Background: Sodium Benzoate (SB) significantly improved positive, negative, and cognitive symptoms as add on treatment in schizophrenia. Olanzapine (Ola), the most effective atypical antipsychotic drug, has been linked to hepatic steatosis, acute kidney injury, reproductive side effects and poor effect on negative symptoms in some patients.

Goals: is to compare the efficacy and check the safety of long-term monotherapy with SB 0.01 mg/Kg versus Ola on male cognitive, memory, hepatic, renal and testicular functions in rat model of schizophrenia.

Methods: 48 young adult male rats were divided into 6 groups; C: control; O: received Ola; SB: received SB; K: received single IP ketamine (Ket) injection; K+O: received Ola and Ket and K+SB: received SB and Ket. Ola and SB given orally for 3 or 10 weeks for behavioral or serological studies respectively. We measured activities of daily life (ADL), spatial learning and memory in radial arm water maze (RAWM), serum parameters of hepatic, renal and testicular functions.

Results: Both Ola and SB significantly improved hoarding and burrowing, caused significant decrease in time to reach target (TRT), working memory errors (WME) in K+O and K+SB groups compared to K group. Ola caused significant increase in ALT, AST and creatinine and decrease in serum LH, testosterone compared to controls. SB caused significant rise in serum LH, ALT, AST and decrease in protein and albumin compared to both C and O groups.

Conclusion: Both Ola and SB improved ADL, cognitive and memory functions. Although SB saved testicular and renal functions, it worsened liver function compared to Ola.

Background: Skeletal muscle injuries with subsequent bleeding is common cause of death on both sports and battle grounds. Application and removal of tourniquet is fast intervention to control hemorrhage resulting ischemia reperfusion (IR) injury. The effect of IR in skeletal muscle is far more severe compared to other body tissues because of the devastating systemic complication. Garlic has beneficial effects in IR of various organs. However, using garlic in IR of skeletal muscle is deficient Goals: To investigate the possible protective effect of garlic in rat model of hind limb IR and its possible mechanisms of action.

Methods: Fifty adult male rats divided into five groups; C: control, IR: ischemia/reperfusion group subjected to 2 hours ischemia followed by 2 hours reperfusion (2/2 hr IR) and three garlic treated groups; G1+IR: 24 hr before I/R, G2+IR: 30 min before IR and G3+IR: immediately before reperfusion. We measured wet to dry weight ratio (W/D) of gastrocnemius muscle, serum creatine kinase (CK), Interleukin 1β (IL-1β), Interleukin-10 (IL-10), gastrocnemius caspase-3 and desmin expression and histopathological damage score.

Results: Garlic treatment caused significant decrease in W/D, serum CK, IL-1β, caspase-3 expression and significant increase in IL-10 as well as desmin expression when compared to IR group. Garlic ameliorated IR-induced histopathological damage and significantly reduced the apoptosis score. Better results obtained with earlier administration before IR.

Conclusion: Garlic protected against IR-induced skeletal muscle damage through reducing inflammation, apoptosis score and elevating desmin expression. We recommend the earlier use of garlic as prophylactic natural medicine in skeletal muscle IR.

Background: Impaired cognitive flexibility is the core manifestation of schizophrenia (SZ). Previous literature raised a claim against the effect of atypical antipsychotic drugs (AAD) on cognitive and executive functions whose cause needs further investigation. Attention set-shifting task (ASST) tests the prefrontal cortex's (PFC) executive and flexibility functions.

Goals: To examine Olanzapine (OLZ) effect on ASST, expression of N-methyl-D-aspartate receptor 1 (NMDR-NR1) in prefrontal cortex (PFC), and metabolic comorbidity in ketamine (KET) model of SZ.

Methods: Sixty-two male rats were divided into three groups: 8 for ASST and 30 for open field, ELISA and immunohistochemistry sub-chronic study, and 24 for regular serological and histopathological examination. Rats treated with V: vehicle; K: KET and KO: OLZ plus KET.

Results: KET caused significant increase in time, trials, and errors to reach criterion. OLZ co-administration reversed effects of KET in ASST with no reduction of locomotor activity. OLZ normalized KET-induced rise of NR1 expression and protected against KET-induced degenerative changes in hippocampus and PFC. Significant increase in serum liver enzymes, total bilirubin, and lipids with chronic compared to sub-chronic OLZ administration. In contrast, insignificant difference between sub-chronic OLZ and vehicle was found.

Conclusions: Current study demonstrated the efficacy of OLZ to reverse KET-induced cognitive deficits in ASST with neither reduction in NR1 expression in PFC nor metabolic malfunction in the sub-chronic study. It also showed the protective effect of OLZ on KET induced neuronal degeneration and necrosis. We suggest that chronic OLZ treatment-induced-metabolic malfunction might be the cause of time-dependent cognitive deterioration.

Keywords: N methyl-D-aspartate receptors (NMDARs); Schizophrenia; attention set shifting task (ASST); ketamine (KET); olanzapine (OLZ).

Backgrounds: Impaired sleep is independent risk factor of neurodegeneration and dementia. Chronic insomnia impairs melatonin (MEL) production that is directly proportionate to its duration. The underlying mechanisms linking sleep loss to dementia and the possible therapeutic effect of melatonin have not been fully elucidated. Previous research showed great controversy concerning the effects of paradoxical sleep deprivation (PSD) on body weight, serum lipoproteins, and inflammatory cytokines.

Goals: To examine the effect of chronic paradoxical sleep deprivation (PSD) with and without MEL supplementation on memory using RAWM, parameters of metabolic syndrome (MS), liver enzymes, serum cortisol, and inflammatory cytokines as well as liver, colon, and brain histopathology.

Methods: Forty rats were divided into four groups ten animals each; C: control, G: grid group, SD: sleep deprivation group, and SD+MEL sleep deprivation treated with melatonin.

Results: MEL supplementation reversed PSD-induced memory deficits (P<0.05), the elevation of serum cortisol (P<0.001), glucose (P<0.05), ALT (P<0.05), AST (P<0.001), TNF-alpha (P<0.001), IL-10 (P<0.01) and improved colon, liver, and brain architecture. Melatonin reduced body weight (P<0.05), total cholesterol, LDL-c, and triglycerides as well as increased HDL-c (P<0.001).

Conclusion: MEL has a protective effect against chronic PSD-induced metabolic malfunction and cognitive deterioration by reducing stress, improving immunity, and maintaining colonic wall integrity.

Maternal diabetes is considered one of the most common causes of defective growth of the fetus. Polyunsaturated fatty acids (PUFAs) help prevent alloxan-induced type 1 diabetes mellitus (type 1 DM). It was found that arachidonic acid (AA) is the most successful PUFA in preventing rats from developing type 1 diabetes brought on by alloxan. The aim of this work is to investigate the effects of maternal diabetes on the prenatal development of rat vertebral columns and the probable protecting role of arachidonic acid. Randomly selected pregnant rats were divided into four groups: control, alloxan-induced diabetes group (150 mg/kg), alloxan + arachidonic acid group (55μg/kg, followed by alloxan injection), and arachidonic acid group (arachidonic acid only). The female pregnant rats were sacrificed at the gestational days 15, 17 and 19. The fetuses were collected and subjected to morphometric analysis. The lumbar vertebrae and the sacrum were removed and managed for light and electron microscopic examination. In the alloxan-induced diabetic group, the offspring exhibited a significant drop in all body measurements. Histologic examination of lumbar and sacral vertebrae in the offspring of the alloxan-induced diabetic group showed delayed chondrification and ossification. Electron microscopic examination of reserve cell of the alloxan-induced diabetic group of the 19-day-old albino rat fetus shows shrinkage of the cell with irregular outline and cytoplasmic vacuolations. In the alloxan + arachidonic acid group, the morphometric measurements of the offspring and the histological picture of their lumbar and sacral vertebrae were more or less similar to the control group.

Keywords:
Diabetes, Vertebral Column, Arachidonic Acid.

Monosodium glutamate (MSG) is a worldwide food flavour enhancer commonly used by the food industry. This feed additive may cause male infertility. Nigella sativa seeds (NSS) is a widely used in herbal medicine as it has many biological benefits and could provide a solution. This work was designed to investigate the histological effects of NSS on rats ingesting MSG. To achieve this aim, adult male albino rats (2- 3 months old) were randomly and equally assigned into three experimental groups. For a period of 21 days, control group received no treatment, MSG group received MSG as 30 g/kg feed, and MSG + NSS group received MSG as 30 g/kg feed and NSS as 30 g/kg feed. Seminal vesicle histopathology in MSG group showed mild seminal vesiculitis with degeneration of smooth muscle fibers in tunica muscularis. In addition, there was an increase in the amount of connective tissue and apoptotic cells count. Periodic Acid Schiff stain indicated irregular and interrupted epithelial basement membranes. Glutathione reductase (GR), superoxide dismutase 2 (SOD2), and caspase-3 immuno-expressions increased in MSG group. It was found that there was an increase in the number of apoptotic cells, intraepithelial lymphocytes and dendritic cells in MSG group. However, treatment with NSS ameliorated these disturbances. NSS mitigated MSG-induced seminal vesicle damage by its histoprotective, cytoprotective and anti-apoptotic activities.

KEYWORDS
Monosodium glutamate, Nigella sativa seeds, Seminal vesicle, Apoptotic cells, Seminal vesiculitis, Dendritic cells, Lymphocytes.

Background

Despite the growing interest in dexmedetomidine as an adjunct to truncal blocks, little is known about the systemic absorption of dexmedetomidine after these blocks and its role in analgesia and in hemodynamics.

Objective

We investigated the pharmacokinetics and pharmacodynamics of dexmedetomidine as an adjunct to transversus abdominis plane (TAP) block in patients undergoing lower abdominal cancer surgery.

Methods

Twenty-four adult patients were randomized to receive a bilateral single-injection TAP block before surgery with 20 mL of bupivacaine 0.5% (TAP group, n = 12) or combined with 1 µg/kg dexmedetomidine (TAP-DEX group, n = 12) and diluted with saline to a volume of 40 mL (20 mL on each side). Plasma concentrations of dexmedetomidine and its pharmacokinetics were investigated using non-compartmental methods, postoperative analgesia, hemodynamics, and adverse