Coronary arteritis in mice following the systemic injection of group B Lactobacillus casei cell walls in aqueous suspension

We describe the induction of an asymmetric, focal, inflammatory coronary arteritis by a single intraperitoneal injection of group B Lactobacillus casei cell wall fragments in various inbred mouse strains. This coronary arteritis resembles the arteritis which is responsible for the 1-2% fatality rate among children with mucocutaneous lymph node syndrome. Coronary arteritis developed in 18 of 26 C57BL/6, 14 of 26 A/J, 7 of 15 Balb/c, and 8 of 15 C3Heb/FeJ mice injected. It also developed in 2 of 4 "nude" A/J background mice and 3 of 4 "nude" C57BL/6 mice, but in 0 of 15 C3H/HeJ mice. Lesions were evident as early as 3 days following injection. The development of arteritis was accompanied by disruption of the arterial intima and media with true aneurysm formation. Measurement of serial IgG and IgM titers indicated no relationship between the development of coronary arteritis and immunoglobulin response to L casei cell walls or the development of antibodies cross-reactive with normal myocardium. The absence of disease in only the C3H/HeJ mice, which are known to have defective macrophages, suggests that macrophages may play an essential role in the pathogenesis of coronary arteritis.     

Attenuated pik3r1 expression prevents insulin resistance and adipose tissue macrophage accumulation in diet-induced obese mice

Obese white adipose tissue (AT) is characterized by large-scale infiltration of proinflammatory macrophages, in parallel with systemic insulin resistance; however, the cellular stimulus that initiates this signaling cascade and chemokine release is still unknown. The objective of this study was to determine the role of the phosphoinositide 3-kinase (PI3K) regulatory subunits on AT macrophage (ATM) infiltration in obesity. Here, we find that the Pik3r1 regulatory subunits (i.e., p85α/p55α/p50α) are highly induced in AT from high-fat diet-fed obese mice, concurrent with insulin resistance. Global heterozygous deletion of the Pik3r1 regulatory subunits (αHZ), but not knockout of Pik3r2 (p85β), preserves whole-body, AT, and skeletal muscle insulin sensitivity, despite severe obesity. Moreover, ATM accumulation, proinflammatory gene expression, and ex vivo chemokine secretion in obese αHZ mice are markedly reduced despite endoplasmic reticulum (ER) stress, hypoxia, adipocyte hypertrophy, and Jun NH(2)-terminal kinase activation. Furthermore, bone marrow transplant studies reveal that these improvements in obese αHZ mice are independent of reduced Pik3r1 expression in the hematopoietic compartment. Taken together, these studies demonstrate that Pik3r1 expression plays a critical role in mediating AT insulin sensitivity and, more so, suggest that reduced PI3K activity is a key step in the initiation and propagation of the inflammatory response in obese AT.     

Telemetry Bed Usage for Patients with Low-risk Chest Pain: Review of the Literature for the Clinician

Background

Telemetry monitoring in patients with low-risk chest pain is highly utilized, despite the lack of quality data to support its use.

Study Objectives

To review the medical literature on the utility of telemetry monitoring in patients with low-risk chest pain and to offer evidence-based recommendations to emergency physicians.

Methods

A PubMed literature search was performed and limited to human studies written in English language articles with keywords of “telemetry” and “chest pain.” Studies identified then underwent a structured review from which results could be evaluated.

Results

There were 114 paper abstracts on telemetry monitoring screened; 30 articles were considered relevant. Twelve appropriate articles were rigorously reviewed and recommendations given.

Conclusions

Insufficient data exist to support telemetry use in low-risk chest pain patients. Telemetry monitoring is unlikely to benefit low-risk chest pain patients with a normal/nondiagnostic electrocardiogram, a normal first set of cardiac enzymes, and none of the following: hypotension, rales above the bases, or pain worse than baseline angina.     

Medial patellofemoral ligament reconstruction in patellar instability

Background:

Medial patellofemoral ligament (MPFL) is one of the major static medial stabilising structures of the patella. MPFL is most often damaged in patients with patellar instability. Reconstruction of MPFL is becoming a common surgical procedure in treating patellar instability. We hypothesised that MPFL reconstruction was adequate to treat patients with patellar instability if the tibial tubercle and the centre of the trochlear groove (TT-TG) value was less than 20 mm and without a dysplastic trochlea.

Materials and Methods:

30 patients matching our inclusion criteria and operated between April 2009 and May 2011 were included in the study. MPFL reconstruction was performed using gracilis tendon fixed with endobutton on the patellar side and bio absorbable interference screw or staple on the femoral side. Patients were followed up with subjective criteria, Kujala score and Lysholm score.

Results:

The mean duration of followup was 25 months (range 14-38 months). The mean preoperative Kujala score was 47.5 and Lysholm score was 44.7. The mean postoperative Kujala score was 87 and Lysholm score was 88.06. None of the patients had redislocation.

Conclusion:

MPFL reconstruction using gracilis tendon gives excellent results in patients with patellar instability with no redislocations. Some patients may have persistence of apprehension.