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Background: Hypertension (HTN) is prevalent in individuals with type 2 Diabetes Mellitus (T2DM), doubling the risk of developing chronic complications. Despite normal routine checks, many patients with diabetes exhibit abnormal blood pressure (BP) profiles identified by 24-hour ambulatory Blood Pressure monitoring (ABPM). This study aimed to analyse blood pressure variability in patients with diabetes to enhance current knowledge and improve clinical practice., Methods: This cross-sectional study obtained ethical approval from Jazan University and involved 58 patients with type 2 Diabetes Mellitus (T2DM) who adhered to the strict inclusion and exclusion criteria. Comprehensive clinical and laboratory data, including demographic, clinical, and essential laboratory parameters, were collected using a standardized form. Blood Pressure (BP) was meticulously monitored using the Sun Tech Oscar 2 ABPMR device, with measurements commencing between 8 am and 10 am, extending over 24 hours. The study calculated averages and evaluated systolic and diastolic percentage dipping during 24-hour, daytime, and night-time intervals. Participants classified as "dippers" experienced a BP reductions of at least 10%., Results: Fifty-eight normotensive T2DM patients, with a mean age of 45.51 ± 6.7 years, were monitored over 24 months. Among the 58 individuals assessed using ABPM, a non-dipping pattern was observed in 45 participants (77.58%), whereas 13 (22.41%) exhibited a dipping pattern. Postprandial and fasting blood sugar levels were distinct; the dipper group demonstrated better post-meal glucose control (p=0.02), whereas the non-dipper group had superior fasting glucose control (p=0.04). The dipper group showed a higher 24-hour average systolic BP (p=0.00) and increased dipping percentages for systolic and diastolic BP during sleep., Conclusion: Over 77% of ABPM-evaluated individuals showed non-dipping patterns, with a higher BMI being strongly associated. Laboratory findings revealed distinct variations in the postprandial and fasting blood sugar levels, suggesting a potential genetic predisposition., Competing Interests: The authors declare no conflicts of interest in this work., (© 2024 Shaphe et al.)

Objective: The purpose of this study was to examine patients' expectations and factors that influence adherence to physiotherapists' treatment recommendations on chronic low back pain (CLBP)., Method: One hundred and forty seven patients with CLBP were included in this study. Predictive indicators including demographic information, views, expectations, and opinions regarding the health status and treatment expectations of patients were derived from questionnaires. The dependent outcome variables were the absence of trust in treatment recommendations provided by physiotherapists, the anticipation of treatment recommendations based on patient expectations, and the resistance to modifying expectations despite efforts by physiotherapists to persuade otherwise. The study was carried out between April 2022 and January 2023 in 2 regions located in India., Results: Multivariate regression analyses show that age, expectations about diagnosis, preference for passive therapies and medical care, and information seeking behavior emerged as independent predictors of a lack of trust in physiotherapists' treatment recommendations. The information-seeking behavior of the patients' alone predicted the anticipation of treatment recommendations based on patient expectations and the reluctance to alter those expectations despite the physiotherapists' persuasion., Conclusion: Our results suggest that information seeking behavior is the most consistent independent predictor of treatment expectations that will align with physiotherapist recommendations. This indicates the importance of screening for such factors and the importance of patient education to optimize the management of CLBP. However, larger studies incorporating all variables associated with patient expectations in similar patient populations are needed to confirm these results., (Copyright © 2024. Published by Elsevier Inc.)

Objectives: The poor prognosis of oral squamous cell carcinoma (OSCC) is vastly due to late diagnosis. The oral submucosal fibrosis (OSMF) is often unnoticed pathology linked with high risk of malignancy. Recently, we demonstrated that the clinicopathological alterations in OSMF and OSCC patients were correlated with cancer stem cell (CSCs) markers (CD133 and CD44). However, the parallel alterations of interleukin-1 beta (IL-1β) with CSCs expression are largely unexplored. Thus, we aimed to investigate the relationship between IL-1β alterations and CSC marker expression in both OSMF and OSCC situations., Materials and Methods: A total of 135 people have signed up for the study. There were sixty each in OSMF and OSCC groups, as well as 15 healthy controls. Levels of serum IL-1β were examined by ELISA. Immunohistochemistry (IHC) was used to examine the expression of CD133 and CD44. For evaluating differential CSCs expression, IHC scoring (0-4) was utilized., Results: The IHC results showed maximum subjects in the OSMF and OSCC displaying CD44 and CD133 positivity, although the extent of expression in terms of IHC scoring found variable. CD133 and CD44-positive subjects showed increased levels of IL-1β in the OSMF and OSCC group. Nevertheless, the enhancement of IL-1β is more pronounced in the OSCC cases. Further, we observed a direct link of IL-1β levels with IHC scoring. Multivariate regression analysis demonstrated a significant role for CD44 and CD133 positivity in the increase of IL-1β levels., Conclusion: We concluded that concurrent simultaneous changes in CSC biomarkers and IL-1β may help with early detection of OSMF and OSCC conditions., Competing Interests: All authors of this work have declared that there is no conflict of interest., (Copyright: © International Journal of Health Sciences.)

Cells constantly adapt to external humoral cues like cytokines and hormones, but practically most cellular behavior is under locally guided control via cell-cell interactions. Galectins (Gals) are one of the most prominent members of the group of molecules involved in this intercellular signaling. They are the family of β-galactoside specific lectins and consist of 15 different types, each with a specific function. They play crucial role in the immune system, inflammation, wound healing and carcinogenesis. In recent times, the role of Gals in the development of cardiovascular disease (CVD) has gained attention. Gals have been reported to act ambiguously by both relieving ischemia and accelerating atherosclerosis. Atherosclerosis can ultimately lead to myocardial infarction or ischemic stroke, which are both associated with Gals. There is also a role for Gals in the development of myocarditis by their influence on inflammatory processes. Moreover, Gal acts as a biomarker for the severity of myocardial ischemia and heart failure (HF). This review summarizes the association between Gals and the development and pathogenesis of CVD like atherosclerosis, stroke, myocardial infarction, and HF. A comprehensive outline of the association between Gals and more general mechanisms such as angiogenesis, arteriogenesis and atherosclerosis has also been provided. Modulation of Gal signaling holds great promise for the treatment of CVD as evident from preclinical studies., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)

The diagnosis of myelodysplastic syndrome (MDS) can be challenging, and may be facilitated by correlation with cytogenetic testing. Microarray analysis using comparative genomic hybridization and/or single-nucleotide polymorphism array can detect chromosomal abnormalities not seen by standard metaphase cytogenetics. We examined the ability of combined comparative genomic hybridization and single-nucleotide polymorphism analysis (hereafter referred to as 'combined array') to detect changes among 83 patients with unexplained cytopenias undergoing pathologic evaluation for MDS and compared results with 18 normal bone marrow controls. Thirty-seven patients (45%) were diagnosed with MDS, 12 patients (14%) were demonstrated to have 'indeterminate dyspoiesis' (insufficient for classification of MDS), 27 (33%) were essentially normal, and 7 patients (8%) had alternative pathologic diagnoses. Twenty-one MDS patients (57% of diagnoses) had effectively normal metaphase cytogenetics, but combined array showed that 5 of these (13% of MDS patients) harbored major cryptic chromosomal aberrations. Furthermore, nearly half of patients with 'indeterminate dyspoiesis' and 1 with normal morphology had clonal cytopenia(s) of undetermined significance by combined array analysis. Cryptic array findings among MDS patients and those with clonal cytopenias(s) included large-scale copy-neutral loss of heterozygosity (up to 118 Mb) and genomic deletion of loci implicated in MDS pathogenesis (eg, TET2 (4q22) and NUP98 (11p15)). By comparison, in MDS patients with abnormal metaphase cytogenetics, microarray mostly recapitulated findings seen by routine karyotype. Combined array analysis has considerable diagnostic yield in detecting cryptic chromosomal aberrations in MDS and in demonstrating aberrant clonal hematopoiesis in cytopenic patients with indeterminate morphologic dysplasia.

The two most common forms of dementia are Alzheimer's disease (AD) followed by vascular dementia (VaD), together accounting for a whopping 60-80% of total dementia cases worldwide. Even though these diseases are recognized as 'common', they still remain underdiagnosed. Recent research suggests that AD and VaD are closely intertwined. The symptoms of AD and VaD can be similar and the two conditions can occur simultaneously. A large number of patients diagnosed with AD have also been reported with VaD-caused brain damage. Moreover, both the diseases have been reported to have similar risk factors. The overlap between these diseases is important because the lifestyle changes and medications prescribed to curb one of these diseases may also help curb the other. In the present review, we present an inclusive outline of parallelism between AD and VaD by exploring the potential commonalities at the mechanistic and therapeutic levels.

Free radicals are generated as byproduct of our body metabolism, and their adverse effect on normal functioning of our body is prevented by body's own antioxidant machinery. Any perturbation in the defense mechanism of antioxidants inside body, its abnormal production or its induction from environment to our body lead to serious threats and is responsible for the development of various neurodegenerative disorders (NDDs). Perturbed antioxidants result in sensory and functional impairments in neuronal cells, which in turn cause NDDs. Free radical attack on neuronal cells plays a catastrophic role in NDDs. Impaired metabolism and generation of excessive reactive oxygen species also lead to a range of NDDs. Free radical induced toxicity is responsible for DNA injury, protein degradation, damage to tissue inflammation and cell death. Besides various genetic and environmental factors, free radical induced oxidative stress is also a major cause of NDDs. Application of upstream and downstream antioxidant therapy to counter oxidative stress can be an effective option in alteration of any neuronal impairment besides free radical scavenging. In the present manuscript, we have presented a comprehensive update on the symptoms, causes and cures of NDDs in relation with their dynamic association with oxidative stress.

Social stressors evolving from individual and population interactions produce stress reactions in many organisms (including humans), influencing homeostasis, altering the activity of the immunological system, and thus leading to various pathological states including cancer and their progression. The present study sought to validate the effectiveness of chronic unpredictable stress (CUS) in cancer promotion and to assess oxidative stress outcomes in terms of various in vivo biochemical parameters, oxidative stress markers, DNA damage, and the development of skin tumors in Swiss albino mice. Animals were randomized into different groups based on their exposure to CUS alone, 7,12-dimethylbenz(a)anthracene (DMBA) alone (topical), and DMBA-12-O-tetradecanoylphorbol-13-acetate (TPA) (topical) and exposure to CUS prior to DMBA or DMBA-TPA treatments and sacrificed after 16 weeks of treatment. Prior exposure to CUS significantly increased the pro-oxidant effect of carcinogen, depicted by compromised levels of antioxidants in the circulation and skin, accompanied by enhanced lipid peroxidation, plasma corticosterone, and marker enzymes as compared to DMBA-alone or DMBA-TPA treatments. DNA damage results corroborated the above biochemical outcomes. Also, the development of skin tumors (in terms of their incidence, tumor yield, and tumor burden) in mice in the presence and absence of stress further strongly supported our above biochemical measurements. CUS may work as a promoter of carcinogenesis by enhancing the pro-oxidant potential of carcinogens. Further studies may be aimed at the development of interventions for disease prevention by identifying the relations between psychological factors and DNA damage.

Mitochondria play a significant role in the pathophysiology of post-traumatic stress disorder (PTSD). Risperidone and paroxetine were evaluated for their effect on mitochondrial dysfunction and mitochondria-dependent apoptosis in discrete brain regions in modified stress re-stress (SRS) animal model of PTSD. Male rats were subjected to stress protocol of 2 h restraint and 20 min forced swim followed by halothane anesthesia on day 2 (D-2). Thereafter, rats were exposed to re-stress (forced swim) on D-8 and at 6-day intervals on D-14, D-20, D-26, and D-32. The rats were treated with risperidone (0.01, 0.1, and 1.0 mg/kg p.o.) and paroxetine (10.0 mg/kg p.o.) from D-8 to D-32. Risperidone at median dose and paroxetine ameliorated modified SRS-induced depressive-like symptom (increase in immobility period) in forced swim, anxiety-like behavior (decrease in percentage of open arm entries and time spent) in elevated plus maze and cognitive deficits (loss in spatial recognition memory) in Y-maze tests on D-32. Risperidone, but not paroxetine, attenuated modified SRS-induced decreases in plasma corticosterone levels. Risperidone ameliorated increase in the activity of mitochondrial respiratory complex (I, II, IV, and V), decreases in the levels of mitochondrial membrane potential, cytochrome-C and caspase-9 in the hippocampus, hypothalamus, pre-frontal cortex, and amygdala. However, both drugs attenuated modified SRS-induced increase in the number of apoptotic cells and caspase-3 levels in all the brain regions indicating anti-apoptotic activity of these drugs. Hence, these results suggest that anti-apoptotic activity could be a common mechanism for anti-PTSD-like effect irrespective of the pathways of apoptosis in the modified SRS model.

Therapies targeting central stress mechanisms are fundamental for the development of successful treatment strategies. Ocimum sanctum (OS) is an Indian medicinal plant traditionally used for the treatment of various stress-related conditions. Previously, we have isolated and characterized three OS compounds; Ocimarin, Ocimumoside A and Ocimumoside B. However, their role in modulating chronic stress-induced central changes is unexplored. Thus, in the present study the efficacy of these OS compounds have been evaluated on the chronic unpredictable stress (CUS)-induced alterations in the monoaminergic and antioxidant systems in the frontal cortex, striatum and hippocampus, along with the changes in the plasma corticosterone levels. CUS (two different types of stressors daily for seven days) resulted in a significant elevation of plasma corticosterone level, which was reversed to control levels by pretreatment with Ocimumoside A and B (40 mg/kg p.o.), while Ocimarin showed no effect. The levels of NA, DA and 5-HT were significantly decreased in all the three brain regions by CUS, with a selective increase of DA metabolites. A significant decrease in the glutathione (GSH) content, the activities of superoxide dismutase and catalase with a significant increase in the glutathione peroxidase activity and lipid peroxidation was observed in all the three regions of the brain by CUS. The OS compounds alone did not cause any significant change in the baseline values of these parameters. However, Ocimumoside A and B (40 mg/kg body p.o.) attenuated these CUS-induced alterations with an efficacy similar to that of standard anti-stress (Panax quinquefolium; 100 mg/kg p.o.) and antioxidant (Melatonin; 20 mg/kg i.p.) drugs. While, Ocimarin failed to modulate these CUS-induced alterations. Therefore, this is the first report which identified the anti-stress activity of novel Ocimumoside A and B at the level of central monoamines and antioxidant properties, implicating their therapeutic importance in the prevention of stress-related disorders., (Copyright © 2012 Elsevier GmbH. All rights reserved.)

Background & Objectives: Ocimum sanctum (OS) is known to possess various therapeutic properties. We have earlier isolated and characterized three OS compounds; Ocimarin, Ocimumoside A and Ocimumoside B. However, their role in modulating stress-induced central changes is unexplored. Thus, the present study was aimed to investigate the effect of these OS compounds on restraint stress (RS)-induced changes in the monoaminergic and antioxidant systems in the frontal cortex, striatum and hippocampus of rats., Methods: RS was produced by immobilizing (restraining) the Sprague Dawley rats for a period of 2.5 h inside cylindrical steel tubes. The monoamine levels and the in vivo antioxidant status in brain regions were evaluated by HPLC-EC and spectrophotometric assays, respectively., Results: RS significantly increased the dopamine levels in the frontal cortex and decreased in the striatum and hippocampus, and accompanied with selective increase of dopamine metabolites compared to the NS control group. The serotonin and its metabolite levels were significantly increased, while noradrenaline levels were decreased by RS in the three brain regions studied. The activities of superoxide dismutase and glutathione peroxidase in the frontal cortex and striatum were significantly increased by RS with decreased glutathione levels and increased lipid peroxidation. Pre-treatment with Ocimumoside A and B (40 mg/kg po) for a period of 3 days prevented the RS-induced changes with an efficacy similar to that of standard anti-stress (Panax quinquefolium; 100 mg/kg po) and antioxidant (Melatonin; 20 mg/kg ip) drugs, while, Ocimarin failed to modulate these changes. OS compounds per se had no effect on these parameters., Interpretation & Conclusions: The present findings showed the anti-stress potential of Ocimumoside A and B in relation to their simultaneous modulatory effects on the central monoaminergic and antioxidant systems implicating their therapeutic importance in stress-related disorders. Further studies are required to understand the mechanism of action of these compounds.

Stress is the leading psychopathological cause for several mental disorders. Physiological and psychological responses to stress are mediated by the hypothalamic?pituitary?adrenal (HPA), sympathoadrenal system (SAS), and brain monoaminergic systems (BMS). Eugenol is reported to substantially modulate brain functions by regulating voltage-gated cation channels and release of neurotransmitters. This study was designed to evaluate the anti-stress effect of eugenol in the 4-h restraint model using rats. Ulcer index was measured as a parameter of the stress response. HPA axis and the SAS were monitored by estimating plasma corticosterone and norepinephrine (NE), respectively. Analysis of NE, serotonin (5-HT), dopamine, and their metabolites in discrete brain regions was performed to understand the role of BMS in the anti-stress effect of eugenol. Stress exposure increased the ulcer index as well as plasma corticosterone and NE levels. Eugenol pretreatment for 7 days decreased the stress-induced increase in ulcer index and plasma corticosterone but not NE levels, indicating a preferential effect on the HPA axis. Furthermore, eugenol showed a ?U?-shaped dose?response curve in decreasing ulcer index and plasma corticosterone levels. Eugenol also reversed the stress-induced changes in 5-HT levels in all brain regions, whereas NE levels were reversed in all brain regions except hippocampus. These results suggest that eugenol possesses significant anti-stress activity in the 4-h restraint model and the effect is due to modulation of HPA and BMS.

Sulfite oxidase [SO; EC 1.8.3.1] catalyses the physiologically vital oxidation of sulfite to sulfate, the terminal reaction in degradation of sulfur containing amino acids, cysteine and methionine. Sulfite oxidase from vertebrate sources is among the best studied molybdenum enzymes. Existence of SO in plants has been established recently by identification of a cDNA from Arabidopsis thaliana encoding a functional SO. The present study was undertaken to identify herbaceous and woody plants (viz., Azardirachta indica L., Cassia fistula L., Saraca indica L., Spinacea oleracea L., and Syzyzium cumini L.), a relatively less explored source, having significant SO activity and to characterize some of its immuno-biochemical properties. The Syzyzium cumini was chosen to characterize SO as it showed maximum enzyme activity in the crude extract as compared to other plants. Absorption spectra of SO revealed two peaks at 235 and 277 nm, but no distinct peak in the visible region could be observed. Crude extract of all the plants were taken into considerations for immuno-biochemical studies. Despite of significant protein structure-functional similarities between plant and animal SO, no cross-reactivity could be established between the two sources of SO. These data suggested that plants SO, however, differed with regards to their immunobiochemical properties.

Sulfite oxidase (EC 1.8.3.1) catalyzes the physiologically vital oxidation of sulfite to sulfate, the terminal reaction in the degradation of sulfur containing amino acids. Genetic deficiency related to human sulfite oxidase is associated with the severe clinical abnormalities with no effective therapies known, making the enzyme of immense biomedical importance. In the present study, sulfite oxidase was been purified from the goat tissues, a hitherto unexplored source, in particular from the liver, and its physico and biochemical properties were characterized. The liver was chosen as it showed the highest activity, compared to kidney and muscle. The enzyme was purified to homogeneity by salting out, gel filtration and ion-exchange chromatography. It was a dimer (113 kDa) having two identical subunits (56 kDa) and did not contain free sulfhydryl groups. Its spectral analysis showed the presence of heme and molybdenum. circular dichroism (CD) spectra in near and far-UV regions showed the presence of significant amounts of secondary structures (45% alpha helix, 9% beta structure and 26% beta turn and remaining random coil) in the native molecule. The kinetic and hydrodynamic properties of the enzyme were also determined. Results also showed that ferricyanide was 8-times more effective electron acceptor than its physiological acceptor cytochrome c. The limited N-terminal analysis of the enzyme revealed the sequence up to six amino acids Trp-Glu-Pro-Ser-Gly-Ala. Together, these results suggested the liver was a major source of sulfite oxidase in goat and most of its physico-chemical, except secondary structure and amino acid sequence from N-terminal and biological properties were fairly similar to the sulfite oxidase isolated from other mammalian species/organs.

Bioactivity-guided purification of n-BuOH soluble fraction from the ethanol extract of Evolvulus alsinoides resulted in the isolation of two new compounds, 2,3,4-trihydroxy-3-methylbutyl 3-[3-hydroxy-4-(2,3,4-trihydroxy-2-methylbutoxy)-phenyl]-2-propenoate (1) and 1,3-di-O-caffeoyl quinic acid methyl ester (2) along with six known compounds, caffeic acid (3), 6-methoxy-7-O-beta-glucopyranoside coumarin (4), 2-C-methyl erythritol (5), kaempferol-7-O-beta-glucopyranoside (6), kaempferol-3-O-beta-glucopyranoside (7) and quecetine-3-O-beta-glucopyranoside (8). The structure of new compounds 1 and 2 were elucidated by spectroscopic analysis, while known compounds were confirmed by direct comparison of their NMR data with those reported in literature. This is the first report of the presence of phenolic constituents in Evolvulus alsinoides. The isolated compounds 1-5 and 8 were screened for anti-stress activity in acute stress induced biochemical changes in adult male Sprague-Dawley rats. Stress exposure has resulted in significant increase of plasma glucose, adrenal gland weight, plasma creatine kinase (CK), and corticosterone levels. Compound 1 displayed most promising antistress effect by normalizing hyperglycemia, plasma corticosterone, CK and adrenal hypertrophy, while compounds 2 and 3 were also effective in normalizing most of these stress parameters, however compounds 4, 5 and 8 were ineffective in normalizing these parameters.