Spontaneous idiopathic bilateral adrenal haemorrhage: a rare cause of abdominal pain.

We describe a case of a 62-year-old woman with a history of chronic obstructive pulmonary disease and gastro-oesophageal reflux disease who presented to the emergency department with left lower quadrant abdominal pain, flank pain with nausea and no history of preceding trauma. The patient had finished a course of azithromycin and oral methylprednisolone 1 day prior to presentation. Abdominal and pelvic CT scan identified changes suggestive of bilateral adrenal haemorrhage. The patient did not show signs of acute adrenal insufficiency but was started on steroid replacement therapy because of concerns about possible disease progression. All recognised causes of adrenal haemorrhage were excluded suggesting this was a case of spontaneous idiopathic bilateral adrenal haemorrhage, a rarely reported phenomenon in the literature. The patient was discharged after clinical improvement following 6 days in hospital, taking oral steroid replacement.

Minocycline-induced hyperpigmentation.

A 62-year-old male with a long history of rosacea, which was well controlled on minocycline, presented to his primary care physician for routine examination. Physical examination was noted for non-palpable, non-pruritic blue patches of hyperpigmentation on the medial aspects of his lower extremities bilaterally. Recognition and management of the findings are discussed.

The Agrobacterium tumefaciens transcription factor BlcR is regulated via oligomerization.

The Agrobacterium tumefaciens BlcR is a member of the emerging isocitrate lyase transcription regulators that negatively regulates metabolism of γ-butyrolactone, and its repressing function is relieved by succinate semialdehyde (SSA). Our crystal structure showed that BlcR folded into the DNA- and SSA-binding domains and dimerized via the DNA-binding domains. Mutational analysis identified residues, including Phe(147), that are important for SSA association; BlcR(F147A) existed as tetramer. Two BlcR dimers bound to target DNA and in a cooperative manner, and the distance between the two BlcR-binding sequences in DNA was critical for BlcR-DNA association. Tetrameric BlcR(F147A) retained DNA binding activity, and importantly, this activity was not affected by the distance separating the BlcR-binding sequences in DNA. SSA did not dissociate tetrameric BlcR(F147A) or BlcR(F147A)-DNA. As well as in the SSA-binding site, Phe(147) is located in a structurally flexible loop that may be involved in BlcR oligomerization. We propose that SSA regulates BlcR DNA-binding function via oligomerization.

Legionella pneumophila inhibits macrophage apoptosis by targeting pro-death members of the Bcl2 protein family.

To establish a vacuole that supports bacterial replication, Legionella pneumophila translocates a large number of bacterial proteins into host cells via the Dot/Icm type IV secretion system. Functions of most of these translocated proteins are unknown, but recent investigations suggest their roles in modulating diverse host processes such as vesicle trafficking, autophagy, ubiquitination, and apoptosis. Cells infected by L. pneumophila exhibited resistance to apoptotic stimuli, but the bacterial protein directly involved in this process remained elusive. We show here that SidF, one substrate of the Dot/Icm transporter, is involved in the inhibition of infected cells from undergoing apoptosis to allow maximal bacterial multiplication. Permissive macrophages harboring a replicating sidF mutant are more apoptotic and more sensitive to staurosporine-induced cell death. Furthermore, cells expressing SidF are resistant to apoptosis stimuli. SidF contributes to apoptosis resistance in L. pneumophila-infected cells by specifically interacting with and neutralizing the effects of BNIP3 and Bcl-rambo, two proapoptotic members of Bcl2 protein family. Thus, inhibiting the functions of host pro-death proteins by translocated effectors constitutes a mechanism for L. pneumophila to protect host cells from apoptosis.