Studies
have found increased rates of dysosmia in patients with
Novel Coronavirus disease 2019 (COVID-19). However, the mechanism
that causes olfactory loss is unknown. The primary objective of this
study was to explore local proinflammatory cytokine levels in the
olfactory epithelium in patients with COVID-19. Biopsies of the olfactory
epithelium were taken from patients with confirmed COVID-19 as well
as uninfected controls. Levels of tumor necrosis factor α (TNF-α)
and interleukin-1-beta (IL-1β) were assessed using ELISA and
compared between groups. Average TNF-α levels were significantly
increased in the olfactory epithelium of the COVID-19 group compared
to the control group (P < 0.05). However, no differences
in IL-1β were seen between groups. Elevated levels of the proinflammatory
cytokine TNF-α were seen in the olfactory epithelium in patients
with COVID-19. This suggests that direct inflammation of the olfactory
epithelium could play a role in the acute olfactory loss described
in many patients with COVID-19.
The
recent coronavirus disease of 2019 (COVID-19) pandemic has
adversely affected people worldwide. A growing body of literature
suggests the neurological complications and manifestations in response
to COVID-19 infection. Herein, we explored the inflammatory and immune
responses in the post-mortem cerebral cortex of patients with severe
COVID-19. The participants comprised three patients diagnosed with
severe COVID-19 from March 26, 2020, to April 17, 2020, and three
control patients. Our findings demonstrated a surge in the number
of reactive astrocytes and activated microglia, as well as low levels
of glutathione along with the upregulation of inflammation- and immune-related
genes IL1B, IL6, IFITM, MX1, and OAS2 in the COVID-19 group. Overall,
the data imply that oxidative stress may invoke a glial-mediated neuroinflammation,
which ultimately leads to neuronal cell death in the cerebral cortex
of COVID-19 patients.
The Cyclin-dependent kinase (CDK) class of serine/threonine kinases has crucial roles in the regulation of cell cycle transition and is mainly involved in the pathogenesis of cancers. The expression of CDKs is controlled by a complex regulatory network comprised of genetic and epigenetic mechanisms, which are dysregulated during the progression of cancer. The abnormal activation of CDKs results in uncontrolled cancer cell proliferation and the induction of cancer stem cell characteristics. The levels of CDKs can be utilized to predict the prognosis and treatment response of cancer patients, and further understanding of the function and underlying mechanisms of CDKs in human tumors would pave the way for future cancer therapies that effectively target CDKs. Defects in the regulation of cell cycle and mutations in the genes coding cell-cycle regulatory proteins lead to unrestrained proliferation of cells leading to formation of tumors. A number of treatment modalities have been designed to combat dysregulation of cell cycle through affecting expression or activity of CDKs. However, effective application of these methods in the clinical settings requires recognition of the role of CDKs in the progression of each type of cancer, their partners, their interactions with signaling pathways and the effects of suppression of these kinases on malignant features. Thus, we designed this literature search to summarize these findings at cellular level, as well as in vivo and clinical levels.
Cholesterol granulomas are rare round or ovoid cysts. They contain cholesterol crystals surrounded by foreign bodies of giant cells and are characterized by chronic inflammation. Large cholesterol granuloma can compress surrounding tissue especially cranial nerves. There are several types of surgery for the resection of cholesterol granuloma. We describe 4 cases of cholesterol granuloma operated on via transnasal endoscopic approach. In this report, we describe radiologic and pathologic features of this lesion and explain the advantages and disadvantages of transsphenoidal endoscopic approach for these rare lesions.
Background
There is evidence regarding the role of two lncRNAs: MEG3 and H19 the pathomechanism of obesity and related disorders. Here, we aimed to evaluate the expression of MEG3 and H19 in visceral adipose tissues (VAT) and subcutaneous adipose tissues (SAT) of obese women (n = 18), as compared to normal‐weight women (n = 17). Moreover, we sought to identify the association of expression of MEG3 and H19 in SAT and VAT with obesity parameters, insulin resistance, and the mRNA expression of possible target genes involved in adipogenesis and lipogenesis including peroxisome proliferator‐activated receptor gamma (PPARγ), fatty acid synthase (FAS), and acetyl‐CoA carboxylase (ACC).
Methods
Real‐time PCR was performed to investigate the mRNA expression of the above‐mentioned genes in VAT and SAT from all participants.
Results
The results showed lower mRNA levels of H19 in SAT of obese women, compared to normal‐weight women, while MEG3 expression was significantly higher in the SAT of the obese group rather than controls. Correlation analysis indicated that the transcript level of H19 had an inverse correlation with obesity indices and HOMA‐IR values. However, MEG3 expression displayed a positive correlation with all the indicated parameters in all participants. Interestingly, a positive correlation was found between transcript level of MEG3 in SAT with FAS and PPARγ. However, there was an inverse correlation between SAT expression of H19 and FAS.
Conclusions
It appears that lncRNAs, MEG3 and H19, are involved in obesity‐related conditions. However, more clinical studies are still required to clarify the relationships between lncRNAs with obesity and related abnormalities.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.