Blunt cardiac injury: case report of salvaged traumatic right atrial rupture.

The incidence of cardiac rupture following blunt trauma is rare, occurring in 0.3%-0.5% of all blunt trauma patients. It can be fatal at the trauma scene, and is frequently missed in the emergency room setting. The severity of a cardiac trauma is based on the mechanism and degree of the force applied. The objective of this study was to report the case of a 32-year-old male patient who was involved in a motor vehicle collision and presented to the emergency room with signs of hypovolemic shock. The patient was found to have severe chest trauma associated with massive hemothorax requiring immediate intervention. The patient had an emergent thoracotomy revealing a right atrial injury. Repair of the atrial injury reversed the state of shock. The patient was discharged after 35 days of hospitalization in good condition.

In vitro assessment of antitumor activities of the PI3K/mTOR inhibitor GSK2126458.

BACKGROUND: Up-regulation of the PI3K/mTOR (phosphatidylinositol-3' kinase/mammalian target of rapamycin) signaling is common in carcinoma. Consistently, targeting these molecules has been shown to halt the growth of many tumors. The main purpose of this study was to develop surrogate biomarkers of the antitumor activity of PI3K/mTOR inhibitors. METHODS: Fragments from eight tumors were collected immediately after resection in ice-cold RPMI gassed with 95% O2 :5% CO2. Viability was determined by measuring tumor cellular respiration (mitochondrial O2 consumption). The specimens were incubated at 37°C with and without 50 nM GSK2126458 (a highly potent and selective inhibitor of PI3K/mTOR) for 90 min. The tissue was then processed for histology, measurement of intracellular caspase-3 activity (using the caspase-3 substrate N-acetyl-asp-glu-val-asp-7-amino-4-methylcoumarin), and immunohistochemical detection of the apoptotic biomarkers caspase-3, cytochrome C, and annexin A2. RESULTS: GSK2126458 induced morphologic changes in four tumors (two invasive ductal carcinomas, one invasive lobular carcinoma, and one ovarian dysgerminoma), intracellular caspase-3 activity in three tumors (two invasive ductal carcinomas and one poorly differentiated signet ring adenocarcinoma of gastric origin), and immunohistochemical evidence of apoptosis in at least four tumors (three invasive ductal carcinomas and one adenocarcinoma of gastric origin). Two tumors (ovarian serous carcinoma and moderately differentiated adenocarcinoma of colorectal origin) demonstrated no treatment effect. CONCLUSION: These preliminary results demonstrate the feasibility of using in vitro biomarkers for detecting antitumor activities of the rapidly emerging PI3K/mTOR inhibitors.

Negative axillary ultrasonography with biopsy may predict non-involvement of the non-sentinel lymph nodes in operable breast cancer patients.

AIM: To evaluate whether axillary ultrasound in combination with a biopsy (AUS +/- Bx) can predict the involvement of the non-sentinel lymph nodes (NSLN). METHODS: A review of all operable breast cancer patients who underwent AUS +/- Bx at our tertiary care center from January 2010 to April 2011 was performed. All patients underwent AUS as part of their pre-operative evaluation. If the AUS was suspicious, a fine-needle aspiration or core-needle biopsy was performed. RESULTS: Of 88 patients included in our final analysis, 20 (23%) had positive AUS + Bx and underwent axillary lymph node dissection (ALND) at time of definitive surgery. In all, 68 of the 88 patients (77.3%) had negative AUS +/- Bx and underwent sentinel lymph node (SLN) Bx at the time of definitive surgery. If the SLN Bx was negative, no further axillary surgery was performed and the NSLN were assumed to be negative. If the SLN Bx was positive, ALND was performed. Of the 68 patients, 62 (91%) had a negative NSLN. Patients with positive AUS + Bx carry a relative risk of 2.02 (P < 0.00002) of having positive NSLN. CONCLUSION: In operable breast cancer patients, a negative AUS+/- Bx may be a predictor of non-involvement of the NSLN.

Widespread expression of the AMPA receptor GluR2 subunit at glutamatergic synapses in the rat spinal cord and phosphorylation of GluR1 in response to noxious stimulation revealed with an antigen-unmasking method.

Glutamate, the principal excitatory neurotransmitter in the spinal cord, acts primarily through AMPA receptors. Although all four AMPA subunits are expressed by spinal neurons, we know little about their distribution at glutamatergic synapses. We used an antigen-unmasking technique to reveal the synaptic distribution of glutamate receptor (GluR) 1-4 subunits with confocal microscopy. After pepsin treatment, punctate staining was seen with antibodies against each subunit: GluR2-immunoreactive puncta were distributed throughout the gray matter, whereas GluR1-immunoreactive puncta were restricted to the dorsal horn and were most numerous in laminas I-II. Punctate staining for GluR3 and GluR4 was found in all laminas but was weak in superficial dorsal horn. Colocalization studies showed that GluR2 was present at virtually all (98%) puncta that were GluR1, GluR3, or GluR4 immunoreactive and that most (>90%) immunoreactive puncta in laminas IV, V, and IX showed GluR2, GluR3, and GluR4 immunoreactivity. Evidence that these puncta represented synaptic receptors was obtained with electron microscopy and by examining the association of GluR2- and GluR1-immunoreactive puncta with glutamatergic boutons (identified with vesicular glutamate transporters or markers for unmyelinated afferents). The great majority (96%) of these boutons were associated with GluR2-immunoreactive puncta. Our findings suggest that GluR2 is almost universally present at AMPA-containing synapses, whereas GluR1 is preferentially associated with primary afferent terminals. We also found a substantial, rapid increase in staining for synaptic GluR1 subunits phosphorylated on the S845 residue in the ipsilateral dorsal horn after peripheral noxious stimulation. This finding demonstrates plastic changes, presumably contributing to central sensitization, at the synaptic level.