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Background Soft tissue filler injections are frequently performed with a relatively low number of severe adverse events reported. While venous complications have been described, the majority of adverse events are generally associated with the arterial vascular system. Intra-arterial product application can present with pain, skin discoloration, and potential tissue loss and/or injection related visual compromise. Aim We present the clinical case and the consecutive symptomology of a 39-year-old woman injected with calcium hydroxylapatite at the zygomatic arch with five perpendicular needle (27G 12mm) supraperiosteal bolus injections of 0.2 cc per site. Methods Immediately after the injections, weakness, nausea, vomiting, and loss of consciousness occurred. Additionally, left-sided loss of sensation of her face, scalp, oral, and nasal mucosa occurred, with absence of left corneal reflex and ipsi-lateral ear congestion. Subsequently, left-sided masseteric atrophy and dysphagia occurred. Results One year after the injection procedure the sensory loss of her facial skin and scalp persisted, while the other symptoms improved. Medications involved in the symptomatic (not causal) partial recovery process were Dexamethasone, Vitamin B complex, Vinpocetine, Pentoxifyllin, and Thioctic acid. Conclusion The symptoms presented and the time-related relationship to the injection procedure increases the likeliness of an association between the administration of the calcium hydroxylapatite product and a lesion of the trigeminal ganglion. The resulting symptoms can altogether be related to the functions of the ganglion. The connecting pathway between the injection site and the ganglion can be explained by the arterial vascular pathway.

CRISPR/cas9 is a popular tool, widely used today for genome editing. However, the modular organization of this tool allows it to be used not only for DNA modifications but also for introducing epigenetic modifications both in DNA (methylation/demethylation) and in histones (acetylation/deacetylation). In these notes we will concentrate on the ways to adapt the CRISPR/cas9 system for epigenetic DNA modification of specific regions of interest. The modular organization represents a universal principal, that allows to create infinite number of functions with a limited number of tools. CRISPR/cas9, in which each subunit can be adapted for a particular task, is an excellent example of this rule. Made of two main subunits, it can be modified for targeted delivery of foreign activity (effector, an epigenetic enzyme in our case) to a selected part of the genome. In doing this the CRISPR/cas9 system represents a unique method that allows the introduction of both genomic and epigenetic modifications. This chapter gives a detailed review of how to prepare DNA for the fully functional CRISPR/cas9 system, able to introduce required modifications in the region of interest. We will discuss specific requirements for each structural component of the system as well as for auxiliary elements (modules), which are needed to ensure efficient expression of the elements of the system within the cell and the needs of selection and visualization.

The aim of this study was to investigate the role of cytokines in light of recently discovered aspects of acne immunopathogenesis. Materials and Methods: The study included 276 patients aged between 16 to 44 years with various forms of acne vulgaris. Severe manifestations of the disease were identified in 126/45.6% patients; disease lasted 1 to 5 years in 157/56.9% patients. The serum levels of cytokines were determined by ELISA using standard kits. The cells were characterized using flow cytometry. Results: The obtained data on an excessive secretion of pro-inflammatory cytokines (IL-1α, IL-2) and VEGF on the background of decreasing the content of anti-inflammatory cytokines (IL-4, IL-10) indicate an insufficient activity of anti-inflammatory immune response. It was concluded that acne is a model of chronic immunodeficiency inflammatory dermatoses with the activation of innate immunity and the subsequent development of the adaptive T-cell immune response.

Introduction Despite advances in screening and early diagnosis, about 15% of colorectal cancers present with acute colonic obstruction. Emergency colorectal surgery is associated with high morbidity and mortality rates. Preoperative decompression (SEMS or trananal decompression tube placement) as a bridge to surgery has been reported to improve short-term outcomes. However, oncological safety of endoscopic interventions is debatable due to the high frequency of perforations and dissemination. There are few retrospective studies of comparative outcomes between SEMS and decompression tube, but the benefits were not clear. The aim of this prospective randomized study is to compare sort-term and especially long term outcome of colorectal stenting and transanal decompression tube as a bridge to surgery. Methods Between December 2012 and December 2017, 72 patients with malignant colon obstruction, which was diagnosed based on radiological and endoscopic findings with pathohistological examination, were consecutively included into the study. Patients were randomized of random sampling numbers and divided into the stent or decompression tube group. Results Technical success rate RR 0.914, 95% CI 0.804–1.039 (p=0.065). Clinical success was significant higher in stent group RR 0.643, 95% CI 0.489–0.846 (p=0.031). Rate of complications was similar in groups RR 0.895, 95% CI 0.755–1.061 (p=0.087). Short-term outcomes in SEMS group were superior to decompression tube group in the following areas: stoma creation rate RR 0.914, 95% CI 0.804–1.039 (p=0.065) (p Conclusions SEMS has some benefits in comparison with decompression tubes in the short-term postoperative period for patients with malignant colorectal obstruction. The overall recurrence rate was higher in the stent group in long-term period. Moreover, the overall survival rate in the group is no different. Need to continue research to material accumulation and analysis of long-term results.

Prader-Willi syndrome (PWS [MIM 176270]) is a neurogenetic disorder characterized by decreased fetal activity, muscular hypotonia, failure to thrive, short stature, obesity, mental retardation, and hypogonadotropic hypogonadism. It is caused by the loss of function of one or more imprinted, paternally expressed genes on the proximal long arm of chromosome 15. Several potential PWS mouse models involving the orthologous region on chromosome 7C exist. Based on the analysis of deletions in the mouse and gene expression in PWS patients with chromosomal translocations, a critical region (PWScr) for neonatal lethality, failure to thrive, and growth retardation was narrowed to the locus containing a cluster of neuronally expressed MBII-85 small nucleolar RNA (snoRNA) genes. Here, we report the deletion of PWScr. Mice carrying the maternally inherited allele (PWScrm−/p+) are indistinguishable from wild-type littermates. All those with the paternally inherited allele (PWScrm+/p−) consistently display postnatal growth retardation, with about 15% postnatal lethality in C57BL/6, but not FVB/N crosses. This is the first example in a multicellular organism of genetic deletion of a C/D box snoRNA gene resulting in a pronounced phenotype., Author Summary Prader-Willi syndrome, or PWS, is a complex neurogenetic disorder and the most common genetic cause of life-threatening childhood obesity. Newborns have poor muscle tone, making suckling difficult, which leads to poor weight gain. After infancy, they experience extreme hunger, leading to obesity. Other symptoms include short stature, mental retardation, and often infertility. In PWS patients, a complex set of genes on the paternal chromosome 15 (in the PWS region) is missing or unexpressed. In an attempt to understand this disorder, various protein-coding genes in this region have been deleted in mice, but none of the resulting phenotypes consistently correlated with the human disease. This region also contains a cluster of genes that encode functional non-protein-coding RNAs. We deleted specifically the MBII-85 small nucleolar RNA (snoRNA) gene cluster on the parental mouse chromosome, which did not affect expression of any of the other snoRNA or protein-coding genes in the PWS region. These mice consistently displayed postnatal growth retardation starting from day 5 to 6, low postnatal lethality only in certain genetic backgrounds (