Lymphoma is generally a nodal disease and arises from lymphoid tissues or organs. Extranodal lymphoma accounts for almost a third of malignant lymphomas. Squamous cell carcinoma accounts for 90 % of laryngeal carcinoma, while extranodal Non Hodgkin Lymphoma (NHL) attributes only less than 1% of laryngeal neoplasms. Less than 100 of such cases been reported in literature since 1952. As to our best knowledge, no such case was ever reported in our country. We report a case of a 58-year-old gentleman who presented the typical history of laryngeal malignancy however the pathology turned out to be as NHLof Diffuse Large B-cell subtype.
This study aimed to identify the prevalence of psychological distress and its association with sociodemographic characteristics, burden of care, and the coping strategies used by childminders in residential homes. A total of 151 childminders (median age = 39; 64.7% female) participated in the study. The prevalence of psychological distress was 59.4%, and 74.0% recorded mild to moderate burden. Multivariate analyses showed that caregiver burden (adjusted beta = 0.464, P = .01), lesser application of problem-focused coping (adjusted beta = -0.292, P = .012), lower salary (adjusted beta = -0.196, P = .040), and lower educational qualification (adjusted beta = -0.212, P = .038) predicted higher psychological distress. Regular screening of psychological distress and burden of care is recommended among this population.
Introduction This appears to be the first biomechanical study that compares the stability of various locations of the crossing points in crossed pinning Kirschner wiring (K-wire) construct in treating pediatric supracondylar humerus fracture (SCHF). Additionally, this study compared the biomechanical stability between crossed pinning K-wire construct and the three-lateral divergent K-wire construct. Methods For the study purpose, 30 synthetic humerus bones were osteotomised at mid-olecranon fossa, anatomically reduced, and pinned using two 1.6-millimeter K-wires in five different constructs. A total of six samples were prepared for each construct and tested for extension, flexion, valgus, varus, internal rotation, and external rotation forces. Results As for crossed pinning K-wire construct, the center crossing point emerged as the stiffest construct in both linear and rotational forces, in comparison to the lateral crossing point, superior crossing, and medial crossing point Conclusion Based on this analysis, it is highly recommended that, if the crossed pinning construct is selected to treat supracondylar humerus fracture, the surgeon should aim for center crossing point as it is the most stable construct. Nevertheless, if lateral and superior crossing points are obtained during the initial attempt of fixation, the fixation may be accepted without revising the K-wire as the stability of these two constructs are comparable and portrayed no significant difference when compared to that of the center crossing point. Additionally, it is essential to avoid the medial crossing point as it is significantly less stable in terms of rotational force when compared to the center crossing point.
Alcohol use disorder (AUD) is characterized by compulsive binge alcohol intake, leading to various health and social harms. Protein Kinase C epsilon (PKCε), a specific family of PKC isoenzyme, regulates binge alcohol intake, and potentiates alcohol-related cues. Alcohol via upstream kinases like the mammalian target to rapamycin complex 1 (mTORC1) or 2 (mTORC2), may affect the activities of PKCε or vice versa in AUD. mTORC2 phosphorylates PKCε at hydrophobic and turn motif, and was recently reported to be associated with alcohol-seeking behavior, suggesting the potential role of mTORC2-PKCε interactions in the pathophysiology of AUD. mTORC1 regulates translation of synaptic proteins involved in alcohol-induced plasticity. Hence, in this article, we aimed to review the molecular composition of mTORC1 and mTORC2, drugs targeting PKCε, mTORC1, and mTORC2 in AUD, upstream regulation of mTORC1 and mTORC2 in AUD and downstream cellular mechanisms of mTORCs in the pathogenesis of AUD.
The long-term binge intake of ethanol causes neuroadaptive changes that lead to drinkers requiring higher amounts of ethanol to experience its effects. This neuroadaptation can be partly attributed to the modulation of numerous neurotransmitter receptors by the various protein kinases C (PKCs). PKCs are enzymes that control cellular activities by regulating other proteins via phosphorylation. Among the various isoforms of PKC, PKCε is the most implicated in ethanol-induced biochemical and behavioral changes. Ethanol exposure causes changes to PKCε expression and localization in various brain regions that mediate addiction-favoring plasticity. Ethanol works in conjunction with numerous upstream kinases and second messenger activators to affect cellular PKCε expression. Chauffeur proteins, such as receptors for activated C kinase (RACKs), cause the translocation of PKCε to aberrant sites and mediate ethanol-induced changes. In this article, we aim to review the following: the general structure and function of PKCε, ethanol-induced changes in PKCε expression, the regulation of ethanol-induced PKCε activities in DAG-dependent and DAG-independent environments, the mechanisms underlying PKCε-RACKε translocation in the presence of ethanol, and the existing literature on the role of PKCε in ethanol-induced neurobehavioral changes, with the goal of creating a working model upon which further research can build.
Multiple alcohol use disorder (AUD)-related behavioral alterations are governed by protein kinase C epsilon (PKCε), particularly in the amygdala. Protein kinase C (PKC) is readily phosphorylated at Ser729 before activation by the mTORC2 protein complex. In keeping with this, the current study was conducted to assess the variations in mTORC2 and PKCε during different ethanol exposure stages. The following groups of rats were employed: control, acute, chronic, ethanol withdrawal (EW), and EW + ethanol (EtOH). Ethanol-containing and non-ethanol-containing modified liquid diets (MLDs) were administered for 27 days. On day 28, either saline or ethanol (2.5 g/kg, 20% v/v) was intraperitoneally administered, followed by bilateral amygdala extraction. PKCε mRNA levels were noticeably increased in the amygdala of the EW + EtOH and EW groups. Following chronic ethanol consumption, the stress-activated map kinase-interacting protein 1 (Sin1) gene expression was markedly decreased. In the EW, EW + EtOH, and chronic ethanol groups, there was a profound increase in the protein expression of mTOR, Sin1, PKCε, and phosphorylated PKCε (Ser729). The PKCε gene and protein expressions showed a statistically significant moderate association, according to a correlation analysis. Our results suggest that an elevated PKCε protein expression in the amygdala during EW and EW + EtOH occurred at the transcriptional level. However, an elevation in the PKCε protein expression, but not its mRNA, after chronic ethanol intake warrants further investigation to fully understand the signaling pathways during different episodes of AUD.