Oral myiasis in a maxillofacial trauma patient

Oral Myiasis is a rare disease that is mostly reported in developing countries. It is primarily caused by the invasion of the human body by fly larvae. The phenomenon is well-documented in the skin, especially among animals. This case report describes the presentation of Oral Myiasis caused by Musca Nebulo (common house fly), in a 28-year-old patient, with recent maxillofacial trauma. The patient was treated by manual removal of the larvae, after topical application of turpentine oil, followed by surgical debridement and oral therapy with Ivermectin.     

Orthopaedic surgeon＇s nightmare： iatrogenic fractures of talus and medial malleolus following tibial nailing

Intramedullary interlocking nailing is the gold standard for treatment of tibial shaft fractures.The growing use of intramedullary nailing has resulted in an increased number of tibial nailing in daily...     

A prospective, randomized, double-blind study to compare the efficacy of lidocaine + metoclopramide and lidocaine + ketamine combinations in preventing pain on propofol injection

Purpose

Propofol injection is known to cause distressing pain, and various methods have been used to decrease this pain. We investigated the efficacy of the lidocaine + metoclopramide and lidocaine + ketamine combinations on modulating propofol injection pain.

Methods

Ninety ASA I/II patients aged 20–60 years were randomly assigned to three groups to receive lidocaine 20 mg (group L), lidocaine 20 mg + metoclopramide 10 mg (group LM), or lidocaine 20 mg + ketamine 5 mg (group LK), respectively, with venous occlusion for 1 min using a forearm tourniquet. Propofol 0.5 mg/kg was subsequently administered into a dorsal hand vein, and pain was assessed during its injection using a verbal rating score. The results were analyzed statistically with analysis of variance, the chi-square test, and the Wilcoxon rank sum test, where appropriate. The significance level was set at p < 0.05.

Results

The incidence of pain was rated to be significantly less in patients in groups LM (40 %) and LK (6.7 %) than in those in group L (83.3 %) (p = 0.001 and p < 0.001, respectively). The pain score [median (range)] was also significantly less in patients in groups LM [0 (0–3)] and LK [0 (0–2)] than in those in group L [2 (0–3)] (p = 0.001 for both groups).

Conclusion

The lidocaine–ketamine combination is most effective for decreasing the pain on propofol injection.     

(ii) Biomechanics of implant fixation

In joint replacement, stability of the implant is provided by a combination of the techniques adopted to fix the implant to the surrounding bone and the geometric features of the implant. Fixation techniques can either use cement or be cementless. Cemented fixation uses PMMA bone cement to grout the implant and bone together, while cementless fixation involves either a press-fit between the implant and bone, or specific design features that encourage bone growth into or onto the implant. Although both of these fixation techniques perform well in terms of longevity, each method functions better than the other in certain patient groups, and each has some positives and negatives. This article reports an overview of the fundamental aspects of the fixation techniques, their clinical advantages and disadvantages, associated clinical concerns and recent trends of fixation in clinical practice. This will be coupled with specific examples on how certain geometric features of an implant help in achieving initial and long-term stability and fixation.     

Saturable Leptin Transport Across the BBB Persists in EAE Mice

We have shown that mice with experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis, have upregulated leptin receptor expression in reactive astrocytes of the hippocampus, a region involved in sickness behavior. Leptin can exacerbate EAE when its serum concentration is high. Although leptin receptors in astrocytes modulate leptin transport across cultured endothelial cell monolayers, it is not known how leptin transport in EAE mice is regulated. Here, we determined brain and cervical spinal cord uptake of leptin in early and recovery stages of EAE, after either intravenous delivery or in situ brain perfusion of ¹²⁵I-leptin and the vascular marker ¹³¹I-albumin. While increased vascular space and general blood–brain barrier (BBB) permeability after EAE were expected, the specific saturable transport system for leptin crossing the BBB also persisted. Moreover, there was upregulation of leptin transport in hippocampus and cervical spinal cord in the early stage of EAE, shown by higher leptin uptake in these regions and by competitive inhibition with coadministered excess unlabeled leptin. We conclude that EAE induced a time- and region-specific increase of leptin transport. The results provide a link between circulating leptin and enhanced leptin signaling that may play a crucial role in disease progression.     

Potato lectin activates basophils and mast cells of atopic subjects by its interaction with core chitobiose of cell-bound non-specific immunoglobulin E

A major factor in non-allergic food hypersensitivity could be the interaction of dietary lectins with mast cells and basophils. Because immunoglobulin E (IgE) contains 10-12% carbohydrates, lectins can activate and degranulate these cells by cross-linking the glycans of cell-bound IgE. The present objective focuses on the effect of potato lectin (Solanum tuberosum agglutinin; STA) for its ability to release histamine from basophils in vitro and mast cells in vivo from non-atopic and atopic subjects. In this study, subjects were selected randomly based on case history and skin prick test responses with food, pollen and house dust mite extracts. Skin prick test (SPT) was performed with STA at 100 microg/ml concentration. Histamine release was performed using leucocytes from non-atopic and atopic subjects and rat peritoneal exudate cells. SPT on 110 atopic subjects using STA showed 39 subjects positive (35%); however, none showed STA-specific IgE; among 20 non-atopic subjects, none were positive by SPT. Maximal histamine release was found to be 65% in atopic subjects (n = 7) compared to 28% in non-atopic subjects (n = 5); the release was inhibited specifically by oligomers of N-acetylglucosamine and correlates well with serum total IgE levels (R(2) = 0.923). Binding of STA to N-linked glycoproteins (horseradish peroxidase, avidin and IgG) was positive by dot blot and binding assay. As potato lectin activates and degranulates both mast cells and basophils by interacting with the chitobiose core of IgE glycans, higher intake of potato may increase the clinical symptoms as a result of non-allergic food hypersensitivity in atopic subjects.