Persistent Cranial Defects After Endoscopic Sagittal Synostosis Surgery.

Introduction: Incomplete cranial ossification is a rare complication of calvarial-vault remodeling for sagittal synostosis often requiring reoperation. Studies show an incidence ranging from 0.5% to 18%.

Neosagittal Suture Formation after Endoscopic Sagittal Strip Craniectomy: A Case Report and Literature Review.

The fate of the excised synostotic suture in craniosynostosis remains relatively understudied. The purpose of this report is to describe a case of neosagittal suture formation following endoscopic excision of a pathology-proven synostotic suture, with CT demonstration of complete reossification in the areas adjacent to the neosagittal suture. We additionally review the existing literature on neosuture formation that has been published over the past 50 years.

Endoscopic Spring-Mediated Distraction for Unilambdoid Craniosynostosis.

Background: Craniosynostosis treatment modalities have changed over time. These have included open calvarial remodeling, suturectomy with helmet molding, hand-powered distraction devices, and spring-mediated distraction. Implantable springs were first described for their use in treatment of craniosynostosis in 1998 (Lauritzen et al, Plast Reconstr Surg 121;2008:545-554).

Artemisinin Bioactivity and Resistance in Malaria Parasites.

Artemisinin is the most widely-used compound against malaria and plays a critical role in the treatment of malaria worldwide. Resistance to artemisinin emerged about a decade ago in Southeast Asia and it is paramount to prevent its spread or emergence in Africa. Artemisinin has a complex mode of action and can cause widespread injury to many components of the parasite.

Live Vaccines Against Plasmodium Preerythrocytic Stages.

Vaccines that target the preerythrocytic phase of malaria hold great promise as elimination tools since they are the sole vaccines that can achieve sterile protection against a challenge. This chapter focuses on preerythrocytic stage vaccines based on live attenuated parasites. It first summarizes the main conclusions that have emerged from studies in rodents, which compared various parasite attenuation methods, and then presents the vaccination regimens that are currently being tested in humans.

The Pushback Pharyngeal Flap: An 18-Year Experience.

Background: The pharyngeal flap is one of the oldest and most popular techniques for correction of velopharyngeal insufficiency. The authors describe a large series using a technique that combines a pharyngeal flap with a palate pushback to avoid common causes of operative failure while restoring the velopharyngeal mechanism.

Methods: A retrospective cohort study was performed of patients who underwent a pushback pharyngeal flap by a single surgeon from 2000 to 2017.

Single Stage Repair of #30 Facial Cleft with Bone Morphogenic Protein.

Tessier #30 clefts (median mandibular clefts) represent a spectrum of deformities ranging from a minor cleft in the lower lip to complete clefts of the mandible involving the tongue, lower lip, hyoid bone, thyroid cartilages, and manubrium. Various techniques have been used to address these problems; the most common procedure involving 2 stages: an initial correction of the soft tissue followed by closure of the mandibular cleft at a later date using bone grafting. This approach was subsequently reduced to a single operation, but still required harvesting of autologous bone graft.

Isolated Intraorbital Frontosphenoidal Synostosis.

Unilateral anterior plagiocephaly is most commonly the result of deformational plagiocephaly or unilateral coronal synostosis, a premature fusion of the frontoparietal suture. However, other sutures within the coronal ring have been implicated in producing anterior cranial asymmetries. These fusions can occur in isolation or in concert with adjacent sutures.

Immunological memory to blood-stage malaria infection is controlled by the histamine releasing factor (HRF) of the parasite.

While most subunit malaria vaccines provide only limited efficacy, pre-erythrocytic and erythrocytic genetically attenuated parasites (GAP) have been shown to confer complete sterilizing immunity. We recently generated a Plasmodium berghei (PbNK65) parasite that lacks a secreted factor, the histamine releasing factor (HRF) (PbNK65 hrfΔ), and induces in infected mice a self-resolving blood stage infection accompanied by a long lasting immunity. Here, we explore the immunological mechanisms underlying the anti-parasite protective properties of the mutant PbNK65 hrfΔ and demonstrate that in addition to an up-regulation of IL-6 production, CD4 but not CD8 T effector lymphocytes are indispensable for the clearance of malaria infection.

Yeast lysates carrying the nucleoprotein from measles virus vaccine as a novel subunit vaccine platform to deliver Plasmodium circumsporozoite antigen.

Background: Yeast cells represent an established bioreactor to produce recombinant proteins for subunit vaccine development. In addition, delivery of vaccine antigens directly within heat-inactivated yeast cells is attractive due to the adjuvancy provided by the yeast cell. In this study, Pichia pastoris yeast lysates carrying the nucleoprotein (N) from the measles vaccine virus were evaluated as a novel subunit vaccine platform to deliver the circumsporozoite surface antigen (CS) of Plasmodium.

Plasmodium Merozoite TRAP Family Protein Is Essential for Vacuole Membrane Disruption and Gamete Egress from Erythrocytes.

Surface-associated TRAP (thrombospondin-related anonymous protein) family proteins are conserved across the phylum of apicomplexan parasites. TRAP proteins are thought to play an integral role in parasite motility and cell invasion by linking the extracellular environment with the parasite submembrane actomyosin motor. Blood stage forms of the malaria parasite Plasmodium express a TRAP family protein called merozoite-TRAP (MTRAP) that has been implicated in erythrocyte invasion.

Vermilion Only Cross-lip Flap for Treating Whistle Deformity in Secondary Bilateral Cleft Lip Repair.

Bilateral cleft lip repairs can result in various secondary deformities. One more commonly seen deformity, the whistle deformity, is characterized by a reduced or absent tubercle, orbicularis muscle diastasis, and abnormalities of the philtrum with notched appearance of cupid's bow. Various techniques have been described to address these problems.

Protection against malaria in mice is induced by blood stage-arresting histamine-releasing factor (HRF)-deficient parasites.

Although most vaccines against blood stage malaria in development today use subunit preparations, live attenuated parasites confer significantly broader and more lasting protection. In recent years, Plasmodium genetically attenuated parasites (GAPs) have been generated in rodent models that cause self-resolving blood stage infections and induce strong protection. All such GAPs generated so far bear mutations in housekeeping genes important for parasite development in red blood cells.

Myeloid Cell Isolation from Mouse Skin and Draining Lymph Node Following Intradermal Immunization with Live Attenuated Plasmodium Sporozoites.

Malaria infection begins when the sporozoite stage of Plasmodium is inoculated into the skin of a mammalian host through a mosquito bite. The highly motile parasite not only reaches the liver to invade hepatocytes and transform into erythrocyte-infective form. It also migrates into the skin and to the proximal lymph node draining the injection site, where it can be recognized and degraded by resident and/or recruited myeloid cells.

Apicomplexa-specific tRip facilitates import of exogenous tRNAs into malaria parasites.

The malaria-causing Plasmodium parasites are transmitted to vertebrates by mosquitoes. To support their growth and replication, these intracellular parasites, which belong to the phylum Apicomplexa, have developed mechanisms to exploit their hosts. These mechanisms include expropriation of small metabolites from infected host cells, such as purine nucleotides and amino acids.

The Plasmodium translocon of exported proteins component EXP2 is critical for establishing a patent malaria infection in mice.

Export of most malaria proteins into the erythrocyte cytosol requires the Plasmodium translocon of exported proteins (PTEX) and a cleavable Plasmodium export element (PEXEL). In contrast, the contribution of PTEX in the liver stages and export of liver stage proteins is unknown. Here, using the FLP/FRT conditional mutatagenesis system, we generate transgenic Plasmodium berghei parasites deficient in EXP2, the putative pore-forming component of PTEX.

Development of Volunteer International Craniofacial Surgery Missions: The Komedyplast Protocol.

Volunteer surgical missions to provide cleft care to patients in developing countries has been done successfully for a number of years. Similar missions that provide craniofacial surgery introduce a dramatic step up in complexity. While articles have addressed protocols for the safe delivery of cleft care around the world, little has been written on volunteer craniofacial surgical missions.

Disruption of Parasite hmgb2 Gene Attenuates Plasmodium berghei ANKA Pathogenicity.

Eukaryotic high-mobility-group-box (HMGB) proteins are nuclear factors involved in chromatin remodeling and transcription regulation. When released into the extracellular milieu, HMGB1 acts as a proinflammatory cytokine that plays a central role in the pathogenesis of several immune-mediated inflammatory diseases. We found that the Plasmodium genome encodes two genuine HMGB factors, Plasmodium HMGB1 and HMGB2, that encompass, like their human counterparts, a proinflammatory domain.

Plasmodium and mononuclear phagocytes.

Plasmodium, the causative agent of malaria, initially multiplies inside liver cells and then in successive cycles inside erythrocytes, causing the symptoms of the disease. In this review, we discuss interactions between the extracellular and intracellular forms of the Plasmodium parasite and innate immune cells in the mammalian host, with a special emphasis on mononuclear phagocytes. We overview here what is known about the innate immune cells that interact with parasites, mechanisms used by the parasite to evade them, and the protective or detrimental contribution of these interactions on parasite progression through its life cycle and pathology in the host.

Plasmodium berghei histamine-releasing factor favours liver-stage development via inhibition of IL-6 production and associates with a severe outcome of disease.

Plasmodium spp., which causes malaria, produces a histamine-releasing factor (HRF), an orthologue of mammalian HRF. Histamine-releasing factor produced by erythrocytic stages of the parasite is thought to play a role in the pathogenesis of severe malaria.

Small-molecule inhibitors of the pseudaminic acid biosynthetic pathway: targeting motility as a key bacterial virulence factor.

Helicobacter pylori is motile by means of polar flagella, and this motility has been shown to play a critical role in pathogenicity. The major structural flagellin proteins have been shown to be glycosylated with the nonulosonate sugar, pseudaminic acid (Pse). This glycan is unique to microorganisms, and the process of flagellin glycosylation is required for H.

ZIPCO, a putative metal ion transporter, is crucial for Plasmodium liver-stage development.

The malaria parasite, Plasmodium, requires iron for growth, but how it imports iron remains unknown. We characterize here a protein that belongs to the ZIP (Zrt-, Irt-like Protein) family of metal ion transport proteins and have named ZIP domain-containing protein (ZIPCO). Inactivation of the ZIPCO-encoding gene in Plasmodium berghei, while not affecting the parasite's ability to multiply in mouse blood and to infect mosquitoes, greatly impairs its capacity to develop inside hepatocytes.

A cysteine protease inhibitor of plasmodium berghei is essential for exo-erythrocytic development.

Plasmodium parasites express a potent inhibitor of cysteine proteases (ICP) throughout their life cycle. To analyze the role of ICP in different life cycle stages, we generated a stage-specific knockout of the Plasmodium berghei ICP (PbICP). Excision of the pbicb gene occurred in infective sporozoites and resulted in impaired sporozoite invasion of hepatocytes, despite residual PbICP protein being detectable in sporozoites.

Local immune response to injection of Plasmodium sporozoites into the skin.

Malarial infection is initiated when the sporozoite form of the Plasmodium parasite is inoculated into the skin by a mosquito. Sporozoites invade hepatocytes in the liver and develop into the erythrocyte-infecting form of the parasite, the cause of clinical blood infection. Protection against parasite development in the liver can be induced by injection of live attenuated parasites that do not develop in the liver and thus do not cause blood infection.