additional 1-3 mm uniform margin expansion of the ITV. The dose was prescribed to the isodose line that completely surrounded the PTV and 6-12 co-planar fields were used to generate the plan Inhibitors,research,lifescience,medical for non-Cyberknife™ treatments. Dose constraints for organs at risk were employed as follows: duodenum—V15Gy<9 cc, V20Gy<3 cc, V33Gy<1 cc; liver—D50%<12 Gy; stomach—D50%<12 Gy, V33Gy<1 cc; spinal cord—V8Gy<1 cc. Institutional standards for patient-specific dosimetric quality assurance were applied. SBRT delivery For non-Cyberknife™-based treatment (N=11), initial patient position was based on cone-beam CT with alignment to spine. Volumetric kV-imaging was then used to align biliary Inhibitors,research,lifescience,medical stent

and/or fiducials to the digitally-reconstructed radiograph. All fiducials were placed specifically for SBRT image guidance using an endoscopic approach (N=11 patients); complications of fiducial placement were observed in only one patient who experienced Inhibitors,research,lifescience,medical laryngospasm and had to return for repeat endoscopy the following day. Common bile duct stents AV-951 were placed endoscopically for relief of symptomatic biliary obstruction and not for purposes of SBRT image guidance, but if a stent was present, then fiducial placement was deemed unnecessary (N=4 patients). If a stent or fiducials were not present, patients were aligned to spine only (N=3). In patients who had previously undergone intra-tumoral fiducial placement, orthogonal kV/MV or kV/kV projection imaging was used to verify fiducial location before first treatment beam delivery and, if indicated, a secondary shift was performed. Active monitoring of treatment delivery accuracy was accomplished using kV and MV projection imaging. For CyberKnife™-based treatment (N=7; fiducials required), initial orthogonal kV/MV or kV/kV projection images were obtained to confirm fiducial location.

In this study, we applied similarity analysis as a quantitative t

In this study, we applied similarity analysis as a quantitative tool to rationalize false positives and false negatives of DOA/Tox screening assays. We have also compiled historical

data on prescription drug usage in the United States to demonstrate how changing patterns of drug use may influence clinical utility of DOA/Tox screening assays. Lastly, we present the results of our own investigation into the causes for positive screening results for PCP and TCA screening assays in our medical center, which has adult and pediatric EDs that serve as a regional toxicology Inhibitors,research,lifescience,medical referral center. Methods Similarity Calculations Similarity searching Inhibitors,research,lifescience,medical uses the ‘find similar molecules by fingerprints’ the site protocol in the library analysis module of Discovery Studio 2.0 (Accelrys, San Diego, CA). The MDL public keys are a fingerprint which uses a pre-defined set of definitions related to structural features [27].

A fingerprint is created based on pattern matching of the structure to this set of 166 keys. These MDL keys are used separately with the Tanimoto similarity coefficient and an input query molecule [21] and will be referred to as ‘Tanimoto similarity’. It should be noted that this type Inhibitors,research,lifescience,medical of similarity algorithm does not recognize differences between stereoisomers (e.g., d- and l-amphetamine or their racemic mixture; citalopram Inhibitors,research,lifescience,medical and escitalopram). Sdf files of the structures of the database compounds are available on request from the authors. Cross-Reactivity Testing and Confirmatory Testing Quetiapine fumarate was obtained from Sequoia Research Products (Pangbourne, United Kingdom). Quetiapine S-oxide, 7-hydroxyquetiapine, Inhibitors,research,lifescience,medical and 11-piperazin-1yl-dibenzo [b, f] [1, 4] thiazepine dihydrochloride (DBTP) were purchased from Molcan (Toronto, Ontario, Canada). These three quetiapine metabolites were tested for cross-reactivity with two different TCA screening immunoassays: (1) Emit® tox™

serum (tricyclic antidepressants) run on Siemens (Dade-Behring) Viva-E analyzers and (2) Biosite Triage® Tox screen. Both assays were performed following manufacturers’ instructions on analyzers used for clinical testing. Urine samples were analyzed by GC/MS to identify a wide range of clinically important drugs and drug metabolites by methods previously described [28]. Patient samples Anacetrapib from five University of Pittsburgh Medical Center hospitals (Children’s, Montefiore, Presbyterian, Shadyside, and Western Psychiatric) showing positive immunoassay screens for PCP or TCAs were followed by GC/MS testing. The studies read FAQ involving human samples in this report qualified as exempt, and the need for informed written consent was waived, as determined by the University of Pittsburgh Medical Center Institutional Review Board.

This is a broader problem in psychiatry, especially with the DSM-

This is a broader problem in psychiatry, especially with the DSM-W. Classification has now moved to the application of a priori criteria derived from panels of experts with a limited evidence base, as opposed to a more empirical approach investigating the occurrence and clustering of individual psychiatric

symptoms as a way of defining selleck inhibitor psychiatric syndromes. This approach is illustrated by recent efforts in AD, which suggest that in neurologic disease empirical classification of psychiatric disorders is more appropriate.37 Such approaches are more replicable across patient populations, better account for the various forms Inhibitors,research,lifescience,medical of comorbidity, and appear to “breed true” over time. In an era where therapy for individual syndromes is

critical in the context of neurologic disease, empirical classification of nosologic entities is more appropriate than the unthoughtful importation of diagnostic entities of DSMTV, which were created for a Inhibitors,research,lifescience,medical different purpose.1 A second common theme is that there appear to Inhibitors,research,lifescience,medical be consistent links between specific types of psychopathology and specific brain areas, no matter what the pathology of the disease. For example, depressive disturbances in neurologic disease are most closely linked to the frontal lobes, the basal ganglia, and the nuclei that produce ascending monoamines such as dopamine, serotonin, and norepinephrine. Other brain structures may be involved when depression presents in other contexts. Delusions appear linked to temporal and to some extent parietal lobes. Cognitive disturbances correlate to more diffuse damage to several areas at once with variation of the cognitive phenotype depending on whether the picture at a given time point is mostly cortical Inhibitors,research,lifescience,medical or subcortical. Syndromes such as apathy and other forms of executive dysfunction appear to reflect

injury in frontal subcortical loop circuits. Thus, psychopathology in neurologic disease seems to have to do more with the specifically affected Inhibitors,research,lifescience,medical brain circuits, rather than the pathology causing the dysfunction in those circuits.1 A more troubling common theme is how selleck chem Crizotinib little is known in this area and what little guidance clinicians have for the detection, treatment, and management of psychopathologic conditions in neurologic disease. This leads to several recommendations that are critical for the advancement of the field: Phenomenology Further empirical study of psychiatric phenotypes Dacomitinib across brain diseases, and over the course of these diseases, is critical. Such study should be broadminded, and attempt to derive disease-specific empirical classifications of psychiatric syndromes rather than importing classifications from DSM-IV or The ICD-10 Classification of Mental and Behavioral Disorders. Clinical descriptions and diagnostic guidelines (ICD 10),50 which were not developed for this purpose.

9) received substantial inhibition in the opener phase and also e

9) received substantial inhibition in the opener phase and also exhibited postinhibitory rebound depolarization. Mutual inhibiting interneurons

that respond with postinhibitory rebound generate rhythmically alternating activity bursts (Perkel and Mulloney 1974; Satterlie 1985). Our data indicate that rebound from opener-phase inhibition triggers closer-interneuron spiking, which in turn temporarily inhibit Inhibitors,research,lifescience,medical opener interneurons during the closer phase. This would explain the tight latency coupling of wing-opener and wing-closer bursts in the motor pattern (Kutsch and Huber 1989). Only opener interneurons (e.g., A3-AO) showed small subthreshold depolarizations following the last syllable cycle

of the chirps, whereas in closer interneurons the depolarization of the last syllable in the chirp slowly decayed (e.g., Fig. 9A). This suggests that once a chirp has started, the alternate bursting of opener and closer interneurons continues until the opener neurons finally fail to generate Inhibitors,research,lifescience,medical a spike burst. Activated by tonic command neuron spike activity, the singing CPG generates Inhibitors,research,lifescience,medical the species-specific calling song pattern with 3–5 syllables grouped to chirps. Constant depolarizing current injection in A3-AO or T3-DO, however, elicited sustained syllable trains, which reliably reset the ongoing chirp rhythm. Subsequent to current elicited syllables, the next chirp always Inhibitors,research,lifescience,medical started after a regular chirp interval. This result contradicts the idea of an independent chirp-cycle generator that periodically drives or inhibits the syllable generating

circuit (Kutsch 1969; Bentley 1969). The chirp rhythm rather originates from activity-dependent inherent network and/or cellular properties (Bentley and Hoy 1972) that regularly silence the syllable generation and let it recover after a normal chirp interval. Additionally, the chirp pattern is stabilized by rhythmic biological activity feedback loops comprising interneurons of the subesophageal and posterior selleckchem abdominal Inhibitors,research,lifescience,medical ganglia (Otto and Hennig 1993; Schöneich and Hedwig 2011) and Entinostat also depends on the activity level of the descending command neurons (Hedwig 2000). Further studies are required to reveal the neural mechanism controlling chirp generation, which probably include activity-dependent slow changes of membrane conductances (El Manira et al. 1994; Harris-Warrick 2010) and/or periodical recovery of strongly depressing synapses (Manor and Nadim 2001). Future prospects Our identification of singing CPG neurons in Gryllus bimaculatus highlights the importance of ganglion A3. The data provide the basis for further studies to establish the functional circuitry of the network and to reveal evolutionary modifications in the singing CPG that account for the distinctive calling song patterns in related cricket species (Alexander 1962).

66) Therapies include medications

66) Therapies include medications lowering heart rate, cardioversion or radiofrequency ablation of arrhythmias, and antiarrhythmic surgery.63) Even though LV function normalizes rapidly with treatment, recurrent tachycardia can cause rapid decline in LV function, development

of heart failure and sudden cardiac death.65) Deficiencies Deficiencies of nutrients, electrolytes or trace elements can cause LV systolic dysfunction. Sometimes these Bortezomib patients exhibit other symptoms of deficiencies, i.e., patients with hypophosphatemia show skeletal muscle weakness.67) These deficiencies are usually associated with malnutrition, intoxication or misuse of illegal drugs. Correction of these Inhibitors,research,lifescience,medical deficiencies can improve LV systolic function with time. Thiamine deficiency Thiamine is a coenzyme that assists in macronutrient oxidation and the production of cellular adenosine till triphosphate.68) Because thiamine is a water soluble B-complex vitamin, thiamine deficiency is usually caused by malnutrition and/or excess diuretic use.68),69) One study Inhibitors,research,lifescience,medical reported thiamine deficiency in about one-third of patients with congestive heart failure.69) Thiamine deficiency is characterized by peripheral vasodilatation,69) and in addition to LV dilatation and dysfunction, these patients may have RV dysfunction with severe pulmonary hypertension.70) The presence Inhibitors,research,lifescience,medical of skeletal muscle edema in patients with

thiamine deficiency induced myopathy can be identified with T2-weighted imaging on magnetic resonance imaging,71) suggesting Inhibitors,research,lifescience,medical the same process may be used to identify myocardial edema in patients with thiamine deficiency and LV dysfunction. With thiamine replacement, the improvement is dramatic and rapid.68),70) Hypophosphatemia Transient Inhibitors,research,lifescience,medical LV systolic dysfunction can occur as a consequence of chronic ingestion

of large quantities of a phosphate, for example as antacid.67) Hypophosphatemia may cause diffuse LV dilatation and dysfunction as well as profound skeletal muscle weakness. After restoration of the serum phosphorus level, LV systolic dysfunction usually normalizes within 2 to 5 weeks.67) Hypocalcemia and hypoparathyroidism Reversible LV systolic dysfunction can be associated with hypocalcemia and hypoparathyroidism.72) The resultant hypocalcemia Batimastat and hypomagnesemia are possible mechanisms of LV systolic dysfunction.72) Carnitine deficiency A small percentage of dilated cardiomyopathy and hypertrophic cardiomyopathy cases result from carnitine deficiency,73) and dietary supplement of L-carnitine improves mortality, especially in children.74) Selenium deficiency Selenium, an essential trace element, is a component of glutathione peroxidase and may prevent oxidative damage to cells. Selenium deficiency has been noted to cause dilated cardiomyopathy, especially in children with poor nutrition.

The non-myocyte cells of the healthy heart account for more than

The non-myocyte cells of the healthy heart account for more than 60% of the cardiac cells, include cardiac fibroblasts (CFs) and endothelial cells (ECs), and are actively involved in the remodeling process. 110,111 Fibroblasts, which are responsible for the synthesis of ECM components, account order Alvocidib for approximately 90% of the non-myocyte cell mass. 110,111 In the stressed

myocardium, fibroblasts differentiate into active myofibroblasts upon a wide range of stimuli (e.g. TGF-β). 89,110 These activated cells can regulate the secretion of ECM components and ECM degrading-enzymes (matrix metalloproteinases, MMPs) and tend to proliferate and migrate, acting to remodel the cardiac interstitium. 89 This process may result in cardiac fibrosis, a hallmark of pathological hypertrophy and HF, which presents with aberrant proliferation of CFs and excessive deposition of ECM proteins in the interstitium and perivascular regions of the myocardium, ultimately impairing

cardiac function. 89 Several lines of evidence indicate that dysregulation of miRNAs during HF occurs in CFs, besides CMCs, thereby contributing to the development of cardiac fibrosis. In particular, the increased miR-21 expression observed in human HF, 70 has been attributed mainly to fibroblasts using the TAC mouse model of HF. 84 Specifically, miR-21 is selectively upregulated in the fibroblasts of the failing heart and has been shown to target Spry1, a negative regulator of ERK-MAPK pathway, which functions to enhance growth factor secretion and fibroblast survival, thus promoting interstitial fibrosis. 84 MiR-21 was also found upregulated in CFs of the infarct zone after ischemia-reperfusion in mice, where it was shown to induce MMP2 (an ECM degrading enzyme) via direct targeting of PTEN, but its role in fibrosis was not further investigated in this model. 112

A more recent study by Liang et al revealed additional evidence supporting a role for mir-21 in fibrosis: miR-21 was upregulated in the border zone of murine hearts after MI, whereas the negative regulator of TGFβ, TGFβRIII, was underexpressed. Further experiments in CFs showed that mir-21 overexpression can enhance collagen production, in part through TGFβRIII suppression, and conversely TGFβRIII overexpression can inhibit mir-21 and reduce collagen production in CFs. 113 Taken together, these studies imply that Batimastat mir-21 upregulation under pathologic conditions in the myocardium may impair cardiac function by contributing to cardiac fibrosis. The miR-29 family has also been found deregulated in the failing heart and associated with the pathological mediator of fibrosis TGFβ. The members of the miR-29 family (miR-29a, b, c) are mainly expressed in the CFs of the murine heart and have been found downregulated in response to a variety of remodeling-inducing stresses (TAC, chronic calcineurin signaling, MI). In vitro experiments in cultured CFs showed that this reduction in miR-29 levels may be triggered upon TGFβ stimulus.

We will then attempt to consider the later stages of dementia, in

We will then attempt to consider the later stages of dementia, in which the patient is promotion information severely demented, and eventually becomes terminally ill. Finally, we will conclude with a discussion of some of the trends in research and health care that will affect our consideration of value conflicts emerging in the future. Approaches in ethics The discipline of bioethics is only a little over 25 years old.5-7 The term ”bioethics“ was introduced into the English language by Potter.8 He coined the term to highlight the need Inhibitors,research,lifescience,medical for broad exploration of the relationship between biology and human values. The use for the term was modified and limited by the Kennedy Institute and others to focus more specifically

on the value considerations associated Inhibitors,research,lifescience,medical with the introduction of new medical technology. Bioethics itself is becoming more unified and professionalized. For example, in the United States, the merging of several organizations has led to the founding

of the new American Society for Bioethics and Humanities. As an inherently interdisciplinary field, defining the knowledge base is challenging. Individuals approach bioethics through philosophy, medicine, nursing, law, empirical social sciences, anthropology, history, Inhibitors,research,lifescience,medical and other disciplines. Appropriate standards for bioethical consultation are being developed. As mentioned above, ethical issues emerge when there are conflicts in what human beings value in a particular social context. They also relate to differences in opinion about what research use only constitutes a virtuous individual or a good life. The dominant mode of ethics practice in the United States is based on an analytical philosophical approach and the application of principles, particularly autonomy, beneficence, Inhibitors,research,lifescience,medical and justice.9; In this secular approach, ethical situations are analyzed in terms of balance among these principles. Autonomy relates to preserving the rights of individuals to make decisions about, their own lives. Beneficence relates to the shared responsibilities we have for each other, particularly the principle

of nonmaleficence, ie, doing no harm. Justice addresses Inhibitors,research,lifescience,medical at the societal level questions of fairness in health care decision making. Ethical decisions arc seen as weighing up these three principles to arrive at the best, course of action in a. particular circumstance. Ethical analysis based on this principled approach is helpful. However, there are other complementary approaches GSK-3 to address biomedical ethical concerns. Discourse or communicative ethics10 is perhaps less abstract and focuses on the practical real-world struggles that individuals face caring for someone with dementia. The focus is on quality communication where the development of trust and clarification of the positions of different parties in the ethical dispute are critical. Casuistry and narrative ethics11 focus on the stories that are told by individuals involved in ethical disputes.

There are some weaknesses in these results, mainly due to the ove

There are some weaknesses in these results, mainly due to the overly simple assumptions used. From the Navitoclax structure perspective of the three constraints mentioned above, we give a brief explanation of the limitations of the earlier works. From the perspective of task and camera constraints, most of the works only consider the coverage of the area while the video resolution and focus are seldom considered; From the perspective of scene constraints, most of the scenes are modeled as a 2D case which is too simple to conduct the real camera network placement, or modeled as a 3D case which is too restrictive because in most of the cases we are only concerned with the surveillance plane area.We give several examples. The surveillance area of [13] is modeled as a rectangle in the 3D cases while we know that in the real circumstances it is a trapezoid which is sensitive to the orientation of the cameras. The constraints in [14,15] only include the coverage rate (FOV is considered), while the resolution and focus are out of the scope of the articles.In this paper, we consider the deployment of homogeneous camera network in the 3D space to surveil a 2D ground plane. For simplicity considerations, the surveillance plane is modeled as a rectangle area which is not essential to our work. We separate the surveillance plane area into n grids, as illustrated in Figure 1. We assume that the probability of choose each grid is the same 1/n and the coverage ratio p can be determined by sampling as illustrated in the next section.Figure 1.The surveillance plane area is divided into n grids no matter the shape of the area.We take a more synthetic constraints set, including the surveillance video resolution, video focus, the camera field of view etc., into consideration. Under the constraints, we propose a probability-inspired particle swarm optimization algorithm to get the optimized camera network placement configuration.The main contributions of this paper can be summarized as follows:-We consider a more realistic problem in that we deploy the cameras in a 3D space to surveil a plane area. Some of the previous works consider the problem in a 2D plane and the FOV of the camera is modeled as a sector which is too simple an assumption, while some works consider the problem in the 3D space and model the FOV of the camera as a cone which is too restrictive an assumption. We can get a more accurate result to solve the camera deployment problem in the 3D space to surveillance of a 2D plane and instruct the real life camera network placement;-We take more constraints into consideration than others, including resolution, focus, FOV.