Death and kidney allograft dysfunction after bacteremia

Background

Some studies have reported causal associations between bacteremia and mortality or allograft loss in kidney transplant recipients (KTR). However, few studies have assessed the clinical course of kidney function and the risk of acute allograft rejection after bacteremia.

Methods

We retrospectively reviewed 902 kidney transplants performed at Nagoya Daini Red Cross Hospital between January 1, 2002 and March 31, 2014. Forty-five living donor kidney transplant recipients with single bacteremia were included. We analyzed death, change in kidney function, and development of acute allograft rejection 12 months after bacteremia according to the following groups: primary source of bacteremia (urinary tract or other sources), site of acquisition (community acquired or nosocomial), severity (not meeting the systemic inflammatory response syndrome criteria and sepsis or severe sepsis and septic shock), empiric antibiotic use (appropriate or inappropriate), and baseline kidney function (estimated glomerular filtration rate ≤44.7 or ≥44.8 ml/min).

Results

Urinary tract infection (UTI) was the leading cause of bacteremia (68.9 %), and Escherichia coli was the most common pathogen. Three cases (6.7 %) died of infection that caused bacteremia within 12 months. Pneumonia accounted for two-thirds. Kidney function declined 1 week after bacteremia (P < 0.05), particularly in severe cases. Thereafter, kidney function was comparable to baseline level in each group (P ≥ 0.05). Severe UTI was associated with subsequent acute allograft rejection (P = 0.03).

Conclusions

Pneumonia in KTR should be managed with caution. Kidney function generally returned to baseline level after bacteremia. However, severe UTI may be associated with subsequent acute allograft rejection.

     

Impairment of the discrimination of the direction of single-whisker stimulation induced by the lemniscal pathway lesion

In the rodent somatosensory system, stimulus information received by the whiskers is relayed to the barrel cortex via two parallel pathways, the lemniscal pathway and the paralemniscal pathway. The lemniscal pathway includes the principal trigeminal nucleus (Pr5) and the ventral posteromedial thalamic nucleus (VPm). The paralemniscal pathway includes the spinal trigeminal subnucleus interpolaris (Sp5i) and the medial division of posterior thalamic nucleus (POm). The purpose of this study was to investigate the roles of those pathways in perceptions of the direction of the single-whisker stimulation in the rat. Rats were trained to perform a go/no-go task that required the discrimination of forward or backward stimulation applied to their single whisker. When a selective lesion was made in VPm or Pr5, error rate for the task performance increased significantly. In contrast, when a selective lesion was made in POm or Sp5i, we found no significant change in performance. These results suggest that the lemniscal pathway plays more important roles in a discrimination of stimulus direction applied to the single whisker.     

Dopamine induces a slow afterdepolarization in lateral amygdala neurons

The amygdala and dopaminergic innervation thereunto are considered to cooperatively regulate emotional states and behaviors. The present experiments examined effects of dopamine on lateral amygdala (LA) neuron excitability by whole cell recordings. Bath application of dopamine induced slow afterdepolarization (sADP). This sADP lasted for >5 s, and its magnitude varied in a concentration-dependent manner. Co-application of the D1 receptor antagonist SKF83566 reduced its amplitude. The D1 receptor agonist SKF38393, applied alone, induced sADP of a smaller amplitude. Induction of the full sADP required 5-HT(2) and noradrenalin alpha(1) receptor activation as well. D2 receptor activation or blockade did not affect sADP induction. The calcium channel blocker cadmium or intracellular calcium chelator bis-(o-aminophenoxy)-N,N,N',N' tetraacetic acid (BAPTA) blocked induction of the sADP, which was suggested to be triggered by calcium influx. Under voltage clamp, membrane conductance decreased at the peak of sADP current (I(sADP)). I(sADP) was suppressed by cesium included in pipettes. The I-V curve of the net I(sADP) was shifted as the external concentration of potassium was raised, and the reversal potential was identical to that of potassium, suggesting that dopamine decreases potassium conductance to induce the sADP. The present sADP may serve as a positive-feedback regulator of excitability in LA neurons.     

Dynamic changes in conjunctival dendritic cell numbers, anatomical position and phenotype during experimental allergic conjunctivitis

Dendritic cells (DCs) are a subset of antigen-presenting cells (APCs) that are involved in the initiation and control of the immune response to antigens present at the interface with the environment. A limited number of groups have studied DCs in human and animal conjunctiva but no data is available concerning the different DC subsets present in the conjunctival tissue. The aims of this study are to characterize the phenotypes and numbers of DCs present in the murine model of allergic conjunctivitis using the technique of immunohistochemistry so as to aid the understanding of the mechanisms involved in allergic eye disease. A double immunofluorescence method was used to analyze the phenotypic distribution and density of DC subsets in the mouse conjunctival tissues of the allergic model using a panel of antibodies: CD11c, as a general marker of DCs, coupled with another DC subset marker such as Langerin for Langerhans cells (LCs), CD11b for myeloid DCs (mDCs) and mPDCA-1 for plasmacytoid DCs (pDCs). In the na?ve conjunctiva, mDCs were consistently detected in the subepithelial layer and substantia propria. In the epithelium and the subepithelial layer, very few LCs and virtually no pDCs were observed. Following allergen challenge, there was a marked influx of mDCs and pDCs, but no LCs, into the subepithelial layer and throughout the substantia propria. These results indicate that conjunctival DC subsets may play an important role in the immune-regulatory processes involved in the inflammatory component of allergic conjunctivitis.     

Acute oral selenium intoxication with ten times the lethal dose resulting in deep gastric ulcer

A 48-year-old woman presented after taking 2000 mg of selenium dioxide, corresponding to 10 times the experimental lethal dose in animals. She presented with mildly altered consciousness and hematemesis. Endoscopy revealed mucosal damage throughout the oral cavity, esophagus, and stomach. There was no evidence of perforation. After intubation and gastric lavage, hemodialysis was performed. The patient was discharged uneventfully on the 16(th) day. This case highlights a very rare acute selenium intoxication. Serum and urinary selenium levels and serum glutathione peroxidase activities during the patient's course were followed, as well as the mucosal corrosive damage caused by the selenium.     

ASO Visual Abstract: Preoperative FDG Positive Lymph Nodes Predict the Postoperative Prognosis in Resectable Biliary Tract Cancers

Annals of Surgical Oncology -     

PKCbeta regulates ischemia/reperfusion injury in the lung

Activation of PKCbetaII is associated with the response to ischemia/reperfusion (I/R), though its role, either pathogenic or protective, has not been determined. In a murine model of single-lung I/R, evidence linking PKCbeta to maladaptive responses is shown in the following studies. Homozygous PKCbeta-null mice and WT mice fed the PKCbeta inhibitor ruboxistaurin subjected to I/R displayed increased survival compared with controls. In PKCbeta-null mice, phosphorylation of extracellular signal-regulated protein kinase-1 and -2 (ERK1/2), JNK, and p38 MAPK was suppressed in I/R. Expression of the immediate early gene, early growth response-1 (Egr-1), and its downstream target genes was significantly increased in WT mice in I/R, particularly in mononuclear phagocytes (MPs), whereas this expression was attenuated in PKCbeta-null mice or WT mice fed ruboxistaurin. In vitro, hypoxia/reoxygenation-mediated induction of Egr-1 in MPs was suppressed by inhibition of PKCbeta, ERK1/2, and JNK, but not by inhibition of p38 MAPK. These findings elucidate key roles for PKCbetaII activation in I/R by coordinated activation of MAPKs (ERK1/2, JNK) and Egr-1.     

Simultaneous Discovery of Cranial and Spinal Intradural Chordomas: Case Report

The present case illustrates the unexpected occurrence of intradural chordomas that were simultaneously discovered in cranial and spinal locations. A 63-year-old female presented with weakness in the left upper extremity. The patient visited a local doctor and underwent brain computerized tomography (CT). CT revealed a brain tumor, and she was referred to our hospital. Brain magnetic resonance imaging (MRI) demonstrated a midline intradural retroclival tumor in addition to an intradural extramedullary mass lesion at the level of C1–C2. The patient developed a spastic gait disturbance that forced her to use a cane. She underwent laminectomy at C1–C2 along with total removal of the tumor and showed no remarkable symptoms after surgery. Histopathological examination confirmed the diagnosis of chordoma. One month after the cervical surgery, the intracranial tumor was subtotally removed in intracranial surgery via the right subtemporal approach. Histopathological data were identical to that of the cervical tumor. The patient consulted another hospital and underwent gamma-knife surgery. Her neurological examination is relatively unchanged 20 months after the cervical surgery. This case suggests that neuroradiological evaluation should also be performed for an intradural spinal chordoma when an intracranial chordoma is detected. Careful determination of the tumor responsible for the symptoms is necessary if an intradural spinal chordoma is simultaneously detected with an intracranial chordoma.