Nanoxel-PM is efficacious and less toxic than free docetaxel formulation and was evaluated in comparison with Taxotere in preclinical studies. Nanoxel-PM can reduce sideeffects of hypersensitivity reactions and fluid retention while retaining antitumor efficacy in cancer patients [22]. Further MK-2206 order studies led to the development of new formulations of liposomal paclitaxel. The special composition of the liposomal membrane which contains high doses

of paclitaxel could reduce the aggregation giving the molecule higher stability and confers an increase of efficacy in animal models as in human tumors [23]. An hydrotropic polymer micelle Inhibitors,research,lifescience,medical system has also been developed for delivery of poorly water-soluble drugs as paclitaxel. This polymer showed not only higher loading capacity but also enhanced physical stability in aqueous media and provides an alternative approach for formulation Inhibitors,research,lifescience,medical of poorly soluble drugs [24, 25]. 3. Nab-Paclitaxel in Breast Cancer Treatment Breast cancer (BC) is the most common cancer in female patients and follows lung cancer as the most common cause of female cancer death. While only 5–7% of BC patients present metastatic disease (mBC) at diagnosis and more than 30% presenting localized disease will eventually recur, 5 year survival of advanced disease is

Inhibitors,research,lifescience,medical less than 20% [33]. Current treatment of advanced breast cancer is mainly aimed to ameliorate quality of life and prolong survival. Treatment choice is not an easy task in terms of drug selection and combination. Chemotherapy plays an essential role for the treatment of Inhibitors,research,lifescience,medical mBC. Among anticancer drugs, taxanes are

considered the most effective, while their use involves long infusion time, neurotoxicity, and high risk of hypersensitivity reactions [8, 34, 35]. These latter effects are due to allergic reactions induced by the use of solubilizing agents (as chromophores) and Inhibitors,research,lifescience,medical today are less common due to the use in the clinical practice of corticosteroids and antihistamines [36]. In order to overcome these important limitations, a major interest is devoted to novel drugs as nab-paclitaxel, eribulin, ixabepilone, PARP inhibitors, and new HER 2 inhibitors as lapatinib, pertuzumab, TDM1, and neratinib [37–43]. Following phase I studies, others by Ibrahim et al. in 2002 [19] and by Teng et al in 2004 [44], which led to MTD identification at 300mg/m2 in the three weekly schedule with neurotoxicity as dose limiting toxicity, Nyman et al. in 2005 [45] identify in the weekly schedule the MTD at 100mg/sqm for highly pretreated patients and 150mg/m2 for nonhighly pretreated patients with grade 4 neutropenia and grade 3 neuropathy as DLT with earlier onset at higher dosages. The pivotal phase 3 study was published in 2005 where Gradishar et al.

2012) as specified by the manufacturer (see the technical information data sheet). Cytochrome oxidase (CO) staining Two rats were used to verify the possibility of using the technique in this series of experiments. Animals were perfused and tissues postfixed and cut as described

above. Brains were freeze sectioned in the sagittal plane. Two consecutive sections, one per stereotaxic plane, were used in two different ways. The first sections (60 μm thick) were incubated at 37°C in the dark for 10–12 Inhibitors,research,lifescience,medical h in a solution containing 50 mg DAB, 30 mg cytochrome C (Type III, Sigma), and 4 g sucrose dissolved in 90 mL PB (0.1 mmol/L, pH 7.4; Wong-Riley 1979). Incubation was arrested when a clear differentiation between cerebral cortex and cc was visible. Sections were rinsed many times in PB, mounted on subbed slides, air-dried, dehydrated Inhibitors,research,lifescience,medical in xylene and then

coverslipped. The adjacent sections (40 μm thick) were counterstained with neutral red (1% in aqueous solution) and then coverslipped. Selected sections from CC-NADPH-1/11, CC-nNOS-1/6 and CC-Fl-1 and -2 were used for CO staining as described above. Data analysis The distribution of NADPH-d+ Inhibitors,research,lifescience,medical and NOSIP neurons in the cc was obtained using a camera lucida attached to a Leitz Orthoplan microscope equipped with a 25× objective. Callosal boundaries were obtained by comparing the sections reacted for COHi with those counterstained with neutral red. The reconstructions thus obtained were

then compared with those of the atlas of Paxinos Inhibitors,research,lifescience,medical and Watson (1982). Counts were performed in serial sagittal sections from two animals (CC-NADPH-10-11; see Table ​Table2).2). The total number of intracallosal NADPH-d+ neurons was calculated on sections from both hemispheres starting from the lateral 4.5 sagittal plane of one hemisphere to reach Inhibitors,research,lifescience,medical the same stereotaxic plane in the contralateral hemisphere. Table 2 (A) Arbitrary subdivisions of the rat cc, (B) Number of NADPH-d+ neurons in the three subdivisions of the rat cc Microscopic studies of the morphology and percentage of intracallosal neurons (three cases: CC-NADPH-d-5; -7; -9; see Tables ​Tables3,3, ​,4)4) were tuclazepam performed using staining criteria Onalespib mw similar to those of previous Golgi and NADPH-d studies (Jacobs and Scheibel 1993; Jacobs et al. 1993; Phillips et al. 2000; Barrera et al. 2001). Selected neurons, drawn using a camera lucida and a 100× oil immersion objective, exhibited the following characteristics: (1) labeled neurons had a clearly distinguishable morphology; (2) cell bodies had a central location within the 60-μm section depth to minimize the cutting of dendritic branches near the section surface; (3) dendrites were not overly obscured by other heavily stained processes from nearby cells; (4) dendritic trees were intensely labeled and did not show discontinuity with their cell bodies.

This clearly explains why the distance between species cannot be measured only by sequence comparisons. Based on such calculations we can indeed conclude that we are closer to chimpanzees than to mice (we know this from other physical traits), but this does not mean that we are 98.77% chimpanzee and 80% mouse. An important message here is Inhibitors,research,lifescience,medical that what counts is not the number of mutations, but where they occur – where they hit the genome. Mutations in regulatory domains are not identical, in term of consequences, to mutations in coding sequences. Their effects will vary depending

on the type of gene under their control; for example a developmental gene or a gene encoding a protein of little physiological importance, eg, eye color. Also in the case of coding sequences, some mutations can have important evolutionary consequences, as will be illustrated in the case of FoxP2, a transcription factor that Inhibitors,research,lifescience,medical may have played a role in the evolution of animal behavior and communication.12 Finally, it must be underlined that, also for coding sequences, some mutations are silent and others possibly dramatic, depending on the similarities or differences between the normal amino acid and the new Inhibitors,research,lifescience,medical one

resulting from the mutation. Technically speaking, some substitutions are synonymous and others nonsynonymous. Point mutations accounting for the 1.23% difference are not the end of the story If one considers the genetic diversity of our species, and its approximate date of appearance (200 000 years ago, more or less), it can be deduced that the founding population was composed of

approximately 10 000 individuals. The fact that we have the same number of genes as the chimpanzees from whom we separated 7 million Inhibitors,research,lifescience,medical years ago leads to the conclusion that mutations in regulatory domains have been decisive. For example, a mutation in a gene regulating the division of neural stem cells in a given region of the brain neuroepithelium will specifically modify the size of this region.10,13 The conclusion is evident: the famous 1.23% implies Inhibitors,research,lifescience,medical sequences of considerable qualitative importance, including regulatory elements of Resveratrol developmental genes, with potentially spectacular effects on the morphology and physiology of the organisms. Most importantly, the differences are not limited to the 1.23% of point mutations, as one must add all genomic deletions and Rucaparib molecular weight insertions, plus the duplications that modify gene dosage. Given the size of the human genome, 1.23% translates into 30 million point mutations (a number not to be underestimated), to which one should add duplications, insertions, and deletions (between man and chimpanzee, gene copy numbers differ by more than 6%). Taken together, mutations, duplications, insertions, and deletions modify the global chromatin structure, and thus the regulation of gene expression.

This can be exemplified by one of the earliest phenomenographic studies carried out in Sweden, which searched for qualitative differences between individual students as to the outcome and process of their learning, based on their written reports after reading

an academic text. The results Selumetinib in vivo revealed a hierarchy of categories in terms of depth of learning (from surface to deep learning), which reflected in turn the qualitatively different ways the students had comprehended the text (Richardson, 1999). Notwithstanding this pedagogical focus, phenomenography has in recent years gained the interest of healthcare researchers as well, as, with its unique empirical approach, it has the potential of adding to knowledge within a healthcare framework (Barnard et al., 1999; Sjostrom & Dahlgren, 2002). In the work presented here, we were interested in the phenomenographic study of patients’ experiences of chronic illness. The prevalence of chronic illnesses worldwide is increasing, as the result of better possibilities PF-02341066 concentration for treatment and survival (Wagner et al., 2001). Chronic illnesses are here defined as illnesses

that are prolonged in duration, do not often resolve spontaneously, and are rarely cured completely. They may require repeated periods of treatment from healthcare providers and may also need to be managed by patients (Audulv, 2013; Wagner et al., 2001). Herein, based on this need to manage the illness, lies the potential of the phenomenographic approach in healthcare research, as the ways that patients experience their illnesses can be used as sources of knowledge in patient education and

patient empowerment (Stattin, 2001). In learning to live with a chronic illness, patients need to understand not only their illness, but the way they experience it. Giving patients the opportunity to reflect upon their ways of experiencing can give them insight into their own needs and reactions, which then can lead to Org 27569 making decisions and taking control (Stattin, 2001). In a preliminary exploratory search for previous research on chronic illnesses with a phenomenographic approach, we found a long series of studies, almost exclusively from Sweden. These studies, which dealt with different chronic illnesses, were each based on the experiences of few informants. Therefore, we decided to synthesize these studies using a meta-ethnographic method which allowed for an interpretation of the results within a phenomenographic framework. Thus, our aim was not to describe patients’ various individual experiences of illness, but instead to identify the different ways chronic illness can be experienced by patients. Method The method chosen for our synthesis of research studies using a phenomenographic approach was meta-ethnography. This method, developed in 1988, is an inductive and interpretive form of knowledge synthesis (Noblit & Hare, 1988).

5-Oxo-ETE is a potent chemoattractant for eosinophils, neutrophils, basophils and monocytes, an activity that is thought to be mediated activation of the Gi/o coupled OXE receptor [38]. Glutathione-S-transferase (GST)-mediated metabolism of 5-oxo-ETE results in the formation of 5-oxo-7-glutathionyl-8,11,14-eicosatrienoic

acid (FOG7), which has similar biological activity to the parent 5-oxo-ETE [39]. In contrast to 5-LOX, which strongly prefers free arachidonic acid as its substrate [40], mammalian 15-LOXs are capable of oxygenating both free and esterified polyunsaturated fatty acids [41]. selleck chemicals 15-LOX can also oxidize more complex lipid-protein assemblies Inhibitors,research,lifescience,medical such as biomembranes and lipoproteins [42,43]. Type 1 human 15-LOX (15-LOX-1), which is mainly expressed

by reticulocytes, eosinophils and macrophages, converts esterified arachidonic Inhibitors,research,lifescience,medical acid to esterified 15(S)-HPETE and a small amount of 12(S)-HPETE; [44]. 15-LOX-1 is a cytoplasmic enzyme with up-regulated expression in atherosclerotic lesions and at sites of macrophage accumulation [45]. Studies of 15-LOX-1 in hematopoietic cells have demonstrated that it translocates to the inner plasma membrane Inhibitors,research,lifescience,medical and other non-nuclear membranes (e.g. sub-mitochondrial membranes) after stimulation with calcium [46]. It has been suggested that 15-LOX-1 plays an important role in angiogenesis and carcinogenesis [47]. This stems from the observation that both angiogenesis and tumor formation in xenograft models were inhibited Inhibitors,research,lifescience,medical in transgenic mice that over-expressed 15-LOX-1 in their endothelial cells [48]. In contrast, 15-LOX has been shown to have both pro-inflammatory and anti-inflammatory effects in cell culture and primary cells and opposite effects on atherosclerosis in animal models [49]. Furthermore, there is substantial evidence that 15-LOX-1 has a pro-atherogenic effect including its direct contribution to LDL oxidation and to the recruitment of monocytes to the vessel wall [49]. The explanation

Inhibitors,research,lifescience,medical for these conflicting observations might reside in the different biological effects of many lipid mediators generated by the 15-LOX-1 pathway. Liothyronine Sodium For example, 15-HETE is converted to 15-oxo-ETE, an anti-proliferative eicosanoid (Figure 1). Similarly, 5-LOX-mediated metabolism of 15-LOX-derived 15(S)-HPETE results in the formation of the anti-inflammatory lipoxins (LX) A4 and LXB4 [50] (Figure 1). Additional 15-LOX-1-derived lipid mediators arising from other polyunsaturated fatty acids such as eicosapentaenoic acid (E-resolvins) and docosahexaenoic acid (D-resolvins) could also potentially be involved [51]. A second human 15-LOX (15-LOX-2) was discovered by the Brash group in 1997, which in contrast to 15-LOX-1, does not efficiently metabolize linoleic acid [52]. 15-LOX-2 has a limited tissue distribution, with mRNA detected in prostate, lung, skin, and cornea, but not in numerous other tissues, including peripheral blood leukocytes [53].

He was really too weak for a third and fourth time, but we said, we’ll just go on, we believe in it; he’ll get better, we won’t stop, we’ll go on (daughter of a Turkish male patient). Whether SB203580 cell line Patients and their families actually believe that they will receive ‘good care’ is affected by previous care experiences. Respondents who have rather low expectations often perceived medical shortcomings that – in their opinion – brought about their present situation. Doubts

about the expertise and the commitment of Dutch doctors are often exacerbated by the stories of other immigrants Inhibitors,research,lifescience,medical who compare Dutch health care with the opportunities in their countries of origin or other European countries. He went to a big professor Inhibitors,research,lifescience,medical in Istanbul. And then they said, why did you let them take away a piece of your lung? That makes it worse. If you hadn’t done that, we could have tried different treatment (son of a Turkish male patient). Maximum care Patients and their families do not just want curative care; ‘good care’ implies maximum medical treatment and diagnosis. Inhibitors,research,lifescience,medical This often means that people want a ‘second opinion’ and will ask for medical tests or (chemo) therapy at a very late stage. We asked for a second opinion and we wanted the chemo cure, just to see whether it would work. Until we said, yes, it’s no good. Of course, you have to accept that. He couldn’t say it, we did that for him. It was a battle,

over and over again, we are still going on. We won’t accept ‘no’. Hoping that it might work, that some other treatment might be possible (sister of a Moroccan male patient). Wanting the best possible treatment and diagnosis

Inhibitors,research,lifescience,medical goes together with the idea that you must fight to the last. Respondents stated that they saw that as a religious commandment. The duty of the patient to fight for his life obliges the family to do everything possible to save their relative. They want the patient to eat and drink and, if possible, to stay mobile. Keeping hope alive Another view of ‘good care’ is that care providers should Inhibitors,research,lifescience,medical not take away the hope of recovery by talking directly and openly about the negative prognosis. If hope is removed, then the family is afraid that the patient will ‘give up’. You can say unless it, but then tell us (relatives), as, if you tell him, he’ll give up (wife of Turkish male patient). Family members want to keep hope alive in the terminally ill patient, because hope can give him strength to get through this very difficult period. When I heard that the tumour was malignant, I couldn’t tell him and I asked my doctor not to discuss this with my father, he needs morale, hope (daughter of Turkish male patient). Some respondents also say that they cannot take away the patient’s hope for religious reasons. According to them, it is for Allah to decide when someone is going to die; life and the possibility of recovery are in Allah’s hands.

8°C), and dyspnea. On admission,

the patient was conscious and reported chills, coughs, and rhinorrhea of two days’ duration. She had developed rash on her face six days after starting epilepsy treatment, with the condition progressing rapidly to her trunk, limbs, neck, and chest over the next four days. The facial rash subsequently evolved into pustules. On examination, there were multiple erosions over the mouth and vulva, and the conjunctiva was inflamed. Nikolsky’s sign Inhibitors,research,lifescience,medical was positive. The total extent of the erythematous rash was 55% of the BSA. Histological investigation of the injured skin revealed an aspect for drug eruption (extensive epidermal necrosis, focal subepidermal necrotic blisters, melanin incontinence, and moderate perivascular lymphocytic infiltrate in the absence of eosinophils, neutrophils, and viral inclusions). Immunofluorescence

Inhibitors,research,lifescience,medical markers showed negative staining. The diagnosis of SJS-TEN caused by antiepileptic drugs was established. On the other hand, laboratory testing Inhibitors,research,lifescience,medical revealed anemia, eosinophilia, increased inflammatory markers, and white blood cell count of 10×109 /µL. Chest X-ray demonstrated multifocal patch consolidations with Panobinostat concentration ground-glass opacity in both lungs. No bacterial pathogen was isolated in the respiratory tract, urine, and blood. Viral serology (HIV and hepatitis B and C) was negative. Real Time Polymerase Chain Reaction (RT-PCR) (R-gène® Kits) of bronchoalveolar lavage (BAL) revealed that the cause of the respiratory symptom was cytomegalovirus (CMV); the finding was thereafter confirmed Inhibitors,research,lifescience,medical by cell culture on MRC-5 cells. Prior serology data showed that our patient had already sustained a primary CMV infection at 6 years old, which was in favour of the current reactivation. As was expected, RT-PCR in blood showed fulminant viremia

with 459 copies/ml (threshold: Inhibitors,research,lifescience,medical 350). The antiepileptic drugs were withdrawn and anticoagulant therapy, parenteral analgesia, eye drops, and mouth antiseptic therapy were initiated. Intravenous Ganciclovir (10 mg/kg/day) was started. Oxygen therapy was initiated with parenteral nutrition and adequate hydration. Serial BAL assays were negative six days after the commencement of antiviral therapy, and the skin lesions began to heal without the need to introduce corticosteroids. The patient’s condition many improved, and she was transferred to the general ward with a prescription of Ganciclovir for a further two weeks. Discussion TEN and SJS are severe adverse cutaneous drug reactions.4,5 Treatment with corticosteroids is recommended but not necessarily effective.5-7 Several drugs are at “high” risk of inducing TEN-SJS.1 Mycoplasma pneumoniae and herpesvirus infections are well-documented causes. In some rare cases, however, the etiology remains unknown.

2006; de Castro et al. 2009b). An assessment of cholinergic tone at the neuromuscular junction has not been BKM120 manufacturer performed in B6eGFPChAT mice. The peripheral expression of the BAC transgene has been previously characterized in B6eGFPChAT mice (Tallini et al. 2006). Using the same mouse model, we found that VAChT is overexpressed in the central nervous system (Fig. ​(Fig.1;1; Nagy and Aubert 2012) and peripheral regions of

the autonomous nervous system (Fig. S1). Our analysis of neuromuscular function in B6eGFPChAT mice reveals that forelimb grip strength and ability to freely support their body weight using an endurance paradigm were maintained. Inhibitors,research,lifescience,medical Furthermore, rotarod performance using an accelerating rod to assess coordination, motor learning, and endurance was essentially identical

between genotypes. The maintenance of motor function in VAChT-overexpressing mice may reflect the tolerance that exists within the neuromuscular junction to withstand changes in cholinergic Inhibitors,research,lifescience,medical transmission. Under normal physiological conditions, peripheral cholinergic neurons maintain cholinergic function through readily releasable pools of ACh-containing synaptic vesicles. During prolonged stimulation, large storage reserves of ACh-containing vesicles can be localized within peripheral cholinergic neurons and used Inhibitors,research,lifescience,medical for synaptic release (Rizzoli and Betz 2005). For these reasons, Inhibitors,research,lifescience,medical the impact of VAChT overexpression on neuromuscular function may require more demanding physical conditions to be resolved. Indeed, previous studies have identified that CHT overexpression improves performance during endurance treadmill paradigms, while CHT deficiency impaired treadmill performance (Bazalakova et al. 2007; Lund et al. Inhibitors,research,lifescience,medical 2010). It remains to be determined whether similar paradigms would elicit an effect in B6eGFPChAT mice. In contrast

to peripheral neurons, central cholinergic neurons have smaller pools of readily releasable vesicles, and as such may be Liothyronine Sodium more dependent on the rapid recycling of vesicles. Under certain physiological scenarios, such as when synaptic vesicles cycle faster than they can be filled (Prado et al. 2002), neurotransmitter transporters may be rate limiting to neurotransmitter release. During these events, the rate of ACh release may be enhanced during VAChT overexpression and as such, central cholinergic functions may be more sensitive to modified levels of VAChT. Spontaneous activity and circadian rhythms ACh is known to play a complex role in the regulation of locomotor control, including acting as a modulator of the dopaminergic system (Rice and Cragg 2004; Drenan et al. 2010; Lester et al. 2010; Threlfell et al. 2010).

30 Reduction in 5-HT1A receptor binding is not. restricted to Abiraterone order patients with TLE. PET studies with the 5-HT1A receptor antagonist carbonyl-carbon

11-WAY-100635 ([11c]WAY-100635) found a decreased binding potential in the dorsolateral prefrontal cortex, raphe nuclei, and hippocampus of 11 patients with juvenile myoclonic epilepsy compared with 11 controls.36 In a recently published study, Hasler et al compared 5-HT1A receptor binding between 37 TLE patients with and without Inhibitors,research,lifescience,medical major depressive disorder (MDD) with interictal PET using the 5-HT1A antagonist [(18)F]FCWAY.37 The MDD was diagnosed by clinical and structured psychiatric interviews. They found that, in addition to a decrease in 5-HT1A receptor binding in the epileptic Inhibitors,research,lifescience,medical focus, patients with TLE and M.DD exhibited a significantly more pronounced reduction in 5-HT1A receptor binding, extending into nonlesional limbic brain areas outside the epileptic focus. The side of the ictal focus and the presence of mesial temporal sclerosis were not associated with the presence of comorbid depression. In a second study in 45 patients with TLE, Theodore et al demonstrated an inverse correlation between increased severity of symptoms of depression identified on the Beck Inhibitors,research,lifescience,medical Depression Inventory and 5-HT1A receptor binding at the ipsilateral hippocampus to the seizure

focus and to a lesser degree at the contralateral hippocampus and midbrain raphe.38 Likewise, Gilliam et al correlated the severity of symptoms of depression using the BDI-II in 31 patients with TLE with the

magnitude of hippocampal abnormalities identified with 1H magnetic resonance spectroscopic imaging (1H-MRSI) technique Inhibitors,research,lifescience,medical at 4.1 Tesla using creatine/N-acety-laspartate ratio maps.39 Clinical implications The existence of common pathogenic mechanisms between mood disorders and epilepsy may explain the higher incidence Inhibitors,research,lifescience,medical of mood disorders in patients with epilepsy. In theory, however, patients with mood disorders should be at greater risk of suffering from epilepsy following the development of 17-DMAG (Alvespimycin) HCl the depressive disorder. Data from three population-based studies appear to confirm this hypothesis. Indeed, while, depression in patients with epilepsy is typically conceptualized as a “complication” of the seizure disorder, such a “unidirectional relationship” between the two disorders was called into question in the last 15 years, first in a Swedish population-based-case control study in which depression was found to be seven times more common among patients with new-onset epilepsy, preceding the seizure disorder, than among age- and sexmatched controls.40 When analyses were restricted to cases with a “localized-onset” seizure, depression was 17 times more common among cases than among controls.

Hartog calls this regime of historicity “presentism” and defines it as an invasion of the present into the realms of the past and future. For instance, Hartog notes that the conception of the past as a bygone time has recently been replaced by that of memory, which revitalizes in the present what would hitherto have been considered as dead or obsolete. Memory thus

appears as a “presentist Inhibitors,research,lifescience,medical instrument,” allowing for a “presentist use of the past.” Hartog also points to the importance given recently to the notion of heritage, which makes traces of the past necessary components of current individual and collective identities. As for the extension of the present into the future, the historian notes that our societies conceive of the time to come as a source of uncertainty and anguish. Inhibitors,research,lifescience,medical The future must be prepared now, in the present, in order to prevent potential environmental, political, health, and other catastrophes from occurring. According to Hartog, this is evident in the emergence of the principle of responsibility and the precautionary principle, which

state, respectively, that the Tyrosine Kinase Inhibitor Library ic50 living are responsible for handing over to future generations a world in which Inhibitors,research,lifescience,medical life will be decent, and that an action should not be undertaken if it is deemed to have serious potential consequences, notably in the long run. For the French historian, presentism differs significantly from previous temporal orders, namely futurism, eschatologism, Inhibitors,research,lifescience,medical and pastism (mentioned here in reverse chronological order). Futurism, which Hartog dates roughly between the French revolution (1789) and the fall of the Berlin Wall (1989), emphasized the present as a step toward the Inhibitors,research,lifescience,medical future; time was seen as a movement of uninterrupted improvement, with an ever-increasing efficiency of technologies and a continuous economic growth. It was an era marked by the idea

of progress and an orientation toward the future. Before the advent of futurism, eschatologism was the dominant temporal order, according to Hartog. It envisaged time above all as a process of salvation. In his theory, the resurrection of Christ marks the beginning of the process—being a fixed, past event, it acts as one of the delimitations of time—which needs to be completed, and this supposedly occurs through the second coming of Christ (parousia), or Judgement Day—representing the other delimitation Idoxuridine of time. In this regime of historicity, the present acts as an in-between stage; it is simultaneously a time of reminiscence about salvation and a time for the expectation of eternal life. “Past, present and future are articulated on the backdrop of eternity,” as Hartog writes (p 75). Finally, pastism, which the historian dates back to ancient times, conceived of the present as the reverberation of a mythical past.