Dissonant Belonging and the Making of Community: Native Hawaiian Claims to Selfhood and Home

In 1898 the United States illegally annexed the Hawaiian Islands over the protests of Queen Liliʽuokalani and the Hawaiian people. American hegemony has been deepened in the intervening years through a range of colonizing practices that alienate Kanaka Maoli, the indigenous people of Hawaiʽi, from their land and culture. Dissonant Belonging and the Making of Community is an exploration of contemporary Hawaiian peoplehood that reclaims indigenous conceptions of multiethnicity from colonizing narratives of nation and race. Drawing from archival holdings at the University of Hawaiʽi, Mānoa and in-depth interviews, this project offers an analysis of public and everyday discourses of nation, race, and peoplehood to trace the discursive struggle over Local identity and politics. A context-specific social formation in Hawaiʽi, “Local” is commonly understood as a multiethnic identity that has its roots in working-class, ethnic minority culture of the mid-twentieth century. However, American discourses of race and, later, multiethnicity have functioned to render invisible the indigenous roots of this social formation. Dissonant Belonging and the Making of Community reclaims these roots as an important site of indigenous resistance to American colonialism. It traces, on the one hand, the ways in which Native Hawaiian resistance has been alternately erased and appropriated. On the other hand, it explores the meanings of Local identity to Native Hawaiians and the ways in which indigenous conceptions of multiethnicity enabled a thriving community under conditions of colonialism.

Na himeni hoolea : he mau mele ma ka uhane, e hoolea ai na kanaka, na keiki, na ohana, na kula, na ekalesia, ia Iehova, ke Akua e ola'i.

First edition, 1823, was "the joint production of Messrs. Ellis and Bingham." cf. H.M. Ballou, Hist. of the Hawaiian mission press, 1908, p.13; cf. also pref. to Lyons' Ka buke himeni hawaii, 1885.

New loci associated with birth weight identify genetic links between intrauterine growth and adult height and metabolism.

Birth weight within the normal range is associated with a variety of adult-onset diseases, but the mechanisms behind these associations are poorly understood. Previous genome-wide association studies of birth weight identified a variant in the ADCY5 gene associated both with birth weight and type 2 diabetes and a second variant, near CCNL1, with no obvious link to adult traits. In an expanded genome-wide association meta-analysis and follow-up study of birth weight (of up to 69,308 individuals of European descent from 43 studies), we have now extended the number of loci associated at genome-wide significance to 7, accounting for a similar proportion of variance as maternal smoking. Five of the loci are known to be associated with other phenotypes: ADCY5 and CDKAL1 with type 2 diabetes, ADRB1 with adult blood pressure and HMGA2 and LCORL with adult height. Our findings highlight genetic links between fetal growth and postnatal growth and metabolism.

Comparative functional analysis of two fibroblast growth factor receptor 1 (FGFR1) mutations affecting the same residue (R254W and R254Q) in isolated hypogonadotropic hypogonadism (IHH).

FGFR1 mutations have been identified in both Kallmann syndrome and normosmic HH (nIHH). To date, few mutations in the FGFR1 gene have been structurally or functionally characterized in vitro to identify molecular mechanisms that contribute to the disease pathogenesis. We attempted to define the in vitro functionality of two FGFR1 mutants (R254W and R254Q), resulting from two different amino acid substitutions of the same residue, and to correlate the in vitro findings to the patient phenotypes. Two unrelated GnRH deficient probands were found to harbor mutations in FGFR1 (R254W and R254Q). Mutant signaling activity and expression levels were evaluated in vitro and compared to a wild type (WT) receptor. Signaling activity was determined by a FGF2/FGFR1 dependent transcription reporter assay. Receptor total expression levels were assessed by Western blot and cell surface expression was measured by a radiolabeled antibody binding assay. The R254W maximal receptor signaling capacity was reduced by 45% (p<0.01) while R254Q activity was not different from WT. However, both mutants displayed diminished total protein expression levels (40 and 30% reduction relative to WT, respectively), while protein maturation was unaffected. Accordingly, cell surface expression levels of the mutant receptors were also significantly reduced (35% p<0.01 and 15% p<0.05, respectively). The p.R254W and p.R254Q are both loss-of-function mutations as demonstrated by their reduced overall and cell surface expression levels suggesting a deleterious effect on receptor folding and stability. It appears that a tryptophan substitution at R254 is more disruptive to receptor structure than the more conserved glutamine substitution. No clear correlation between the severity of in vitro loss-of-function and phenotypic presentation could be assigned.

The design, synthesis, and evaluation of molecules that enable or enhance cellular uptake: Peptoid molecular transporters

Certain proteins contain subunits that enable their active translocation across the plasma membrane into cells. In the specific case of HIV-1, this subunit is the basic domain Tat49–57 (RKKRRQRRR). To establish the optimal structural requirements for this translocation process, and thereby to develop improved molecular transporters that could deliver agents into cells, a series of analogues of Tat49–57 were prepared and their cellular uptake into Jurkat cells was determined by flow cytometry. All truncated and alanine-substituted analogues exhibited diminished cellular uptake, suggesting that the cationic residues of Tat49–57 play a principal role in its uptake. Charge alone, however, is insufficient for transport as oligomers of several cationic amino acids (histidine, lysine, and ornithine) are less effective than Tat49–57 in cellular uptake. In contrast, a 9-mer of l-arginine (R9) was 20-fold more efficient than Tat49–57 at cellular uptake as determined by Michaelis–Menton kinetic analysis. The d-arginine oligomer (r9) exhibited an even greater uptake rate enhancement (>100-fold). Collectively, these studies suggest that the guanidinium groups of Tat49–57 play a greater role in facilitating cellular uptake than either charge or backbone structure. Based on this analysis, we designed and synthesized a class of polyguanidine peptoid derivatives. Remarkably, the subset of peptoid analogues containing a six-methylene spacer between the guanidine head group and backbone (N-hxg), exhibited significantly enhanced cellular uptake compared to Tat49–57 and even to r9. Overall, a transporter has been developed that is superior to Tat49–57, protease resistent, and more readily and economically prepared.

Oxalate Exudation by Taro in Response to Al1

Roots of taro (Colocasia esculenta [L.] Schott cvs Bun-long and Lehua maoli) exuded increasing concentrations of oxalate with increasing Al stress. This exudation was a specific response to excess Al and not to P deficiency. Addition of oxalate to Al-containing solutions ameliorated the toxic effect of Al.

Les canaques de la Nouvelle-Calédonie /

In Revue d'ethnographie, t. 2, no. 4 (July-August). Paris : Ernest Leroux, 1883.