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A close reading of the popular spiritual Sufi qawwali “Dama Dam Mast Qalandar” reveals how the spatial, aural and trans-textual dimensions of the qawwali span Urdu poetics, performance studies, affect theory, among other fields of critical translation and theory. Celebrating antinomianism in a trans-ethos, “Dama Dam Mast Qalandar” blurs boundaries between text and sound, written word and body. It explores how perception of and participation in spiritually constructed mehfils involves ongoing interplay with the text of the qawwali, its performers, and its receiving audience. In its exploration, this qawwali allows for ambiguity within a typically gendered performance genre through sound and intervenes in hegemonic spiritual concerns of Sunni succession. Circulated as a ‘living text’ in the subcontinent, “Dama Dam Mast Qalandar'' takes on a transtextual element, especially in its 1990’s performance by acclaimed musician Abida Parveen, transcending rigid boundaries between written and embodied aspects of its own text. In doing so, it complicates distinctions between performer and audience, man and woman, and the inner self with the outer world. Navigating these complex blurrings, this qawwali divulges the aural atmosphere that it emerges from, encouraging participation and reidentification with devotionalism in through its text, as well as its performance. Both the close reading analysis of “Dama Dam Mast Qalandar” and its performance by Abida Parveen reveal broader notions of antinomian spirituality that dialogically undoes normative distinctions and weaves together multiple aspects of performance and texts through the construction of its aural atmosphere.

Mutations in the intraflagellar transport-A (IFT-A) gene, THM1, have been identified in skeletal ciliopathies. Here, we report a genetic interaction between Thm1, and its paralog, Thm2, in postnatal skeletogenesis. THM2 localizes to primary cilia, but Thm2 deficiency does not affect ciliogenesis and Thm2-null mice survive into adulthood. However, by postnatal day 14, Thm2(−/−); Thm1(aln/+) mice exhibit small stature and small mandible. Radiography and microcomputed tomography reveal Thm2(−/−); Thm1(aln/+) tibia are less opaque and have reduced cortical and trabecular bone mineral density. In the mutant tibial growth plate, the proliferation zone is expanded and the hypertrophic zone is diminished, indicating impaired chondrocyte differentiation. Additionally, mutant growth plate chondrocytes show increased Hedgehog signaling. Yet deletion of one allele of Gli2, a major transcriptional activator of the Hedgehog pathway, exacerbated the Thm2(−/−); Thm1(aln/+) small phenotype, and further revealed that Thm2(−/−); Gli2(+/−) mice have small stature. In Thm2(−/−); Thm1(aln/+) primary osteoblasts, a Hedgehog signaling defect was not detected, but bone nodule formation was markedly impaired. This indicates a signaling pathway is altered, and we propose that this pathway may potentially interact with Gli2. Together, our data reveal that loss of Thm2 with one allele of Thm1, Gli2, or both, present new IFT mouse models of osteochondrodysplasia. Our data also suggest Thm2 as a modifier of Hedgehog signaling in postnatal skeletal development.

We examined the changes in mechanical strain response of male and female mouse tibia and ulna, using axial compression tests, to assess age-related changes in tibiae and ulnae by a non-contact strain measurement technique called the digital image correlation (DIC) and the standard strain gage. A unique aspect of the study was to compare bones from the same animal to study variations in behavior with aging. This study was conducted using male and female C57Bl/6 mice at 6, 12 and 22 months of age (N=6-7 per age and sex) using three load levels. The DIC technique was able to detect a greater number of statistically significant differences in comparison to the strain gaging method. Male ulna showed significantly higher DIC strains compared to strains captured from strain gage at all three levels of load at 6 months and in the lowest load at 12 months. DIC measurements revealed that the ulna becomes stiffer with aging for both males and females, which resulted in 0.4 to 0.8 times reduced strains in the 22-month group compared to the 6 month group. Male tibia showed three-fold increased strains in the 22 months group at 11.5 N load compared to 6 months group (p

Ciliopathies are genetic syndromes that link osteochondrodysplasias to dysfunction of primary cilia. Primary cilia extend from the surface of bone and cartilage cells, to receive extracellular cues and mediate signaling pathways. Mutations in several genes that encode components of the intraflagellar transport-A ciliary protein complex have been identified in skeletal ciliopathies, includingTHM1. Here, we report a role for genetic interaction betweenThm1and its paralog,Thm2,in skeletogenesis. THM2 localizes to the ciliary axoneme, but unlike its paralog,Thm2deficiency does not affect ciliogenesis andThm2-null mice survive into adulthood. Since paralogs often have redundant functions, we crossed aThm1null (aln) allele into theThm2colony. After 5 generations of backcrossing the colony onto a C57BL6/J background, we observed that by postnatal day 14,Thm2-/-; Thm1aln/+mice are smaller than control littermates.Thm2-/-; Thm1aln/+mice exhibit shortened long bones, narrow ribcage, shortened cranium and mandibular defects. Mutant mice also show aberrant architecture of the tibial growth plate, with an expanded proliferation zone and diminished hypertrophic zone, indicating impaired chondrocyte differentiation. Using microcomputed tomography,Thm2-/-; Thm1aln/+tibia were revealed to have reduced cortical and trabecular bone mineral density. Deletion of one allele ofGli2, a major transcriptional activator of the Hedgehog (Hh) pathway, exacerbated the small phenotype ofThm2-/-; Thm1aln/+mice and caused small stature inThm2-null mice. Together, these data revealThm2as a novel locus that sensitizes to Hh signaling in skeletal development. Further,Thm2-/-; Thm1aln/+mice present a new postnatal ciliopathy model of osteochondrodysplasia.

Aging is known to reduce bone quality and bone strength. We sought to determine how aging affects the biomechanical and architectural properties of various long bones, and if sex influences age related differences/changes. While researchers have extensively studied these changes in individual bones of mice, there is no comprehensive study of the changes in the bones from the same mice to study the changes with aging. We performed three point bending tests and microcomputed tomography (microCT) analysis on femurs, tibiae and ulnae. Three point bending tests were utilized to calculate biomechanical parameters and imaging was also performed using high resolution microCT to reveal both cortical and trabecular microarchitecture C57BL/6N mice were divided into three age groups: 6, 12 and 22 months. Each age and sex group consisted of 6–7 mice. The ultimate load to failure (UL), elastic stiffness (ES), modulus of elasticity (E) and the moment of inertia about bending axis (MOI) for each bone was calculated using three point bending test. MicroCT scans of all the bones were analyzed to determine cortical bone volume per tissue volume (C.BV/TV), trabecular bone volume per tissue volume (Tb.BV/TV), cortical bone area (B.Ar) using CTAn's microCT analysis and tested for correlation with the biomechanical parameters. Mean (standard error) values of UL in femur decreased from 19.8(0.6) N to 12.8(1.1) N (p, Highlights • Assess age/gender related biomechanical property changes in femur, tibiae and ulnae. • C57Bl/6 mice were divided into three age groups: 6, 12 and 22 months. • Significant decline in the biomechanical response of femurs and tibiae at the age of 22 months. • Ulnae showed some improved properties with aging. • Aging affected biomechanical rather than microCT properties and female bones