Helicobacter pylori (H. pylori) is one of the most common human pathogens, affecting half of the world’s population. Approximately 20% of the infected patients develop gastric ulcers or neoplastic changes in the gastric stroma. An infection also leads to the progression of epithelial–mesenchymal transition within gastric tissue, increasing the probability of gastric cancer development. This paper aims to review the role of H. pylori and its virulence factors in epithelial–mesenchymal transition associated with malignant transformation within the gastric stroma. The reviewed factors included: CagA (cytotoxin-associated gene A) along with induction of cancer stem-cell properties and interaction with YAP (Yes-associated protein pathway), tumor necrosis factor α-inducing protein, Lpp20 lipoprotein, Afadin protein, penicillin-binding protein 1A, microRNA-29a-3p, programmed cell death protein 4, lysosomal-associated protein transmembrane 4β, cancer-associated fibroblasts, heparin-binding epidermal growth factor (HB-EGF), matrix metalloproteinase-7 (MMP-7), and cancer stem cells (CSCs). The review summarizes the most recent findings, providing insight into potential molecular targets and new treatment strategies for gastric cancer.

Background: This meta-analysis outlines the role of elevated lactate dehydrogenase (LDH) levels in assessing the severity of coronavirus disease 2019 (COVID-19). Methods: The current study was designed as a systematic review and meta-analysis. Embase, PubMed, Web of Science, Scopus and Cochrane Central Register of Controlled Trials were searched to identify the usefulness of LDH as a marker of COVID-19 severity. All extracted data were analyzed using RevMan V.5.4 or STATA V.14 software. Results: A total of 264 records were selected for this meta-analysis. Pooled analysis showed that LDH levels were statistically significantly lower in the group of survivors compared to patients who died in hospital (standardized mean differences [SMD] = –3.10; 95% confidence interval [CI]: –3.40 to –2.79; I² = 99%; p < 0.001). Lower LDH levels were observed in non-severe groups compared to severe course of COVID-19 (SMD = –2.38; 95% CI: –2.61 to –2.14; I² = 99%; p < 0.001). The level of LDH was statistically significantly lower in the severe group compared to the critical group (SMD = –1.48; 95% CI: –2.04 to –0.92; I² = 98%; p < 0.001). Patients who did not require treatment in the intensive care unit (ICU) showed significantly lower levels of LDH compared to patients who required treatment in the ICU (SMD = –3.78; 95% CI: –4.48 to –3.08; I² = 100%; p < 0.001). Conclusions: This meta-analysis showed that elevated LDH was associated with a poor outcome in COVID-19. Background: This meta-analysis outlines the role of elevated lactate dehydrogenase (LDH) levels in assessing the severity of coronavirus disease 2019 (COVID-19). Methods: The current study was designed as a systematic review and meta-analysis. Embase, PubMed, Web of Science, Scopus and Cochrane Central Register of Controlled Trials were searched to identify the usefulness of LDH as a marker of COVID-19 severity. All extracted data were analyzed using RevMan V.5.4 or STATA V.14 software. Results: A total of 264 records were selected for this meta-analysis. Pooled analysis showed that LDH levels were statistically significantly lower in the group of survivors compared to patients who died in hospital (standardized mean differences [SMD] = –3.10; 95% confidence interval [CI]: –3.40 to –2.79; I² = 99%; p < 0.001). Lower LDH levels were observed in non-severe groups compared to severe course of COVID-19 (SMD = –2.38; 95% CI: –2.61 to –2.14; I² = 99%; p < 0.001). The level of LDH was statistically significantly lower in the severe group compared to the critical group (SMD = –1.48; 95% CI: –2.04 to –0.92; I² = 98%; p < 0.001). Patients who did not require treatment in the intensive care unit (ICU) showed significantly lower levels of LDH compared to patients who required treatment in the ICU (SMD = –3.78; 95% CI: –4.48 to –3.08; I² = 100%; p < 0.001). Conclusions: This meta-analysis showed that elevated LDH was associated with a poor outcome in COVID-19.

Hydroxyapatite possesses desirable properties as a scaffold in tissue engineering: it is biocompatible at a site of implantation, and it is degradable to non-toxic products. Moreover, its porosity enables infiltration of cells, nutrients and waste products. The outcome of hydroxyapatite implantation highly depends on the extent of the host immune response. Authors emphasise major roles of the chemical, morphological and physical properties of the surface of biomaterial used. A number of techniques have been applied to transform the theoretical osteoconductive features of HAp into spinal fusion systems—from integration of HAp with autograft to synthetic intervertebral implants. The most popular uses of HAp in spine surgery include implants (ACDF), bone grafts in posterolateral lumbar fusion and transpedicular screws coating. In the past, autologous bone graft has been used as an intervertebral cage in ACDF. Due to the morbidity related to autograft harvesting from the iliac bone, a synthetic cage with osteoconductive material such as hydroxyapatite seems to be a good alternative. Regarding posterolateral lumbar fusion, it requires the graft to induce new bone growth and reinforce fusion between the vertebrae. Hydroxyapatite formulations have shown good results in that field. Moreover, the HAp coating has proven to be an efficient method of increasing screw fixation strength. It can decrease the risk of complications such as screw loosening after pedicle screw fixation in osteoporotic patients. The purpose of this literature review is to describe in vivo reaction to HAp implants and to summarise its current application in spine surgery.

Background: Acute myeloid leukemia (AML) is a heterogenic lethal disorder characterized by the accumulation of abnormal myeloid progenitor cells in the bone marrow which results in hematopoietic failure. Despite various efforts in detection and treatment, many patients with AML die of this cancer. That is why it is important to develop novel therapeutic options, employing strategic target genes involved in apoptosis and tumor progression. Methods: The aim of the study was to evaluate PARP1, PARP2, PARP3, and TRPM2 gene expression at mRNA level using qPCR method in the cells of hematopoietic system of the bone marrow in patients with acute myeloid leukemia, bone marrow collected from healthy patients, peripheral blood of healthy individuals, and hematopoietic stem cells from the peripheral blood after mobilization. Results: The results found that the bone marrow cells of the patients with acute myeloid leukemia (AML) show overexpression of PARP1 and PARP2 genes and decreased TRPM2 gene expression. In the hematopoietic stem cells derived from the normal marrow and peripheral blood after mobilization, the opposite situation was observed, i.e. TRPM2 gene showed increased expression while PARP1 and PARP2 gene expression was reduced. We observed positive correlations between PARP1, PARP2, PARP3, and TRPM2 genes expression in the group of mature mononuclear cells derived from the peripheral blood and in the group of bone marrow-derived cells. In AML cells significant correlations were not observed between the expression of the examined genes. In addition, we observed that the reduced expression of TRPM2 and overexpression of PARP1 are associated with a shorter overall survival of patients, indicating the prognostic significance of these genes expression in AML. Conclusions: Our research suggests that in physiological conditions in the cells of the hematopoietic system there is mutual positive regulation of PARP1, PARP2, PARP3, and TRPM2 genes expression. PARP1, PARP2, and TRPM2 genes at mRNA level deregulate in acute myeloid leukemia cells.

This study aimed to assess the relationship between the occurrence of cervical myofascial pain with active myofascial trigger points (MTrPs) within the upper trapezius muscle and the electromyographic asymmetry index (AsI) of masticatory muscles: temporalis anterior (TA), superficial part of the masseter muscle (MM), and anterior belly of the digastric muscle (DA). The study group comprised 100 subjects (80 women and 20 men) aged 18 to 30 years (mean 23 ± 2.6 years) reporting pain in the neck muscles, diagnosed with myofascial pain with active MTrPs only within the upper trapezius muscle. The control group comprised 60 healthy, pain-free subjects (42 women and 18 men) aged 20 to 30 years (mean 22.8 ± 2.6 years) without MTrPs in the upper trapezius muscle. The palpation measurement, based on the diagnostic criteria of Travell and Simons, was used to diagnose active MTrPs. The masticatory muscle activity was recorded using an 8-channel device for surface electromyography—BioEMG III^TM. Significant differences in electromyographic patterns between the group with MTrPs in the right side of upper trapezius muscle and the control group were observed within resting activity for the AsI TA (MTrPs: 8.64 vs. controls: −3.22; p = 0.001) and AsI MM (MTrPs: 7.05 vs. controls: −2.09; p = 0.018). Controls presented different electromyographic patterns during maximum voluntary clenching with cotton rolls between teeth within masseter muscle compared to the MTrPs group (MTrPs: 9.27 vs. controls: −0.43 vs. p = 0.041). Participants with MTrPs in the left side of upper trapezius muscle presented predomination of left-sided electromyographic patterns at rest within temporalis anterior in comparison to controls (MTrPs: −19.22 vs. controls: −3.22; p = 0.001). MTrPs within the trapezius muscle may be related to asymmetry within the masticatory muscle activity, suggesting that the presence of myofascial pain within the cervical muscles plays a role in the imbalance of the stomatognathic system. A unilateral active MTrPs within the trapezius muscle may increase the sEMG activity on the same side of the temporalis anterior and masseter muscles.

CD44, a multi-isoform adhesion receptor for hyaluronic acid (HA), plays a crucial role in regulating cell interactions with the extracellular matrix, cell migration, differentiation, and survival in both physiological and pathological contexts. Accumulating experimental evidence suggests that CD44 is not merely a passive marker of mesenchymal cell activation but rather an active signaling hub driving fibrosis in many organs, including the lung, skin, heart, and liver. Its involvement in fibroblast differentiation into myofibroblasts, as well as induction of the invasive phenotype of these cells, shows striking analogies to the mechanisms of epithelial-to-mesenchymal transition (EMT) known from cancer progression. In this paper, we discuss both the molecular mechanisms of CD44-dependent signaling (including through EGFR, MAPK/ERK, CaMKII, lipid rafts, and Smad) and the influence of its modulation (knockout, antibodies, blockade of HA synthesis) on the course of fibrosis in in vitro and in vivo models. In addition, we present the influence of environmental pollutants—such as heavy metals, particulate matter, endocrine disruptors, and microplastics—on the activation of the HA-CD44 axis in connective tissue, with particular emphasis on their role in the induction of chronic inflammation, EMT, and extracellular matrix deposition. The collected evidence suggests that CD44 serves as a central integrator of inflammatory and fibrogenic signals, and its pharmacological modulation may represent a novel therapeutic strategy for treating fibrotic diseases and chronic inflammatory conditions.