Cancellation of Elective Oral and Maxillofacial Surgery, a Tertiary Hospital Experience.

Background: Cancellation of elective surgery is said to occur when a patient's name appears on the operation list, but the operation is not done on the intended date. Cancelling elective surgeries is a long-standing problem faced by many countries worldwide. Reasons for cancellation of surgery vary from one hospital to another. The goal of this study was to identify factors associated with the cancellation of scheduled Oral and maxillofacial surgeries in the Lagos State University Teaching Hospital. Methodology: Cancellations of elective scheduled operations from January 2021 to July 2022 were reviewed retrospectively. All cancellations were recorded in a predesigned form which included information about the age of the patient, hospital identification number, date of cancellation, type of operation, the Surgeon and the Anaesthetist, preoperative anaesthetic evaluations, any associated medical problems and the presumed reasons for cancellations for in-patients and day case surgery. Patients who died before the time of their scheduled surgery were excluded. Result: 80 patients had their operation cancelled on the day of surgery, and the rate of cancellations was 44.2%. The most common causes of cancellations were patient-related (50%), accounting for up to half of the cancellations. The major reason for cancellation under the administrative category was insufficient time in the theatre to complete the operation list (18.8%). Financial constraint (16.3%) on the day of the surgery was noted more among planned day case procedures and delayed laboratory results (12.5%); oftentimes, covid test results were the major reasons for cancellations under the patient-factors category. Conclusion: The rate of cancellation in this study was high, most of which are patients related. Administrative-related reasons were also identified. However, in most cases, these cancellations can be avoided.

Combined cerium and zinc oxide nanoparticles induced hepato-renal damage in rats through oxidative stress mediated inflammation.

The toxicity profiles of nanoparticles (NPs) used in appliances nowadays remains unknown. In this study, we investigated the toxicological consequences of exposure to cerium oxide (CeO2) and zinc oxide (ZnO) nanoparticles given singly or in combination on the integrity of liver and kidney of male Wistar rats. Twenty (20) rats were allotted into four groups and treated as: Control (normal saline), CeO2NPs (50 µg/kg), ZnONPs (80 µg/kg) and [CeO2NPs (50 µg/kg) + ZnONPs (80 µg/kg)]. The nanoparticles were given to the animals through the intraperitoneal route, three times per week for four repeated weeks. Results revealed that CeO2 and ZnO NPs (singly) increased serum AST and ALT by 29% & 57%; 41% & 18%, and co-administration by 53% and 23%, respectively. CeO2 and ZnO NPs increased hepatic and renal malondialdehyde (MDA) by 33% and 30%; 38% and 67%, respectively, while co-administration increased hepatic and renal MDA by 43% and 40%, respectively. The combined NPs increased hepatic NO by 28%. Also, CeO2 and ZnO NPs, and combined increased BAX, interleukin-1ß and TNF-α by 45, 38, 52%; 47, 23, 82% and 41, 83, 70%, respectively. Histology revealed hepatic necrosis and renal haemorrhagic parenchymal in NPs-treated rats. Summarily, CeO2 and ZnO NPs produced oxidative injury and induced inflammatory process in the liver and kidney of experimental animals.

Comparative study of piroxicam and nitroglycerin on prostaglandin-modulated blood and electrolyte indices during di-estrous in female Wistar Rats.

OBJECTIVE: Endogenous prostaglandins are involved in hemostasis, renal excretion of electrolytes, and implicated in dysmenorrhea. Piroxicam and Nitroglycerin are common drugs used in treating dysmenorrhea by inhibiting the cyclooxygenase pathway involved in prostaglandin production. However, studies comparing the effects of these drugs on prostaglandin-modulated hemostasis and renal function are lacking. METHODS: Fifteen female rats (120-160g) were divided into 3 groups (20 per group), namely Control (distilled water, 0.3 mL), Piroxicam treated (3mg/kg) and Nitroglycerin treated (1 mg/kg). Di-estrous phase was confirmed in animals in each group using the Pipette smear method. Treatment was administered for 4 days covering the estrous cycle. Bleeding and clotting time were assessed and blood concentrations of sodium, potassium, urea and platelet counts were evaluated in all phases. Data were analyzed using one-way ANOVA and Newman-Keuls post-hoc test. Statistical significance was considered at p<0.0. RESULTS: The nitroglycerin-treated group showed significant increases in blood potassium during di-estrous while the piroxicam-treated group showed significant increases in blood potassium, urea and clotting time with a significant decrease in sodium levels during di-estrous compared to controls. Results obtained in other phases were not significant compared to controls. CONCLUSIONS: The study showed that Nitroglycerin produces minimum alteration of blood and electrolyte indices compared to piroxicam during di-estrous.

Multivariant Transcriptome Analysis Identifies Modules and Hub Genes Associated with Poor Outcomes in Newly Diagnosed Multiple Myeloma Patients.

The molecular mechanisms underlying chemoresistance in some newly diagnosed multiple myeloma (MM) patients receiving standard therapies (lenalidomide, bortezomib, and dexamethasone) are poorly understood. Identifying clinically relevant gene networks associated with death due to MM may uncover novel mechanisms, drug targets, and prognostic biomarkers to improve the treatment of the disease. This study used data from the MMRF CoMMpass RNA-seq dataset (N = 270) for weighted gene co-expression network analysis (WGCNA), which identified 21 modules of co-expressed genes. Genes differentially expressed in patients with poor outcomes were assessed using two independent sample t-tests (dead and alive MM patients). The clinical performance of biomarker candidates was evaluated using overall survival via a log-rank Kaplan-Meier and ROC test. Four distinct modules (M10, M13, M15, and M20) were significantly correlated with MM vital status and differentially expressed between the dead (poor outcomes) and the alive MM patients within two years. The biological functions of modules positively correlated with death (M10, M13, and M20) were G-protein coupled receptor protein, cell-cell adhesion, cell cycle regulation genes, and cellular membrane fusion genes. In contrast, a negatively correlated module to MM mortality (M15) was the regulation of B-cell activation and lymphocyte differentiation. MM biomarkers CTAG2, MAGEA6, CCND2, NEK2, and E2F2 were co-expressed in positively correlated modules to MM vital status, which was associated with MM's lower overall survival.

Ameliorative effects of hexane extract of Garcinia kola seeds Heckel (Clusiaceae) in cisplatin-induced hepatorenal toxicity in mice.

Garcinia kola seed is used to manage liver diseases in ethnomedicine. However, there is limited information on its role in Cisplatin (CIS)-induced toxicity. Here, we investigated the potential of hexane extract of Garcinia kola (HEGK) in lessening CIS-induced hepatorenal- and gene- toxicity. Male mice (22 ± 3 g) randomly assigned into groups (n = 5) were treated for five days: Corn oil only, HEGK (200 mg/kg), CIS (20 mg/kg; i.p; 48-hours), CIS + HEGK (100 mg/kg), CIS + HEGK (200 mg/kg), CIS + Quercetin (25 mg/kg), and Quercetin(25 mg/kg). Corn oil, HEGK, and Quercetin were administered daily by gavage. GC-MS revealed the presence of 9,19-Cyclolanost-24-en-3-ol as the most abundant component in HEGK, with an LC50 of 1023 µg/mL. HEGK significantly (p < 0.05) scavenged DPPH, inhibited lipid peroxidation and exhibited reducing activity dose-dependently. CIS treatment increased (p < 0.05) urinary albumin and creatinine by 18 and 56%, respectively, serum levels of total bilirubin, creatinine, and hepatic transaminases, while albumin decreased (p < 0.05) by 57%. CIS treatment increased renal and hepatic malondialdehyde (MDA) levels by 67 and 70% individually, while the activities of glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT) and reduced glutathione (GSH) levels were decreased (p < 0.05). Furthermore CIS-induced the formation of mononucleated polychromatic erythrocytes (mnPCEs) 150% in the bone marrow of mice. Histology revealed necrosis of hepatocytes, congestion of renal interstitial vessel, and hyperplasia of the Kupffer cells. Pretreatment with HEGK reduced the levels of MDA, mnPCEs, and increased the activities of antioxidant enzymes and restored GSH to levels comparable in control mice. Taken together, HEGK ameliorated CIS-toxicity via the activation of the antioxidative pathways and mitigated genotoxicity by mitigating mnPCEs formation in mice.

Differential miRNA Profiles Correlate With Disparate Immunity Outcomes Associated With Vaccine Immunization and Chlamydial Infection.

Vaccine-induced immune responses following immunization with promising Chlamydia vaccines protected experimental animals from Chlamydia-induced upper genital tract pathologies and infertility. In contrast, primary genital infection with live Chlamydia does not protect against these pathologies. We hypothesized that differential miRNA profiles induced in the upper genital tracts (UGT) of mice correlate with the disparate immunity vs. pathologic outcomes associated with vaccine immunization and chlamydial infection. Thus, miRNA expression profiles in the UGT of mice after Chlamydia infection (Live EB) and immunization with dendritic cell (DC)-based vaccine (DC vaccine) or VCG-based vaccine (VCG vaccine) were compared using the NanoString nCounter Mouse miRNA assay. Of the 602 miRNAs differentially expressed (DE) in the UGT of immunized and infected mice, we selected 58 with counts >100 and p-values < 0.05 for further analysis. Interestingly, vaccine immunization and Chlamydia infection induced the expression of distinct miRNA profiles with a higher proportion in vaccine-immunized compared to Chlamydia infected mice; DC vaccine (41), VCG vaccine (23), and Live EB (15). Hierarchical clustering analysis showed notable differences in the uniquely DE miRNAs for each experimental group, with DC vaccine showing the highest number (21 up-regulated, five down-regulated), VCG vaccine (two up-regulated, five down-regulated), and live EB (two up-regulated, four down-regulated). The DC vaccine-immunized group showed the highest number (21 up-regulated and five down-regulated compared to two up-regulated and four down-regulated in the live Chlamydia infected group). Pathway analysis showed that the DE miRNAs target genes that regulate several biological processes and functions associated with immune response and inflammation. These results suggest that the induction of differential miRNA expression plays a significant role in the disparate immunity outcomes associated with Chlamydia infection and vaccination.

Cerium oxide nanoparticles elicit antitumourigenic effect in experimental breast cancer induced by N-methyl-N-nitrosourea and benzo(a)pyrene in female Wistar rats.

The use of cerium oxide nanoparticles [CeO2 NPs] in the biomedical field has continued to gain prominence due to its potent antioxidant property. This study was designed to assess the antitumorigenic effect of CeO2 NPs in rats administered N-methyl-N-nitrosourea [NMU] and benzo(a)pyrene (BaP). Twenty four female Wistar rats were equally assigned into four groups and treated with normal saline (control), [NMU + BaP], [NMU + BaP+CeO2 NPs], and [NMU + BaP + vincristine]. Animals were pretreated with NMU and BaP three times (age 7, 10, and 13 weeks). Thereafter, vincristine and CeO2 NPs were administered twice and three times per week, respectively, for 13 weeks. Results showed that the administration of NMU and BaP increased serum nitric oxide [NO] and myeloperoxidase [MPO] by 220% and 132%, respectively, whereas the activities of aspartate and alanine aminotransferases and level of total bilirubin remained unchanged. Furthermore, mammary inflammatory [NO and MPO] and oxidative stress (LPO) markers were increased by 37%, 19%, and 24%, respectively. Mammary superoxide dismutase, catalase, reduced glutathione, and glutathione-S-transferase were significantly decreased in [NMU + BaP]-administered rats by 165%, 146%, 35%, and 36%, respectively. Immunohistochemistry showed downregulation of Bax, p53, and caspase-3, while histology revealed the presence of malignant epithelial cells with pyknotic nuclei and high nucleocytoplasm in [NMU + BaP]-administered rats. Treatment with CeO2 NPs attenuated oxidative stress, apoptosis, and inflammation and restored the cytoarchitecture of the tissue. Overall, CeO2 NPs show an antitumourigenic effect in experimental breast cancer by targeting pathways linked to inflammation and apoptosis.

Cerium Oxide Nanoparticles Attenuate Oxidative Stress and Inflammation in the Liver of Diethylnitrosamine-Treated Mice.

The catalytic activity of cerium oxide nanoparticles (CeO2NPs) is responsible for its application as an antitumor agent. This activity may be due to its ability to switch between III and IV oxidation states thereby conferring pro- and antioxidant properties. This study was designed to assess the hepatoprotective potential of CeO2NPs in male BALB/c mice administered diethylnitrosamine (DEN). Thirty-six mice were divided equally into six groups and treated intraperitoneally with normal saline (control), DEN (200 mg/kg) alone, CeO2NPs 1 (100 µg/kg) + DEN (200 mg/kg), CeO2NPs 2 (200 µg/kg) + DEN (200 mg/kg), CeO2NPs 1 alone, and CeO2NPs 2 alone. Animals were pretreated with CeO2NPs daily for eight consecutive days, while DEN was administered 48 h before the animals were sacrificed. Administration of DEN caused a significant increase in serum alanine aminotransferase (ALT) and urea by 51% and 96%, respectively. Markers of oxidative stress (malondialdehyde) and inflammation (nitric oxide and myeloperoxidase) in hepatic tissues of DEN-treated mice were increased by 60%, 16%, and 38%, respectively. The activities of hepatic superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, and level of reduced glutathione were significantly decreased in DEN-treated mice by 50%, 123%, 23%, 419%, and 78%, respectively. In addition, DEN increased the expression of hepatic Bcl2 and COX-2, while p53, Bax, and iNOS were mildly expressed. Pretreatment with CeO2NPs attenuated the activities of antioxidant enzymes and expression of Bcl2 and COX-2. Overall, CeO2NPs confers protection from DEN-induced liver damage via antioxidative activity.

P311, a novel intrinsically disordered protein, regulates adipocyte development.

Adipocyte development and adipose tissue expansion have many implications for human diseases, including obesity. Obesity is a debilitating disorder and a risk factor for metabolic disorders including insulin resistance and diabetes mellitus, due in part to an overabundance of adipocytes and adipocyte dysfunction. In recent years, obesity has become a global pandemic with approximately one-third of US adults classified as obese. Adipose tissue has recently been identified as a major metabolic organ, classified into white adipose tissue (WAT) and brown adipose tissue (BAT). Other than lifestyle modifications and invasive surgeries, only a very limited number of drugs are available to treat obesity and overweight. P311 has been shown to play a key role in blood pressure regulation, vascular contractility and tissue remodeling. Here we present a role for P311 in adipogenesis using a 3T3-L1 cell culture model. P311 expression is initiated with the induction of adipogenesis and increased during adipogenesis. This increase correlates with an increase in the expression of the key adipogenic transcriptional factors PPARγ2 and C/EBPα. In addition, siRNA-mediated P311 knockdown inhibits adipogenic differentiation in 3T3-L1 cells. Finally, P311 binds to the PPARγ2 promoter, implicating P311 mediates adipogenesis partly through PPARγ activation.

First-line antituberculosis drugs disrupt endocrine balance and induce ovarian and uterine oxidative stress in rats.

BACKGROUND: The first-line antituberculosis (anti-TB) drugs, isoniazid (INH), rifampicin (RIF), ethambutol (EMB), and pyrazinamide (PZA), are effective in the treatment of pulmonary tuberculosis. However, the toxicity of these drugs in the clinical setting limits their use. Here, we evaluated the effects of anti-TB drugs on the reproductive system in female rats. METHODS: Thirty-five female Wistar rats were assigned into five groups of seven animals each. The control group received normal saline, whereas others received INH (5 mg/kg), RIF (10 mg/kg), EMB (15 mg/kg), and PZA (15 mg/kg) through gavage thrice a week for 8 consecutive weeks. RESULTS: Administration of anti-TB drugs significantly (p<0.05) reduced uterine and ovarian weight, as well as the relative weight of the uterus when compared with controls. In addition, anti-TB drugs increased the activities of alanine aminotransferase as well as the level of total bilirubin. Treatment with INH, RIF, and PZA significantly (p<0.05) reduced the levels of follicle-stimulating and luteinizing hormones, estrogen, and prolactin. The INH, RIF, EMB, and PZA caused significant (p<0.05) increases in uterine malondialdehyde (MDA) levels by 281%, 214%, 273% and 190%, respectively, whereas INH and EMB increased the ovarian malondialdehyde by 111% and 129%, respectively. These drugs significantly (p<0.05) decreased the activities of ovarian glutathione-S-transferase and uterine glutathione peroxidase, superoxide dismutase, and catalase. Histology revealed the erosion of uterine mucosa, debris in the lumen of the uterus, congestion, and underdeveloped follicles in ovaries. CONCLUSIONS: The first-line anti-TB drugs elicited reproductive toxicity in the uterus and ovaries of rats through mechanisms that involved oxidative stress.

Biflavonoid fraction from Garcinia kola seed ameliorates hormonal imbalance and testicular oxidative damage by anti-tuberculosis drugs in Wistar rats.

BACKGROUND: Tuberculosis (TB) is a global health problem. The effects of anti-TB drugs on male reproductive system have not been properly evaluated. We investigated the effects of anti-TB drugs on testicular antioxidant indices, sperm characteristics and hormonal levels in rats, and the protective role of kolaviron (KV), a biflavonoid from Garcinia kola seed. METHODS: Twenty-eight male Wistar rats were assigned into four groups and orally treated with corn oil (control), anti-TB drugs [4-Tabs=isoniazid (5 mg/kg), rifampicin (10 mg/kg), pyrazinamide (15 mg/kg) and ethambutol (15 mg/kg) in combination], anti-TB drugs +KV and KV alone (200 mg/kg). Anti-TB drugs and KV were given three times per week for 8 weeks. In vitro, reducing power, inhibition of lipid peroxidation (LPO), diphenyl-1-picrylhydrazyl (DPPH) and hydroxyl radical scavenging effects of KV were examined. RESULTS: KV at 10, 20, 50 and 100 µg/mL showed strong reducing potential and effectively scavenged DPPH and OH radicals in a concentration-dependent manner. Furthermore, KV significantly inhibited LPO in rats' liver homogenate. In vivo, administration of 4-Tabs caused a significant (p<0.05) decrease in body weight gain and weight of testis of rats. Body weight gain and weight of testis decreased by 45% and 36%, respectively, in the 4-Tabs-treated rats. Also, 4-Tabs increased testicular lipid peroxidation by 82%, with a concomitant decrease in antioxidant indices. Testicular reduced glutathione, superoxide dismutase and glutathione peroxidase decreased by 2.2-, 1.9- and 1.6-folds, respectively. Likewise, 4-Tabs markedly decreased sperm count, motility, luteinizing hormone and testosterone. Co-administration of KV with 4-Tabs normalized body weight, enhanced antioxidant system and improved sperm characteristics. CONCLUSIONS: Kolaviron protects male reproductive system from oxidative damage by anti-tuberculosis drugs via the antioxidative mechanism.

Antimalarial, hematological, and antioxidant effects of methanolic extract of Terminalia avicennioides in Plasmodium berghei-infected mice.

Terminalia avicennioides Guill. & Perr. (Combretaceae) is used traditionally to treat malaria in Nigeria. To establish its efficacy, methanolic extract of T. avicennioides bark was investigated for antimalarial activity against Plasmodium berghei (NK-65) in mice. Twenty-five mice in five groups were used for this study. Group 1 was uninfected normal control. Twenty mice infected with P. berghei were grouped as untreated negative control (group 2), 5 mg/kg b.w. p.o. artesunate-treated positive control (group 3), and 100 and 200 mg/kg b.w. p.o. T. avicennioides-treated infected mice (groups 4 and 5, respectively). Four-day suppressive effects on P. berghei and hematological and oxidative statuses of the mice were assessed. Suppression of parasitemia by artesunate and methanolic extract of T. avicennioides (at 100 and 200 mg/kg b.w.) after 1 day of treatment was 10, 18, and 11% respectively; at day 5, the level of suppression was 77, 82, and 84% respectively. P. berghei infection decreased hemoglobin, red blood cell, and lymphocyte counts and increased neutrophil count; artesunate and medicinal plant treatment restored these parameters to normal control levels. Also, artesunate and medicinal plant treatment of infected mice significantly (p < 0.05) increased serum and liver superoxide dismutase activities and significantly (p < 0.05) reduced serum malondialdehyde concentration compared to untreated infected mice. The antimalarial effect of T. avicennioides is comparable to that of artesunate. The restoration of oxidative and hematological statuses, to normal values by T. avicennioides, may provide better protection against the malaria severity and complications.