[Risk factors and construction of a nomogram model for cirrhotic portal vein thrombosis combined with esophagogastric variceal bleeding].

Objective: To investigate the risk factors and construct a nomogram model for predicting the occurrence of cirrhotic portal vein thrombosis in patients combined with esophagogastric variceal bleeding (EVB). Methods: Clinical data on 416 cirrhotic PVT cases was collected from the First Hospital of Lanzhou University between January 2016 and January 2022. A total of 385 cases were included after excluding 31 cases for retrospective analysis. They were divided into an esophagogastric variceal bleeding group and a non-esophagogastric variceal bleeding group based on the clinical diagnosis. The esophagogastric variceal group was then further divided into an EVB group and a non-bleeding group. All patients underwent gastroscopy, serology, and imaging examinations. The risk factors of PVT combined with EVB were identified by univariate analysis using SPSS 26. The prediction model of cirrhotic PVT in patients combined with EVB was constructed by R 4.0.4. The prediction efficiency and clinical benefits of the model were evaluated by the C-index, area under the receiver operating characteristic curve, calibration plots, and decision curve. The measurement data were examined by a t-test or Mann-Whitney U test. The counting data were tested using the χ(2) test or the Fisher exact probability method. Results: There were statistically significant differences in the etiology, Child-Pugh grade,erythrocyte count, hematocrit, globulin, and serum lipids between the esophageal and non-esophageal varices groups (P < 0.05). There were statistically significant differences in etiology, erythrocyte count, hemoglobin, hematocrit, neutrophil percentage, total protein, globulin, albumin/globulin, urea, high-density lipoprotein cholesterol, calcium, and neutrophil lymphocyte ratio (NLR) between the EVB and non-bleeding groups (P < 0.05). Multivariate logistic regression analysis showed that etiology (OR = 3.287, 95% CI: 1.497 ~ 7.214), hematocrit (OR = 0.897, 95% CI: 0.853 ~ 0.943), and high-density lipoprotein cholesterol (OR = 0.229, 95% CI: 0.071 ~ 0.737) were independent risk factors for cirrhotic PVT patients combined with EVB. The constructed normogram model predicted the probability of bleeding in patients. The nomogram model had shown good consistency and differentiation (AUC = 0.820, 95% CI: 0.707 ~ 0.843), as verified by 10-fold cross-validation (C-index = 0.799) and the Hosmer-Lemeshow goodness of fit test (P = 0.915). The calibration plot and the decision curve suggested that the prediction model had good stability and clinical practicability. Conclusion: The risk factors for EVB occurrence include etiology, erythrocyte, hemoglobin, hematocrit, percentage of neutrophils, total protein, globulin, albumin/globulin, urea, high-density lipoprotein cholesterol, calcium, and NLR in patients with cirrhotic liver. The constructed prediction model has good predictive value, and it can provide a reference for medical personnel to screen patients with high bleeding risk for targeted treatment.

Prevention of etomidate-induced myoclonus during anesthetic induction by pretreatment with dexmedetomidine

Myoclonus induced by etomidate during induction of general anesthesia is undesirable. This study evaluated the effect of dexmedetomidine (DEX) pretreatment on the incidence and severity of etomidate-induced myoclonus. Ninety patients undergoing elective surgical procedures were randomly allocated to three groups (n=30 each) for intravenous administration of 10 mL isotonic saline (group I), 0.5 µg/kg DEX in 10 mL isotonic saline (group II), or 1.0 µg/kg DEX in 10 mL isotonic saline (group III) over 10 min. All groups subsequently received 0.3 mg/kg etomidate by intravenous push injection. The incidence and severity of myoclonus were recorded for 1 min after etomidate administration and the incidence of cardiovascular adverse events that occurred between the administration of the DEX infusion and 1 min after tracheal intubation was recorded. The incidence of myoclonus was significantly reduced in groups II and III (30.0 and 36.7%), compared with group I (63.3%). The incidence of severe sinus bradycardia was significantly increased in group III compared with group I (P<0.05), but there was no significant difference in heart rate in groups I and II. There were no significant differences in the incidence of low blood pressure among the 3 groups. Pretreatment with 0.5 and 1.0 µg/kg DEX significantly reduced the incidence of etomidate-induced myoclonus during anesthetic induction; however, 0.5 µg/kg DEX is recommended because it had fewer side effects.

Prevention of etomidate-induced myoclonus during anesthetic induction by pretreatment with dexmedetomidine.

Myoclonus induced by etomidate during induction of general anesthesia is undesirable. This study evaluated the effect of dexmedetomidine (DEX) pretreatment on the incidence and severity of etomidate-induced myoclonus. Ninety patients undergoing elective surgical procedures were randomly allocated to three groups (n=30 each) for intravenous administration of 10 mL isotonic saline (group I), 0.5 µg/kg DEX in 10 mL isotonic saline (group II), or 1.0 µg/kg DEX in 10 mL isotonic saline (group III) over 10 min. All groups subsequently received 0.3 mg/kg etomidate by intravenous push injection. The incidence and severity of myoclonus were recorded for 1 min after etomidate administration and the incidence of cardiovascular adverse events that occurred between the administration of the DEX infusion and 1 min after tracheal intubation was recorded. The incidence of myoclonus was significantly reduced in groups II and III (30.0 and 36.7%), compared with group I (63.3%). The incidence of severe sinus bradycardia was significantly increased in group III compared with group I (P<0.05), but there was no significant difference in heart rate in groups I and II. There were no significant differences in the incidence of low blood pressure among the 3 groups. Pretreatment with 0.5 and 1.0 µg/kg DEX significantly reduced the incidence of etomidate-induced myoclonus during anesthetic induction; however, 0.5 µg/kg DEX is recommended because it had fewer side effects.

[Effects and clinical significance of virus load on red blood cell parameters in different stage of hepatitis B].

OBJECTIVE: To evaluate the effect of the viral load on the red blood cell parameters in chronic hepatitis B patients and its clinical significance. METHODS: In the study, 373 chronic hepatitis B patients were recruited, including 123 alanine transaminase (ALT) normal patients (ALT<40 U/L),128 ALT greater than or equal to the upper limit of normal, and less than 2 times higher than the upper limit of normal patients(40 U/L ≤ALT<80 U/L), and 122 ALT greater than or equal to 2 times higher than the upper limit of normal patients (ALT≥80 U/L). The blood routine parameters were measured by automatic blood cell counter. The liver function parameters were measured by automatic biochemical analyzer, the hepatitis B virus loads were measured by quantitative PCR analyzer and the results were analyzed by covariance analysis. RESULTS: In the ALT normal chronic hepatitis B patients group, the viral load had minor effects on the red blood cell parameters.But in the ALT abnormal chronic hepatitis B patients group, the viral load had a significant effect on the red blood cell parameters, and the effect was most manifest in the ALT≥ double upper limit of normal group. The specific performance was that with the viral load increasing, the red blood cell [low copies group (4.10±0.67)×10(12)/L,medium copies group (3.92±0.69)×10(12)/L,high copies group (3.54±0.90) ×10(12)/L], the hemoglobin[low copies group (129.66±21.12 ) g/L, medium copies group (126.23±23.38) g/L, high copies group (112.98±27.77) g/L], the hematocrit (low copies group 37.66±5.68, medium copies group 37.03±6.03, high copies group 33.34±8.15) decreased(P=0.006,0.007,0.010),the mean corpuscular volume [low copies group (92.17±6.53) fL, medium copies group (94.85±7.95) fL, high copies group (101.63±11.33) fL], the mean corpuscular hemoglobin [low copies group (31.70±2.22) pg, medium copies group (33.11±3.62) pg, high copies group (34.65±3.13) pg], the mean corpuscular hemoglobin concentration [low copies group (344.28±17.17) g/L, medium copies group (351.33±16.90) g/L, high copies group (358.12±15.67) g/L], and the red blood cell distribution width-standard deviation [low copies group (52.49±9.04) fL, medium copies group (56.96±7.19) fL, high copies group (61.23 ±7.23) fL] increased(P=0.000,0.000,0.002,0.000). CONCLUSION: Observing the effect of the viral load on the red blood cell parameters in chronic hepatitis B patients can reflect the effect of hepatitis B virus on the immune response and liver function in the different pathological stages, providing theoretical support for the clinical antiviral treatment.

MicroRNA-922 promotes tau phosphorylation by downregulating ubiquitin carboxy-terminal hydrolase L1 (UCHL1) expression in the pathogenesis of Alzheimer's disease.

Decreased levels of soluble ubiquitin carboxy-terminal hydrolase L1 (UCHL1) have been reported in the brains of sporadic Alzheimer's disease (AD) patients, and the introduction of UCHL1 rescued the synaptic and cognitive function of AD model mice. Obviously, a reduction in the levels of UCHL1 may play a role in the pathogenesis of AD. However, the mechanisms underlying the regulation of UCHL1 levels in AD have not been fully elucidated. MicroRNAs (miRs) have been shown to participate in the process of AD. In our study, we discovered that microRNA-922 decreased the levels of UCHL1. Neurofibrillary tangles (NFTs) mainly consisting of the hyperphosphorylated microtubule-associated protein tau are the defining pathological features of AD. In the present study, we found the levels of UCHL1 affected the levels of phosphorylated tau: the phosphorylated tau levels increased after knockdown of UCHL1 expression, and the phosphorylated tau levels decreased when UCHL1 was overexpressed. Furthermore, overexpression of microRNA-922 increased the phosphorylated tau levels. In conclusion, miR-922 increasing the levels of phosphorylated tau by regulating UCHL1 levels contributed to the pathogenesis of AD. Our study partly explained one of the mechanisms underlying the downregulation of UCHL1 levels in AD patients and could enrich the content of tau pathology in the pathogenesis of AD.

Soluble polycyclic aromatic hydrocarbons in raw coals.

Polycyclic aromatic hydrocarbons (PAHs) are considered to be a group of compounds that pose potential health hazards since some PAHs are known carcinogens. During coal utilization processes, such as coal combustion and pyrolysis, PAHs released may be divided into two categories according to their formation pathways. One category is derived from complex chemical reactions and the other is from free PAHs transferred from the original coals. PAHs released from complex chemical reactions during combustion and pyrolysis have received considerable attention in recent years. However, free PAHs contained in raw coals have not been seriously considered as a source of these materials to be released during the utilization of coal. The goal of this study was to observe the relation between the content of PAHs in different coals and the elemental composition of the coals. In this study, eight bituminous coals with dry, ash-free carbon values varying from 65% to 90% were selected. Each coal was extracted with dichloromethane in a Soxhlet extractor for 6 h. The extracts were quantitatively analyzed with a gas chromatograph/mass spectrometer (GC-MS). More than 20 kinds of PAHs were identified. The total amount of PAHs determined varied from 1.2 to 28.3 mg/kg from the various coal types. The maximum total PAHs extracted was reached when the carbon content exceeded 84% by weight.

Prolactin-secreting pituitary adenomas with mammary dysplasia in New Zealand white rabbits.

Nine aged (mean age = 3.2 years) nulliparous New Zealand white rabbit does were found to have markedly enlarged teats. The teats were frequently engorged with fluid but were not hot and did not cause signs of pain. The number of affected teats per animal ranged from 1 to 8 (mean = 4). The teats and associated glandular tissue were typically discolored grey, blue, or greenish black (n = 6). Prolactin concentrations were evaluated by radioimmunoassay. Serum prolactin concentrations ranged from 22.4 ng/ml to 2.21 micrograms/ml (mean = 397.3 ng/ml), which was 10- to 1000-fold greater than normal values in nonpregnant rabbits. Conventional radiography of the skull of six rabbits did not reveal pituitary enlargement. Necropsy revealed an enlarged pituitary gland and sella turcica in six of nine does. The diaphragma sellae had ruptured in two rabbits. All nine rabbits had pituitary acidophil adenomas. The neoplastic portions of the pituitaries were diffusely immunoreactive when stained immunohistochemically for prolactin. In contrast, only small clusters of five to seven cells stained positively in normal pituitaries selected as controls. Histologic examination of the mammary glands revealed numerous large dilated cystic spaces containing proteinaceous fluid. Many cysts had numerous papillary epithelial infoldings. The cystic dilations extended into and included the teat canal producing the gross appearance. Prolactin-secreting acidophil adenomas have not been previously reported in the rabbit, and the association with mammary dysplasia is unique.

Methyl prednisolone acetate modulation of infection and subsequent pulmonary pathology in hamsters exposed to parainfluenza-1 virus (Sendai).

Parainfluenza-1 virus (PI-1) has a wide host range; the disease process observed varies with the age, previous exposure, and species. This study was performed to determine possible effects of the corticosteroid methyl prednisolone acetate (MPA) on PI-1 infection in hamsters. Hamsters serologically negative for PI-1 were exposed to virus alone or were exposed to virus the day after pretreatment with a single subcutaneous injection of MPA. Serum antibodies to PI-1 were present in virus-only exposed hamsters by Day 8 and increased up to Day 20. PI-1 was recovered from lungs of virus-only exposed hamsters on Day 2 to 8. Virus antigen was detected by immunocytochemistry on Days 2 to 10 in lungs of virus-only exposed hamsters. Virus-associated lesions in these hamsters began as acute bronchiolar epithelium degeneration and necrosis on Day 4 and were foci of fibrosis by Days 12 to 20. Hamsters exposed to virus after MPA treatment developed no antibodies to virus, had no virus detectable by plaque assays or immunocytochemistry, and had no pulmonary lesions. Hamsters treated with MPA had decreased total lymphocyte counts up to Day 20 after treatment. Treatment of hamsters with MPA one day prior to PI-1 virus exposure is associated with no detectable evidence of viral infection. Humoral and cellular immunity mediated by MPA-sensitive lymphocytes may mediate some of the manifestations of PI-1 pulmonary disease.