Slipping rib syndrome: case report of an iatrogenic result following video-assisted thoracic surgery and chest tube placement.

The aim of this case report is to shed light on slipping rib syndrome (SRS), a painful and overlooked condition. A 62-year old man reported intermittent, self-resolving sharp rib pain that began after a video-assisted thoracic surgery and chest tube placement 4 years prior to presentation. The patient's pain was associated with a rigid protrusion in the right upper quadrant, and home use of acetaminophen provided no relief. After physical examination, multiple imaging and lab tests, the patient was diagnosed with SRS and was referred to physical therapy and thoracic surgery for further evaluation. SRS is an under-recognized cause of upper abdominal and lower thoracic pain that should be considered if a patient's history includes previous trauma or abdominal surgery.

Lay abstract This is a case report of slipping rib syndrome (SRS). It is a painful medical condition. A 62-year old man after a video-assisted thoracic surgery and chest tube placement had recurrent, self-resolving sharp rib pain. The pain was associated with a rigid lump in the right lower rib cage. Acetaminophen and narcotics provided no relief. After physical examination, multiple imaging and lab tests, he was diagnosed with SRS and was referred to physical therapy and thoracic surgery for further evaluation. SRS is an under-recognized cause of rib pain that should be considered if a patient's history includes previous trauma or abdominal surgery.

Botulinum toxin a injection to facial and cervical paraspinal muscles in a patient with stiff person syndrome: a case report.

Stiff person syndrome (SPS) is a rare neurologic disorder of unknown etiology characterized by increased resting muscle tone, progressive rigidity, and stiffness of the axial musculature. We present a case of a 48-year-old male patient with SPS who experienced facial and neck muscle spasms that were uncontrolled with oral medications and the use of an intrathecal baclofen pump. Botulinum toxin A injections into the bilateral masseter and neck paraspinal muscles provided pain relief and spasm control, illustrating the use of botulinum toxin A injections in the small muscles of face and neck in patients with SPS.

Deciphering the key molecular and cellular events in neutrophil transmigration during acute inflammation.

Recruitment of leukocytes circulating in our blood to the sites of infection or tissue damage is the key phenomenon in the acute inflammatory response(s). Among the leukocytes, neutrophils are primarily recruited into the areas of acute inflammation. When neutrophils interact with activated endothelium of the blood vessels, they become migratory and cross the endothelial layer of the blood vessel wall in a process called as leukocyte extravasation. Identifying and understanding the gene regulation of this extravasation phenomenon is one of the key objective of biomedical research aimed at ameliorating or alleviating the symptoms of various diseases, such as rheumatoid arthritis, asthma, anaphylaxis, atherosclerosis, ulcerative colitis etc., that are exacerbated by inappropriate inflammatory stimuli. Here, we decipher and discuss the key genes implicated in the leukocyte transmigration using the acute inflammation model called as the Dextran Sulphate Sodium (DSS) induced Colitis in mice as a classic paradigm.

Induction of PDE5 and de-sensitization to endogenous NO signaling in a systemic resistance artery under altered blood flow.

In the classical pathway, the opposing activities of guanylyl cyclases (GC) and phosphodiesterases (PDE), and the effect of the cGMP-dependent protein kinase (cGK) on its targets, determine the biological responses to NO signaling. Here we tested the hypothesis that vascular dysfunction may be due to altered expression and activity of these effectors of NO signaling. Every other set of rat second order mesenteric resistance arteries (MA) were ligated, resulting in chronic low flow (LF) in the upstream MA1 and high flow (HF) in the adjacent MA1 without tissue ischemia. eNOS and iNOS were up-regulated in HF and LF MA1, respectively, in the sub-acute phase (four days) of vascular remodeling. The Day4 HF/LF MA1s were under increased control of NO as indicated by reduced sensitivity to the vasoconstrictor phenylephrine and its normalization with the NOS antagonist L-NAME. PDE5 mRNA and protein were also significantly up-regulated in the HF/LF MA1 with no change in sGC or PKG1, an effect that was dependent upon NO synthesis. The PDE5 inhibitor Sildenafil was several-fold more powerful in relaxing the HF/LF MA1s, and pre-treatment with Sildenafil uncovered an increased responsiveness of HF/LF MA1s to the NO donor DEA/NO. We conclude that induction of PDE5 de-sensitizes this systemic resistance artery to sustained NO signaling under chronic HF/LF. Treatment with PDE5 antagonists, in contrast to NO donors, may more specifically and effectively increase blood flow to chronically hypo-perfused tissues.