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Two much-discussed trends in academe -- the adoption of corporate values and the decline in the percentage of faculty jobs that are on the tenure track -- are closely linked and require joint examination. That is the thesis of a new book, The Last Professors: The Corporate University and the Fate of the Humanities, just published by Fordham University Press. Frank Donoghue, the author, is associate professor of English at Ohio State University. Donoghue recently responded to e-mail questions about the themes of his book.
Q: What prompted you to write this book? Does your career fit these trends?
A: More than any other factor, the career decision that prompted me to write The Last Professors was my move to Ohio State in 1989. I'd spent my prior academic life (undergrad, graduate school, my first teaching job) at elite private universities. Coming to a public, land grant university meant working at an institution that has no vast endowment, that is often strongly affected by the state's economy and politics, and that is frequently forced to make very tough financial decisions. This new climate gave me an unmediated look at "how the university works," to borrow the title phrase of Marc Bousquet's new book. I reacted by reading everything I could find on the topic of academic labor (not much in 1990, other than Richard Ohmann's English in America and Evan Watkins' Work Time), and then began teaching courses on the subject. The book really grew out of those graduate seminars on academic labor, and I'm deeply grateful to the students who took them.
Q: What are the main reasons for the erosion of the tenure-track career?
A: I believe that tenure and the kind of career it makes possible are disappearing largely for financial reasons. Opponents of tenure are less likely to make political arguments against it -- except in very inflammatory cases like Ward Churchill's -- but instead are now inclined to argue that professors' labor costs too much. The casualization of labor is the global norm, practiced by employers everywhere. Academia is one of the last workplaces to come almost completely under this management philosophy, where payment by the job replaces the traditional salary, benefits and, in the case of professors, job security. Medicine and the law are currently engaged in less acute versions of this transition from one management system to another. Among the professions, only the clergy and the officer ranks of the military seem to be immune to the erosion of tenure or its equivalent.
Q: Many advocates for adjuncts say that tenure-track (and especially tenured) professors did nothing or far too little as academe was restructured. Is this true? Why do you think this happened?
A: Certainly most tenure-track professors were oblivious as the teaching workforce was restructured, and very few predicted how dire a problem it would become. Had we identified the casualization of the teaching workforce as a problem when it began to take hold in the 1980s, we might have been able to correct it. Paul Lauter referred to the misuse of adjuncts as a "scandal" in 1991 in Canons and Contexts, and he may have been the first to use language that strong. That we could have done much about it over the past twenty years presupposes that professors set hiring policies. At most institutions, professors have a lot of input in the hiring of other professors, but not in the hiring of adjuncts, either the people themselves or the terms of their contracts. Decisions about adjunct labor have, by and large, never been made by faculty, but have instead been part of larger administrative policies.
Q: How have humanities professors fared, compared to those in other fields?
A: The liberal arts, and the humanities in particular, suffer the most because they lack any connection to sources of funding outside the university. Humanists typically don't do consulting work, they don't compete for large corporate or government grants, they don't have the option of working in the private sector (and thus insisting that universities pay a competitive wage). These factors conspire to put humanists in a bad bargaining position: We depend entirely on our home institutions not only to pay us a fair salary but to determine both the kinds of work and the amount of work we have to do (publishing, teaching, service, outreach) in order to earn that salary.
Q: You have a chapter on the role of prestige -- how does this figure into your analysis?
A: For a hundred years, humanists claimed to follow Matthew Arnold's exhortation to promulgate the best that has been thought and said. As universities have more and more come to function as occupational training centers, places where students come for vocational credentials, this charge has been emptied of any real meaning. It's no longer relevant to the mission of most universities. And at those institutions where the liberal arts still flourish, prestige has taken the place of the Arnoldian mottoes. That is, the best universities now steer prospective students away from the content of the curriculum (literature, philosophy, history) and toward the signaling power of the institution itself. U.S. News & World Report has, since its annual America's Best Colleges issue debuted in 1983, fixed this new principle by implying that the abstract notion of prestige can be converted into an assortment of rank-ordered lists. As a result, many universities present the narrative of their ambitions as a quest for prestige. It's now one of the principal organizing fictions of American higher education.
Q: What are key steps that could be taken to restore the tenure-track professoriate?
A: The tenure-track professoriate will never be restored. Two factors seal its fate. First, the hiring of adjuncts continues to outpace the hiring of tenure-track professors by a rate of three to one. It's silly to think we can reverse the trend toward casualization when, despite a great deal of attention and effort, we can't even slow it down. Second, the demographics of American higher education don't help us either. For 40 years, students have been moving away from the humanities toward vocationalism. This trend has been accompanied by an equally pronounced shift in enrollments from four-year schools (with English and History majors) to community colleges, where the humanities have never had a strong presence. Tenure-track professors don't have a place in this new higher education universe. Much as it pains me to say it, I never considered putting a question mark at the end of my title, The Last Professors.


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Gastrointestinal Inflammation and Repair: Role of Microbiome, Infection, and NutritionView this Special Issue
Nutrition and Helicobacter pylori: Host Diet and Nutritional Immunity Influence Bacterial Virulence and Disease Outcome
Helicobacter pylori colonizes the stomachs of greater than 50% of the world's human population making it arguably one of the most successful bacterial pathogens. Chronic H. pylori colonization results in gastritis in nearly all patients; however in a subset of people, persistent infection with H. pylori is associated with an increased risk for more severe disease outcomes including B-cell lymphoma of mucosal-associated lymphoid tissue (MALT lymphoma) and invasive adenocarcinoma. Research aimed at elucidating determinants that mediate disease progression has revealed genetic differences in both humans and H. pylori which increase the risk for developing gastric cancer. Furthermore, host diet and nutrition status have been shown to influence H. pylori-associated disease outcomes. In this review we will discuss how H. pylori is able to create a replicative niche within the hostile host environment by subverting and modifying the host-generated immune response as well as successfully competing for limited nutrients such as transition metals by deploying an arsenal of metal acquisition proteins and virulence factors. Lastly, we will discuss how micronutrient availability or alterations in the gastric microbiome may exacerbate negative disease outcomes associated with H. pylori colonization.
1. H. pylori Infects the Human Stomach
Helicobacter pylori is a Gram-negative member of the Epsilonproteobacteria class. Over 50% of the global human population is colonized with H. pylori, which inhabits the gastric niche of human hosts and is commonly acquired early in life. Furthermore, evidence indicates that H. pylori has colonized human hosts and coevolved for at least a thousand centuries [1–4]. The human stomach provides numerous nutritional opportunities and challenges for an invading prokaryote. To colonize the stomach successfully, H. pylori must survive the acidic pH in the lumen of the stomach, move through the mucus lining of the gastric tissue via chemotactic flagellar-mediated motility, attach to gastric epithelial cells using a repertoire of adhesins, and deploy cytotoxins to alter the gastric environment and create a hospitable niche for bacterial proliferation [3]. These bacterial toxins promote necrosis, autophagy, and proinflammatory signaling cascades [4, 5]. However, H. pylori persists in the stomach despite a robust inflammatory response, indicating that this organism has evolved elaborate mechanisms to circumnavigate the onslaught of host immunity [4–6].
2. H. pylori Infection and Disease Outcomes
Virtually all hosts infected with H. pylori experience gastritis while a smaller subset of these patients develop more serious outcomes such as peptic or duodenal ulcer, MALT lymphoma, or gastric adenocarcinoma. Nearly 75% of all gastric cancer and 5.5% of all malignancies worldwide can be attributed to H. pylori [4]. H. pylori infection is the strongest risk factor for developing gastric cancer [5]. It is proposed that the profound proinflammatory signaling initiated by H. pylori infection leads to atrophic gastritis, intestinal metaplasia, dysplasia, and finally gastric cancer [6]. This process, termed the "Correa pathway" is predicated on the chronic inflammation of the gastric mucosa which fosters a cascade of genotypic perturbations that ultimately lead to carcinogenesis [6–9]. It is increasingly appreciated that carcinogenesis is established due to a constellation of factors including host genetics, environment, and bacterial strain differences [6–10]. A better understanding of how these factors intersect to promote disease progression could yield novel preventative or therapeutic strategies to ameliorate the global disease burden, which costs hundreds of thousands of human lives each year [10]. In this review we consider how nutrition, or the process by which an organism derives cofactors and metabolic precursors, impacts the progression of H. pylori-associated disease outcomes and gastric homeostasis. Furthermore, we discuss how host micronutrients can alter bacterial growth and virulence and ultimately influence pathogenesis.
H. pylori has an ancient association with human beings [1]. Although H. pylori strains exhibit remarkable genetic diversity, phylogenetic analyses have revealed that strains can be classified into distinct phylogeographic clades indicative of their origin [2, 3]. These results indicate that H. pylori strains have coevolved with their hosts, observations which are supported by results indicating that H. pylori has undergone reductive evolution during its association with man [11]. However, prolonged coevolution is commonly associated with commensal adaptation and concurrent loss of virulence [12, 13]. Because H. pylori exhibits strain-specific virulence and potential to cause disease, this supports a model in which the coevolution of H. pylori and its cognate human host has been perturbed [2, 3].
In some geographical settings, such as Asia, H. pylori infection and gastric cancer rates are correlative. However, in other areas, such as Africa, Malaysia, India, and Costa Rica, infection rates are high and gastric cancer rates are low [14–17]. These are collectively referred to as "enigmas" because the protective mechanisms in these populations are obscure. It is proposed that H. pylori potentially coevolves with its host to dampen pathogenic effects and promote immunological tolerance which facilitates protection against numerous autoimmune diseases including allergic airway disease [18, 19]. However, the role of geography, nutrition, and host genetics remains ill-defined in this model. Furthermore, regions within a single country, such as Colombia, experience differential disease outcomes [20]. Recent assessments of genetic variations in both host and H. pylori strain by multilocus sequence typing analyses (MLST) were performed to ascertain how the coevolutionary relationships between hosts and pathogens were shaping development of gastric cancer [2]. This work demonstrated that low-risk coastal Colombians exhibit phylogenetic variations consistent with an admixture of Amerindian, European, and African populations. Similarly, H. pylori strains recovered from these individuals primarily represented an African lineage of H. pylori that was concordant with the host genetic background [2, 3]. Conversely, mountain-dwelling Colombians exhibit phylogenetic variations consistent with Amerindian heritage and their H. pylori strains predominantly were associated with a European phylogenetic clade [2, 3]. The authors conclude that infection with a strain of H. pylori that is discordant with host phylogenetic background is predictive for increased risk of gastric cancer [2].
3. H. pylori Virulence Factors
Besides phylogenetic differences between host and pathogen, there are specific strain differences that have been associated with increased risk of gastric disease. H. pylori strains that harbor a 40 kb genomic island termed the "cag-pathogenicity island" (cag-PAI) have been associated with increased risk of gastric disease outcome [21]. The cag-PAI encodes a type IV secretion system (cag-T4SS) which is a macromolecular nanomachine that spans both the inner and outer membrane of H. pylori. The cag-T4SS functions to transport substrates, such as peptidoglycan, and effector molecules, such as the oncogenic cytotoxin CagA, from the bacterial cytoplasm into the host epithelial cell. The activity of the T4SS has multiple effects on the host including nuclear factor activation, IL-8 chemokine secretion, host cytoskeletal rearrangement, and recruitment of innate immune cells to the site of infection [22–25]. In addition to the cag-T4SS cytotoxin secretion, H. pylori also secretes a pore-forming cytotoxin, VacA [26]. VacA is an 88-kDa protein that is secreted through type V, or autotransporter secretion pathway [27]. It causes a variety of alterations in target cells including vacuolation, depolarization of membrane potential, permeabilization, disruption of endosomal and lysosomal trafficking, autophagy, programmed necrosis, and immune modulation including inhibition of T cell activation and proliferation. Interestingly, VacA and CagA appear to have antagonistic properties: CagA is highly proinflammatory, while VacA is immunosuppressive, and VacA induces CagA degradation via autophagic pathways [22, 27, 28]. Interestingly, both VacA and CagA are often coregulated in response to nutritional signals, indicating that H. pylori has evolved to utilize both of these toxins in concert under certain nutritional stresses [29]. Together, these two cytotoxins promote H. pylori-dependent pathogenesis.
Additionally, H. pylori utilizes a repertoire of outer membrane proteins to facilitate host-pathogen interactions. The adhesin BabA binds mucosal ABO/Lewis-B blood group carbohydrates and consequently facilitates adhesion to gastric surfaces. Adherence to the gastric mucosa and/or epithelial surface is a critical first step in colonization and ultimately aids bacterial virulence by promoting the interaction of the cag-T4SS with host cells [30, 31]. Another adhesin, SabA, binds to laminin and sialyl-dimaric-Lewis × glycosphingolipid receptor and is a member of the BabA protein family [32]. Upon binding to the receptor, SabA promotes hemagglutination via sialyl-Lex binding, a process that is critical for survival within the hostile gastric environment [33]. Additionally, H. pylori outer membrane protein and Hop-family proteins such as outer membrane inflammatory protein A (OipA, encoded by hopH) or HopZ protein are both required for gastric epithelial cell binding [33]. Although the host receptors for these proteins have not yet been identified, both proteins have been implicated in inflammation and/or carcinogenesis [34, 35]. Interestingly, there is a high degree of variation in the sequence of CagA, VacA, BabA, SabA, OipA, and HopZ, indicating that H. pylori adapts to its host by modifying the repertoire of virulence factors to accommodate niche-specific challenges [36].
4. H. pylori and Nutrition
In addition to host or strain genetic differences, environmental factors, such as host diet, are emerging as important components of the ecology within the gastric environment. It is likely that the gastric environment is highly influenced by host nutrient intake. Epidemiological studies have revealed that dietary habits such as high intake of green tea, fruits, or vegetables are protective against gastric cancer risk [37–39]. Conversely, case-controlled and cohort studies reveal that high intake of red meat and/or processed meat (which are high in transition metals) and preserved foods (pickled, dried, smoked, or salted) which are often high in salt is associated with increased risk of noncardia gastric cancer [40, 41]. Furthermore, the advent of refrigeration has radically changed the manner in which food is prepared for storage. Case-controlled population studies have demonstrated that access to refrigeration is protective against gastric cancer [42]. This is attributed to the fact that refrigeration leads to prolonged access to fresh foods such as fruits and vegetables, which would otherwise be unavailable. It is hypothesized that carotenoids, folate, vitamin C, and phytochemicals from fruits and vegetables have a protective role against carcinogenesis. Conversely, salt and the availability of some transition metals can alter H. pylori virulence and accelerate carcinogenesis [43, 44]. The contribution of these individual micronutrients to H. pylori-dependent diseases will be reviewed in detail below.
4.1. Salt
Gastric cancer is the third leading cause of death from cancer worldwide. While large geographic and ethnic differences in gastric cancer incidence exist, a common risk factor for gastric cancer development is high levels of dietary salt intake. A meta-analysis of studies analysing the association between diets rich in salt and gastric cancer risk concluded that salt consumption is directly associated with the risk of gastric cancer [45]. Furthermore, the risk of developing cancer increases with increased salt ingestion in a dose-dependent manner [46]. Studies included in this meta-analysis looked at the association between high salt diets and gastric cancer across a spectrum of countries and ethnicities. For example, the meta-analysis included studies which found a correlation between consumption of salty foods, such as miso soup, pickled vegetables, and salted fish within Japanese people, and a study conducted in Norway evaluating the risk of total salt intake and gastric carcinoma. Also included in this meta-analysis are studies which show no correlation between excessively salted foods and cancer; however the strain of H. pylori endemic to these regions lacks cagA and is associated with a decreased risk of gastric cancer as compared to strains harboring cagA. Additional studies indicated that the association between salt consumption and gastric cancer risk was highest amongst individuals who were habitual consumers of high salt foods [45]. The rationale for this association between heavy salt intake and gastric cancer is multifaceted and includes that salt perturbs the integrity and viscosity of gastric mucosa and promotes colonization by H. pylori both of which ultimately contribute to increased inflammation and subsequent gastric cell proliferation and endogenous DNA mutations [47–49]. One such study compared gastric tissue morphology of mice maintained on a standard diet compared to mice sustained on a high salt diet and found that animals within the high salt cohort had increased gastric epithelial cell hyperplasia and concomitant loss of parietal cells [49].
While high levels of salt consumption in the absence of H. pylori infection are associated with gastric cancer, the alterations to the gastric tissue mediated by high salt intake are further exacerbated by H. pylori colonization and drive disease progression. Studies aimed at elucidating the molecular mechanisms responsible for this increased susceptibility to cancer development have revealed a complex relationship whereby increased salt ingestion potentiates H. pylori carcinogenesis. In addition to promoting H. pylori colonization of the gastric mucosa high dietary salt exacerbates H. pylori induced inflammation. Studies performed in a Mongolian gerbil model determined that H. pylori infected animals maintained on a high salt diet had increased inflammation when compared to infected animals maintained on a normal diet [50]. The increase in inflammation was assessed using both histological examination of gastric tissue and comparing levels of the proinflammatory cytokine, IL-1β. Importantly, this increase in inflammation mediated by high salt levels was CagA dependent, and animals infected with a cagA deficient strain of H. pylori had significantly less inflammation, even in the context of high salt [50]. Studies investigating the regulation of cagA have found that its expression is increased in response to multiple environmental changes including increases in environmental salt concentrations [51]. In fact, this increase in cagA expression was detected in vivo, using RT-PCR on gastric tissue samples from infected animals. Accompanying the increase in inflammation, infected animals on a high salt chow were found to have augmented dysplasia and invasive gastric adenocarcinoma [50]. Concomitant with this disruption in tissue architecture and inflammation is an increase in H. pylori induced hypochlorydia in animals fed excessive salt [50]. Alterations in salt concentration also enhance production of several H. pylori outer membrane proteins notably, including HopQ, which is upregulated in response to high salt stress, and VacA which is upregulated in low salt conditions [52]. Together these studies indicate that increases in salt consumption result in alterations to both the host and H. pylori and this constellation of changes stimulates carcinogenesis.
4.2. Iron
Iron is an essential nutrient for nearly every living organism including H. pylori [53]. Iron is frequently used as an enzymatic cofactor and plays a critical role in respiration and electron transport [54]. To prevent bacterial growth, the human body exploits this need for iron by limiting bacterial access to this vital metal and sequestering iron intracellularly in a process referred to as nutritional immunity [55]. The majority of iron within the human body is localized within erythrocytes in the form of heme, a tetrapyrrole ring with a coordinated iron center. Heme is then further complexed within hemoglobin [56]. Any extracellular iron is rapidly removed by high-affinity iron binding proteins such as lactoferrin and transferrin [57]. Nutritional immunity is a dynamic process capable of responding to pathogenic assaults on the host. Iron absorption and distribution are regulated through the hepatic peptide hormone, hepcidin. During the infectious process, inflammation can mediate increases in hepcidin leading to a hypoferremic response that depletes even further the available iron present within the host [58]. Together lactoferrin, transferrin, hepcidin, and numerous other proteins ensure that the human body has an inhospitably low level of iron available to invading bacteria.
While the human stomach is a unique organ in that it experiences large influxes of iron during digestion, the specific niche occupied by H. pylori is within the gastric mucosa, an area predicted to have little available iron [59]. H. pylori has evolved sophisticated mechanisms to circumvent the host's sequestration of iron and responds to the scarcity of this metal with a coordinated upregulation of iron acquisition systems and virulence factors [59–66]. One way that H. pylori mediates gene regulation in response to low environmental iron levels is through the global ferric uptake regulator (Fur), a transcriptional regulator [61–63]. H. pylori Fur is unique in that it can bind DNA sequences both when complexed to ferric iron and in its apo form [60]. Consequently, H. pylori Fur can regulate gene expression in response to conditions of both high and low iron. Many of the Fur regulated genes that are transcriptionally upregulated upon iron starvation facilitate the acquisition and trafficking of iron within the bacterial cell [60–62]. For example, when iron availability is low H. pylori increases the transcription of the high-affinity iron transporters feA1, fecA2, frpB1, and feoB facilitating an influx of iron into the cytoplasm [60–65]. Additionally, H. pylori increases binding of the host chelating proteins, lactoferrin and transferrin, upon iron starvation, both of which can be used as a source of nutrient iron. This increase in lactoferrin and transferrin binding is presumably through increasing transcription of the receptors for these proteins [59]. Together this coordinated upregulation of iron acquisition genes allows H. pylori to respond to and survive the iron deplete environment of the human host.
Many pathogenic bacteria coordinate the expression of virulence factors to the detection of changes in iron availability and H. pylori is no exception. Two of the most important virulence factors expressed by H. pylori, VacA and CagA toxin, are transcriptionally regulated in part by iron [63, 64]. Similar to VacA, once inside the cytoplasm, CagA mediates a cascade of changes within the cell including changes to cell morphology and immune signaling. Importantly, the activity of CagA in concert with VacA has been shown to initiate a perturbation in the inner leaflet of the cell membrane which results in the rerouting of transferrin receptors to the apical surface, ostensibly making all bound transferrin available to the bacterium [67]. Similarly, the human antimicrobial protein lactoferrin, which serves as an iron source for H. pylori, has been shown to repress the expression of both cagA and vacA, indicating that the human antimicrobial response can directly alter H. pylori virulence by altering the micronutrient gradient available to this bacterial pathogen [59, 68]. Recently, our work has indicated that the biogenesis and activity of the cag-T4SS increase upon iron starvation [65, 66]. Together these findings indicate that regulation of H. pylori toxin secretion is mediated by iron availability and that both toxins play a critical role in iron homeostasis.
Iron availability not only modulates expression and deployment of both vacA and cagA-T4SS in vitro but recent research utilizing a Mongolian gerbil infection model indicates that dietary iron levels augment disease progression and cancer development in vivo. In this infection model gerbils were maintained on iron replete and iron deplete diets beginning two weeks prior to infection and were maintained on these diets throughout the duration of the infection. Analysis of animals treated with a low iron diet revealed that they had markedly less hepatic iron present, as well as significantly less iron binding proteins, ferritin and hemoglobin, within their serum [66]. Iron levels within gastric tissue were also measured using Inductively Coupled-Plasma Mass-Spectrometry (ICP-MS) which demonstrated that iron concentrations within the replicative niche of H. pylori were drastically reduced upon subjection to an iron deplete diet [66]. Together these results confirm that an iron poor diet results in a global decrease in iron stores throughout the body, including the stomach. Within the same study, when comparing the disease outcome of animals fed an iron deficient diet to that of animals maintained on an iron sufficient diet, it was clear that the animals with decreased iron had greater immune cell infiltrate to the site of infection, a more rapid onset of gastritis, and a higher rate of cancer development, compared to the animals maintained on an iron rich diet [66]. The mechanisms driving these differences in inflammation and cancer development were found to be similar in vivo as they are in vitro, in the fact that the increased inflammation and disease severity are attributable to the deployment of the cagT4SS pili [65, 66]. The number of pili found in animals maintained on low iron diets versus high iron diets was determined using SEM to visualize and subsequently enumerate the amount of pili formation under both conditions. Consistent with this finding, strains harvested from iron deplete animals translocated a greater amount of CagA into host cells than strains from animals fed an iron rich diet. Together these data demonstrate that the diet of the host, specifically iron intake, has a large impact on the availability of nutrients for invading pathogens and consequently influences disease outcomes.
The correlation between reduced dietary iron and increased disease severity demonstrated in an animal model is mirrored within the human population. Individuals with low serum levels of the iron binding protein, ferritin, have more severe disease outcomes in the context of an H. pylori infection than individuals with adequate ferritin serum levels [69]. The mechanisms by which iron deficiency can arise are varied and include not only diets lacking necessary iron but also blood loss. Some strains of H. pylori are associated with hemorrhagic gastritis which may contribute to blood loss and successive iron deficiency. Furthermore, chronic H. pylori infection is associated with hypochlorhydria, an increased stomach pH, which may impede iron absorption as iron is more soluble at lower pHs. Importantly, case control studies have shown an inverse relationship between dietary iron intake and gastric cancer suggesting that iron deficiency arising from both dietary factors and blood loss contributes to cancer progression during an H. pylori infection [70, 71].
4.3. Zinc
Similar to iron, zinc is gaining appreciation as a micronutrient that exerts great influence at the host-pathogen interface. Zinc is required for cellular processes in all domains of life, and the mammalian host exploits this requirement by chelating nutrient zinc within host innate immune S100A-family proteins, including EN-RAGE (calgranulin C, S100A12) or calprotectin (MRP-8, S100A8/A9) [72, 73]. This process, termed "nutritional immunity," tightly regulates zinc availability in response to infection and essentially starves the invading prokaryote. Both EN-RAGE and calprotectin are significantly elevated in H. pylori infected gastric tissues compared to uninfected tissues, and these proteins primarily localize to polymorphonuclear cells (neutrophils) recruited to the site of infection [72, 73]. The severity of inflammation, specifically the infiltration of neutrophils in response to H. pylori infection, was inversely proportional to mucosal zinc levels [74]. The authors conclude that low zinc levels could enhance inflammation, but it is equally plausible that the S100A-family proteins deposited by neutrophils at the site of infection could be contributing to the chelation and subsequent removal of zinc from the gastric mucosa.
H. pylori has a strict nutritional requirement for zinc to grow and both calprotectin and EN-RAGE have been shown to inhibit H. pylori growth and viability via zinc sequestration activity [72, 73]. In response to zinc sequestration (by calprotectin or synthetic chelators), H. pylori forms tenacious biofilms and alters its lipid A structure [75]. The alterations in lipid A structure under conditions of zinc starvation indicate that LpxF, LpxL, and LpxR enzyme functions are diminished [75]. This results in the presence of a lipid A structure which is penta-acylated and contains both a phosphoethanolamine residue at 1′-position and a 4′-phosphate which decorates the outer membrane [75]. These alterations in lipid A structure confer decreased cell surface hydrophobicity which enhances bacterial fitness in the presence of calprotectin. These results indicate that H. pylori modifies its lipopolysaccharide endotoxin production in response to nutrient zinc availability to circumnavigate the host immune response [75].
Interestingly, H. pylori exposure to EN-RAGE or calprotectin prior to coculture with gastric epithelial cells also results in diminished cag-T4SS activity including CagA translocation into host cells and proinflammatory IL-8 chemokine secretion. Additionally, the downregulation of cag-T4SS activity is associated with abrogation of cag-T4SS pilus deployment, results that were reversed by the addition of an exogenous source of nutrient zinc [65, 72, 73]. Together, these results indicate that H. pylori senses nutrient zinc in the gastric environment and has evolved to deploy the cag-T4SS in response to the presence of this transition metal. Epidemiological data supports a model in which zinc enhances the carcinogenic cag-T4SS activity, as high zinc intake has been associated with gastric noncardia adenocarcinoma [76]. Concordantly, high serum zinc levels and high zinc intake have been associated with H. pylori infection and antibody response, respectively [77]. Similar studies in pediatric patients have revealed no association between H. pylori and iron or zinc nutritional status but significant association between H. pylori infection status and copper nutritional status as determined by serum metal concentrations [78, 79].
Besides regulating endotoxin and cytotoxin secretion, zinc has also been implicated as an important cofactor for urease and nickel-iron hydrogenase (Ni, Fe-hydrogenase), enzymes that are critical for H. pylori survival in the low pH of the stomach [80–82]. Zinc is required for dimerization of the chaperone UreG, which participates in nickel trafficking to promote urease activation. The accessory protein UreE utilizes either nickel or zinc as a cofactor which is critical for activity [83]. The metallochaperone, HypA, binds zinc for appropriate structural stabilization and interacts with HypB to deliver nickel to both urease and Ni, Fe-hydrogenase, indicating that zinc is critical for bacterial physiology in vivo [84–86].
H. pylori has clearly evolved to experience zinc stress in the gastrointestinal environment due to evidence that this pathogen encodes multiple proteins involved in zinc efflux in its genome. CadA, CznABC, CrdB, and CzcAB proteins protect H. pylori from zinc toxicity [87–89]. CznABC efflux function is required for colonization in a gerbil model of H. pylori infection. These studies underscore the critical role that detoxification strategies play in bacterial metal homeostasis during pathogenesis. It is likely that H. pylori encounters transition metals including zinc in the micromolar range from the host diet [89]. Studies on short term supplementation with zinc sulfate reveal that cohorts maintained on zinc supplementation exhibit less gastritis than cohorts without zinc supplementation. However, bacterial burden was not altered by this addition of zinc, as would be expected with increased zinc toxicity within the bacterial cell [90]. The numerous epidemiological studies of dietary zinc intake and zinc supplementation have yielded heterogeneous results, and a recent meta-analysis concluded that no firm conclusions about dietary zinc could be reached at this time [91]. It is interesting to note that, of the studies which have shown a correlation between zinc intake and H. pylori-dependent disease progression, most have been on populations in Asia, which are commonly associated with cag-PAI-positive strains of H. pylori [16].
4.4. Nickel
In addition to zinc and iron, H. pylori requires the transition metal nickel for full virulence. H. pylori exploits nickel-containing metalloenzymes such as NiFe-hydrogenase and urease to circumnavigate the low pH environment of the human stomach [92]. Urease, one of the most abundant enzymes in H. pylori proteome requires 24 nickel atoms for activity [93]. However, excess nickel in the bacterial cell results in mismetallation of cellular enzymes, which can abrogate physiological activity. Consequently, H. pylori manages its cellular nickel economy by tightly controlling both nickel import and export functions [94]. Nickel is transported into the bacterial cell in Helicobacter spp. via a NixA permease, and the FrpB4 outer membrane protein in a TonB-dependent fashion [95–98]. Nickel efflux is achieved by the promiscuous CznABC transporter, which promotes nickel resistance in H. pylori cells [89]. It is likely that H. pylori will encounter micromolar concentrations of transition metals such as nickel from host diet, which could ultimately influence the activity of these critical enzymes and nickel homeostasis functions [89]. Recent work by Campanale et al. indicates maintenance of patients on a nickel-free diet enhanced H. pylori eradication rate, supporting the essentiality of nickel for H. pylori pathogenesis [92].
5. Microbiome
Chronic H. pylori colonization leads to dramatic changes within the gastric environment including a reduction in parietal cells and subsequent increases in stomach pH and altered nutrient availability and local immune responses. Together, these H. pylori mediated changes in gastric physiology and immunology likely induces perturbations in the microbiome composition. While H. pylori-associated changes in microbiome structure are not fully understood, recent advances in both DNA sequencing and computational analysis have revealed an exceptionally complex microbiota in the human stomach. H. pylori colonization in specific pathogen-free female BALB/c mice leads to a decrease in the quantity of Lactobacillus species within the gastric microbiota when compared to noninfected mice [99]. In contrast H. pylori infection did not significantly alter the overall stomach microbiota composition within female C57BL/6N mice. Infection models using Mongolian gerbils found that H. pylori colonization altered both the number and localization of indigenous gastric microbiota ultimately leading to more severe gastritis [100]. Analysis of the microflora following a 12-week infection found dramatic differences in composition including the appearance of S. aureus and Enterococci and a decrease in number of Lactobacilli as well as an increase in number of Bacteroides [100]. Furthermore, gerbil studies have shown that H. pylori infected animals had alterations in the distribution of Bifidobacteria which was greater in the corpus than the antrum when compared to uninfected animals. Similarly, Aebischer et al. found that the stomachs from H. pylori-positive animals were colonized by bacterial species typically confined to the lower gastrointestinal tract [99]. Underscoring the complex relationship that exists between H. pylori and the indigenous microflora are studies indicating that some resident microbes may inhibit H. pylori growth, specifically Lactobacilli spp. [101, 102]. Discrepancies between studies may be because the ability of H. pylori to alter the stomach microbiome is influenced by the species of animal used, genetic background of the animal, specific strain of H. pylori, and length of infection. Together these findings indicate that H. pylori mediates changes to the host both directly as discussed previously and indirectly by altering the composition and distribution of its natural microbiota.
There are a limited number of studies investigating what effect H. pylori has on the microbiome within the human host. One analysis found that the microbial profiles of patients infected with H. pylori had increased numbers of non-Helicobacter Proteobacteria, Spirochetes, and Acidobacteria as compared to H. pylori-negative patients [103]. However, another study examining the effect of H. pylori colonization on the gastric microflora showed that H. pylori infection causes a shift in the microbiome such that there is an enrichment of Proteobacteria and a decrease in Actinobacteria [104]. Discrepancies in findings may be attributable to variations in bacteria surveillance techniques. As sequencing and analysis technologies improve and become more accessible the perturbation of host flora caused by H. pylori colonization will become more clearly defined.
In addition to defining how H. pylori alters the composition of the resident microbiome another issue to be resolved is elucidating what impact H. pylori mediated dysbiosis has on disease outcome. Specifically, it remains unclear if the gastric microbiota induces a more virulent H. pylori or if H. pylori induced changes in gastric flora promote carcinogenesis. In the transgenic insulin-gastrin (INS-GAS) mouse model of spontaneous gastric cancer, H. pylori drove disease progression and the development of intraepithelial neoplasia. Mice given antibiotics 8 weeks after infection to eradicate H. pylori had neoplasia significantly less than mice who received the antibiotics at 12 and 22 weeks after infection. Interestingly, H. pylori-free mice given similar antibiotics also displayed a decrease in the development of neoplasia. Taken together these observations indicate that gastric atrophy mediated by H. pylori or other factors predisposes to gastric carcinogenesis. The finding that earlier antibiotic treatment was more protective against gastric cancer both in the presence and in the absence of H. pylori may be attributable to the eradication of additional, unidentified cancer-potentiating microbes [105]. These findings are further supported by research which showed that germ-free INS-GAS mice had delayed onset of both gastritis and neoplasia compared to specific pathogen-free INS-GAS mice. In the same study H. pylori-monocolonization was found to accelerate disease progression resulting in early onset of neoplasia as compared to germ-free mice; however the gastritis was delayed and less severe than H. pylori infected mice that maintained a diverse microbiota [106]. The mechanism by which H. pylori-associated dysbiosis induces disease progression remains poorly defined. One rationale is that changes in the microbe community include increases of nitrosylating bacterial species which convert nitrogen compounds in gastric fluid to carcinogens such as N-nitrosamines or nitric oxide. Additionally the overgrowth of some bacteria may result in increases in DNA-damaging reactive oxygen species and reactive nitrogen species, which are potent mutagens and can contribute to gastric cancer. Lastly, the dysbiosis created by H. pylori may promote host inflammatory responses and accelerate metaplasia, atrophy, and cancer.
6. Conclusions
The intersection of host genetics, immune response, bacterial virulence expression, diet, micronutrient availability, and microbiome structure and composition undoubtedly influence the disease outcomes associated with chronic H. pylori infection. However, the complex relationship that each of these variables has with each other remains poorly defined. Future studies will seek to determine how these dynamic factors influence each other and can be exploited to ameliorate disease risk and promote gastric health as the age of antibiotics begins to wane.
The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.
Competing Interests
The authors declare that they have no competing interests.
This work has been funded primarily by a Career Development Award IK2BX001701 (to Jennifer A. Gaddy) from the Office of Medical Research, Department of Veterans Affairs. Additional support was provided by the Childhood Infections Research Program T32-AI095202 (to Kathryn P. Haley) and Vanderbilt University Medical Center's Digestive Disease Research Center supported by NIH Grant P30DK058404 and Vanderbilt Institute for Clinical and Translational Research Program supported by the National Center for Research Resources, Grant UL1 RR024975-01, and the National Center for Advancing Translational Sciences, Grant 2 UL1 TR000445-06.
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subset: commoncrawl


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MIPS Technologies Joins the Multicore Association to Drive Standards for Next-Generation Embedded Designs
MIPS Technologies, Inc., (NASDAQ: MIPS), a leading provider of industry-standard architectures, processor cores and analog IP for digital consumer, home networking, wireless, communications and business applications, today announced it has joined the Multicore Association, a global non-profit organization developing standards to help speed time-to-market for products that feature multi-core implementations.
MIPS Technologies has extensive experience in multi-processing, with the MIPS® architecture being widely used in multi-core systems ranging from deeply embedded, low-power applications to massively parallel supercomputers. As developers increasingly turn to multi-core implementations to either boost performance or decrease power consumption, there is a growing requirement for software interface and tool standards.
According to industry analyst firm Venture Development Corporation (VDC), revenue growth of the market for multi-core CPUs in embedded applications is projected to be strong through 2011. VDC projects 2007 revenues to be $372 million, and estimates 2011 revenues will be more than six times that amount. The firm says that revenues will surpass the billion dollar mark as early as 2009.
Our customers have long been successful in both homogenous and heterogeneous multi-core implementations, and we will continue to support the configurations that best suit their design parameters and applications, said Jack Browne, vice president of marketing for MIPS Technologies. Standards, like those proposed by the Multicore Association, are essential for the future development and progression of the SoC market. Standards-based communication and debug will help ease the transition to the software models needed for next-generation multi-core designs.
As a leading provider of processor architectures and cores for the embedded industry, were very pleased to welcome MIPS Technologies to the Multicore Association, said Markus Levy, Multicore Association president. MIPS Technologies renowned leadership in the embedded market as well as its commitment to multi-processing systems will be invaluable in helping us define future standards for multi-core communication, resource and task management, and debug.
About The Multicore Association
The Multicore Association provides a neutral forum for vendors who are interested in, working with, and/or proliferating multicore-related products, including processors, infrastructure, devices, software, and applications. Currently, the organization is set up with three working groups: Communications API (CAPI), Debug API, and Transparent Inter Process Communication (TIPC) protocol. Members include ARC International, Codeplay, Enea, eSOL, Freescale Semiconductor, Imperas, Intel, Mentor Graphics, MIPS Technologies, NEC Electronics America, Nokia Siemens Networks, PolyCore Software, QNX, Texas Instruments, Tilera, the University of York, and Wind River. Further information is available at www.multicore-association.org.
About MIPS Technologies
MIPS Technologies, Inc. (NASDAQ: MIPS) is a leading provider of industry-standard architectures, processor cores and analog IP for digital consumer, networking, personal entertainment, communications and business applications. The company drives the broadest architectural alliance that delivers 32- and 64-bit embedded RISC solutions to the embedded market, and in combination with its licensees, offers the widest range of robust, scalable processors in standard, custom, semi-custom and application-specific products worldwide. MIPS Technologies currently owns more than 400 patent properties (patents and applications) worldwide and licenses its intellectual property to todays leading semiconductor companies, ASIC developers and system OEMs.
Today, MIPS-BasedTM designs are integrated in millions of products around the world, including broadband devices from Linksys, digital cameras from Canon, DTVs and entertainment systems from Sony, DVD Recordable devices from Pioneer, digital set-top boxes from Motorola, network routers from Cisco and laser printers from Hewlett-Packard. Founded in 1998, MIPS Technologies is based in Mountain View, California, with offices worldwide. For more information, please contact (650) 567-5000 or visit http://www.mips.com.
MIPS and MIPS-Based are trademarks or registered trademarks of MIPS Technologies, Inc. in the United States and other countries. All other trademarks referred to herein are the property of their respective owners.
This news content was configured by WebWire editorial staff. Linking is permitted.
News Release Distribution and Press Release Distribution Services Provided by WebWire.


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Book directly from your current position by tapping "TRAVEL NOW". If you want to be picked up somewhere else, just move around on the map or search for the address. You can also pre-book a trip by tapping "PRE-BOOK" and select what time you want to be picked up or when you want to arrive at your destination.
Add your destination address and get a fixed price. Before you book your trip you will be able to select how you want to pay and you can add a via address. Tap on "BOOK TRIP" to confirm the booking. You will be notified both when the car is on its way and when it has arrived at the pickup location. You can also follow the car directly on the map.


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The Truth in Losing Belly Fat!
Ladies, regardless of our shapes and sizes, we all face the same issue of wanting to lose that belly fat. It is a dream to create a flat tummy and toned abs, and this is not limited to those who have a slim silhouette. Due to the busy lifestyle and advanced technologies, it is easy to have stubborn fats accumulating around our hips and belly. The long hours of sitting behind a desk and reduce in mobility is all part of the contributing factors.
There are many tips and myths on how to reduce belly fat by doing abdominal exercises for 5 or 10 minutes a day. In reality, do these abdominal exercises really help to lose belly fats?
The Truth…
By doing these abdominal exercises such as crunches, planking or leg lifts, it does not provide the result of a toned abs nor will it reduce your belly fat. What these exercises provides, is strengthening of your muscles but if you have a thick layer of belly fat under your skin, these abs will not surface and be seen no matter how many reps of crunches you do per day.
So What Should You Do?
What you do need to achieve is losing overall fat by doing cardio or moderate-high intensity workout to burn off the fats and core exercises at the end to create a toned body. The results will not be visible if you target to do only abdominal exercises without a holistic fitness plan and diet.
Foods to Eat to Reduce Belly Fat
After all the sweat and tears, you do not want to go and eat a heavy meal and ruin the earlier efforts. Include food that increases your metabolism rate and help to burn off the fat even when you're not exercising. Here are lists of foods that you should eat to help reduce belly fat:
- Oat meal and whole grains and nuts
- Eggs
- Lean meat
- Berries
- Green tea
- Apple cider vinegar
Foods such as garlic, cucumber, tomato and apples are great at inducing metabolism which helps to burn overall fats. You need to take note that the calories intake should not be higher than the calories you burn off in order to lose those fats.
Tips on How to Reduce Belly Fat Without Exercise
Increase in physical activity will definitely help in burning extra calories, slowly but surely, you should be able to see a difference in your body. For example, instead of taking a bus home, opt for that 15-20 minute walk back. Instead of taking the lift, opt for taking the stairs to burn off the fats.
Other than turning to these exercises to burn belly fat, there are other options that will help in the daily maintenance of reducing our belly fat.
Protein to Help Lose Belly Fat
One study showed that the amount and quality of protein consumed was inversely related to fat in the belly. That is, people who ate more and better protein had much less belly fat.
Protein has been shown to reduce cravings by 60%, and boost metabolism by 80-100 calories per day and help you eat up to 441 fewer calories per day! Not only will it help you lose these calories, it can also help you avoid rebound weight.
So make an effort to increase your intake of unprocessed eggs, fish, seafood, meats, poultry and dairy products. These are the best protein sources in the diet. Eat smart and get the maximized results with minimal effort.
Reduce Carbs in Your Diet Plan
Carb restriction is a very effective way to lose fat. When people cut carbs, their appetite goes down and they lose weight. Low-carb diets also lead to quick reductions in water weight, which gives people near instant results. There are also studies comparing low-carb and low-fat diets, showing that low-carb diets specifically target the fat in the belly, and around the organs and liver.
Just avoiding the refined carbs (white breads, pastas, etc) should be sufficient, especially if you keep your protein high. However, if you need to lose weight fast, then consider dropping your carbs down to 50 grams per day. This will put your body into ketosis, killing your appetite and making your body start burning primarily fats for fuel.
Cut Down on Alcoholic Beverages and Sugared Drinks
Cutting down on beer or other alcoholic beverages is an effective way to lose belly fat, as alcohol is basically pure concentrated sugar which will eventually be stored in the belly area. Alcohol also causes low blood sugar levels and dehydration, leading to an increase in appetite and binge eating at the end of a drinking session. Now you know why there is an increase in hunger pangs after a night of drinking!
Besides these, the liver also processes alcohol before other carbohydrates and protein, thus the presence of alcohol in the body slows down fat burning. For instance, studies have shown that your body's ability to burn belly fat decreases up to 73% for a few hours after having a couple of drinks and drinking more than a couple of drinks can lower your fat burning ability for up to 4 days.
Sugar is half glucose, half fructose and fructose can only be metabolized by the liver in any significant amount. When you eat a lot of refined sugar, the liver gets flooded with fructose, and is forced to turn it all into fat. Numerous studies have shown that excess sugar, mostly due to the large amounts of fructose, can lead to increased accumulation of fat in the belly.
A can of coke gives you 140 calories, and that extra calories per day could make you gain 6.3kg more per year. In order to burn off the excess calories, you will need to walk at medium pace for at least 40 minutes. Do not reach for the coke if you are not ready to work for it.
Are You Heading in The Right Direction?
So instead of thinking that abdominal exercise itself can help lose belly fats, you now know that those crunches or planking challenges will not provide the result you wish to achieve without losing overall and belly fats.
Once you have accomplished in losing the fats that harbours underneath your skin, the abdominal exercises should pay off and you will be able to achieve that toned abs that you desire.


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Monatsschr. Kakteenk. 16: 41. 1906
Family: CACTACEAE
Accepted Scientific Name: Mammillaria formosa subs. chionocephala (J.A.Purpus) D.R.Hunt
Mammillaria Postscripts 7: 3 (1998)
Origin and Habitat: Highlands of central Mexico (Coahuila, Nuevo Leon, and Durango).
Type locality: Sierra de Parras, Coahuila, Mexico.
Altitude range: 1450-2400 metres above sea level.
Habitat and ecology: Mammillaria formosaSN|15832]]SN|15832]] subs. chionocephala grows in rocky areas together with Thelocactus macdowellii, Ferocactus steinesii, Hamatocactus hamatacanthus, Echinocactus horizonthaloniusSN|1711]]SN|1711]], Fouquieria splendensSN|15717]]SN|15717]], Thelocactus phymatothele, Neolloydia conoideaSN|10089]]SN|10089]], Agave striataSN|562]]SN|562]], Yucca filifera, Ariocarpus retususSN|2079]]SN|2079]] and Lophophora williamsiiSN|1117]]SN|1117]], amongst others.
- Mammillaria formosa subs. chionocephala (J.A.Purpus) D.R.Hunt
- Mammillaria chionocephala J.A.Purpus
- Neomammillaria chinocephala (J.A.Purpus) Britton & Rose
Mammillaria formosa Galeotti ex Scheidw.
Bull. Acad. Roy. Sci. Bruxelles v. (1838) 497 [et: Allg. Gartenzeitung (Otto & Dietrich) 12: 186. 1844 ]
Synonymy: 7
- Mammillaria formosa Galeotti ex Scheidw.
- Cactus formosus Kuntze
- Neomammillaria formosa Britton & Rose
- Mammillaria arroyensis Repp.
- Mammillaria formosa var. dispicula Monv. ex Labour.
- Mammillaria formosa var. gracilispina Monv. ex Labour.
- Mammillaria formosa var. laevior Monv. ex Labour.
Mammillaria formosa subs. chionocephala (J.A.Purpus) D.R.Hunt
Mammillaria Postscripts 7: 3 (1998)
Synonymy: 10
- Mammillaria formosa subs. chionocephala (J.A.Purpus) D.R.Hunt
- Mammillaria chionocephala J.A.Purpus
- Neomammillaria chinocephala (J.A.Purpus) Britton & Rose
- Mammillaria acanthophlegma Lehm.
- Cactus acanthophlegmus (Lehm.) Kuntze
- Mammillaria caerulea R.T.Craig
- Mammillaria ritteriana Boed.
- Neomammillaria ritteriana (Boed.) Y.Itô
- Mammillaria ritteriana var. quadricentralis R.T.Craig
- Neomammillaria ritteriana var. quadricentralis (R.T.Craig) Y.Itô
Mammillaria formosa subs. microthele (Muehlenpf.) D.R.Hunt
Mammillaria Postscripts 6: 9 (1997)
Synonymy: 8
- Mammillaria formosa subs. microthele (Muehlenpf.) D.R.Hunt
- Cactus bispinus J.M.Coult.
- Mammillaria formosa var. microthele Salm-Dyck
- Mammillaria microthele Muehlenpf. & Tiegel
- Mammillaria formosa subs. microthele var. superfina hort.
Mammillaria formosa subs. pseudocrucigera (R.T.Craig) D.R.Hunt
Mammillaria Postscripts 6: 10 (1997)
Synonymy: 2
- Mammillaria formosa subs. pseudocrucigera (R.T.Craig) D.R.Hunt
- Mammillaria pseudocrucigera R.T.Craig
UKRAINIAN (Українська): Мамілярія xіоноцефала, Мамілярія сніжнобілоголова
Description: Mammillaria formosaSN|15832]]SN|15832]] subs. chionocephala (firstly described as Mammillaria chionocephalaSN|13998]]SN|15848]] by J.A.Purpus 1906) is an attractive globose pincushion cactus simple or rarely proliferous, sometimes 10 cm in diameter and typically wrapped on the upper part with a dense snow-white wool, so that only the tips of the tubercles visible. Each head is surrounded by a complete ring of star-like pink flowers. Even without flowers it is an extremely attractive plant, and one of the most beautiful mammillarias. Young plants start producing their wool only when they reach the flowering stage. There are several similar looking Mammillarias but far from being so woolly like the real "chionocephala".
Note. It was distributed by Pringle in 1890 as Mammillaria acanthophlegmaSN|15848]]SN|31354]] and has been in collections for many years. In 1906 Dr. J. A. Purpus described it as Mammillaria chionocephalaSN|31354]]SN|15848]]. It resembles very much a large plant of Mammillaria elegansSN|15848]]SN|13998]], but the tubercles are milky and bear dense hairs and wool in their axils. Some people consider Mammillaria formosaSN|15832]]SN|15832]] subs. chionocephala to be good species.
Stem: Symmetrical, solitary, slowly becoming branched, flattened-globular to short cylindrical, rounded or depressed at the summit, light to dark green, 15-20 cm high, 9-10 cm in diameter with a milky juice.
Tubercles: Tubercles arranged in 13-21 series, low, crowded, obtusely tetragonal-pyramidal, very milky, axils of tubercles densely filled with white wool and numerous hair-like bristles up to 20 mm long.
Radial spines: 22-24, occasionally as many as 40, rigidly bristle-like, white, to 8 mm long, somewhat pectinate, spreading.
Central spines: Usually 2-4, rarely as many as 7, straight or somewhat curved, more or less divergent, much stouter than the radials, rigid, white with brownish tips.
Flowers: About 1 cm long and in diameter, white to rose-red, in a circle near the summit.
Blooming season: Spring.
Fruit: Clavate, carmine red, to 10 mm long.
Seeds: Small, brown.
Subspecies, varieties, forms and cultivars of plants belonging to the Mammillaria formosa group
- Mammillaria formosa Galeotti ex Scheidw.: has pale pink flowers and 20-22 white radial spines. Distribution: Coahuila, Aguascalientes, Guanajuato, Zacatecas, Tamaulipas, Nuevo Leon, and San Luis Potosi.
- Mammillaria formosa subs. chionocephala (J.A.Purpus) D.R.Hunt: is typically wrapped on the upper part with a dense snow-white wool, so that only the tips of the tubercles visible. Distribution: Highlands of central Mexico (Coahuila, Nuevo Leon, and Durango).
- Mammillaria formosa subs. microthele (Muehlenpf.) D.R.Hunt: has nearly pure white flowers and 22-24 flattened and bristle-like radials. Description: Coahuila, Guanajuato, Tamaulipas, and San Luis Potosi.
- Mammillaria formosa subs. microthele var. superfina hort.: it is a particular nice selected form with very small tubercles and spines.
- Mammillaria formosa subs. pseudocrucigera (R.T.Craig) D.R.Hunt: has distinctly pink flowers with white margins and only 18 radials, often lacking on mature areoles. Distribution: Queretaro and Guanajuato.
Bibliography: Major references and further lectures
1) Fitz Maurice, B, Fitz Maurice, W.A., Hernández, H.M., Sotomayor, M. & Smith, M. 2013. Mammillaria formosa. The IUCN Red List of Threatened Species. Version 2015.2. <www.iucnredlist.org>. Downloaded on 18 July 2015.
2) David Hunt, Nigel Taylor "The New Cactus Lexicon" DH Books, 2006
3) Edward F. Anderson "The Cactus Family" Timber Press, 2001
4) James Cullen, Sabina G. Knees, H. Suzanne Cubey "The European Garden Flora Flowering Plants: A Manual for the Identification of Plants Cultivated in Europe, Both Out-of-Doors and Under Glass"Cambridge University Press, 11/August/2011
5) Nathaniel Lord Britton, Joseph Nelson Rose "Cactaceae: Descriptions and Illustrations of Plants of the Cactus Family" vol. 4 The Carnegie Institution of Washington, Washington 1923
6) Bulletin of Miscellaneous Information, page 71, H.M. Stationery Office, 1974
7) Kakteen und andere Sukkulenten, Volume 53, page 126, Steinhart KG, 2002
8) Alfred Byrd Graf "Exotica 3: Pictorial Cyclopedia of Exotic Plants from Tropical and Near-tropic Regions : 12,000 Illustrations, 204 Plants in Color, Guide to Care of Plants Indoors, Horticultural Color Guide, Plant Geography" Parte 2 Roehrs Company, 1976
- A young specimen still without wool in the axils of tubercles. (Mammillaria formosa subs. chionocephala) Photo by: Valentino Vallicelli
The gallery now contains thousands of pictures, however it is possible to do even more. We are, of course, seeking photos of species not yet shown in the gallery but not only that, we are also looking for better pictures than those already present. Read More...
Cultivation and Propagation: Mammillaria formosaSN|15832]]SN|15832]] subs. chionocephala is easy to cultivate and make interesting specimens for any collection, and over time (in 12-15 years) it may form colonies up to 50 cm or more in diameter, and doesn't require any special treatment, except for the need for frequent transplanting, in order to manage its exuberance. It needs as much light as possible without burning the plant, to keep the stems compact. Provide a well-drained soil mix. Water well and then allow to dry thoroughly before watering again during the growing season. It doesn't like much, if any, winter water, but can survive short exposures to freezing temperatures (-4° C.) if properly hardened off and kept dry.
Propagation: It is best propagated from seed. Seed readily germinates at 20°-22°C, or by offsets if available. The white wool between the areoles makes this species a pleasure to look at and grow, but the diversity among individual specimens is considerable and the best plants have abundant white axillary wool. Hence, it is worth raising a batch of seedlings and selecting one or two that have the most wool.
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Trestman emerges as candidate for Colts job
Colts owner Jim Irsay considered Montreal Alouettes G.M. Jim Popp for the job that went to Ryan Grigson. Maybe Irsay was simply looking for insight on the guy whom Popp hired four years ago to coach the CFL team.
According to ESPN, via the Toronto Star, Alouettes coach Marc Trestman has landed on the list of candidates for the job. Trestman reportedly was interviewed over the weekend.
Trestman, a 56-year-old lawyer who obtained his degree while serving as an assistant coach at the University of Miami, worked at the NFL level from 1985 through 2004. He specializes in offense, working as a quarterbacks coach and offensive coordinator.
After two years at North Carolina State and one year out of football, Trestman emerged as the Alouettes head coach in 2008, leading the team to Grey Cup titles in 2009 and 2010.


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A thorough guide to making a menagerie of charming fondant creatures.
Fondant-decorated cakes are an important part of today's celebrations and now more than ever, bakers are choosing to make specialty cakes at home.
100 Fondant Animal Cake Toppers is a practical guide to making charming fondant toppers for any occasion. Straightforward instruction and hundreds of step-by-step photographs make it easy for both expert and beginner bakers.
The introduction explains all of the essential techniques and describes the materials used, along with recipes for all of the cakes, fillings, frostings and fondants used in the book.
The 50 projects are presented with these features for easy reference:
100 Fondant Animal Cake Toppers features whimsical decorations for every kind of celebration, including a panda bear munching on bamboo, cuddly teddy bears, a mouse with a piece of cheese, a fluffy lamb, a freckled turtle and colorful clownfish.
100 Fondant Animal Cake Toppers is an essential, easy-to-use guide to creating delightful decorations that will never fail to impress.
Helen Penman has been making fondant cakes for more than 15 years. She designs cakes for Cakes and Sugarcraft magazine and runs her own cake-decorating business, Too Nice to Slice. She is the author of Fondant Modeling for Cake Decorators.


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NeMLA 2015 Panel Seeing is Believing: Antiquity and Beyond Abstract due Sept. 30th
The relationship between the visual and the literary traces its origins to antiquity. In Rhetoric, Aristotle famously defines rhetoric as 'the ability to see the available means of persuasion' (I.2.1). Sight is a vital component of the human cognitive experience; neither education nor persuasion can take place without visualization. Throughout antiquity, philosophical concepts were often conveyed by artistic terminology and visual language and all genres of Classical literature contain lengthy ekphrases.