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The number of patients with oral lichen planus (OLP) has increased due to the raise of aggressive forms of the disease (erosive, ulcerative and hyperkeratotic forms) with a possible risk of malignancy. There are isolated researches which indicate a genetic determinism to OLP, but more often these conclusions are based on insufficiently adequate and out of date methods, which make it impossible to correctly interpret the obtained data. The aim was to identify a genetical predisposition with a programmed risk to the oral lichen planus. The main group – 278 patients with the OLP (aged 26-65 years). The control group – 298 people (blood donors) who didn’t have dental diseases, as well as diseases of internal organs and systems. The groups were homogeneous by gender and age. In our research we used such methods: clinical, radiological, immunogenetic, statistical methods were used. The erosive form of OLP was associated with 0(I) group in 54.2±0.4% of cases, while the hyperkeratotic form was associated with group 0(I) only in 28.7±1.8% of cases. B(ІІІ) and AB(ІB) groups were less often associated with the erosive form of OLP and were observed in 17.3±0.1% and 2.0±0.1% of cases, respectively. The integration of A(ІІ) group in the erosive form of OLP was 30.5±0.1%, but the indicator was higher than in individuals with B(III) and AB(IV) groups. Hyperkeratotic form of OLP was more often observed in A(II) carriers than in 0(I) and was 44.1±0.1% versus 28.7±1.8%, respectively. With blood group B (ІІІ), the relationship with OLP is not traced. Correlative relationship with erythrocyte blood antigens of the ABO system in patients with oral lichen planus was established. Risk groups for the development of erosive and hyperkeratotic forms of lichen planus in patients with gastrointestinal tract pathology O(I)>A(II)>B(III) – with erosive form and A(II)>O(I)>B(III)) – with hyperkeratosis. [ABSTRACT FROM AUTHOR]

A range of issues related to using English attributive phrases formed by the prefix + noun model in dental literature by modern scientists is considered. Such words' syntactic structure does not correspond to the disease's pathogenesis, which creates certain difficulties in terms of the perception of these syntactic constructions by General Practitioners and Pathologists Our work is devoted to finding an adequate equivalent replacement for the ingrained semantics of phrases that are implicit in nature. Using the term "discoloration", in our opinion, is due to the simplicity of explaining to the patient the change in tooth color under the influence of various exogenous and endogenous factors. Using the term 'pigment dystrophy' for dental patients is a complicated psychological factor. Therefore, there is a substitution of 'pigment dystrophy' to "discoloration" in modern dental literature. The term 'pigment dystrophy' is more pathologically and pathogenetically determined and is more suitable for explaining pathological processes in the teeth' hard tissues. There is no concept of "pigment dystrophy" and "discoloration" of teeth in the current classification of diseases World Health Organization (WHO) ICD-10. As a result of the analysis of the rules and semantics of the terms used by scientists, they are incorrect in many cases., (© 2022 MEDPRESS.)

Aberrant expression of noncoding RNAs plays a critical role during tumorigenesis. To uncover novel functions of long non-coding RNA (lncRNA) in lung adenocarcinoma, we used a microarray-based screen identifying LINC00673 with elevated expression in matched tumor versus normal tissue. We report that loss of LINC00673 is sufficient to trigger cellular senescence, a tumor suppressive mechanism associated with permanent cell cycle arrest, both in lung cancer and normal cells in a p53-dependent manner. LINC00673-depleted cells fail to efficiently transit from G1- to S-phase. Using a quantitative proteomics approach, we confirm the modulation of senescence-associated genes as a result of LINC00673 knockdown. In addition, we uncover that depletion of p53 in normal and tumor cells is sufficient to overcome LINC00673-mediated cell cycle arrest and cellular senescence. Furthermore, we report that overexpression of LINC00673 reduces p53 translation and contributes to the bypass of Ras-induced senescence. In summary, our findings highlight LINC00673 as a crucial regulator of proliferation and cellular senescence in lung cancer.

Long noncoding RNAs (lncRNAs) are major regulators of many cellular processes including cell cycle progression and tumorigenesis. In this study, we identify a novel lncRNA, MA-linc1, and reveal its effects on cell cycle progression and cancer growth. Inhibition of MA-linc1 expression alters cell cycle distribution, leading to a decrease in the number of G1 cells and a concomitant increase in all other stages of the cell cycle, and in particular G2/M, suggesting its involvement in the regulation of M phase. Accordingly, knock down of MA-linc1 inhibits M phase exit upon release from a mitotic block. We further demonstrate that MA-linc1 predominantly functions in cis to repress expression of its neighboring gene, Purα, which is often deleted in human cancers and whose ectopic expression inhibits cell cycle progression. Knock down of Purα partially rescues the MA-linc1 dependent inhibition of M phase exit. In agreement with its suggested role in M phase, inhibition of MA-linc1 enhances apoptotic cell death induced by the antimitotic drug, Paclitaxel and this enhancement of apoptosis is rescued by Purα knockdown. Furthermore, high levels of MA-linc1 are associated with reduced survival in human breast and lung cancer patients.Taken together, our data identify MA-linc1 as a novel lncRNA regulator of cell cycle and demonstrate its potential role in cancer progression and treatment.

Numerous studies have investigated the relationship between surface electromyogram (EMG) and torque exerted about a joint. Most studies have used conventional EMG amplitude (EMGamp) processing, such as rectification followed by low-pass filtering, to pre-process the EMG before relating it to torque. Recently, advanced EMGamp processors that incorporate signal whitening and multiple-channel combination have been shown to significantly improve EMGamp processing. In this study, we compared the performance of EMGamp-torque estimators with and without these advanced EMGamp processors. Fifteen subjects produced constant-posture, non-fatiguing, force-varying contractions about the elbow while torque and biceps/triceps EMG were recorded. EMGamp was related to torque using a linear FIR model. Both whitening and multiple-channel combination reduced EMG-torque errors and their combination provided an additive benefit. Using a 15th-order linear FIR model, EMG-torque errors with a four-channel, whitened processor averaged 7.3% of maximum voluntary contraction (MVC) (or 78% of variance accounted for). By comparison, the equivalent single-channel, unwhitened (conventional) processor produced an average error of 9.9% of MVC (variance accounted for of 55%). In addition, the study describes the occurrence of spurious peaks in estimated torque when the torque model is created from data with a sampling rate well above the bandwidth of the torque. This problem occurs when the torque data are sampled at the same rate as the EMG data. The problem is corrected by decimating the EMGamp prior to relating it to joint torque, in our case to an effective sampling rate of 40.96 Hz.