Conservation challenges in a threatened hotspot: agriculture and plant biodiversity losses in Baja California,Mexico

Modern agricultural practices pose serious threats to biodiversity worldwide. Species losses from habitat conversion are well documented, but indirect impacts such as reduced water availability to adjacent ecosystems are less known. San Quintín is an important agricultural valley in the mediterranean climate region of Baja California, Mexico. The region is also a hotspot of plant species richness and endemism. Plant species in the region are here analyzed by comparison of the contemporary flora to historical botanical collections to identify extirpations. Historical collections indicate that habitat loss to agriculture has been a direct cause of species losses. As importantly, the unsustainable extraction of groundwater has apparently led to salt water intrusion, resulting in the loss of 22 native plant taxa, including 13 rare plants. Seventy-eight percent of all the vernal pool taxa have been lost from the flora (including 85 % of the rare taxa) and 11 % of plants of riparian and pond habitat (including 25 % of the rare taxa) are no longer found in the region. Unsustainable agricultural practices continue to threaten fragile coastal ecosystems and are a serious challenge to current and future conservation efforts. Ironically, these same practices frequently result in abandonment of cultivated areas. Owing to indirect impacts, conservation of biodiversity and large-scale agricultural operations are even less compatible on a regional scale than indicated by direct impacts. It is vital that sustainable agricultural practices be adopted locally and globally to avoid further losses of biodiversity.     

Structural analysis of polymers of sickle cell hemoglobin. III. Fibers within fascicles

We have examined the structure of hemoglobin S fibers, which are associated into large bundles, or fascicles. Electron micrographs of embedded and cross-sectioned fascicles provide an end-on view of the component fibers. The cross-sectional images are rotationally blurred as a result of the twist of the fiber within the finite thickness of the section. We have applied restoration techniques to recover a deblurred image of the fiber. The first step in this procedure involved correlation averaging images of cross-sections of individual fibers in order to improve the signal-to-noise ratio. The rotationally blurred image was then geometrically transformed to polar co-ordinates. In this space, the rotational blur is transformed into a linear blur. The linearly blurred image is the convolution of the unblurred image and a point spread function that can be closely approximated by a square pulse. Deconvolution in Fourier space, followed by remapping to Cartesian co-ordinates, produced a deblurred image of the original micrograph. The deblurred images indicate that the fiber is comprised of 14 strands of hemoglobin S. This result provides confirmation of the fiber structure determined using helical reconstruction techniques and indicates that the association of fibers into ordered arrays does not alter their molecular structure.     

Systems analysis of primary Sjögren's syndrome pathogenesis in salivary glands identifies shared pathways in human and a mouse model

Bone tissue has an exceptional quality to regenerate to native tissue in response to injury. However, the fracture repair process requires mechanical stability or a viable biological microenvironment or both to ensure successful healing to native tissue. An improved understanding of the molecular and cellular events that occur during bone repair and remodeling has led to the development of biologic agents that can augment the biological microenvironment and enhance bone repair. Orthobiologics, including stem cells, osteoinductive growth factors, osteoconductive matrices, and anabolic agents, are available clinically for accelerating fracture repair and treatment of compromised bone repair situations like delayed unions and nonunions. Preclinical and clinical studies using biologic agents like recombinant bone morphogenetic proteins have demonstrated an efficacy similar or better than that of autologous bone graft in acute fracture healing. A lack of standardized outcome measures for comparison of biologic agents in clinical fracture repair trials, frequent off-label use, and a limited understanding of the biological activity of these agents at the bone repair site have limited their efficacy in clinical applications.     

Determinants of fruit and seed set in Pavonia dasypetala (Malvaceae)

Summary Measurements of foliage quality, physiological, and phenological condition of sample trees were used as independent variables in multiple correlation analyses to determine their effect on female and male spruce budworm larval dry weights. Female budworm from trees high in foliar concentrations of beta-pinene, myrcene and total nitrogen weighed less than those from trees lacking these characteristics. Male budworm from trees high in foliar concentrations of alpha-pinene, myrcene, terpinolene, citronellyl acetate, and bornyl acetate weighted less than those from trees lacking these characteristics. Additionally, relatively vigorous and productive trees tended to be less susceptible (as evidenced by reduced larval weight) to budworm of either sex.     

Sequence analysis of the 17-kilodalton-antigen gene from Rickettsia rickettsii.

DNA obtained from the Sheila Smith strain of Rickettsia rickettsii was digested to completion with the restriction endonucleases BamHI and SalI and ligated with the plasmid vector pUC19. The ligation mixture was used to transform Escherichia coli. A total of 465 bacterial clones were screened for antigen production with hyperimmune rabbit serum. One of the reactive clones, containing a recombinant plasmid designated pSS124, was solubilized and subjected to immunoblot analysis and revealed expression of a 17-kilodalton protein reactive with anti-R. rickettsii serum that comigrated with an antigen from R. rickettsii. A 1.6-kilobase PstI-BamHI fragment from pSS124 was subcloned and continued to direct synthesis of the 17-kilodalton antigen. The nucleotide sequence was determined for this 1.6-kilobase subclone, which encompassed the gene encoding the polypeptide as well as flanking regions containing potential regulatory sequences. The open reading frame consisted of 477 nucleotides that specified a 159-amino-acid protein with a calculated molecular weight of 16,840. The deduced amino acid sequence contained a hydrophobic sequence near the amino terminus that resembled signal peptides described for E. coli. The carboxy terminus was hydrophilic in nature and probably contained the exposed epitopes.     

Individual wealth rank, community wealth inequality, and self-reported adult poor health: a test of hypotheses with panel data (2002-2006) from native Amazonians, Bolivia

Growing evidence suggests that economic inequality in a community harms the health of a person. Using panel data from a small-scale, preindustrial rural society, we test whether individual wealth rank and village wealth inequality affects self-reported poor health in a foraging-farming native Amazonian society. A person's wealth rank was negatively but weakly associated with self-reported morbidity. Each step up/year in the village wealth hierarchy reduced total self-reported days ill by 0.4 percent. The Gini coefficient of village wealth inequality bore a positive association with self-reported poor health that was large in size, but not statistically significant. We found small village wealth inequality, and evidence that individual economic rank did not change. The modest effects may have to do with having used subjective rather than objective measures of health, having small village wealth inequality, and with the possibly true modest effect of a person's wealth rank on health in a small-scale, kin-based society. Finally, we also found that an increase in mean individual wealth by village was related to worse self-reported health. As the Tsimane' integrate into the market economy, their possibilities of wealth accumulation rise, which may affect their well-being. Our work contributes to recent efforts in biocultural anthropology to link the study of social inequalities, human biology, and human-environment interactions.     

Does Cosleeping Contribute to Lower Testosterone Levels in Fathers? Evidence from the Philippines

Because cross-species evidence suggests that high testosterone (T) may interfere with paternal investment, the relationships between men''s transition to parenting and changes in their T are of growing interest. Studies of human males suggest that fathers who provide childcare often have lower T than uninvolved fathers, but no studies to date have evaluated how nighttime sleep proximity between fathers and their offspring may affect T. Using data collected in 2005 and 2009 from a sample of men (n = 362; age 26.0 ± 0.3 years in 2009) residing in metropolitan Cebu, Philippines, we evaluated fathers'' T based on whether they slept on the same surface as their children (same surface cosleepers), slept on a different surface but in the same room (roomsharers), or slept separately from their children (solitary sleepers). A large majority (92%) of fathers in this sample reported practicing same surface cosleeping. Compared to fathers who slept solitarily, same surface cosleeping fathers had significantly lower evening (PM) T and also showed a greater diurnal decline in T from waking to evening (both p<0.05). Among men who were not fathers at baseline (2005), fathers who were cosleepers at follow-up (2009) experienced a significantly greater longitudinal decline in PM T over the 4.5-year study period (p<0.01) compared to solitary sleeping fathers. Among these same men, baseline T did not predict fathers'' sleeping arrangements at follow-up (p>0.2). These results are consistent with previous findings indicating that daytime father-child interaction contributes to lower T among fathers. Our findings specifically suggest that close sleep proximity between fathers and their offspring results in greater longitudinal decreases in T as men transition to fatherhood and lower PM T overall compared to solitary sleeping fathers.     

Determination of Antibiotic Susceptibility of Rickettsia by the Plaque Assay Technique

Plaque formation by various rickettsiae was completely inhibited by commercial antibiotic discs impregnated with tetracycline, chloramphenicol, nitrofurantoin, and erythromycin; partial inhibition was observed around discs containing nalidixic acid and sulfisoxazole, but no inhibition was seen around discs containing cephalothin, ampicillin, oxacillin, kanamycin, polymyxin B, streptomycin, or penicillin.     

Granzyme M has a critical role in providing innate immune protection in ulcerative colitis

Inflammatory bowel disease (IBD) is an immunoregulatory disorder, associated with a chronic and inappropriate mucosal immune response to commensal bacteria, underlying disease states such as ulcerative colitis (UC) and Crohn''s disease (CD) in humans. Granzyme M (GrzM) is a serine protease expressed by cytotoxic lymphocytes, in particular natural killer (NK) cells. Granzymes are thought to be involved in triggering cell death in eukaryotic target cells; however, some evidence supports their role in inflammation. The role of GrzM in the innate immune response to mucosal inflammation has never been examined. Here, we discover that patients with UC, unlike patients with CD, display high levels of GrzM mRNA expression in the inflamed colon. By taking advantage of well-established models of experimental UC, we revealed that GrzM-deficient mice have greater levels of inflammatory indicators during dextran sulfate sodium (DSS)-induced IBD, including increased weight loss, greater colon length reduction and more severe intestinal histopathology. The absence of GrzM expression also had effects on gut permeability, tissue cytokine/chemokine dynamics, and neutrophil infiltration during disease. These findings demonstrate, for the first time, that GrzM has a critical role during early stages of inflammation in UC, and that in its absence colonic inflammation is enhanced.Inflammatory bowel disease (IBD) is a gut-associated inflammatory disorder, which stems from a dysfunctional mucosal immune response to commensal bacteria.¹ As a multifactorial disease, IBD is the consequence of a complex interplay between environmental triggers, genetic susceptibility, and immunoregulatory defects, resulting in a pathogenesis that is still poorly understood.² These interactions result in the inability of an individual to control the normal inflammatory response to pathogens in the gut, leading to a chronic state of sustained and inappropriate inflammation. IBD underlies disease states such as ulcerative colitis (UC) and Crohn''s disease (CD), with symptoms including weight loss, abdominal pain, diarrhea, and rectal bleeding which often require intensive medical therapy and resective surgery.³ The pathogenesis of IBD, characterized by a defective mucosal immune response to microbial exposure in the gastrointestinal tract, is thought to be caused by a dysfunctional immune response to host microbiota, infection by specific pathogens, and/or a defective mucosal barrier to luminal pathogens.^{1, 2} IBD patients also have a high risk of developing colitis-associated colon cancer (CAC).⁴ Additionally, histological assessment of inflamed ileal and colonic segments from IBD patients typically shows increased infiltration of immune cells, particularly neutrophils, as well as crypt abscesses, mucin depletion, and ulcers—all correlating with the severity of small bowel and colonic tissue damage.⁵Cytotoxic pathways mediated by lymphocytes directly trigger cell death in target cells.⁶ These cytotoxic pathways are mediated by proteins such as perforin, which mediates pore formation in the target cell surface and allows granzyme (Grz)s to enter the intracellular compartment and induce cell death.⁷ To date, five different Grzs have been identified in humans (GrzA, GrzB, GrzH, GrzK, and GrzM), whereas mice express eleven Grzs (GrzA, GrzB, GrzC, GrzD, GrzE, GrzF, GrzG, GrzK, GrzL, GrzM, and GrzN).^{8, 9} Walch et al.¹⁰ recently demonstrated that Grzs (GrzA and GrzB) directly kill bacteria through granulysin-mediated delivery, suggesting that Grzs act as microbial modulating factors. Moreover, recently GrzA was shown to be increased in the colon biopsies of UC patients undergoing treatment with Etrolizumab, a monoclonal antibody targeting the β7 integrin subunit. Higher levels of GrzA could predict which patients were more likely to benefit from the therapy; however, the precise mechanism of action of GrzA in UC remains to be addressed.¹¹ GrzM was initially described as being constitutively expressed by natural killer (NK) cells,^{12, 13} and specifically associated with inflammation.¹⁴ This enzyme has been shown to preferentially cleave methionine and leucine residues in target cells, mediating direct, non-specific cell death.^{15, 16} More recently, GrzM was also shown to be an important mediator for the release of MIP-1α from NK cells, inducing NK cell and neutrophil recruitment during early microbial infection.¹⁷ We now observe that GrzM expression is increased in inflamed colon tissue samples from UC, but not CD patients. Further, GrzM-deficient (GrzM^−/−) mice are more sensitive to a mouse model of IBD and IBD-induced colorectal cancer (CRC). These findings demonstrate, for the first time, that GrzM has a critical role in mediating the early stages of the gut mucosal immune response.