Heat shock protein (Hsp)-27 is a small-sized, ATP-independent, chaperone molecule that is overexpressed under conditions of cellular stress such as oxidative stress and heat shock, and protects proteins from unfolding, thus facilitating proteostasis and cellular survival. Despite its protective role in normal cell physiology, Hsp27 overexpression in various cancer cell lines is implicated in tumor initiation, progression, and metastasis through various mechanisms, including modulation of the SWH pathway, inhibition of apoptosis, promotion of EMT, adaptation of CSCs in the tumor microenvironment and induction of angiogenesis. Investigation of the role of Hsp27 in the resistance of various cancer cell types against doxorubicin, herceptin/trastuzumab, gemcitabine, 5-FU, temozolomide, and paclitaxel suggested that Hsp27 overexpression promotes cancer cell survival against the above-mentioned chemotherapeutic agents. Conversely, Hsp27 inhibition increased the efficacy of those chemotherapy drugs, both in vitro and in vivo. Although numerous signaling pathways and molecular mechanisms were implicated in that chemotherapy resistance, Hsp27 most commonly contributed to the upregulation of Akt/mTOR signaling cascade and inactivation of p53, thus inhibiting the chemotherapy-mediated induction of apoptosis. Blockage of Hsp27 could enhance the cytotoxic effect of well-established chemotherapeutic drugs, especially in difficult-to-treat cancer types, ultimately improving patients’ outcomes.

Cancer is a leading cause of death worldwide, with approximately 19 million new cases each year. Lately, several novel chemotherapeutic drugs have been introduced, efficiently inhibiting tumor growth and proliferation. However, developing a new drug is a time- and money-consuming process, requiring around 1 billion dollars and nearly ten years, with only a minority of the initially effective anti-cancer drugs experimentally finally being efficient in human clinical trials. Drug repurposing for cancer treatment is an optimal alternative as the safety of these drugs has been previously tested, and thus, in case of successful preclinical studies, can be introduced faster and with a lower cost into phase 3 clinical trials. Antipsychotic drugs are associated with anti-cancer properties and, lately, there has been an increasing interest in their role in cancer treatment. In the present review, we discussed in detail the in-vitro and in-vivo properties of the most common typical and atypical antipsychotics, along with their mechanism of action.

Traumatic brain injury (TBI) is a leading cause of disability worldwide. Traumatic axonal injury (TAI) is a subtype of TBI resulting from high-impact forces that cause shearing and/or stretching of the axonal fibers in white matter tracts. It is present in almost half of cases of severe TBI and frequently associated with poor functional outcomes. Axonal injury results from axonotomy due to mechanical forces and the activation of a biochemical cascade that induces the activation of proteases. It occurs at a cellular level; hence, conventional imaging modalities often fail to display TAI lesions. However, the advent of novel imaging modalities, such as functional magnetic resonance imaging and fiber tractography, has significantly improved the detection and characteristics of TAI. Furthermore, the significance of several fluid and structural biomarkers has also been researched, while the contribution of omics in the detection of novel biomarkers is currently under investigation. In the present review, we discuss the role of imaging modalities and potential biomarkers in diagnosing, classifying, and predicting the outcome in patients with TAI.

Background: Chronic subdural hematoma (CSDH) is a common neurosurgical condition that usually occurs in the elderly. Surgical evacuation of the hematoma with burr holes is considered the standard of care for the treatment of patients with CSDH. However, a high risk of recurrence, up to 34%, after hematoma evacuation has been reported, while the risk factors linked with recurrence have not been studied in depth. In the present study, we set out to identify risk factors of recurrence in patients surgically treated for CSDH. Methods: We retrospectively studied patients with symptomatic CSDH who were treated surgically in our institute during a five-year period. All the patients were treated by single or double burr hole drainage. The data for this study were extracted by the pre-operative and post-operative CT scan of each patient. These data include the sex, the midline shift, the width, and the presence of acute clots and subdural air collection post-operatively. A univariate analysis was performed. A receiver operating characteristic (ROC) analysis was utilized to detect the hematoma’s width more efficiently, differentiating patients that developed recurrence. Results: A total of 222 patients were included in this study. Recurrence occurred in 20 (9.0%) patients. The univariate analysis showed that the presence of acute clots post-operatively are significant factors related with recurrence (OR = 4.01, CI 95% 1.55–10.33, and p = 0.002). There was no significant relationship between the recurrence rate and the hematoma’s width, sex, the midline shifts pre-operatively or post-operatively, the subdural space, and air collection post-operatively. Conclusions: The presence of acute clots in the post-operative CT scan is a potential, previously unexplored, risk factor associated with the recurrence of CSDH.

Background: Routine admission inflammatory and metabolic biomarkers have been proposed as adjunctive tools in mild traumatic brain injury (mTBI). However, their association with specific traumatic intracranial lesion types remains unclear. Methods: We conducted a prospective observational study including adult patients with isolated mTBI who underwent head computed tomography (CT) on admission. Admission laboratory parameters included the platelet-to-lymphocyte ratio (PLR), systemic immune-inflammation index (SII), and glucose-to-potassium ratio (GPR). Two predefined endpoints were assessed. The first compared biomarker values between CT-positive and CT-negative patients. The second evaluated associations between biomarkers and individual intracranial lesion subtypes, including analyses restricted to isolated lesions. Results: A total of 125 patients were included, of whom 95 (76%) were CT-positive. No significant differences were observed between CT-positive and CT-negative patients for PLR (p = 0.793), GPR (p = 0.531), or SII (p = 0.291). In lesion-specific analyses including all intracranial injuries, subdural hematoma (SDH) was associated with higher GPR compared with patients without SDH (p = 0.016). In analyses restricted to patients with isolated lesions, SDH was associated with higher PLR (p = 0.018) and higher GPR (p = 0.015). No significant associations were observed between any biomarker and intraparenchymal hemorrhage, subarachnoid hemorrhage, or epidural hematoma (all p > 0.05). Patients with multiple intracranial injuries exhibited higher PLR (p = 0.012) and higher SII (p = 0.021) compared with those with isolated lesions. After correction for multiple comparisons, none of the observed associations remained statistically significant. Conclusions: These findings suggest that routine systemic biomarkers have limited global discriminatory value in mTBI. Exploratory lesion-specific associations with SDH did not remain significant after correction for multiple comparisons, underscoring the preliminary nature of these findings.