Subacute thyroiditis after SARS-CoV-2 vaccination: A case report.

Key Clinical Message: Subacute thyroiditis which is typically characterized by cervical pain and fever is caused by viral infection and is seen after SARS-CoV-2 vaccination. Here we report a post-vaccination subacute thyroiditis after SARS-CoV-2 vaccination. Abstract: Subacute thyroiditis (SAT) is possibly caused by a viral infection and is typically characterized by cervical pain and fever. SAT associated with SARS-CoV-2 infection or SARS-CoV-2 vaccination has been reported, albeit in limited numbers. A 34-year-old woman was referred to our clinic with typical SAT symptoms. The diagnosis was confirmed through thyroid scintigraphy after receiving the SARS-CoV-2 vaccination, despite testing negative for COVID-19 via RT-PCR. There is a theoretical correlation between SARS-CoV-2 vaccination and SAT. Vaccination may have a direct or indirect impact on the thyroid, but further studies are required to confirm this relationship. A systematic review of the literature of similar cases was performed for comparison. Ultimately, the overall benefits of SARS-CoV-2 vaccination outweigh the potential adverse effects. Therefore, these types of reports should not divert attention from the actual reality.

Morphine attenuates neuroinflammation and blood-brain barrier disruption following traumatic brain injury through the opioidergic system.

Endogenous opiates are suggested to have a role in the pathophysiology of traumatic brain injury (TBI). Furthermore, administration of opioidergic agents in TBI injured animals have been shown to affect the brain injury and provide neuroprotection post-TBI. This study aims to investigate the potential neuroprotective effects of morphine through inhibition of neuroinflammatory pathways in acute severe TBI. Male Wistar rats were divided into seven groups (24 rats per group): Sham, Vehicle (TBI + intraperitoneal (i.p) injection of normal saline), TBI + i.p injection of morphine in 1, 5 and 10 mg/kg doses (MOR 1, MOR 5 and MOR 10 groups), TBI + morphine (5 mg/kg i.p) + Naloxone (NAL + MOR), and TBI + morphine (5 mg/kg i.p) + Naltrindole (NALT + MOR). A severe diffuse TBI model (weight dropping Marmarou model) was used to induce TBI in rats. The veterinary coma scale (VCS), beam-walk, and beam-balance tasks were used to assess short-term neurological deficits. Histolopathological changes of brain tissue was evaluated using light microscopy and hematoxilin and eosin staining. Blood-Brain barrier (BBB) disruption was evaluated by the Evans Blue method 6 h post-injury. Brain water content and cerebrospinal fluid (CSF) content of IL-1ß and IL-10 were assessed by the wet-dry method and enzyme-linked immunosorbent assay (ELISA), respectively. Morphine (1 and 5 mg/kg doses) attenuated BBB leakage, improved VCS score, pathological changes of brain tissue, and vestibulomotor function compared to the vehicle group (p < 0.0001). Only 5 mg/kg morphine attenuated brain edema (p < 0.0001). Furthermore, 1 and 5 mg/kg morphine significantly changed CSF concentration of IL-1ß and IL-10 compared to the vehicle group (p < 0.0001). Inhibition of opioid receptors by naloxone and naltrindole abolished morphine neuroprotective effects (p < 0.0001 vs. MOR 5 group). This study suggests that morphine administration inhibits TBI-mediated neuroinflammation via opioid receptors and improves neurobehavioral function following TBI, which provides a potential therapeutic opportunity in the treatment of traumatic brain injury.

Expression Analysis of Fyn and Bat3 Signal Transduction Molecules in Patients with Chronic Lymphocytic Leukemia.

BACKGROUND: Chronic lymphocytic leukemia (CLL) is correlated with defects in T-cell function resulting imparity in antitumor immune responses. Tim-3 is a co-inhibitory immune checkpoint receptor expressed on exhausted T-cells during tumor progression. Fyn and Bat3 are two important adaptor molecules involved in inhibition and activation of Tim-3 downstream signaling, respectively. In this study, the expression of Tim-3, Fyn, and Bat3 mRNA was evaluated in CLL patients. METHODS: Peripheral blood mononuclear cells (PBMCs) were isolated from 54 patients with CLL and 34 healthy controls. Total RNA was extracted from all samples and applied for cDNA synthesis. The relative expression of Tim-3, Fyn, and Bat3 mRNA was determined by TaqMan Real-Time PCR using GAPDH as an internal control. RESULTS: Tim-3 mRNA expression was not significantly different between CLL patients and healthy controls. Fyn mRNA expression was significantly lower in CLL patients and conversely, Bat3 mRNA expression was higher in CLL patients compared to healthy controls. Interestingly, the mRNA expression of Fyn inhibitory adaptor molecule was remarkably associated with expression of Tim-3 in CLL patients. CONCLUSION: We have highlighted for the first time the expression of Fyn and Bat3 adaptor molecules in CLL patients. Our data demonstrated the strong correlation between the expression of Tim-3 and Fyn inhibitory molecules in CLL implying an important role for Tim-3-Fyn cooperation in induction of T-cell exhaustion.