Bilateral coracoclavicular joints as a rare cause of bilateral thoracic outlet syndrome and shoulder pain treated successfully by conservative means.

The coracoclavicular joint (CCJ) is a rare anomalous joint. Symptomatic CCJ, being an exceptional rarity, makes it difficult to formulate a standard set of practice or guidelines. We report a 50-year-old Indian man, a machine operator by profession, who experienced bilateral shoulder pain and arm paraesthesia for two years, and was diagnosed with bilateral CCJ. The symptoms gradually increased, affecting his daily activities. Dynamic magnetic resonance imaging revealed the compression of the brachial plexus in extreme shoulder abduction. After a thorough search of the literature, we retrieved four similar cases, all of them treated with individualised protocols. None of the cases was bilateral. The lack of clear evidence in any particular direction and the patient's medical condition prompted us to give a conservative trial, before embarking on more invasive methods. He showed rapid response to the conservative treatment with remission of all symptoms. To the best of our knowledge, this is the first reported case of bilateral symptomatic CCJ with bilateral thoracic outlet syndrome, that was managed conservatively.

Traumatic bilateral atlantoaxial rotatory subluxation mimicking as torticollis in an adult female.

Rotatory subluxation of the atlantoaxial joint in adults is a rare, but potentially life-threatening injury. Delayed or missed diagnosis can lead to catastrophic consequences. Early recognition and prompt treatment is paramount to avoid long-term morbidity and disability. We report on an instance of bilateral atlantoaxial rotatory subluxation (AARS) in a 25-year-old female who presented to the Casualty Department with a painful neck, right-sided hemiparesis and torticollis after a road traffic collision. Reduction was achieved by controlled cervical traction followed by immobilization in a four-post Halo brace, with complete resolution of her symptoms. At the 12-month follow-up, she had normal neck movements with no signs of instability.

The tumor suppressor p53 associates with gene coding regions and co-traverses with elongating RNA polymerase II in an in vivo model.

Sequence-specific transcriptional regulators function by stably binding cognate DNA sequences followed by recruitment of both general and specialized factors to target gene promoters. The tumor suppressor p53 mediates its anti-oncogenic effect on cells by functioning as a sequence-specific regulator. p53 employs a secondary mechanism to suppress tumor formation by permeabilizing the outer mitochondrial membrane, thereby releasing pro-apoptotic factors. Here, we report a potential third biological function of p53: as a transcriptional elongation factor. Using chromatin immunoprecipitation, we demonstrate that human p53 robustly associates with RNA polymerase II (Pol II), but neither Pol I- nor Pol III-transcribed regions in the budding yeast, Saccharomyces cerevisiae. p53's association with open reading frames is mediated by its physical interaction with elongating Pol II, with which p53 travels in vivo and co-immunoprecipitates in vitro. When similarly expressed, the potent acidic activator VP16 cannot be cross-linked to Pol II coding regions. p53 levels comparable to those found in induced mammalian cells confer synthetic sickness or lethality in combination with deletions in genes encoding transcription elongation factors; p53 likewise confers hypersensitivity to the anti-elongation drug 6-azauracil. Collectively, our results indicate that p53 can physically interact with the transcription elongation complex and influence transcription elongation, and open up new avenues of investigation in mammalian cells.