METHODS: Baseline characteristics and laboratory results were collected and analyzed. Receiver operating characteristic (ROC) curve analysis was used to joint detection of inflammatory markers for influenza positive children, and the scatter-dot plots were used to compare the differences between severe and non-severe group.
RESULTS: Influenza B positive children had more bronchitis and pneumonia (P count, lymphocyte count, neutrophil-to-lymphocyte ratio (NLR), and platelet parameters performed differently among
Methods: This retrospective study involved 215 children aged 12 years and below with the initial diagnosis of AA and PA. Clinical factors studied were demographics, presenting symptoms, body temperature on admission (BTOA), white cell count (WCC), absolute neutrophil count (ANC), platelet count and urinalysis. Simple and multiple logistic regressions were used to determine the odds ratio of the statistically significant clinical factors. Results: The mean age of the included children was 7.98 ± 2.37 years. The odds of AA increased by 2.177 times when the age was ≥ 8 years (P = 0.022), 2.380 times when duration of symptoms ≥ 2 days (P = 0.011), 2.447 times with right iliac fossa (RIF) pain (P = 0.007), 2.268 times when BTOA ≥ 38 °C (P = 0.020) and 2.382 times when neutrophil percentage was ≥ 76% (P = 0.045). It decreased by 0.409 times with non-RIF pain (P = 0.007). The odds of PA was increased by 4.672 times when duration of symptoms ≥ 2 days (P = 0.005), 3.611 times when BTOA ≥ 38 °C (P = 0.015) and 3.678 times when neutrophil percentage ≥ 76% (P = 0.016). There was no significant correlation between WCC and ANC with AA and PA.
Conclusion: Older children with longer duration of symptoms, RIF pain and higher BTOA are more likely to have appendicitis. The risk of appendiceal perforation increases with longer duration of symptoms and higher BTOA.
METHODS AND RESULTS: The goats were experimentally infected with a low dose of 2400 Haemonchus contortus, Trichostrongylus spp. and Oesophagostomum spp. at a 6:1:1 ratio. Faecal egg counts (FEC), packed cell volume (PCV), IgA activity against third-stage larvae and peripheral eosinophilia were measured twice a week for eight weeks. The infection generated an IgA response but did not significantly increase peripheral eosinophilia in the 25 infected kids compared with the 4 control animals. FEC was not associated with IgA activity or eosinophilia.
CONCLUSION: A detailed analysis of IgA and eosinophil responses to deliberate nematode infection in Boer goats showed that there was an increase in nematode-specific IgA activity but no detectable eosinophil response. In addition, there was no association between increased IgA activity or eosinophilia with egg counts and worm burdens. These suggest that IgA and eosinophils do not act to control nematode infection in goats.
Methods: Seventy-two postmenopausal women with stage I, II, or III breast cancer from the Oncology Clinic, Universiti Sains Malaysia Hospital were treated with anastrozole (1 mg/day). Patients were randomly assigned to one of the two groups (n = 36/group): a control group (no honey) and a honey group (20 g/day of honey for 12 weeks). Fasting blood samples were obtained pre- and post-intervention to investigate differences in the haematological, renal, and liver profiles of patients in both the groups.
Results: Post-intervention, alanine aminotransferase levels were significantly higher in the control group than in the honey group. In the honey group, white blood cell counts, platelet counts, and creatinine levels were significantly higher following honey supplementation for 12 weeks. Nevertheless, the values were still within normal ranges.
Conclusions: The present study suggests that honey supplementation of 20 g/day for 12 weeks is safe and beneficial for postmenopausal breast cancer patients.
METHODS: Thirty-two healthy volunteers were randomly allocated to receive saline (Control) or dexamethasone 2 mg, 4 mg or 8 mg intravenously. Venous blood samples were collected at baseline before administration of treatment, and at 4 h, 24 h and one-week post-treatment. At each time point, measurements included blood glucose and macrophage migration inhibition factor (MMIF), full blood count including lymphocyte subsets, monocytes, neutrophils, eosinophils and basophils by flow cytometry, and plasma SPM using liquid chromatography tandem mass spectrometry. The effect of dexamethasone dose and time on all measures was analysed using linear mixed models.
RESULTS: There was a dose-dependent increase in neutrophil count after dexamethasone that persisted for 24 h. In contrast, there was a dose-dependent reduction in counts of monocytes, lymphocytes, basophils and eosinophils 4 h after dexamethasone, followed by a rebound increase in cell counts at 24 h. Seven days after administration of dexamethasone, all cell counts were similar to baseline levels. MMIF concentration, glucose and natural killer cell counts were not significantly affected by dexamethasone. There was a significant gender effect on plasma SPM such that levels of 17-HDHA, RvD1, 17R-RvD1 and RvE2 in females were on average 14%-50% lower than males. In a linear mixed model that adjusted for neutrophil count, there was a significant interaction between the dose of dexamethasone and time, on plasma 17R-RvD1 such that plasma 17R-RvD1 fell in a dose-dependent manner until 4 h after administration of dexamethasone. There were no significant effects of dexamethasone on the other plasma SPM (18-HEPE, RvE2, 17-HDHA, RvD1, RvD2 and 14-HDHA) measured.
DISCUSSION: This is the first study in healthy volunteers to demonstrate that commonly employed antiemetic doses of dexamethasone affect immune cell populations and plasma levels of 17R-RvD1 an SPM with anti-nociceptive properties. If similar changes occur in surgical patients, then this may have implications for acute infection risk in the post-operative period.
Methods: The control group was administered with phosphate buffer solution (PBS) while the other two groups received PCM alone (1000 mg/kg) and PCM + 25 mg/kg ZER, respectively, at 0 h and 4 h after PCM injection. After 24 h, the blood and liver were collected for differential white blood cell count, liver histological observation and biochemical analysis including alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total protein concentration in serum and liver.
Results: Treatment with ZER was found to significantly reduce ALT (P = 0.041), AST (P = 0.044) and total hepatic protein (P = 0.045) in comparison to PCM-induced rats. Rats treated with ZER exhibited the normal structure of hepatocytes with no vacuolisation or necrosis and showed significantly reduced neutrophil count (P = 0.037). This finding suggests its ability to suppress the inflammatory processes caused by PCM overdosage and decrease the hepatocytes tendency to go through necrotic processes.
Conclusion: ZER possessed protective activity against PCM-induced acute hepatotoxicity in a rat model.
METHODS: This study included 159 septic patients admitted to an intensive care unit. Leukocytes count, procalcitonin (PCT), interleukin-6 (IL-6), and paraoxonase (PON) and arylesterase (ARE) activities of PON-1 were assayed from blood obtained on ICU presentation. Logistic regression was used to derive sepsis mortality score (SMS), a prediction equation describing the relationship between biomarkers and 30-day mortality.
RESULTS: The 30-day mortality rate was 28.9%. The SMS was [еlogit(p)/(1+еlogit(p))]×100; logit(p)=0.74+(0.004×PCT)+(0.001×IL-6)-(0.025×ARE)-(0.059×leukocytes count). The SMC had higher area under the receiver operating characteristic curve (95% Cl) than SOFA score [0.814 (0.736-0.892) vs. 0.767 (0.677-0.857)], but is not statistically significant. When the SMS was added to the SOFA score, prediction of 30-day mortality improved compared to SOFA score used alone [0.845 (0.777-0.899), p=0.022].
CONCLUSIONS: A sepsis mortality score using baseline leukocytes count, PCT, IL-6 and ARE was derived, which predicted 30-day mortality with very good performance and added significant prognostic information to SOFA score.