The impact of glucocorticoids on brain structures can be expected to vary not only with age and disease selleck Crizotinib status, but also with individual genetic and environmentallyimparted selleckbio differences influencing hippocampal volume and connectivity, HPA reactivity, and other neurobiologie factors.39,51 Besides the possibility of persistent synapse or neuron loss induced directly by prolonged hypercortisolemia, glucocorticoid-related derangement of hippocampal Inhibitors,research,lifescience,medical physiology, as described above, may increase vulnerability to damage through other pathophysiologic mechanisms. This latter effect may become clinically relevant

in older persons with co-occurring neuronal insults such as accumulating AD pathology or cerebrovascular Inhibitors,research,lifescience,medical disease, promoting synapse or neuron loss through a synergistic relationship with these factors. The loss of hippocampal volume and memory function observed in some elders with late -life depression suggests the possibility that depression may be a predispositional risk

factor for AD in particular. Indeed, lower hippocampal volumes independently predict subsequent AD in groups of MCI and cognitively normal elderly subjects.52 Likewise, deficits Inhibitors,research,lifescience,medical in verbal learning and memory, similar to those described in cuthymic patients with history of major depression,30 also predict AD (eg, ref 53). While a primary causal role for depression in AD pathogenesis seems unlikely, depression-associated hypercortisolemia leading to decline in hippocampal size, connectivity and cognitive function may represent one of multiple links between depression

and dementia as described below (also see Figure 1). Biologic relationships between depression and Alzheimer’s Inhibitors,research,lifescience,medical disease The association between depression and dementia suggested by epidemiologic data10,11 may be partially explained by one or more direct, mechanistic links between late-life depression-related processes and ADspecific neuropathology (focal and diffuse Inhibitors,research,lifescience,medical cortical neuronal loss, P-amyloid plaques, and neurofibrillary tangles). Emerging evidence from neuroimaging studies, postmortem neuropathology analyses, and animal models provides support, for such links. Some structural GSK-3 magnetic resonance imaging (MRI) studies find that hippocampal atrophy is more strongly associated with late-onset than early-onset depression, suggesting that early AD-related pathophysiology could generate both hippocampal atrophy and depressive symptoms in some elderly persons.54,55 In addition, one of these studies failed to find a significant correlation between hippocampal volume and Cortisol level among elders with depression. Furthermore, the late-life depression subjects showed persistent memory and cognitive impairment at 6-month follow-up despite effective treatment of mood symptoms and normalization of Cortisol levels.

2007; Colom et al. 2012). We have also demonstrated the spatiotemporal localization of JAM-C following sciatic nerve crush injury in rats, and shown a strong selleckchem Ponatinib correlation with the process of remyelination after injury. Furthermore, we have shown that, at 56 days after injury, there is

a persistent upregulation of JAM-C in the distal nerve Inhibitors,research,lifescience,medical and the morphology of JAM-C immunoreactive paranodes and incisures appeared abnormal compared to the controls. In addition, we observed significant numbers of JAM-C immunoreactive paranodes that did not express the nodal marker, jacalin, and this may indicate that JAM-C localization precedes node formation. The spatiotemporal http://www.selleckchem.com/products/z-vad-fmk.html pattern of JAM-C localization after sciatic nerve injury Our observations at various time points postinjury demonstrate a transient loss of JAM-C localization followed by a progressive gradual reappearance, which is in keeping with previous studies of paranodes (Burnett and Zager 2004). Inhibitors,research,lifescience,medical This temporal pattern of localization was further corroborated by the changes expressed spatially ranging from the highest levels of JAM-C close to the site of crush, with ensuing decline through the remaining distal nerve. This occurred at all time points except the longest (56 days), Inhibitors,research,lifescience,medical when the density of JAM-C immunoreactive paranodes was highest in the most distal region of the nerve. Three days after

injury, we expected that the level of JAM-C localization Inhibitors,research,lifescience,medical would have decreased dramatically in the distal nerve. However, although JAM-C localization was very low in the most distal regions, there remained significant JAM-C localization in the region just distal to the crush site. It is probable that this pattern of JAM-C localization was caused by Wallerian Inhibitors,research,lifescience,medical degeneration progressing in a retrograde direction with fragmentation beginning at the distal end, resulting in slightly higher numbers of JAM-C immunoreactive paranodes and incisures at the near-distal region than more distally along

the nerve. The progressive nature of Wallerian degeneration has long been controversial, with conflicting reports over the directionality and whether the distal stumps of the injured axons degenerate anterogradely, retrogradely, or simultaneously (reviewed in Joseph 1973; Lubinska 1975; Chaudhry et al. 1992). Consistent with recent reports (Lunn et al. 1990; Beirowski et al. 2005), we show the progressive nature of Wallerian degeneration begins distally after Entinostat crush injury. The reason for this is not known, but may be due to the distal end of the nerve being more vulnerable to compromised anterograde axonal transport (Beirowski et al. 2005). At later time points (e.g., 28 days), the proximo-distal gradient of JAM-C localization is consistent with regeneration proceeding in the anterograde direction, and Schwann cells re-expressing JAM-C as they mature into a myelinating phenotype.

19 To date, this has not been explored in Iranian populations. Therefore, we investigated the association between DNMT3B genotype and the risk of breast cancer

incidence among sporadic breast cancer patients in Fars Province, Southern Iran. Materials and Methods Study selleck chemicals Vismodegib subjects A total of 100 sporadic breast tumor samples (95 fresh and 5 paraffin-embedded) were obtained from the Department of Pathology, Shiraz University of Medical Sciences, Shiraz, Iran Inhibitors,research,lifescience,medical from 2003 to 2006. Fresh samples were snap-frozen immediately after surgery and stored at -70°C. All samples were subjected to re-evaluation of the original histological diagnosis by an expert pathologist who also selected Inhibitors,research,lifescience,medical representative areas of the tissue sections for DNA extraction and further molecular analysis. Each patient’s clinicopathological information that included age, tumor size, type, grade and site, estrogen and progesterone receptor and lymph node involvement status was obtained from hospital records. The 138 healthy control females, matched for age with the case subjects, were selected from a pool

of cancer-free subjects who volunteered to join the epidemiology Inhibitors,research,lifescience,medical survey during the same period. For the control group, normal genomic DNA was prepared from blood lymphocytes. This investigation was approved by the Ethics Committee of Shiraz University of Medical Sciences. DNA Extraction Inhibitors,research,lifescience,medical and DNMT3B Genotyping Genomic DNA was isolated from tumor samples (case group) and peripheral blood

lymphocytes (control group) using a www.selleckchem.com/products/AZD2281(Olaparib).html Cinnagen genomic DNA purification kit (Cinnagen, Iran). The purity and concentration of DNA were assessed by spectrophotometric measurement of absorbance at 260 and 280 nm. DNMT3B C/T polymorphism was analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The PCR sense (5´-TGCTGTGACAGGCAGAGCAG-3´) and antisense (5´-GGTAGCCGGGAACTCCACGG-3´) primers were used to amplify the target DNA Inhibitors,research,lifescience,medical as previously described.18 Briefly, we used 25 μl of PCR mixture that contained 100-300 ng of DNA template, 12.5 pmol of each primer (Takapoo Zist Company, Iran), Brefeldin_A 0.1 mmol/L of each deoxynucleotide triphosphate, 1×PCR buffer (50 mmol/L KCl, 10 mmol/L tris-HCl, and 0.1% Triton X-100), 2.0 mmol/L MgCl2, and 1.25 U Taq polymerase (Cinnagen Company, Iran). The PCR amplification profile consisted of an initial denaturation step at 95°C for 5 min, 35 cycles of denaturation at 95°C for 30 s, annealing at 65°C for 30 s, and extension at 72°C for 30 s. This was followed by a further extension step at 72°C for 10 min. The 380 bp PCR products were digested overnight with 5 units of AvrII (Vivantis Company, Malaysia) at 37°C and separated on 2% agarose gels. The digested product was visualized by red gel staining under UV illumination.

76 The BNST is considered to be part of the extended amygdala.77

It appears to be a center for the integration of information originating from the amygdala and the hippocampus (Figure 1), and is clearly involved in the modulation of the neuroendocrine stress response.78,79 Activation of the BNST, notably by corticotropin-releasing factor (CRF), may be more specific for anxiety than fear. Studies in rats with the startle reflex suggest that explicit cues such as light, tone, or touch activate the amygdala, which then activates hypothalamic and brainstem target areas involved in the expression of Inhibitors,research,lifescience,medical fear, whereas less specific (or more complex) stimuli of longer duration, such as exposure to a threatening environment or intraventricular administration of CRF, may preferentially involve the BNST.73 The PFC and the control of emotional responses The primary roles of the PFC appear to be the analysis of complex stimuli or situations and the control of emotional responses. In a revised version of his Inhibitors,research,lifescience,medical original BIS model, Gray postulated that the PFC may modulate septohippocampal activity, and Inhibitors,research,lifescience,medical that lesions to this area would impair the processing of vital information for the subicular comparator, and subsequently

affect behavioral inhibition and anticipatory anxiety.51 He also suggested that the role Inhibitors,research,lifescience,medical of cortical structures in anxiety was probably more prominent in primates, based on the increased anatomical relationship between the septohippocampal system and the prefrontal and cingulate selleck cortices observed in monkeys. Recent studies in humans and primates have largely confirmed Gray’s hypothesis, and it is now clear that the various subdivisions of the human PFC

(dorsolateral, ventromedial, and orbital sectors) have specific roles in representing affect in the absence of immediate rewards or punishments and in controlling emotional responses.80,81 Inhibitors,research,lifescience,medical There appear to be important functional this explanation differences between the left and right sides within each of these sectors. Earlier studies on patients with unilateral brain lesions have GSK-3 already emphasized the role of cerebral lateralization in emotional information processing.82 More recently, brain electrical activity measures and positron emission tomography (PET) studies have indicated that negative affect and anxiety are associated with increased activation of the right PFC; moreover, individual differences in baseline levels of asymmetric activation in the PFC may be associated with individual differences in affective styles and vulnerability to mood and anxiety disorders.81 There is also increasing evidence that the PFC plays an important role in controlling anxiety and the associated stress response in rats, and that cerebral laterality is an important feature of the PFC system.

This number was 5.5% in the Roushan17 study (table 6). Table 6 Frequency of sacroiliac involvement (percentage of all skeletal involvement Spondylitis Spondylitis possesses an insidious nature and produces mild pain despite the presence of obvious radiological signs.28 There is local tenderness or limitation of motion, or both. With an increase in the severity and extent of the disease, difficulty in walking and symptoms of pressure

on the spinal cord may be reported on physical examination. The lumbar region is the most common site of involvement. Sometimes para-spinal abscesses also occur, though with a smaller size than that of tuberculous abscesses. An incidence rate of even Inhibitors,research,lifescience,medical up to 16% for these Inhibitors,research,lifescience,medical abscesses in brucellosis has been reported. Spondylolisthesis, paraplegia, and sphincter malfunction

as a result of brucellosis have been reported. Unlike sacroiliac involvement, spinal involvement in brucellosis is often associated with graphic signs. Most of the time, brucellosis involves Inhibitors,research,lifescience,medical the anterior superior vertebral endplate, resulting in the epiphysitis of the anterior superior angle. Al-Eissa4 observed no case of brucellosis spondylitis in 40 children with skeletal complications. In a research by Geyik,6 17.94% of the children and 24.59% of the adults suffering from the skeletal complications of brucellosis had spondylitis. In both age groups, the most common sites of involvement were the lumbar, dorsal, and cervical areas, respectively. Inhibitors,research,lifescience,medical In another study by Gür,5 very similar figures were obtained: 17% of the children and 24% of the adults with skeletal complications of brucellosis had spondylitis. Some clinical and paraclinical findings of children and adults with brucellosis are compared in tables 7 and ​and88. Table 7 Comparison of the frequency of paraclinical

Inhibitors,research,lifescience,medical findings (reported in percentages) between children and adults with skeletal involvement of brucellosis Table 8 Comparison of the frequency of clinical findings (reported in percentages) between children and adults with skeletal involvement of brucellosis Limitations Sorafenib Tosylate Raf Paucity of articles on the skeletal involvement of B. melitensis in children is the most important limitation of this review. Conclusion Brucellosis is a protean disease and is reported to involve various areas Carfilzomib of the skeletal system. Nevertheless, clarification of all the Ceritinib chemical structure aspects of this issue in children requires a thorough and precise observation and documentation of the relevant data in the future. Conflict of Interests: None declared.
Dear Editor, Stroke is truly an important disease, especially because of its morbidity and mortality the world over. Wiwanitit and Wiwanitkit also confirmed this opinion and pointed out some important features of stroke in tropics in their review article published in the Journal.

Each

of these steps leads to concomitant changes in protein complexes, starting from the phosphotransfer http://www.selleckchem.com/products/CHIR-258.html system to carbohydrate metabolizing enzyme complexes. However, as these two examples already show, the sequence of changes depends on the succession of concentration changes, the last example would refer well to a situation where there are high concentrations of glucose and, in the end, there is some lactose available to profit from the switch. The prokaryotic response to changing metabolic conditions is thus condition dependent (see e.g., Jozefcuk [6] for data on E. coli). However, our overall current Inhibitors,research,lifescience,medical understanding of the involved, fine-tuned regulation and feedback, as well as feedforward, loops is limited. More studies to elucidate the details of such physiological changes in protein complexes and bacterial responses to metabolic changes are clearly needed. In fact, system switching states occur often fast in bacteria. Whole cascades or even larger networks are rapidly reorganized as the whole network is controlled often

by one master regulator. A good example is the Inhibitors,research,lifescience,medical pathogenicity switch by the PrfA protein Inhibitors,research,lifescience,medical of Listeria which simultaneously accomplishes (i) adaptation of a number of virulence pathways, and (ii) reorganization of nutrient utilization, thus facilitating adaptation of L. monocytogenes from a more saprophytic to an intracellular lifestyle. Also in Staphylococci (and many other bacterial species), such major system changes in metabolism (stress response or growth behavior) are mediated with tight control just by the activation of transcription factors (including repressors such as the Rex family). Other switching states include diauxic shift, glucose limitation under aerobic or anaerobic conditions, Inhibitors,research,lifescience,medical differentiation (e.g., biofilm formation) or amino acid limitation. In a full “on” state for sellectchem pathways and networks (e.g., growth on full medium and central carbohydrate metabolism)

correlation between gene expression and metabolite flux is high. For not-so-central pathways, Inhibitors,research,lifescience,medical gene expression data may provide a lower limit as the metabolite flux can still become higher when enzymes are regulated Drug_discovery to be more active. However, for such a system-switching state the correlation in activity for the pathways changed simultaneously is high, as seen both for S. aureus [41], as well as in other organisms (e.g., Jozefcuk [6] for E. coli). Besides the high correlation between the concerned pathways, there are structural changes in complexes such as pyruvate dehydrogenase complex, central for carbohydrate metabolism to accompany such system changes (see examples above). However, the involvement for transcription and regulatory factors, changes in the respective protein complexes, correlated pathway changes and correlation between different data sets also apply to other major system changes such as bacterial differentiation (sporulation, apoptosis) and adaptation in general.

Conversely, postmortem AD studies suggest an association between more severe plaque and tangle pathology and lifetime depression history MG132 133407-82-6 preceding AD diagnosis,56 offering support for the idea that, prior depression is a true, etiologic risk factor for AD, as suggested by other epidemiologic data (eg, ref 11). Furthermore, both stress and exogenous glucocorticoids increase P-amyloid production in rodent, models of AD, consistent, with a direct. biologic role of human depression in AD pathogenesis. ‘Ihesc disparate hypothesized relationships arc not exclusive of one another. Given the tremendous Inhibitors,research,lifescience,medical heterogeneity of late-life depression, various

dementia pathologies, and the other clinical or subclinical

disease inevitably present in older individuals, depressive symptoms should be expected to bear an inconsistent relationship with cognitive decline, dementia in general, and AD specifically. Such symptoms Inhibitors,research,lifescience,medical in a given elderly individual may potentially represent either prodromal AD, or an independent process interacting with AD-related pathophysiology. As discussed in this manuscript, Inhibitors,research,lifescience,medical depression may furthermore contribute to cognitive decline and AD through glucocorticoid-relatcd hippocampal toxicity and interrelationships with other types of pathology such as vascular disease. Role of vascular disease in late-life depression, cognitive decline, and dementia Substantial data exist showing an association between latelife

depression and cerebrovascular changes. In separate reports, Alexopoulos65 and Krishnan66 Inhibitors,research,lifescience,medical pointed to the thennascent evidence that a subgroup of individuals with latelife depression showed evidence of cerebrovascular changes. Alexopoulos coined the term “vascular depression,” positing that, a subgroup of individuals experience Inhibitors,research,lifescience,medical disruption of prefrontal systems that mediate both mood and executive functions, by either single vascular lesions or accumulation of lesions. ‘Ihc concept of vascular depression has subsequently been supported and expanded by a growing literature. Depression and vascular disease display Brefeldin_A an interesting bidirectional relationship. Depression increases risk for first-ever myocardial, infarction (MI) and stroke, and has been shown to predict worse selleck compound outcomes in a wide range of concurrent vascular disease states (reviewed in ref 67). Notably, clinical diagnosis of major depression confers significant relative risk for MI,68 stroke,69 and post-MI cardiac mortality.70,71 Moreover, major depression confers greater relative risk than diagnosis of dysthymia or indices of self -reported depressive symptoms, suggesting a possible dose-response relationship between severity of depressive illness and excess cardiovascular risk.67 Diverse mechanisms have been proposed to explain the link between prior depression and subsequent vascular disease.

Therefore, dye method alone may not be suitable for SLN mapping in oesophageal cancer (35).

With the use of three selleck kinase inhibitor serial sections and immunohistochemistry on negative SLNs, 14% (3/22) of http://www.selleckchem.com/products/Sorafenib-Tosylate.html patients were upstaged (35) and Lamb et al. also found that 12% (3/25) of pN0 patients were upstaged following immunohistochemistry Inhibitors,research,lifescience,medical analysis (27). The routine use of SLN biopsy in oesophageal cancer cannot alter or limit the extent of lymphadenectomy in the same way as is seen in breast cancer and melanoma. And in oesophageal cancer, preoperative access to sentinel nodes may be as invasive, and as morbid, as the operation itself. But, if one agrees that isolated tumour cells have prognostic significance in oesophageal cancer and are detected in 12-14% of node-negative patients using serial sections and immunohistochemistry, then the SLN concept becomes the only practical method of improving pathological staging

(35). So, although sentinel node biopsy has not yet Inhibitors,research,lifescience,medical been shown to minimize the extent of lymphadenectomy, it may influence postoperative therapy for a substantial number of patients. Perhaps the key drawback with SLN biopsy in oesophageal cancer is the variety of SLN tracer authorized Inhibitors,research,lifescience,medical for clinical use in each nation (54). The vastly diverse particle sizes hinder wide application of the model and design of a uniform practice. For instance, Japan’s 99mTc-tin colloid (100 nm in size) Inhibitors,research,lifescience,medical allows for lymphoscintigraphy 24 h before surgical resection (23), while other smaller radio colloids (like Australia’s 99mTc-antimony trisulphide colloid) have much shorter transit periods in the sentinel nodes (54,55). We observed that Inhibitors,research,lifescience,medical the parameters like sensitivity, accuracy and detection rates were higher in radioisotopes

when compared to methylene blue or patent blue dyes (Table 6). Facilitating preoperative lymphoscintigraphy in between endoscopic peritumoural injection and same-day surgery is often not practical. Table 6 Information about the particle property, injection technique and pathological analysis Skip metastases Another criticism in the literature GSK-3 about SLN biopsy in oesophageal cancer is the described high frequency of skip metastases, although most of these outcomes have been in patients with squamous cell carcinomas (27,35). If SLNs without metastasis are identified only in abdominal lymph nodes, especially in the tumours limited to the lower third of the oesophagus, cervical lymph nodes dissection may be omitted, such as left thoracotomy or trans-hiatal approach. SLN navigation surgery also is unacceptable for patients who have had neoadjuvant therapy (25). Limitations The studies included in the meta-analysis are predominantly from Japan and hence generalization of such results cannot be made.

Parenthetically, the issue at hand is whether we can select our patients better so as to (I) identify patients with strictly borderline/locally advanced non-metastatic disease a priori and treat them with chemoradiation therapy and (II) intensify

this local therapy in those patients who are likely to have local tumor progression as the predominant source of disease-related mortality? Improvements in imaging techniques Inhibitors,research,lifescience,medical have significantly enhanced our ability to identify the extent of locoregional disease in the pancreas and stratify pancreatic cancer into potentially resectable, borderline resectable, and locally advanced. Nevertheless, accurate identification of metastatic disease remains a challenge because of the frequent occurrence of occult metastatic deposits in the liver and peritoneum that are not readily visualized non-invasively by current imaging Inhibitors,research,lifescience,medical technology. We and others have addressed this therapeutic dilemma by using induction chemotherapy to either treat micrometastatic disease or give occult metastatic disease an opportunity to manifest itself on subsequent imaging (7,8). By excluding patients with metastatic disease identified Inhibitors,research,lifescience,medical on repeat imaging after chemotherapy, the pool of patients who undergo consolidative chemoradiation therapy is

enriched with those who are most likely to have localized non-metastatic disease. Concentrating a localized treatment modality on these patients offers the possibility of these patients reaping the maximum benefit of standard chemoradiation therapy. With the advent of newer chemotherapeutic regimens with greater systemic efficacy like FOLFIRINOX and gemcitabine-abraxane, this sequencing of chemotherapy followed Inhibitors,research,lifescience,medical by chemoradiation

therapy may further select patients for maximum benefit from chemoradiation therapy. The next challenge is to further select these patients for intensification of local therapy with a focal radiation boost in those patients predicted to have Inhibitors,research,lifescience,medical a pattern of failure where local relapse is the dominant site of recurrence. Indeed, there is converging evidence that, contrary to the pathway signaling widespread perception that all patients with pancreatic cancer die as a result of distant metastatic disease, complications of local tumor progression are a product information significant source of disease-related mortality. Selecting these patients for intensified radiation therapy is therefore a viable therapeutic strategy if a biomarker of local-dominant biology can be identified and validated. A recent Batimastat autopsy study of pancreatic cancer patients noted that intact Smad4 expression in tumors predicts for a predominantly loco-regional failure pattern (9). This correlation was also observed in locally advanced pancreatic cancer patients treated with chemotherapy followed by chemoradiation therapy (10). This provides a rationale for potentially personalizing and intensifying radiation therapy via a focal boost in patients with intact Smad4.

At this point we suggest repeating the vascular imaging examination every 5 years, which is about the mean follow-up in previous randomized clinical studies, during which no major cardiovascular event occurred in these very-low-risk patients. Further prospective

studies are required to determine if and when repeated examination is required, but this time-frame Inhibitors,research,lifescience,medical is reasonable in light of the position stated by the panel of radiologists who recommended that patients who have normal carotid ultrasound (US) studies but marked risk factors, thus not low risk, might be evaluated every 3–5 years.15 In Israel, many thousands of subjects with very low FRS (less than 6%), mostly women, are selleck chemicals llc treated with statins (personal knowledge). Inhibitors,research,lifescience,medical In a recently published study,16 half of low-risk patients who underwent CCTA showed no vascular pathology. Thus, a large proportion of subjects from this category will be treated

with statins, and, of these subjects, at least 10%–15% suffer from myopathy but are still encouraged by their physicians to continue the medication. We suggest that in these very-low-risk subjects, if vascular imaging shows no CAC or normal CIMT without plaques, statin treatment need not be administered, with the exception of subjects with Inhibitors,research,lifescience,medical low FRS with a family history of CAD at young age. In our view, vascular imaging is also cost-effective, especially in the long run. The cost of CT for evaluation of CAC or Inhibitors,research,lifescience,medical US carotid artery examination in our institution is about $130, which is about the equivalent of 1 year of treatment with low-dose generic statins, blood tests, and visits to the physician. In summary, we suggest using vascular imaging as a method to reduce significantly the number of subjects who, in our opinion, would not benefit from Inhibitors,research,lifescience,medical statins and only suffer from their side-effects. As P.K. Shah has previously well formulated17:

“If the goal of using a statin is to reduce atherothrombotic cardiovascular events, then it is unrealistic to expect those patients without significant atherosclerosis to benefit from statin therapy even if they have hyperlipidemia. In such subjects, one can only expect side effects.” Abbreviations: CAC www.selleckchem.com/products/Tubacin.html coronary artery calcification; CAD coronary artery disease; CCTA cardiac CT angiography; CIMT carotid artery intima-media thickness; CV cardiovascular; CVD cardiovascular disease; FRS Framingham Risk Score; US ultrasound. Footnotes Anacetrapib Conflict of interest: No potential conflict of interest relevant to this article was reported.
In the last 50 years our technological abilities have expanded in an unprecedented way and have undergone several phases that have dramatically changed our lives. Advances have been made in material sciences, chemical analysis, physics and imaging, communications, energy transmission, miniaturization of devices and material structures, and nanotechnology.