Reversible central respiratory events induced by valproic acid treatment: A case report.

Valproic acid holds a prominent position as the primary therapeutic option for epilepsy cases. The utilization of antiepileptic agents like valproic acid has been linked to disturbances in sleep architecture. Although scant, there exists a subset of studies that allude to the potential manifestation of sleep apnea as an adverse effect of valproic acid administration. In this context, we present a case report of a 76-year-old man with a past medical history of arterial hypertension, atrial fibrillation, and obstructive sleep apnea syndrome treated with continuous positive airway pressure since 2020. Following the commencement of valproic acid treatment for vascular epilepsy, obstructive sleep apnea evolved toward to central sleep apnea. This case exemplifies the need for a heightened awareness of the multifaceted implications of valproic acid therapy on sleep patterns.

Anesthetic Management of Cesarean Section in the Case of a Sextuplet Pregnancy and Polycystic Ovarian Syndrome.

Cesarean section in a mother with a sextuplet pregnancy is challenging for an anesthesiologist. Several perioperative complications are likely because of the overdistended uterus and associated changes in the mother. We are reporting the case of a woman with a sextuplet pregnancy who came for an emergency cesarean. She also had a background history of polycystic ovarian syndrome (PCOS) and ovulation induction for conception. Early pregnancy was complicated by ovarian hyperstimulation syndrome. She required cervical cerclage in early pregnancy. The emergency cesarean was done as she went into preterm labor and six premature babies were delivered at 29 weeks of gestation. Cesarean was done under spinal anesthesia. Preeclampsia and postpartum hemorrhage complicated the perioperative period.

The protective effects of sesamol and/or the probiotic, Lactobacillus rhamnosus, against aluminum chloride-induced neurotoxicity and hepatotoxicity in rats: Modulation of Wnt/ß-catenin/GSK-3ß, JAK-2/STAT-3, PPAR-γ, inflammatory, and apoptotic pathways.

Introduction: Aluminium (Al) is accumulated in the brain causing neurotoxicity and neurodegenerative disease like Alzheimer's disease (AD), multiple sclerosis, autism and epilepsy. Hence, attenuation of Al-induced neurotoxicity has become a "hot topic" in looking for an intervention that slow down the progression of neurodegenerative diseases. Objective: Our study aims to introduce a new strategy for hampering aluminum chloride (AlCl3)-induced neurotoxicity using a combination of sesamol with the probiotic bacteria; Lactobacillus rhamnosus (L. rhamnosus) and also to test their possible ameliorative effects on AlCl3-induced hepatotoxicity. Methods: Sprague-Dawley male rats were randomly divided into five groups (n = 10/group) which are control, AlCl3, AlCl3 + Sesamol, AlCl3 + L. rhamnosus and AlCl3 + Sesamol + L. rhamnosus. We surveilled the behavioral, biochemical, and histopathological alterations centrally in the brain and peripherally in liver. Results: This work revealed that the combined therapy of sesamol and L. rhamnosus produced marked reduction in brain amyloid-ß, p-tau, GSK-3ß, inflammatory and apoptotic biomarkers, along with marked elevation in brain free ß-catenin and Wnt3a, compared to AlCl3-intoxicated rats. Also, the combined therapy exerted pronounced reduction in hepatic expressions of JAK-2/STAT-3, inflammatory (TNF-α, IL-6, NF-κB), fibrotic (MMP-2, TIMP-1, α-SMA) and apoptotic markers, (caspase-3), together with marked elevation in hepatic PPAR-γ expression, compared to AlCl3 -intoxicated rats. Behavioral and histopathological assessments substantiated the efficiency of this combined regimen in halting the effect of neurotoxicity. Discussion: Probiotics can be used as an add-on therapy with sesamol ameliorate AlCl3 -mediated neurotoxicity and hepatotoxicity.

E-cigarette dependence in former smoker: A Tunisian survey.

INTRODUCTION: Since its appearance, E-cigarette (EC) has experienced a strong craze among those seeking to reduce their conventional cigarette (CC) consumption. AIM: This study aimed to compare EC to CC addictive power in actual users of EC and former smokers of CC. METHODS: We conducted a comparative cross-sectional study including 65 EC users and former smokers. They were collected on Facebook using a questionnaire including Fagrestrom score (FS). RESULTS: The average total of FS was estimated at 3.45 ± 2 with EC vs 3.89±2.45 with CC (p=0.04). The dependence on the EC was strong in 8%, average in 25%, and weak in 35% of cases. The predictive factors of a medium to high dependence on EC were the duration of its consumption (p=0.008) and the daily quantity of e-liquid (p=0.009). The presence of medical history was inversely correlated with EC addiction. The duration of EC use was the only independent factor of dependence with an OR of 4.25 IC95% [1.019-17.729]. EC users continued to smoke TC in 68% of cases. CONCLUSION: Our study shows that even if it remains less important than that of CC, the dependence on EC is not negligible.

The protective effect of thymoquinone or/and thymol against monosodium glutamate-induced attention-deficit/hyperactivity disorder (ADHD)-like behavior in rats: Modulation of Nrf2/HO-1, TLR4/NF-κB/NLRP3/caspase-1 and Wnt/ß-Catenin signaling pathways in rat model.

Both thymoquinone (TQ) and thymol (T) have been proved to possess a positive impact on human health. In this research, we aimed to investigate the effect of these compounds separately and together on the Attention-deficit/hyperactivity disorder (ADHD)-like behavior induced by monosodium glutamate (MSG) in rats. Forty male, Spargue Dawley rat pups (postnatal day 21), were randomly allocated into five groups: Normal saline (NS), MSG, MSG+TQ, MSG+T, and MSG+TQ+T. MSG (0.4 mg/kg/day), TQ (10 mg/kg/day) and T (30 mg/kg/day) were orally administered for 8 weeks. The behavioral tests proved that rats treated with TQ and/or T showed improved locomotor, attention and cognitive functions compared to the MSG group with more pronounced effect displayed with their combination. All treated groups showed improvement in MSG-induced aberrations in brain levels of GSH, IL-1ß, TNF-α, GFAP, glutamate, calcium, dopamine, norepinephrine, Wnt3a, ß-Catenin and BDNF. TQ and/or T treatment also enhanced the mRNA expression of Nrf2, HO-1 and Bcl2 while reducing the protein expression of TLR4, NFκB, NLRP3, caspase 1, Bax, AIF and GSK3ß as compared to the MSG group. However, the combined therapy showed more significant effects in all measured parameters. All of these findings were further confirmed by the histopathological examinations. Current results concluded that the combined therapy of TQ and T had higher protective effects than their individual supplementations against MSG-induced ADHD-like behavior in rats.

Yellow nail syndrome: a genetic Disorder?

BACKGROUND: Yellow nail syndrome is a very rare disorder. The classic clinical presentation includes a triad involving yellow nail discoloration, chronic pulmonary manifestations and lower limb lymphedema. Its etiology remains unknown and the genetic disorder is still controversial. OBSERVATION: We report a case of a young man diagnosed with this syndrome and for who the same affection was found in several members of his family Conclusion: The diagnosis of yellow nail syndrome in several members of the same family supports the fact that it is a genetic disorder.

The impact of pharmacist telephone calls after discharge on satisfaction of oncology patients: A randomized controlled study.

Purpose The aim of the study was to determine the impact of telephone follow-up calls on satisfaction in oncology patients after hospital discharge. Method A randomized controlled study, in which patients were randomized into two groups: The experimental group with the telephone follow-up (TFU) calls (intervention) and the control group (no intervention). The telephone follow-up call was conducted within 72 h after discharge. During the call, patients were asked about their medications, namely, whether they received them, understood how to take them, and whether they developed any medication-related adverse effect. Both groups were contacted by phone two weeks later to assess their satisfaction with the discharge medication instructions and the provided pharmaceutical services, using the 5-point Likert scale. In addition, hospital records were reviewed for emergency room visits and hospital readmissions within 30 days after discharge. Results There was no difference in the percentage of patients who reported being very satisfied between both the intervention and the control groups (45% intervention vs. 48% control, P = 0.68). The mean time of the intervention phone call was 3 ± 1.7 (SD) min. During the telephone follow-up call, medication-related problems were identified in 20% of the patients. There was no significant difference in emergency room visits and hospital readmissions in the intervention group vs. control (44% vs. 53%, P = 0.123) and (37% vs. 43%, P = 0.317), respectively. Conclusion Telephone follow-up calls conducted by a pharmacist to discharged oncology patients did not improve patients' satisfaction, emergency room visits or hospital readmissions; however, they helped to identify medication-related adverse effects in the oncology patients.

Serum biomarkers for early detection of hepatocellular carcinoma associated with HCV infection in egyptian patients.

BACKGROUND: Early detection of hepatocellular carcinoma using serological markers with better sensitivity and specificity than alpha fetoprotein (AFP) is needed. AIMS: The aim of this study was to evaluate the diagnostic value of serum sICAM-1, ß-catenin, IL-8, proteasome and sTNFR-II in early detection of HCC. MATERIALS AND METHODS: Serum levels of IL-8, sICAM-1, sTNFR-II, proteasome and ß-catenin were measured by ELISA assay in 479 serum samples from 192 patients with HCC, 96 patients with liver cirrhosis (LC), 96 patients with chronic hepatitis C (CHC) and 95 healthy controls. RESULTS: Serum levels of proteasome, sICAM-1, ß-catenin and αFP were significantly elevated in HCC group compared to other groups (P-value<0.001), where serum level of IL-8 was significantly elevated in the LC and HCC groups compared to CHC and control groups (P-value <0.001), while no significant difference was noticed in patients with HCC and LC (P-value=0.09). Serum level of sTNFR- II was significantly elevated in patients with LC compared to HCC, CHC and control groups (P-value <0.001); also it was significantly higher in HCC compared to CHC and control groups (P-value <0.001). ROC curve analysis of the studied markers between HCC and other groups revealed that the serum level of proteasome had sensitivity of 75.9% and specificity of 73.4% at a cut-off value of 0.32 µg/ml with AUC 0.803 sICAM-1 at cut off value of 778ng/ml, the sensitivity was 75.8% and the specificity was 71.8% with AUC 0.776. ß-catenin had sensitivity and specificity of 70% and 68.6% respectively at a cut off value of 8.75ng/ml with an AUC of 0.729. sTNFR-II showed sensitivity of 86.3% and specificity of 51.8% at a cut off value of 6239.5pg/ml with an AUC of 0.722. IL-8 had sensitivity of 70.4% and specificity of 52.3% at a cut off value of 51.5pg/ml with AUC 0.631. CONCLUSIONS: Our data supported the role of proteasome, sICAM-1, sTNFR-II and ß-catenin in early detection of HCC. Also, using this panel of serological markers in combination with αFP may offer improved diagnostic performance over αFP alone in the early detection of HCC.

Disease progression from chronic hepatitis C to cirrhosis and hepatocellular carcinoma is associated with increasing DNA promoter methylation.

BACKGROUND: Changes in DNA methylation patterns are believed to be early events in hepatocarcinogenesis. A better understanding of methylation states and how they correlate with disease progression will aid in finding potential strategies for early detection of HCC. The aim of our study was to analyze the methylation frequency of tumor suppressor genes, P14, P15, and P73, and a mismatch repair gene (O6MGMT) in HCV related chronic liver disease and HCC to identify candidate epigenetic biomarkers for HCC prediction. MATERIALS AND METHODS: 516 Egyptian patients with HCV-related liver disease were recruited from Kasr Alaini multidisciplinary HCC clinic from April 2010 to January 2012. Subjects were divided into 4 different clinically defined groups - HCC group (n=208), liver cirrhosis group (n=108), chronic hepatitis C group (n=100), and control group (n=100) - to analyze the methylation status of the target genes in patient plasma using EpiTect Methyl qPCR Array technology. Methylation was considered to be hypermethylated if >10% and/or intermediately methylated if >60%. RESULTS: In our series, a significant difference in the hypermethylation status of all studied genes was noted within the different stages of chronic liver disease and ultimately HCC. Hypermethylation of the P14 gene was detected in 100/208 (48.1%), 52/108 (48.1%), 16/100 (16%) and 8/100 (8%) among HCC, liver cirrhosis, chronic hepatitis and control groups, respectively, with a statistically significant difference between the studied groups (p-value 0.008). We also detected P15 hypermethylation in 92/208 (44.2%), 36/108 (33.3%), 20/100 (20%) and 4/100 (4%) , respectively (p-value 0.006). In addition, hypermethylation of P73 was detected in 136/208 (65.4%), 72/108 (66.7%), 32/100 (32%) and 4/100 (4%) (p-value <0.001). Also, we detected O6MGMT hypermethylation in 84/208 (40.4%), 60/108 (55.3%), 20/100 (20%) and 4/100 (4%), respectively (p value <0.001. CONCLUSIONS: The epigenetic changes observed in this study indicate that HCC tumors exhibit specific DNA methylation signatures with potential clinical applications in diagnosis and prognosis. In addition, methylation frequency could be used to monitor whether a patient with chronic hepatitis C is likely to progress to liver cirrhosis or even HCC. We can conclude that methylation processes are not just early events in hepatocarcinogenesis but accumulate with progression to cancer.

Gene expression profiling of non-hodgkin lymphomas.

BACKGROUND: Chromosomal translocations are genetic aberrations associated with specific non-Hodgkin lymphoma (NHL) subtypes. This study investigated the differential gene expression profile of Egyptian NHL cases based on a microarray approach. MATERIALS AND METHODS: The study included tissue samples from 40 NHL patients and 20 normal lymph nodes used as controls. Total RNA was extracted and used for cDNA microarray assays. The quantitative real time polymerase chain reaction was used to identify the aberrantly expressed genes in cancer. RESULTS: Significant associations of 8 up-regulated and 4 down-regulated genes with NHL were observed. Aberrant expression of a new group of genes not reported previously was apparent, including down-regulated NAG14 protein, 3 beta hydroxy-delta 5-c27 steroid oxi-reductase, oxi-glutarate dehydrogenase (lipo-amide), immunoglobulin lambda like polypeptide 3, protein kinase x linked, Hmt1, and caveolin 2 Tetra protein. The up-regulated genes were Rb binding protein 5, DKFZP586J1624 protein, protein kinase inhibitor gamma, zinc finger protein 3, choline ethanolamine phospho-transferase CEPT1, protein phosphatase, and histone deacetylase-3. CONCLUSIONS: This study revealed that new differentially expressed genes that may be markers for NHL patients and individuals who are at high risk for cancer development.

Do desipramine [10,11-dihydro-5-[3-(methylamino) propyl]-5H-dibenz[b,f]azepine monohydrochloride] and fluoxetine [N-methyl-3-phenyl-3-[4-(trifluoromethyl)phenoxy]-propan-1-amine] ameliorate the extent of colonic damage induced by acetic acid in rats?

The present study was designed to compare the anti-inflammatory and antioxidant effects of two antidepressant drugs, desipramine [10,11-dihydro-5-[3-(methylamino) propyl]-5H-dibenz-[b,f]azepine monohydrochloride] and fluoxetine [N-methyl-3-phenyl-3-[4-(trifluoromethyl)phenoxy]-propan-1-amine], administered with variable doses, on experimentally induced colitis in rats. Two doses for each drug (10 and 20 mg/kg/day i.p.) were injected in 48 adult male albino rats for 2 weeks after induction of colitis by intracolonic administration of 2 ml of 3% acetic acid. Several parameters, including macroscopic (ulcer score index) and biochemical such as myeloperoxidase (MPO), reduced glutathione (GSH), tumor necrosis factor (TNF)-alpha, and interleukin (IL)-1beta, were measured using standard assay procedures. The study demonstrates that both desipramine and fluoxetine significantly attenuated the extent and the severity of the macroscopic signs of cell damage. Both drugs significantly reduced tissue MPO activity in a dose-dependent manner. Both desipramine and fluoxetine, at either dose, significantly increased GSH in colonic tissue. Desipramine and fluoxetine, at either dose, significantly reduced TNF-alpha and IL-beta. Desipramine at the dose of 20 mg/kg produced more decrease in the level of TNF-alpha compared with the effect of the smaller dose, but fluoxetine at 10 mg/kg diminished more in the level of IL-1beta compared with the effect of the larger dose. The present data indicate that both desipramine and fluoxetine have anti-inflammatory and antioxidants effects in experimentally induced colitis in rats, opening the avenue to their possible protective role in patients with inflammatory bowel disease.