International journal of physiology, pathophysiology and pharmacology最新文献

Background: Sleep disorders can significantly impair the quality of life and daily functions. Evaluating sleep quality can provide valuable information about working conditions. This study aims to evaluate the sleep quality of faculty members at Isfahan University of Medical Sciences (IUMS).

Methods: This descriptive-analytic study was conducted from 2020 to 2021, involving 106 faculty members from the medical school. A questionnaire collected demographic information, including age, sex, height, weight, body mass index (BMI), level of education, history of faculty membership, major, working hours during the day and night, residency place, and medical history. The Pittsburgh Sleep Quality Index (PSQI) and Symptom Checklist-25 (SCL-25) questionnaire were used to assess participants' sleep quality. Data were compared between clinicians and basic science faculty members.

Results: PSQI subtypes were examined among the participants. The total PSQI score was 6.20±3.4. A comparison of PSQI scores and subtypes based on age categories did not show any significant differences (P > 0.05 for all). Clinicians had significantly lower total PSQI scores (P=0.044), sleep latency (P=0.024), sleep disturbances (P=0.012), and daytime dysfunction (P=0.022). Additionally, clinicians had a lower severity of sleep latency (P=0.024), sleep disturbances (P=0.012), and total PSQI score (P=0.044). However, clinicians exhibited a higher intensity of daytime dysfunction (P=0.022).

Conclusion: Faculty members exhibited a high prevalence of sleep disorders, with the most common disorders being sleep disturbance and high sleep latency. The prevalence of sleep disorders was higher among basic science faculty members compared to clinicians.

Obstructive sleep apnea (OSA) is a sleep disorder of significant health concern with a high prevalence in the general population. It has been found to exhibit a high incidence of comorbidity with epilepsy, the exact underlying pathophysiology of which still remains poorly understood. OSA is characterized by apnea/hypopnea spells and arousals, leading to intermittent hypoxemia and sleep deprivation. Both sleep deprivation and hypoxemia adversely affect the cortical excitability and favor epileptogenesis and worsening of pre-existing epilepsy, if any. In patients with OSA, deprivation of rapid eye movement sleep (REMS) phase (known for its strong antiepileptic influence) is relatively more than that non rapid eye movement sleep phase leading to postulation of REMS deprivation as a significant factor in the development of epilepsy as a comorbidity in patients with OSA. Furthermore, OSA and epilepsy both have shown to exercise a bidirectional influence on one another and are also likely to exacerbate each other through a positive feedback mechanism. This is especially based on the reports of improved control of epilepsy upon treatment of comorbid OSA. This brief paper attempts to present an underlying pathophysiological basis of the comorbidity of OSA and epilepsy based upon sleep deprivation and hypoxemia that are characteristic features observed in patients with OSA.

There is conflicting data regarding the ability of nitric oxide (NO) to promote or inhibit colorectal cancer cell proliferation. Furthermore, NO reacts rapidly with endogenous superoxide at a diffusion-controlled rate to give peroxynitrite (ONOO^-), a strong oxidant and nitrating agent. The aim of this study was to assess the effects of exogenous NO and ONOO^- on the proliferation of the colorectal cancer cell line Caco-2. NOR5 and SIN-1 were used as NO and ONOO^- donors, respectively. Both NOR5 and SIN-1 inhibited the proliferation of the Caco-2 cells; however, the effect of NOR5 was slightly stronger than that of SIN-1. The results also indicated that NO plays a major role in the inhibition of SIN-1-induced proliferation of Caco-2 cells. The results of a terminal deoxynucleotidyl transferase dUTP nick end labeling assay, cell cycle analysis, and p21 protein expression measurement further indicated that NO induced S-G₂/M phase arrest, but not apoptosis, in the Caco-2 cells. The results suggest that NO, rather than ONOO^-, has the potential to repress the proliferation of Caco-2 cells by inducing S-G₂/M cell cycle arrest.

Alcohol consumption afflicts men and women differently. However, the underlying neuronal mechanisms that contribute to the difference are mostly unexplored. Although more men suffer from alcohol use disorders (AUD), women more frequently accelerate to dependence and develop adverse consequences of alcoholism sooner than men. Women also exhibit more significant negative emotions that cues more reactivity and alcohol-craving than men. Despite ample evidence that women are vulnerable to AUD, results of preclinical studies on sex differences in alcohol consumption and withdrawal-related behaviors are inconclusive. In this study, we trained adult male and female Sprague-Dawley rats to drink alcohol in the intermittent access to 20% ethanol two-bottle free-choice paradigm for two months. Their behaviors and Fos expression in related brain regions were measured at acute (24 h) and after prolonged (28 days) abstinence. We found that female rats drank more alcohol than males. After acute abstinence, rats of both sexes showed higher sensitivity to depressive, thermal, and mechanical stimuli. Females also displayed higher anxiety levels. After prolonged abstinence, rats of both sexes displayed depressive-like behaviors; the males displayed allodynia; the females showed higher anxiety levels and drank more alcohol upon reaccess to alcohol. Furthermore, during acute withdrawal, Fos-positive nuclei were increased in the prefrontal cortex, anterior cingulate cortex (ACC), nucleus accumbens (NAc), amygdala and lateral habenula (LHb) in the females, versus only in the ACC, amygdala, and LHb in the males. Conversely, after prolonged abstinence, Fos-positive nuclei were decreased in the prefrontal cortex, ACC, and NAc in the females, but fell in the ACC, NAc, and LHb of the males. Thus, adaptations in diverse brain regions may contribute to the sex differences in behaviors in ethanol-withdrawn rats.

Multiple Sclerosis (MS) is an autoimmune, inflammatory disease of the central nervous system (CNS) mostly affecting young adults. The exact mechanism and pathogenesis of MS remain still undiscovered but there have been useful treatments with different efficacy rates. Most of these therapies are divided into the first line, second line and third line, impact on the immune system and immune cells. These drugs are approved to be useful in MS, but like any other therapies, adverse effects (AE) are associated with these drugs. In this review, we continue the survey over mechanisms of actions and AEs of MS drugs. Physicians must be aware of such AEs and complications to choose the best drug for each patient.

Diabetes mellitus has been recognised as one of the four major non-communicable diseases that demands urgent attention from all key shareholders globally in an effort to address its prevalence and associated complications. It is considered as a top 10 cause of death globally, killing about 1.6 million people worldwide and is seen as the third highest risk factor for worldwide premature mortality due to hyperglycaemia and hyperglycaemic-induced oxidative stress and inflammation. There is a strong link between hyperglycaemia, hyperglycaemic-induced oxidative stress, inflammation and the development and progression of type 2 diabetes mellitus. Various reports have shown that chronic low-grade inflammation is associated with the risk of developing type 2 diabetes and that sub-clinical inflammation contributes to insulin resistance and is linked to the characteristics of metabolic syndrome which include hyperglycaemia. Oxidative stress stimulates the generation of inflammatory mediators and inflammation in turn enhances the production of reactive oxygen species. This interaction between diabetes, oxidative stress and inflammation is the primary motivation for the compilation of this review. Based on previous studies, the review examines the interaction between diabetes, oxidative stress and inflammation, factors promoting prevalence of diabetes mellitus, mechanisms involved in hyperglycaemia-induced oxidative stress with particular focus on type 2 diabetes and selected diabetic complications.

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.

Inflammatory bowel disease (IBD) is a condition describing chronic gastrointestinal inflammation. Chronic inflammation in colon can develop into colon cancer. Lunasin has been known to inhibit inflammatory reactions induced by lipopolysaccharide in vitro. The effect of lunasin to inhibit inflammation in vivo is not widely known. In this study, we analyzed the effect of lunasin from soybean to decrease the risk of inflammation by analyzing histopathologic feature and the expression of COX-2. 30 mice are divided into 6 groups. Normal group was not induced by dextran sodium sulfate (DSS). The other groups were induced by 2% DSS through drinking water for 9 days. After 9 days, negative control group did not receive any treatment. The other groups received treatment given lunasin dose 20 mg/kg body weight (BW) and 40 mg/kg BW, commercial lunasin and positive control given aspirin. Treatment was performed for 5 weeks. Inflammatory colon histopathologic examination and immunohistochemical score of COX-2 proteins were analyzed using statistical tests. Lunasin dose 20 mg/kg BW and 40 mg/kg BW were able to significantly reduce inflammation (P<0.05) performed by histopathologic feature with an average score of 2.52 and 2.16 COX-2 expression decreased significantly (P<0.05) with an average score of 43.674 and 33.349. Lunasin dose 20 mg/kg BW and 40 mg/kg BW were able to inhibit inflammation and decrease the expression of COX-2 in colon induced by DSS.

Parkia biglobosa seed an important household spice commonly consumed in Nigeria is believed to possess antioxidant activity that may exert modulatory effects in diabetes and diabetic complications. This study investigated the modulatory potential of Parkia biglobosa protein isolate (PBPi) on serum testosterone (sTT) level as well as its influence on biomarkers of oxidative stress in brain and testes of streptozotocin-induced diabetic male rats. Animals were made diabetic by single intraperitoneal administration of streptozotocin (STZ; 60 mg/kg body weight). PBPi (200 or 400 mg/kg body weight) was given orally by gavage or insulin (5 U/kg, i.p.) was administered daily to STZ-induced diabetic rats for 28 days. The results revealed a significant elevation in thiobarbituric acid reactive substances (TBARS) levels in the brain and testes of diabetic rats. This was closely associated with a concomitant reduction in levels of sTT and reduced testes weight, a noticeable decline in the glutathione-S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT) as well as total glutathione (Total GSH) level in the brain and testes of diabetic rats. Interestingly, treatment with PBPi efficiently prevented the alterations witnessed in the serum sTT and also ameliorated various alterations in the biomarkers of oxidative stress (TBARS, Total GSH, GST, SOD and CAT) in brain and testes of diabetic rats. These results provide evidence that PBPi could protect the brain and testicular tissues against oxidative stress induced by STZ, via modulation of serum testosterone concentration and also by enhancing antioxidant defence system in STZ-diabetic rats.