Traumatic 6th Nerve Palsy Managed with Medial Rectus Recession with Hangback Sutures and Hummelsheim Procedure

Traumatic paralytic esotropia due to 6th nerve palsy is not uncommon but difficult to manage. We reported a case of 38‑year‑old male who sustained head injury in road traffic accident 15 years ago and inward deviation of his left eye. His vision in right eye was 20/20 and counting fingers at one foot in the left eye. He had >70 prism diopters esotropia in the left eye with restriction of movements in all directions of gaze except adduction. His forced duction test was positive. Examinations of the anterior and posterior segments of both eyes were within normal limits. Magnetic resonance imaging suggested old traumatic insult in the left eye. Diagnosis of left eye traumatic 6th nerve palsy with medial rectus contracture was made. Left medial rectus recession with hangback sutures and Hummelsheim procedure were performed. Postoperatively, the patient’s vision in the left eye had improved to 20/80 the esotropia had reduced to 15 prism diopters (delta).Keywords: Abducent nerve, esotropia, traum

Checking the Goldbach conjecture on a vector computer

bibliographical data to be processed -- Number theory and applications (Banff, AB, 1988) Pages: 423--433 Series: NATO Adv. Sci. Inst. Ser. C Math. Phys. Sci. Vol: 265 -- Kluwer Acad. Publ. (Dordrecht) -- 1

Dynamics of neuroinflammation in the macrosphere model of arterio-arterial embolic focal ischemia: an approximation to human stroke patterns

<p>Abstract</p> <p>Background</p> <p>Neuroinflammation evolves as a multi-facetted response to focal cerebral ischemia. It involves activation of resident glia cell populations, recruitment of blood-derived leucocytes as well as humoral responses. Among these processes, phagocyte accumulation has been suggested to be a surrogate marker of neuroinflammation. We previously assessed phagocyte accumulation in human stroke by MRI. We hypothesize that phagocyte accumulation in the macrosphere model may resemble the temporal and spatial patterns observed in human stroke.</p> <p>Methods</p> <p>In a rat model of permanent focal ischemia by embolisation of TiO₂-spheres we assessed key features of post-ischemic neuroinflammation by the means of histology, immunocytochemistry of glial activation and influx of hematogeneous cells, and quantitative PCR of TNF-α, IL-1, IL-18, and iNOS mRNA.</p> <p>Results</p> <p>In the boundary zone of the infarct, a transition of ramified microglia into ameboid phagocytic microglia was accompanied by an up-regulation of MHC class II on the cells after 3 days. By day 7, a hypercellular infiltrate consisting of activated microglia and phagocytic cells formed a thick rim around the ischemic infarct core. Interestingly, in the ischemic core microglia could only be observed at day 7. TNF-α was induced rapidly within hours, IL-1β and iNOS peaked within days, and IL-18 later at around 1 week after ischemia.</p> <p>Conclusions</p> <p>The macrosphere model closely resembles the characteristical dynamics of postischemic inflammation previously observed in human stroke. We therefore suggest that the macrosphere model is highly appropriate for studying the pathophysiology of stroke in a translational approach from rodent to human.</p

Cell lineage-specific mitochondrial resilience during mammalian organogenesis

Mitochondrial activity differs markedly between organs, but it is not known how and when this arises. Here we show that cell lineage-specific expression profiles involving essential mitochondrial genes emerge at an early stage in mouse development, including tissue-specific isoforms present before organ formation. However, the nuclear transcriptional signatures were not independent of organelle function. Genetically disrupting intra-mitochondrial protein synthesis with two different mtDNA mutations induced cell lineage-specific compensatory responses, including molecular pathways not previously implicated in organellar maintenance. We saw downregulation of genes whose expression is known to exacerbate the effects of exogenous mitochondrial toxins, indicating a transcriptional adaptation to mitochondrial dysfunction during embryonic development. The compensatory pathways were both tissue and mutation specific and under the control of transcription factors which promote organelle resilience. These are likely to contribute to the tissue specificity which characterizes human mitochondrial diseases and are potential targets for organ-directed treatments

Fast Bounds on the Distribution of Smooth Numbers

In this paper we present improvements to Bernstein’s algorithm, which finds rigorous upper and lower bounds for (x, y)

Primeless Factoring-Based Cryptography

Factoring-based public-key cryptosystems have an overall complexity which is dominated by the key-production algorithm, which requires the generation of prime numbers. This is most inconvenient in settings where the key-generation is not an one-off process, e.g., secure delegation of computation or EKE password-based key exchange protocols. To this end, we extend the Goldwasser-Micali (GM) cryptosystem to a provably secure system, denoted SIS, where the generation of primes is bypassed. By developing on the correct choice of the parameters of SIS, we align SIS's security guarantees (i.e., resistance to factoring of moduli, etc.) to those of other well-known factoring-based cryptosystems. Taking into consideration different possibilities to implement the fundamental operations, we explicitly compare and contrast the asymptotic complexity of well-known public-key cryptosystems (e.g., GM and/or RSA) with that of SIS's. The latter shows that once we are ready to accept an increase in the size of the moduli, SIS offers a generally lower asymptotic complexity than, e.g., GM or even RSA (when scaling correctly the number of encrypted bits). This would yield most significant speed-ups to applications like the aforementioned secure delegation of computation or protocols where a fresh key needs to be generated with every new session, e.g., EKE password-based key exchange protocols