br Data Fig shows the photographs of the

Data
Fig. 1 shows the photographs of the developed porous Co3O4 films on the FTO/glass substrate. Co3O4 films were masked using Kapton tape to define the working area (60 mm2) for electrochemical experimentation are shown in Fig. 1b. Polarization curve for water oxidation cycle (as shown in Fig. 2) are presented for the natural sea water. Tafel analysis is presented in Fig. 2b. Linear sweep voltammetry (LSV) measurement of the porous Co3O4 electrode was measured under a pulsed light (100mW/cm2) condition with 0.1M Na2S2O3 electrolyte in cathodic direction, as shown in Fig. 3. Fig. 4 shows the spectral photoresponse of Co3O4/FTO photocathode with natural sea water at over potential of 0.3V vs RHE. Photoinduced seawater splitting using the porous Co3O4 working electrode is demonstrated in the moving clip. In this video current density is 20mA/cm2 @ −0.8V vs RHE.

Experimental design, materials and methods
Preparing Co3O4 electrode: Co3O4 working electrodes were prepared using the Kirkendall diffusion method [1]. Initially the sputtered pure Co film was grown for the porous and semitransparent Co3O4 film by the heat treatment (550°C for 10minutes in air condition). Photographs of Co3O4 samples are shown in Fig. 1.
Electrolytes:
Electrochemical Measurements: All measurements were done using the three electrode electrochemical cyclobenzaprine hcl (Reference electrode: Ag/AgCl (KCl, 3M), Counter electrode: platinum gauze, and working electrode: Co3O4/FTO/glass) attached to the Potentiostat/Galvanostat (PG-stat) (WonA Tech, ZIVE SP1). Linear sweep voltammetry was applied to measure the anodic polarization and photocathode properties. Chronoamperometry technique was applied to measure the transient photoresponses at an applied potential of 0.33V vs RHE in the natural seawater. The white light (5800K, Bridgelux, ES Star Array, BXRA-56C0700-A) was applied for photoinduced electrochemical measurement. This was calibrated by a power meter (KUSAMMECO, KM-SPM-11). The illuminating light source was calibrated for one-sun light intensity (100mW/cm2) and was applied in the pulse mode or the continuous mode. For transient photoresponses, a monochromatic light source of wavelength 365nm (2mW/cm2), 460nm (3mW/cm2), 520nm (6mW/cm2), and 620nm (15mW/cm2) were applied to working electrode from the front direction.

Acknowledgements
This research was supported by Basic Science Research Program through the National Research Foundation (NRF) of Korea by the Ministry of Education (NRF-2015R1D1A1A01059165), Korea Research Fellowship Program through the NRF by the Ministry of Science, ICT and Future Planning (NRF-2015H1D3A1066311) and Korea Institute of Energy Technology Evaluation and Planning by the Ministry of Knowledge Economy (KETEP-20168520011370)

Data
Chemical analyses of the prepared SnS thin film based upon XPS analysis are provided in Figs. 1–3. XPS survey spectra including the Sn3d and the S2p spectra confirm the chemical states corresponding to the Sn+2 and S-2 states. The thickness-dependent surface morphology and cross-sectional FESEM images of vertical layers of SnS stacked on Si wafer are shown in Fig. 4. Cross-sectional images of SnS samples demonstrated the length extension of the vertical SnS layer for a wafer-scale application [1]. This vertical SnS could be one of emerging 2D materials, such as HfS2, [2] MoS2, [3] MoSe2 and WSe2, [4] ReS2, [5] and SnS2, [6]. The thickness of multilayers of SnS was estimated by using the FESEM image, as shown in Fig. 5. Refractive index of the grown SnS films was calculated using the reflectance data. Both reflectance and refractive index data of SnS film are shown in Fig. 6. Photoresponse data of SnS/n-Si device and light switching frequency dependent are shown in Fig. 7. The light source of wavelength 850nm was used to acquire Linkage data.

Experimental design, materials and methods

Acknowledgements

br Case Report A year old woman presented with symptoms

Case Report
A 73-year-old woman presented with symptoms of massive hematochezia and abdominal pain. Her blood pressure was 116/58 mmHg, pulse rate 78 beats/min, and temperature 36.4°C. Abdominal examination revealed: distension, board-like rigidity, and muscular defense in the right upper quadrant; no liver dullness; inaudible bowel sounds; and a palpable mass over the right upper quadrant. Moreover, rectal examination revealed an empty ampulla. Blood tests showed a Sirolimus level of 8.2 g/dL, white blood cell count of 14.57 × 109/L, and C-reactive protein of 0.1 mg/dL. Colonoscopic and gastroscopic evaluations were normal and did not reveal the origin of the bleeding. An abdominal enhanced computed tomography (CT) scan revealed a 9.2 cm × 10 cm solid tumor with a low density area, suggesting necrosis or abscess (Figure 1). A radiological diagnosis suspected a carcinoid or GIST arising from the jejunum. No free fluid was identified around the mass in the abdominal cavity.
During hospitalization, the patient was treated with intravenous administration and blood transfusion. The patient subsequently registered improvement in her clinical condition and laboratory tests. However, sudden diffuse abdominal pain with peritonitis was noted 4 days later; we suspected that the peritonitis was induced by mass rupture and we thus performed emergency laparotomy under general anesthesia. Intraoperative findings showed an excessive bloody fluid collection, ∼1600 mL in the peritoneal cavity. An outgrown mass ruptured in the jejunum, ∼5 cm from the Treitz ligament without seeding to nearby soft tissues (Figure 2). We performed segmental resection of the jejunum with the tumor and end-to-end anastomosis. The resected mass was a well-circumscribed tumor measuring approximately 10 cm × 8 cm (Figure 3). Hematoxylin–eosin staining showed an intramuscular tumor (Figure 4), with focal hemorrhage and necrosis (Figure 5), composed of spindle-shaped and epithelioid cell proliferation (Figure 6). The mitosis index was 6 in 50 higher power fields and of a high grade (over 50 high-power fields). Immunohistochemical staining showed positive results for c-kit and DOG1 (Figure 7). The largest dimension of the tumor was 9.5 cm (pT3), and cellular atypia was moderated. We deemed the tumor to be a moderately differentiated GIST originating from the jejunum. The pathological tumor–node–metastasis stage of spontaneous rupture of the GIST of the jejunum was IIIB. The patient expired because of intestinal obstruction with community-associated pneumonia and septic shock in the postoperative period.

Discussion
The annual incidence of GIST is one in 10–20 million persons, with a malignant potential of 20–30%. GISTs have a wide range of malignancy rates, and it is preferable to consider and treat them as potentially malignant. Approximately 60–70% of cases occur in the stomach, 25–35% in the small intestine, and 10% in the jejunum, whereas the esophagus, colon, rectum, and appendix are rarely affected.
The clinical symptoms of a GIST range from mild to severe, and complications include vague abdominal pain, hematemesis, and intestinal obstruction. Common presentations include abdominal pain, palpable mass, gastrointestinal bleeding, fever, anorexia, weight loss, and anemia. The symptoms and signs are not disease-specific; therefore, ∼50% of GISTs have already metastasized at diagnosis, typically to the liver or peritoneum.
Over the past decade, several studies have reported spontaneous perforation of jejunal GISTs.
An isolated jejunal GIST associated with perforation and peritonitis is rare. GISTs originating in the jejunum seldom cause perforation and acute diffuse peritonitis.
Most GISTs are > 5 cm in diameter at diagnosis; a diameter of 10 cm is associated with a higher risk of local or distant metastasis.
Considering the exophytic growth of tumors, intestinal obstruction occurs because of compression rather than luminal obstruction. Pressure necrosis and an ulceration of the overlying mucosa may cause gastrointestinal bleeding, and patients with considerable blood loss may experience malaise and fatigue. Gastrointestinal bleeding is the most common presentation (50%) of GISTs and is typically associated with an ulceration of the tumor into the lumen. Perforation is generally attributed to: the replacement of the bowel wall by tumor cells; tumor embolization, leading to ischemia; and necrosis in addition to increased intraluminal pressure.

Analgesia is an important ancillary property of all anti inflammatory

Analgesia is an important ancillary property of all anti-inflammatory agents. Most of the anti-inflammatory drugs increased pain threshold in various animal models [44]. This is natural because many endogenous chemical mediators of inflammation play a part in generating pain impulses (for example, histamine, serotonin and prostaglandins) and some other mediators such as bradykinin and cytokines, are involved in prolongation of the sensation of the pain [45].
RA is an inflammatory condition of the joint that is associated with hyperalgesia and functional impairment [46]. Joint inflammation induced by AIA is associated with hyperalgesia and slight compression of the joint which caused leg withdrawal and squeaking. The hyperalgesia associated with arthritis has been reported to involve prostaglandin synthesis [47]. Increased levels of substance P, R115777 gene-related peptide and up-regulation of neurokinin-1 receptor in the dorsal horn of the rat spinal cord have been reported to play an important role in modulating both inflammation and hyperalgesia in the FCA model [48]. However, in the present study, TAPP did not prevent reduction pain latency in Randall–Selitto assay. Therefore, nociception-related mediators (substance-P, calcitonin gene-related peptide and neurokinin-1) are not involved in mechanism of action of TAPP. This also pointed toward the possibility of disease modification as possible mechanism of action of TAPP against RA.
AIA has been generally believed to be the result of a delayed-type hypersensitivity (DTH) response to a disseminated antigen probably derived from the injected bacterial cell wall [49]. AIA in rats is a useful model of inflammatory cachexia that mimics the human pathophysiology in many important ways [50]. AIA induces inflammation as primary lesion which reached to peak after 3–5d with secondary lesions occur after a delay of about 11–12d. Secondary reactions in AIA are characterized by immune responses, inflammation and decrease of weight (cachexia). In our study, the test R115777 compound, TAPP significantly protected rats from cachexia because of arthritis induction.
In the past, many plant-derived procyanidines reported to have cytokine inhibitory effect in vitro[51,52]. Similar effects were also attributed to Cinnamon bark extract and polyphenols [16,53]. In vitro pre-challenge with cinnamon extract is reported to suppress lipopolysaccharide (LPS)-induced cytokines expression [54]. Recently, immune regulatory action of TAPP in mouse 3T3-L1 adipocytes is attributed to TTP (tristetraprolin) [55]. Besides, TAPP is capable of affecting immune responses by regulating anti-inflammatory mediators as well as the TTP gene expression in macrophages [16]. Taken together, cytokine inhibition emerges as a probable mechanism of TAPP responsible for cachexia reducing effects in AIA-induced established polyarthritis in rats. This probability is also supported by our result that TAPP reduces serum C-reactive protein (CRP) levels of rats on day-21 compared to day-12 levels (Table 2) whereas AIA control rats showed sustained increase in CRP till day-21 (Table 2).
CRP is an acute-phase protein and has been identified as an important biomarker for various inflammatory, degenerative, and neoplastic diseases [56,57]. Elevated levels of CRP have been found in the blood during almost all diseases associated with active inflammation or tissue destruction, particularly in RA patients [57,58]. Sustained increase in serum CRP levels suggests a lasting production and stimulation of acute-phase proteins during disease progression.
In our study, serum turbidity (showed by absorbance of serum samples) of AIA control rats was found to be significantly reduced compared with normal rats (Fig. 1). Treatment from day-12 to day-21 with TAPP but not diclofenac sodium (an NSAID) prevented AIA-induced fall in turbidity (Fig. 1). The decrease in serum turbidity in AIA control rats, is known to be caused by denatured products and was shown to be correlated with severity [59] and immune response seen in AIA [60]. Further, increased levels of serum lysozyme levels were reported to be strongly correlated with decreases in serum turbidity in AIA [59]. Therapeutically useful anti-inflammatory drugs were shown to reverse this decrease in serum turbidity [32]. Taken together, our results strongly pointed to disease-modifying properties of TAPP and its potential to slow down the RA progression.

Introduction Botulinum neurotoxins BoNTs composed of seven biochemically distinct serotypes

Introduction
Botulinum neurotoxins (BoNTs), composed of seven biochemically distinct serotypes (BoNT/A–G) secreted by Staurosporine bacteria Clostridium botulinum, are extremely potent inhibitors of neurotransmitter exocytosis at neuromuscular junctions (Neale et al., 1999; Rossetto et al., 2006; Montecucco and Molgo, 2005). Furthermore, BoNTs have been weaponized (Arnon et al., 2001), and there is a significant concern that one or more of these toxins could easily be used during an act of bioterror (Wein and Liu, 2005). Indeed, BoNTs, as the most poisonous of known bacteria toxins (Lamanna, 1959), are listed as category A bio-threat agents by the Centers for Disease Control and Prevention (Centers for Disease Control and Prevention, 2010).
On the other hand, and despite their unmatched toxicities, pharmaceutical grade BoNT serotypes A and B are widely used, in quantitatively minute, localized doses: (i) to treat various movement and hyperactivity disorders and (ii) cosmetically for wrinkle reduction (Jankovic, 2004; Dolly et al., 2009; Brin, 2009). In fact, Botox (BoNT/A) treatment is FDA approved and, according to statistics provided by the American Society for Aesthetic Plastic Surgery (American Society for Aesthetic Plastic Surgery, 2010), is one of the top nonsurgical cosmetic procedures performed in the United States. Furthermore, to extend BoNT potency for clinical neurology applications, chimeric and modified BoNTs have been generated using protein engineering methods to expedite the toxin\’s cellular entry, increase its substrate specificity, and extend its duration of activity in neuronal and possibly nonneuronal cells (Dolly et al., 2009; Chen and Barbieri, 2009; Wang et al., 2008; Foster et al., 2006).
However, as BoNTs are increasingly being used for medical and cosmetic purposes, the possibility of accidental overdosing in the clinic, in addition to unintentional environmental exposure through contaminated food or liquids, is also increasing. Moreover, as indicated above, BoNTs represent a major concern with regard to counter-bioterrorism efforts. Yet, there is still no effective therapeutic means for countering these toxins postneuronal internalization (Montecucco and Molgo, 2005). To date, there are only two FDA approved anti-BoNT antibodies: babyBIG (human serum-derived anti-BoNT immunoglobulins) and bivalent (BoNT A/B) equine toxin (Infant Botulism Treatment and Prevention Program, 2010; Larsen, 2009). However, the antibody treatments must be administered to intoxicated individuals within a very narrow time frame to prevent the progression of neuronal paralysis—since the antibodies cannot inhibit the toxins postneuronal penetration. As a result, the antibodies are only marginally beneficial for recovery, since patients still require respiratory aid for weeks. Hence, there is an urgent need to develop novel and more effective medical treatments to limit/counter BoNT intoxication (Burnett et al., 2005).
Mechanistically, BoNTs inhibit neurotransmitter exocytosis by cleaving specific soluble N-ethylmaleimide-sensitive fusion protein attachment (SNARE) proteins. The cleavage of SNARE proteins results in impaired muscle function, respiratory arrest, and, if mechanical respiration is not available, death (Neale et al., 1999; Baldwin and Barbieri, 2009; Rossetto et al., 1994). Structurally, BoNTs are composed of a heavy chain (HC) (100 kDA), which is mainly responsible for neuronal internalization, and a light chain (LC) metalloprotease (50kDa) (Grumelli et al., 2005; Simpson, 2004). The HC and the LC are linked by a disulfide bridge (Montecucco and Molgo, 2005). The C-terminal region of the BoNT HC interacts with SV2 (Synaptic Vesicle Protein 2) receptors, and mediates toxin endocytosis (Dong et al., 2006; Mahrhold et al., 2006). Following cellular entry, the LC dissociates from the HC and cleaves SNARE proteins in the neuronal cytosol (Rossetto et al., 2006). Importantly, it is the LC\’s proteolytic activity that is responsible for the extreme potencies of these toxins; LC at very low concentrations is sufficient to block the activity of a motoneuron. For example, BoNT/A specifically removes 9 amino acids from the C-terminus of SNARE component synaptosomal-associated protein of 25 kDA (SNAP-25), and this simple cleavage is sufficient to inhibit neurotransmitter release (Kalandakanond and Coffield, 2001; Apland et al., 1999, 2003; Blasi et al., 1993; Bajohrs et al., 2004). Moreover, while BoNT/A mainly targets motoneurons, it is stable in cells for weeks (Adler et al., 2001; Keller et al., 1999; Fagan et al., 2009), and its active form can travel in the nervous system and reach distant synapses through retrograde transportation (Caleo et al., 2009; Antonucci et al., 2008).

Introduction Using the cell surface marker CD Yin et

Introduction
Using the cell surface marker, CD133 (Yin et al., 1997; Yu et al., 2002), we identified a subpopulation of cells from a variety of human mini prep tumors, termed brain tumor initiating cells (BTICs), which exhibit stem cell properties in vitro (Singh et al., 2003; Reynolds and Weiss, 1992; Tropepe et al., 1999) and in vivo (Singh et al., 2004; Wang et al., 2010). Similar to neural precursor cells (NPCs), BTICs generate all neural cell types through the process of differentiation, during which CD133+ stem and early progenitor cells lose their CD133 expression, giving rise to late progenitors, and finally differentiated progeny. Currently, there is a lack of definitive markers defining NPC and BTIC early and late progenitors. However, molecular markers which capture cells during the intermediate stages of differentiation, just as CD133 expression levels begin to decline, may improve our understanding of signaling pathways that promote BTIC cell fate determination.
The mini prep Bmi1 signaling pathway is not only required for execution of key stem cell programs in mammals, but is also consistently dysregulated or overexpressed in numerous emerging cancer stem cell populations (Cui et al., 2007; Lessard and Sauvageau, 2003; Liu et al., 2006a; Mihic-Probst et al., 2007; Song et al., 2006). The Bmi1 gene, first isolated as an oncogene in mouse lymphoma (van Lohuizen et al., 1991), was also identified as a key regulator of hematopoietic (Lessard and Sauvageau, 2003) and neural stem cell self-renewal (Fasano et al., 2007, 2009; Molofsky et al., 2005). Bmi1 has been implicated in the pathogenesis of brain tumors such as gliomas (Bruggeman et al., 2007) and medulloblastoma (Leung et al., 2004; Michael et al., 2008; Wiederschain et al., 2007), and as an important epigenetic regulator of fate determination in stem cell populations (Bracken et al., 2006; Valk-Lingbeek et al., 2004). However, a targeted study of the potential role of Bmi1 in further defining BTIC populations has yet to be performed.
Here, we use pre-existing BTIC assays and Bmi1 siRNA-mediated knockdown to characterize the expression and stem cell regulatory role of Bmi1 in primary minimally cultured human glioblastoma (GBM) patient isolates prospectively sorted for CD133. We show that Bmi1 governs key stem cell properties in different cellular compartments: self-renewal in CD133+ stem and early progenitor cells, and proliferation, differentiation and cell fate determination in CD133− progenitors. Our work demonstrates that Bmi1 differentially regulates stem cell function and cell identity in BTIC-enriched (CD133+) and BTIC-depleted (CD133−) compartments of human glioblastoma. Interestingly, in our minimally cultured GBM BTICs, we find that Bmi1 mRNA expression level is significantly higher in CD133− cell subpopulations, suggesting that Bmi1 may play a previously uncharacterized role in CD133− late progenitor populations, in addition to its known role in CD133+ stem cells (Abdouh et al., 2009; Molofsky et al., 2003). While contributing to stem cell self-renewal in CD133+ BTIC populations, Bmi1 may also play a role in regulating proliferation, differentiation and tumor maintenance in CD133− populations. Furthermore, in vitro stem cell assays are predictive of clinical outcome for GBM patients, and Bmi1 expression in BTIC patient isolates may contribute to current molecular classifications of GBM.

Results

Discussion
We have analyzed Bmi1 expression and function in human GBM patient isolates prospectively sorted for CD133, rather than in whole spheres, which are heterogeneous stem cell colonies that contain a mixture of stem, progenitor and differentiated cells. We called our experimental model system “BTIC patient isolates” to emphasize the fact that these cells are not cell lines, but rather minimally cultured under conditions to select for stem cell populations. BTICs are assayed immediately after primary sphere formation, and grown briefly in human NPC media with LIF. Under these conditions, we find that CD133 reliably marks stem or early progenitor populations (Singh et al., 2003, 2004; Wang et al., 2010; Uchida et al., 2000) (Fig. 1A), although this finding may not pertain to human BTICs propagated in long-term culture (Abdouh et al., 2009; Chen et al., 2010).

br Results and Discussion br Experimental Procedures

Results and Discussion

Experimental Procedures

Acknowledgments

Introduction
Insights into potential mechanisms for the regulation of mammalian tissue repair have come from studies of animals that can regenerate limbs, tails, and even the spinal cord, such as NSC59984 manufacturer and reptiles. One major conclusion from these studies is that tissue regeneration requires nerve innervation (Kumar and Brockes, 2012). These findings have led to the idea that peripheral nerves may regulate tissue repair in mammals. This possibility has important implications because every tissue in the body is innervated. Indirect support for this intriguing idea comes from recent studies showing that innervation regulates the biology of some adult tissue precursors (Yamazaki et al., 2011; Brownell et al., 2011).
How might nerves regulate tissue repair and regeneration? In newts, neural-crest-derived Schwann cells migrate into the regenerating limb and secrete factors that regulate mesenchymal cell proliferation and regeneration itself (Kumar and Brockes, 2012). In mammals, nerve injury leads to a dramatic dedifferentiation of Schwann cells into a precursor cell state, which is important for appropriate nerve regeneration (Jessen and Mirsky, 2008). Here, we asked whether nerve-derived neural crest precursor cells (NCPCs) play a role in mammalian tissue repair, focusing on adult murine skin. We describe nerve-associated NCPCs in adult skin and show that NCPCs contribute to the regenerating dermis in a Sox2-dependent fashion, and that when Sox2 is ablated, this NCPC response is perturbed concomitantly with aberrant skin repair. Thus, Sox2 regulates skin repair, likely via its actions in Sox2-positive NCPCs, suggesting that nerve-derived NCPCs may play a general role in promoting mammalian tissue repair.

Results

Discussion
The data presented here support a number of conclusions. First, we identify a population of Sox2-positive neural-crest-derived NT cells around the hair follicle bulge. These cells express an NCPC phenotype and contribute cells to the regenerating dermis following skin injury. Second, we show that skin injury induces expression of Sox2 in skin nerve cells (likely dedifferentiated Schwann cells), and that these cells likely provide the major source of NCPCs in the regenerating dermis. Third, we show that Sox2 is important for this NCPC response, because when Sox2 is genetically ablated, the number of NCPCs within the regenerating dermis is reduced 2- to 3-fold. Finally, we show that an aberrant NCPC injury response, caused by genetic ablation of Sox2, is coincident with significant deficits in skin repair. Thus, Sox2-positive NCPCs contribute to the regenerating dermis. This contribution depends upon normal levels of Sox2, and when this injury response is perturbed, skin repair is aberrant.
One question that arises from this work involves the nature of the NT cells. We show here that these bulge-associated cells are located at nerve terminals, that they resemble NCPCs phenotypically, and that they contribute cells to the regenerating skin. Intriguingly, previous publications have identified NCPC stem cell activity in the hair follicle bulge region (Sieber-Blum and Hu, 2008; Amoh et al., 2005). Moreover, during development, NCPCs migrate into the skin via nerves, where they contribute melanocytes to hair follicles (Adameyko et al., 2009). We therefore propose that NT cells are NCPCs that arrive in the embryonic skin via nerves, are maintained in a precursor state by their hair follicle niche, and function as a reservoir of adult NCPC activity.
A second question involves the origin of the Sox2-positive NCPCs within the regenerating dermis. The Sox2-CreERT2-mediated lineage tracing shows that a large majority of these NCPCs are induced to express Sox2 following skin injury. Because the only neural-crest-derived skin cells that express Sox2 following injury are NT cells and cutaneous nerve cells, it is likely that many of these NCPCs derive from the injured nerve, perhaps from dedifferentiated Schwann cell precursors that express Sox2 (Parrinello et al., 2010; Jessen and Mirsky, 2008). It is, however, formally possible that these Sox2-positive NCPCs originate outside of the skin and are trafficked into the regenerating dermis from a distance, perhaps via the circulation.

Since the function entering in integral

Since the function entering in integral (27) takes the form
in a symmetric problem (when ), the stress singularity with r → 0 occurs when the angle governing the region with the harder material exceeds 180°.

Conclusion

Introduction
The order Talabostat mesylate of plastic flow, which has currently gained wide application, assumes that the unloading of a material has no effect on plastic strain. However, the results of a number of studies [1–19] have revealed that plastic strain accumulates under passive loading (unloading, loading within the loaded surface and tangential to it). Plastic strain under passive loading is described by the endochronic theory of plasticity [4,5] and the generalized Prandtl model (the Mazing model) [6]. The formulations of the constitutive equations of the above theories are primarily aimed at refining the description of active strain, while the parameters of the material are determined without taking into account the specifics of the processes occurring under passive loading.
Experimental studies into the properties of the plastic compliance field [20] laid the foundations for developing a multi-surface theory of plasticity with one active surface [14–19]. The concept of plastic compliances is directly or indirectly used by multi-surface theories of plasticity [21,22]. At the same time, not nearly enough experimental research has been accumulated on the properties of plastic compliances of materials. This mainly concerns strain with passive loading paths. The accumulation of residual strain under such loads must be taken into account not only in stress–strain analysis [14–19], but also in calculations of damage accumulation [13,23,24], studies of superplasticity processes [25] or in assessing the operating capacity and precision of machine units [26].

Constitutive equations for describing passive loading

Experimental procedure and samples
The experiments were carried out for a multiaxial stress state, using a modernized setup [27] consisting of a high-pressure chamber, pressure sources, high- and low-pressure hydraulic systems, control and measurement devices and various maintenance tools.
Segments of seamless tubes with a length of 4m, made from one batch of a Cr–Ni–Ti steel alloy synthesized by vacuum arc remelting (VAR) were used to prepare the samples. Sample sizes:

This ratio corresponds to the recommended values and provides a good uniformity in the distribution of circumferential and radial stresses along the thickness of the wall. This makes pilus possible to calculate the stresses in the middle layer by the formulae for membrane shells. The chemical composition of the tube material (steel) is presented in Ref. [18].
The basis of the experimental procedure is that the loading process is considered in the Σ1, Σ2 stress space, and the deformation process in the , plastic strain space:
where are the nonzero components of the stress tensor in a cylindrical coordinate system that coincide with the principal stresses; , , are the principal plastic strains.
To calculate the length of the plastic strain path (Odqvist\’s parameter ), we used the relation

The hydrostatic pressure (mean stress) was determined based on the dependence

The loading procedure was based on the step-by-step application of loads, allowing to perform loading along any direction in the Σ1, Σ2 space, which is characterized by a state parameter on the deviatoric plane:

Loading may be achieved in a tubular sample (i.e., with ψ= 0, …, 120°). The stress state of the sample is governed by the deviatoric state parameter ψ(13), by the stress intensity and by the ratio of the invariants /.
The experiments were carried out in a high-pressure chamber and included sample loading and unloading along straight radial paths in the stress space, with the varying parameter ψ. As the first step, axial tension was applied at ψ= 0° to a certain chosen stress intensity 0, followed by complete unloading, circumferential tension at ψ= 115–120° to approximately the same stress intensity, and then again complete unloading to = 0 (see rays 0–1, 1–0, 0–4, 4–0 in Fig. 3a).

Our study found a link between

Our study found a link between screening and delay in seeking medical advice. Attending regular BC screening aid in the self-awareness process and helped women understand the seriousness of their condition, three women in our study had BC screening before and knew about BC, this knowledge prompted them to seek advice earlier than other women in the study. Screening helped women evaluate the condition properly and women who understood the seriousness of their condition, tried to seek medical care to confirm the diagnosis (Adam & Soutar, 2003; Taib, Yip, & Low, 2011).
Similar to studies conducted in Muslim countries, talking about breast as a sexual reproductive organ is culturally taboo (Babu, Samari, Cohen, et al., 2011). Fatality is also a concern and a reason for delay resulting from the perception of incurability of cancer (Sabih et al., 2012; Taib, Yip, & Low, 2011). In our study, some women suggested feeling inferior to men in the SP 600125 and being less powerful, as their role in the family obliges them to please their husbands. The husband׳s relationship with a woman diagnosed with BC is a very sensitive issue. The attitude of husbands and the perspective of men in regards to women with BC was not addressed in our study. However, some aspects of the intimate relationship of women with their husbands was explored in our study. Our study provided an opportunity for women with BC to openly talk about their feelings, behavior and relationships.

Strengths and limitations

Implications for future research

Conclusion
Our findings suggest that culture has a great effect on the decision making of women with BC. The lack of awareness about signs and symptoms of BC and routine screening has a major effect on symptom appraisal and consequently informed decision making. However, national efforts are needed to address specific benefits of early detection and to increase the awareness about these benefits.

Funding
This study was supported by a grant from United Arab Emirates University, College of Medicine and Health Sciences.

Acknowledgment

Introduction
Sub-Saharan African women are increasingly entering marriage at older ages (Garenne, Tollman, & Kahn, 2000). Given the commonality of premarital sex in the region (Mensch, Grant, & Blanc, 2006), the trend toward later marriage means many African women are at risk of premarital childbearing for increasingly long durations of later adolescence and early adulthood. Indeed, the rise in women’s age at first marriage corresponds with higher levels of premarital childbearing in select sub-Saharan African contexts (Harwood-Lejeune, 2001).
Evidence that premarital childbearing has become more common in some sub-Saharan African countries (Barker & Rich, 1992; Gage-Brandon, & Meekers, 1993; Ocholla-Ayayo, Wekesa, & Ottieno, 1993) and is normative in many settings (Garenne et al., 2000; Garenne & Zwang, 2006a; Meekers & Ahmed, 2000; Xu, Mberu, Goldberg, & Luke, 2013; Zwang & Garenne, 2009), raises concerns over its consequences for population health. Premarital childbearing is tied to disadvantages at the aggregate and individual levels (Garenne & Zwang, 2006a). At the individual level, premarital childbearing places women at risk of numerous health problems (Kaufman, Wet, & Stadler, 2001), including an elevated risk of sexually transmitted infections (Garenne & Zwang, 2006a; Nzioka, 2004), and even penalizes women in the marriage market (Calvès, 1999; Ikamari, 2005, Klein Hattori & Larsen, 2007).
Premarital childbearing also adversely affects the health and developmental trajectory of the resulting child. The childhood consequences of being born premaritally are especially severe in sub-Saharan Africa: compared to their peers born to formally married parents, these children are often born in the absence of medical supervision (Gage, 1998), are un/under-vaccinated (Gage, 1997), and are malnourished (Gage, 1997), each of which may help explain their high risk of death under age 5 (Clark & Hamplová, 2013).

Finally this analysis also contributes

Finally, this analysis also contributes to our knowledge of the determinants of limited physical functioning at older ages. The prevalence of functional limitations is increasing in many countries simply because of rapid purchase PHA-793887 aging. In some countries, such as the U.S. and Mexico, functional limitations may also become more prevalent because of the dramatic growth in obesity and increased sedentariness during the past several decades (Himes & Reynolds, 2012; Rtveladze et al., 2014; Vincent, Vincent, & Lamb, 2010). Thus, old age functional limitations and other forms of disability are a key issue in public health policy and more research on ways to reduce old age functional limitations is essential (Chatterji, Byles, Cutler, Seeman, & Verdes, 2015; Jette & Field, 2007; Martin & Schoeni, 2014).

Work conditions and health
Workers with less education and from lower income backgrounds are more likely to have jobs that include heavy physical demands (e.g., carrying or moving heavy loads), repetitive movements, tiring or painful positions, ergonomic strain, extensive vibrations, noise, and heat, exposure to toxic or hazardous substances, and/or physical dangers. For example, blue collar jobs even in higher income countries often still involve exposure to heavy physical demands (Clougherty et al., 2010). Physical work conditions are typically worse in middle and lower income countries that have more limited occupational health and safety regulation and a higher proportion of workers in the unregulated informal sector (Haro-García, Juárez-Pérez, Sánchez-Román, & Aguilar-Madrid, 2014; Verbeek & Ivanov, 2013). In Mexico, for example, Sánchez-Román, Juárez-Pérez, Madrid, Haro-Gárcia, & Borja-Aburto (2006) report that high levels of underemployment (e.g., 39% in 2004) have favored informal and unregulated work.
A number of studies in higher income countries have shown that physically demanding work is associated with poorer health and functional ability in later adulthood. For example, in a U.S. national sample of individuals aged 65 or older, those whose occupation involved high levels of physical activity were less likely to be able to perform activities of daily living (ADLs) (Missikpode, Michael, & Wallace, 2016). Studies in other countries report similar results for older adult ADLs, physical functioning, and/or disability (da Costa & Vieira, 2010; Lahelma et al., 2012; Li, Wu, & Wen, 2000; Møller et al., 2015; Polvinen, Gould, Lahelma, & Martikainen, 2013; Russo et al., 2006). However, in a national Swedish sample, Rydwik et al. (2013) found little association between midlife occupation and later adult ADL or IADL disability.
A number of recent studies, mostly from European countries, have assessed the contributions of physical work conditions to socioeconomic inequalities in health. Using nationally representative survey and register data in Finland, Polvinen et al. (2013) found Meissner’s corpuscles socioeconomic inequalities in disability retirement – and particularly for musculoskeletal conditions – could be accounted for, in part, by differences in physical work requirements. Several studies based on the GAZEL cohort data in France found that physical work conditions contributed to socioeconomic inequalities in quality of life after retirement (Platts et al., 2013), back pain (Plouvier, Leclerc, Chastang, Bonenfant, & Goldberg, 2009), and sick days (Melchior et al., 2005). In the Netherlands, Monden (2005) showed that adverse physical work conditions, particularly over a lifetime, accounted for a significant portion of educational inequality in self-reported health (SRH) for men, but not for women. The sex difference appears to be due to educational differences in time out of the workforce (e.g., maternity and family leave) for women and limited educational variation in the physical work conditions to which women are exposed. Results of a study by Goh et al. (2015) in the United States also suggest that physical work conditions may contribute to socioeconomic inequalities in premature mortality.

br Acknowledgement br Introduction Evidence has long been

Acknowledgement

Introduction
Evidence has long been accumulating about the association between social relationships and health and well-being at all ages (Cornwell & Waite, 2009; House, Landis, & Umberson, 1988; Kawachi & Berkman, 2001; Umberson, Crosnoe, & Reczek, 2010). Among life\’s most intimate relationships, being married (Kawachi & Berkman, 2001) has been found to be positively associated with better health for a number of reasons. For example, Goldman, Korenman, and Weinstein (1995:1718) argue that:
Thus resources are attained through being married and crises are incurred through marital dissolution. Among older adults, strong family ties and friendship networks are also considered to be crucial for emotional and physical welfare, and researchers have identified negative health consequences of being unmarried (never-married, divorced, or widowed), being childless, and/or living alone (Lillard & Waite, 1995; Ross, 1995; Umberson, Pudrovska, & Reczek, 2010; Waite & Gallagher, 2000; Wilcox et al., 2003; Williams & Umberson, 2004). Indeed, “[for] many older adults, becoming widowed is perhaps the most difficult, yet inevitable role transition” (Li, Liang, Toler, & Gu: 2005: 637).
These matters have been recognized as important in a number of geographical contexts, including locations in Asia where researchers have found that 3X FLAG tag manufacturer living with or near children can significantly improve elderly welfare (Knodel & Debavalya, 1997; Hermalin, 1997). In Japan, Okabayashi, Liang, Krause, Akiyama, and Sugisawa (2004) have found that among older married adults, spousal support is more important for an individual\’s well-being than is children\’s support, but help from children is particularly beneficial for welfare outcomes among those without a spouse. Family support networks and living arrangements are likely to continue to be important where populations are aging and social safety nets remain uneven (Teerawichitchainan, Pothisiri, & Long, 2015).
Despite all the positive associations identified to date between social ties and health indicators, Umberson, Crosnoe, and Reczek (2010: 143) argue that a thorough examination of the literature “yields a clear image of the double-edged nature of social ties – as a source of support and sustenance and as a source of stress and worry.” The authors detail the various pathways through which either stress or social support may result, and argue that many of the adverse effects of social ties have been observed among those at younger ages, while among the elderly, it is again often the loss of ties (e.g., through widowhood), and the potentially harmful health consequences of those experiences (weight loss, etc.), that are of particular concern. At the same time, it seems clear that older adults may experience diminished control over their lives as younger people assume responsibility in realms previously the domain of the older person (Tucker, Klein, & Elliott, 2004; Umberson, Pudrovska, & Reczek, 2010; Williams, 2004). Kawachi and Berkman (2001: 461) contend that both lost ties and aid from children can affect well-being:
Our research focuses on physical and mental health indicators among older adults in China, the most populous nation in the world, and where, as of the year 2000, one fifth of family households had an adult aged 65 or older in residence. Both the number and percentage of elderly adults in the population are projected to rise considerably over the next several decades in China, where the family remains the principal institution for support of older adults (Yi & Wang, 2003: 98). Chinese parents continue to be held entirely accountable for the well-being of their children when they are young, and children continue to be fully responsible for their parents’ physical and emotional care when parents become old (Li et al., 2005). As in much of East and Southeast Asia, however, rising rates of migration to cities, in combination with very low fertility and expanding female labor force participation have been in the spotlight, as the government expects these changes to lead to declining family support for the elderly, and as it attempts to devise plans for long term care among the oldest members of the population (ESCAP, 2015). In particular, a shortage of grown children in a context of shifting attitudes and economic conditions is expected to be important for co-residence patterns in the years ahead (Logan, Bian, & Bian, 1998; Yi & Wang, 2003). Sun, Lucas, Meng, and Zhang (2011) argue that culturally, China appears ill-prepared for what is likely to be a growing number of older empty-nest families.