At the end of 2019, the world met with the coronavirus disease 2019 (COVID-19), which will affect all humanity. Later in the course, the genetic variants of SARS-CoV-2 have emerged, bringing new questions and concerns. This study investigated differences between patients infected with the B.1.1.7 (UK variant) and the B.1.617.2 (Delta variant) regarding patient complaints, intensive care unit (ICU) admission and stay time, intubation, severe disease, mortality rates, and laboratory parameters. Hospitalized 205 patients infected with B.1.1.7 and 207 patients infected with B.1.617.2 were included in the study. Laboratory parameters, admission complaints, and the percent saturation of oxygen in the blood (SpO₂) were recorded on the same day as the diagnosis and clinical findings during their follow-up. Cough and fever were more common complaints in the B.1.1.7 infected group, whereas tiredness, joint pain, and gastrointestinal complaints were more frequent in patients infected with B.1.617.2. The B.1.617.2 infected group had higher severe disease, acute coronary syndrome (ACS), mortality rates, neutrophil, troponin, and ferritin levels. In conclusion, patients infected with B.1.617.2 had a higher risk of intubation, ACS, and mortality rates. Cough and fever were more common in B.1.1.7 infected group, whereas tiredness was more frequent in B.1.617.2 infected group. Vaccination with at least one dose of Pfizer-BioNTech or CoronaVac is independently associated with a decreased mortality risk caused by two variants (Odds Ratio 0.4).

We evaluated the protective effect of epifriedelinol against breast cancer and postulated an underlying mechanism. Breast cancer was induced by a single dose of 50 mg/kg 7,12-Dimethylbenanthracene (DMBA), and rats were treated with 100 or 200 mg/kg (i.p.) epifriedelinol for 4 weeks. We then evaluated the effect of epifriedelinol on tumor growth, oxidative stress and serum inflammatory cytokine levels in DMBA-induced breast cancer. Protein and mRNA levels were determined using western blotting and quantitative reverse transcription polymerase chain reaction, respectively. The tumor volume and weight were significantly (p < 0.01) decreased in the epifriedelinol-treated group compared to the negative control group. Epifriedelinol decreased the altered levels of oxidative stress and serum inflammatory cytokines in rats with DMBA-induced breast cancer. Protein levels of PI3K, AKT and mTOR and mRNA levels of PI3K, AKT, Map3k1, Erbb2 and Pdk1 were decreased in the mammary tissue of epifriedelinol-treated rats with DMBA-induced breast cancer. Apoptosis was significantly induced in the epifriedelinol-treated group compared to the negative control group. In conclusion, epifriedelinol ameliorates DMBA-induced breast cancer by regulating the PI3K/AKT pathway.

One of the most important steps for preventing deaths due to snake bites is to administer snake antivenom to the eligible patients in a swift manner. In our study, we aimed to investigate whether procalcitonin is useful for predicting the clinical severity and the necessity of antivenom therapy at the early stages in patients presenting with snake bite. A total of 78 patients over the age of 18 who applied to the emergency department within the first 24 hours were included in this retrospective cross-sectional study. Age and sex of patients, severity of snake bites, total antivenom vials administered, observation periods and outcomes were recorded. Patients were graded according to their clinical severity after the snake bite. Procalcitonin, complete blood count and biochemical parameters of the patients were recorded. According to their clinical severity, the patients’ grades were as follows: 21 (26.9%) patients were grade 0; 21 patients (26.9%) were grade 1; 16 patients (20.5%) were grade 2; and 20 patients (25.6%) were grade 3. Snake antivenom was administered to 57 (73.1%) patients. There was a statistically significant difference between procalcitonin levels of patients in respect to their grade (P < 0.001). Sensitivity and specificity of procalcitonin levels of 13.45 and above were 100% and 100% respectively, both for the need of antivenom administration and for the blister formation in the patients. According to our study, we believe that elevated procalcitonin levels should alert the clinicians for possible blister formation, higher clinical severity, and increased requirement for antivenom administration.

Leucine-rich alpha-2 glycoprotein (LRG) is a novel biomarker for monitoring disease activity in inflammatory bowel disease (IBD). The aim of this study was to evaluate its utility in monitoring disease activity. In this retrospective study based on case records between August 2020 and July 2021 at our two centers, we examined the correlation between serum levels of LRG and C-reactive protein (CRP) with disease activity in IBD patients. Background factors related to serum LRG levels were also analyzed. Overall, 47 Crohn’s disease (CD) and 123 ulcerative colitis (UC) patients were evaluated. In patients with CD, LRG and CRP levels correlated with Harvey-Bradshaw Index (HBI) and Simple Endoscopic Score for CD (SES-CD) (LRG and HBI, r = 0.397; LRG and SES-CD, r = 0.637; CRP and HBI, r = 0.253; CRP and SES-CD, r = 0.332). In patients with UC, LRG and CRP significantly correlated with the partial Mayo score (PMS) and Mayo endoscopic subscore (MES) (LRG and PMS, r = 0.3; CRP and PMS, r = 0.282; LRG and MES, r = 0.424; CRP and MES, r = 0.459). In CD patients with normal CRP, serum LRG level was significantly higher in those with mucosal inflammation than in those with mucosal healing (16.4 vs. 10.7 μg/ mL). Stenosis was associated with serum LRG levels in CD group using multiple regression analysis. Therefore, LRG is a useful biomarker for monitoring disease activity and mucosal inflammation, and indicates the status of intestinal stenosis in IBD patients.

Eosinophilic gastrointestinal disorders are diseases that cause inflammation and dysfunction due to infiltration of eosinophils into various regions of the gastrointestinal tract. Symptoms and treatment vary depending on lesion severity. We describe the first pediatric case of an eosinophilic duodenal ulcer with esophageal involvement that was effectively treated using proton pump inhibitor monotherapy. A 12-year-old boy with no relevant family or medical history presented with a one-month history of epigastric pain. Laboratory test results were as follows: white blood cell count, 4,700/µL; eosinophil count, 150/µL (3.2%); and total IgE, 151.6 IU/L; and IgG antibodies for Helicobacter pylori were absent. Esophagogastroduodenoscopy revealed longitudinal linear furrows in the esophagus, indicating eosinophilic esophagitis with an A1 ulcer from the duodenal bulb to the descending duodenum. The patient was diagnosed with an eosinophilic duodenal ulcer with esophageal involvement based on pathological findings. Esomeprazole, a common proton pump inhibitor, was orally administered, after which the symptoms promptly improved. After two months, the esophagogastroduodenoscopy and pathological examination results showed improvement in both the esophagus and duodenum. There have been no previous reports of an eosinophilic duodenal ulcer with esophageal involvement without post-duodenal involvement at the time of diagnosis. The possibility of eosinophilic gastrointestinal disorders should be investigated in patients with duodenal ulcers by means of active biopsy, and patients should be investigated for other types of gastrointestinal lesions. Proton pump inhibitor monotherapy may be considered a first-line treatment for eosinophilic duodenal ulcers with esophageal involvement, depending on lesion severity.

Multiple myeloma (MM) is a common hematological malignancy. Bortezomib (BTZ) is a traditional medicine for MM treatment, but there are limitations for current treatment methods. Trifluoperazine (TFP) is a clinical drug for acute and chronic psychosis therapy. Lately, researchers have found that TFP can suppress tumor growth in many cancers. We attempted to study the effects of BTZ and TFP on MM in vivo and in vitro. We concentrated on the individual and combined impact of BTZ and TFP on the proliferation and apoptosis of MM cells via Cell Counting kit-8 assay, EdU assay, western blot, and flow cytometry. We found that combination therapy has a strong synergistic impact on MM cells. Combination therapy could induce cell arrest during G2/M phase and induce apoptosis in MM cells. Meanwhile, BTZ combined with TFP could play a better role in the anti-MM effect in vivo through MM.1s xenograft tumor models. Furthermore, we explored the mechanism of TFP-induced apoptosis in MM, and we noticed that TFP might induce MM apoptosis by inhibiting p-P38 MAPK/NUPR1. In summary, our findings suggest that TFP could synergistically enhance the BTZ-induced anti-cancer effect in multiple myeloma, which might be a promising therapeutic strategy for MM treatment.

The liver is an organ that is frequently injured by blunt trauma. In clinical medicine, contrast-enhanced computed tomography (CT) is useful for diagnosing liver damage. However, detection of liver injury is difficult with postmortem CT (PMCT) that does not use contrast media. This study aims to identify findings that are useful for diagnosing liver injury with PMCT. This study included 97 high-energy trauma cases that underwent both PMCT without contrast and forensic autopsy between July 2009 and November 2020. PMCT findings in and around the liver in cases of liver injury were collected. The diagnostic accuracy of each finding was calculated. Of 97 cases, 62 had liver injury on autopsy. PMCT detected hepatic surface gas in 31 cases, intrahepatic focal gas in 19 cases, high-density fluid accumulation around the liver in 12 cases, and fracture of a right lower (9th-12th) rib in 48 cases. Abnormal PMCT findings in and around the liver had insufficient diagnostic sensitivity, ranging from 19.4% to 38.7%. By contrast, the finding of a right lower rib fracture was more sensitive for suspected liver injury. Our results indicate that abdominal liver findings (hepatic surface gas, intrahepatic focal gas, and high-density fluid accumulation around the liver) are of limited utility for the diagnosis of liver injury, whereas a right lower rib fracture is a useful indirect finding.

Fibroepithelial polyps are benign tumors of mesodermal origin. They rarely occur in the nasal cavity, with only four such cases reported in the relevant English literature. The location was the inferior turbinate in three cases and anterior nasal septum in one case. The etiology has been suggested in other organs; however, it is entirely unknown in the nasal cavity. Pathological findings play an essential role in the diagnosis of fibroepithelial polyps. We report the case of a 76-year-old woman with fibroepithelial polyps originating from the posterior part of the nasal septum. The fibroepithelial polyps were white-yellow lobular masses that differed from a common inflammatory polyp. We made the diagnosis by excluding the other possible tumors based on a pathological examination. This is the first report about fibroepithelial polyps arising from the posterior nasal septum. She had no potential risk factors that might trigger fibroepithelial polyps in the nasal cavity. This case is a valuable example when considering the potential causes (e.g., female hormones and mechanical pressure) of nasal fibroepithelial polyps.

Carney complex is a rare, autosomal dominant disease accompanied by multiple endocrine neoplastic syndromes. Mutations in the PRKAR1A gene have recently been reported as a cause of Carney complex, but genotype-phenotype correlations vary widely. A 15-year-old Japanese man (Case 1) with short stature visited our hospital with suspected Cushing’s syndrome. Biochemical investigations suggested corticotropin-independent Cushing’s syndrome. Computed tomography revealed multiple bilateral adrenal tumors, and a two-staged partial adrenalectomy was performed. Pathological findings revealed primary pigmented nodular adrenocortical disease (PPNAD). The patient also exhibited distinctive spotty skin pigmentation. Based on these features, the patient was diagnosed as Carney complex. Cascade screening of family members was performed, and the mother (Case 2) and elder brother (Case 3) were diagnosed as Carney complex. Case 2 showed cardiac myxoma, acromegaly, spotty skin pigmentation, and mammary myxoid fibroadenoma. Case 3 exhibited gigantism, spotty skin pigmentation, and thyroid nodules. Target gene testing in Case 1 and 2 revealed the same novel mutation in PRKAR1A gene (c.503G>T, p.Gly168Val). This mutation was predicted as a pathogenic variant by multiple in silico analyses. Here, we present a family of Carney complex cases with a novel PRKAR1A pathogenic variant exhibiting varied clinical phenotypes within each case. In these cases, some specific phenotypes of Carney complex, such as pigmentary disorders, myxomas, and PPNAD are important as clues for diagnosis and prognostic factors. Clinicians should consider further examination in patients with Carney complex-specific phenotypes.

The 8p inverted duplication deletion [inv dup del(8p)] is a complex structural rearrangement in chromosome 8. Patients with this chromosomal abnormality exhibit developmental delay, facial dysmorphism, central nervous abnormalities, hypotonia, orthopedic abnormalities, and congenital heart defects. However, cellular immune function in inv dup del(8p) syndrome has never been reported. We present the case of a 1-month-old boy with inv dup del(8p) syndrome who had severe respiratory syncytial (RS) virus bronchiolitis. Natural killer (NK) cells are recruited to airway epithelium in the early phase of RS viral infection. A cluster of defensin genes (DEFs), which are deleted in inv dup del(8p), are located in 8p23.1. Human defensins are involved in antiviral activity through the NK cell-mediated cytotoxic pathway and envelope disruption in the normal immune response. This patient showed lower NK cell activity and α-defensin level compared with healthy controls. These results suggest that decreased NK cell activity can result from DEF haploinsufficiency. In addition to a skeletal deformity with chromosomal abnormality, NK cell-mediated immune deficiency may account for the exacerbation of RS virus bronchiolitis.