In conclusion, all the results revealed that curcumin attenuated CS-induced inflammation both in vivo and in vitro, presumably by modulating the PPARγ-NF-κB pathway.

Thus, curcumin may be a potential antioxidant and anti-inflammatory therapeutic agent against chronic inflammatory lung diseases.

Curcumin supplementation effectively mitigates inflammation in patients suffering from chronic SM-induced cutaneous complications.

Our results indicate that curcumin interferes with colonic inflammation partly through inhibition of the chemokine expression and through direct inhibition of neutrophil chemotaxis and chemokinesis.

Curcumin could be used in the prevention or therapy of cardiovascular disease, respiratory diseases, cancer, neurodegeneration, infection, and inflammation based on cellular biochemical, physiological regulation, infection suppression and immunomodulation.

Conclusion Our findings provide new evidence for the therapeutic potential of curcumin to treat human NAFLD.

Despite mostly unclear outcomes for standard physiological determinants of performance, 8 d of NO3- supplementation resulted in likely beneficial improvements to 4-km TT performance in well-trained male endurance cyclists.

These results indicate that acute dietary NO3(-) supplementation can elevate plasma NO3(-) and NO2(-) concentrations, improve exercise performance, and reduce blood pressure in COPD patients.

Thus, the present study indicates that dietary NO3 - supplementation improves physical performance in non-athletes, particularly during long-duration open-ended tests.

In conclusion, low‐dose dietary NO3− supplementation does not enhance the effects of intermittent hypoxic training on endurance exercise performance at sea level.

Nitrate treatment may improve exercise performance, in part, by stimulating the preferential use of fuels that require less oxygen for energy production.

The current analysis indicates that NO3– supplementation can enhance exercise performance with an ergogenic effect more likely in untrained subjects and as the duration of supplementation increases.

Dietary supplementation with NO3(-)-rich BR juice speeds VO2 kinetics and enhances exercise tolerance during severe-intensity exercise when initiated from an elevated metabolic rate.

Our results provide new evidence that chronic high-dose NO3- supplementation improves cycling performance of well-trained cyclists in both normoxia and hypoxia.

The results indicate that both strong and weak antibacterial agents suppress the rise in plasma [NO2-] observed following the consumption of a high NO3- diet and the former can influence the BP response during low-intensity exercise.

These findings suggest that the NO3 (-)-NO2 (-)-NO pathway is a significant modulator of muscle energetics and O2 delivery during hypoxic exercise and subsequent recovery.

Conclusion In middle to older-aged well-trained adults, NO3- supplementation has non-significant, albeit highly variable, effects on exercise tolerance.

In conclusion, an acute dose of ∼13 mmol NO3- does not affect physiological or performance responses to submaximal or maximal treadmill roller-skiing in competitive cross-country skiers exercising in N and H.

However, nitrate supplementation does not enhance muscle V̇O2 kinetics during exercise, nor does it improve time to exhaustion when exercising with a small muscle mass.

We conclude that acute increases in circulating NO3− and NO2− via BR increases muscle blood flow during moderate‐ to high‐intensity handgrip exercise via local vasodilation.

Thus, while NO3‐ supplementation may have performance benefits, especially in elite athletes exercising at high intensities, in recreationally active males, there appears to be little impact on changes in VO2 due to submaximal prolonged exercise.

Therapeutic strategies that improve elimination of Aβ and other soluble metabolites from the brain may prevent cognitive decline in Alzheimer's disease.

However, prevention and manipulation of adiposity may also provide a means to prevent Alzheimer's disease.

The findings of this review validate the importance of some nutritional interventions as possible approach to prevent or delay simultaneously progression of Alzheimer's disease and obesity.

Treatment with vitamin D may be an independent protecting factor in the progression of Alzheimer's disease.

Individual interventions should be considered to delay institutionalization in Alzheimer's disease.

Our findings provide new insights that may help to establish preventive strategies against Alzheimer's disease.

Risk of Alzheimer's disease.

Reducing homocysteine levels in healthy older people may help to prevent Alzheimer's disease.

These results suggest that treatment at very early stages of Alzheimer's disease could prevent later irreversible neuronal degeneration.

This mechanism could be impaired in patients with Alzheimer's disease.

However, as a therapeutic strategy for Alzheimer's disease, it may only be effective for removing Aβ from the brain.

Interferring with neuronal differentiation control might, thus, be a potential strategy to prevent neurodegeneration in Alzheimer's disease and related disorders.

Overall, evidence from trials of cholinesterase inhibitors and memantine suggests that when these agents are optimized for the various stages of Alzheimer's disease, they can also prevent the emergence of neuropsychiatric symptoms.

This work suggests novel avenues for the immunotherapy of Alzheimer's disease.

This method is expected to be helpful in the early diagnosis of Alzheimer's disease in clinical practice.

This finding is essential for furthering the prevention and treatment of neurodegenerative diseases such as Alzheimer's disease (AD) and stroke.

AIMS The aims of KADSS are: (1) to determine whether an aqueous standardised extract of kava is effective for the treatment of anxiety; (2) to assess the effects of kava on differing levels of depression; and (3) to explore participants' experience of taking kava via qualitative research.

The data support the safety of kava in treating anxiety at 280 mg kava lactones/day for 4 weeks.

The results of the study may be of benefit to sufferers of anxiety and the future economy of the Pacific islands, potentially providing an important step in the way forward with kava.

Thus, unlike conventional benzodiazepine‐type anxiolytics, which tend to impair cognitive performance and to increase the occurrence of negative affective states, Kava is a potent anxiolytic agent, which, additionally, can facilitate cognitive functioning and can increase positive affectivity related to exhilaration.

Kava holds promise for decreasing anxiety in peri- and postmenopausal women; however, women should be careful in the amount and duration of use.

Kava Kava was shown to be more effective than placebo in 3 of the 7 trials.

Kava-kava extract is an herbal medicine having not only hypnotic effects, but also sleep quality-enhancement effects.

It is concluded that when taken as a short-term monotherapy at recommended doses, kava extracts appear to be well tolerated by most users.

The aqueous Kava preparation produced significant anxiolytic and antidepressant activity and raised no safety concerns at the dose and duration studied.

If the findings are confirmed, kava may be a useful component to the treatment of addictions, especially for Native Hawaiian and Pacific peoples.

The results suggest that kava and valerian may be beneficial to health by reducing physiological reactivity during stressful situations.

Although kava was not superior to placebo, it would be premature to rule it out as efficacious in GAD.

Our findings indicate that Ashwagandha root powder possesses free radical scavenging activity, which may be responsible for its pharmacological effects.

Overall, the strongest evidence for therapeutic efficacy of ashwagandha is the alleviation of stress and anxiety symptoms.

Conclusion Ashwagandha could be a powerful antioxidant and a promising anticancer agent against HCC.

Ashwagandha may be effective in enhancing both immediate and general memory in people with MCI as well as improving executive function, attention, and information processing speed.

Ashwagandha (Withania somnifera) is an important herb in the Indian traditional system of medicine for neurological disorders.

A Case Series from Iceland and the U. S. Drug-Induced Liver Injury Network" which illustrated the hepatotoxic potential of Ashwagandha seems to be quiet misleading1 .

This case study suggests that thyrotoxicosis is a potentially serious side effect of ashwagandha.

They found ashwagandha to exhibit anti-apoptotic, anti-metastatic, anti-invasive and anti-inflammatory properties and gave the evidence that ashwagandha has a capability for averting and treating breast cancer.

Therefore, the present investigation is showed that Ashwagandha can prevent the diabetes-induced hormonal dysfunction by inhibiting hyperglycemia and hyperlipidemy.

Patients with anxiety can also benefit from Ashwagandha Keyword: Ashwgandha, Sedative, Diuretic, Cognitive and Neurological Disorders

DESIGN This review is in a narrative format and consists of all publications relevant to ashwagandha that were identified by the authors through a systematic search of major computerized medical databases; no statistical pooling of results or evaluation of the quality of the studies was performed due to the widely different methods employed by each study.

It is thus logical to extend the Ashwagandha model to other high demand medicinal plants and its feasibility.

The outcome of this study suggests that Ashwagandha root extract can be used for body weight management in adults under chronic stress.

This comparison, depicted in (Table 1), provides evidence to classify Ashwagandha in TCM accurately and establishes a methodology by which other relevant herbal medicines can be joined with Chinese medicine and classified under TCM categories and terms.

Men tend to have a larger but more collapsible airway during mandibular movement than women and this, in part, may play a role in the positional dependency and severity of OSA in men.

In conclusion, while obesity does not appear to alter airway size, women may have larger airways compared with men when mid-expiratory flow is maximal.

Therefore it was concluded that the relationship between tracheal area and lung volume is consistent with the hypothesis that in men and women lung parenchyma grows independently of the airways; furthermore, in women the airways grow faster than the lung parenchyma.

The larger airways appear to respond faster than the smaller airways and the response of the smaller airways appears to be more prolonged.

Secondly, they show that while smaller airways are more responsive than larger ones, the reduction of responsiveness diminishes with each increase of lung size.

These physiologic data support the concepts that neonates have proportionately larger airways relative to their lung volume at FRC, infants have size-corrected flows similar to those in older children and adults, and female infants have proportionately larger airways relative to their lung size than do male infants.

Our data also suggest that smaller rodents have proportionately wider airways than do larger animals.

We conclude that there are differences in swallowing between men and women, with women having a longer oropharyngeal transit than men for a 5-ml bolus.

Men had a significantly higher prevalence of chronic wheeze compared with women.

The cerebellar hemispheres and the area of the anterior vermis may be larger in men than in women regardless of differences in body size.

Women encounter their GP more frequently with respiratory symptoms than men and GPs perform more diagnostic investigations in men.

In conclusion, men have the capacity to place a larger volume of water inside their mouth than women.

The larger conducting airways in females are significantly smaller than those of males even after controlling for lung size.

Furthermore, the influence of the epithelium exhibits regional differences, being greater in larger airways.

These findings suggest that increasing the supply of market rate housing has beneficial spillover effects for incumbent renters, reducing rents and displacement pressure while improving neighborhood quality.

We provide empirical evidence on two potential mechanisms for these findings: Excess demand for low-income housing puts upwards pressure on rental prices; increasing supply of high-income housing coupled with rising homicide rates put downwards pressure on rental prices.

Further studies show that the development of the capital market and housing rental market are somewhat helpful in mitigating the associations between income inequality and the housing price-to-income ratio and vacancy rate.

We show that a contraction of mortgage supply after the Great Recession has increased housing rents.

Interestingly, our findings show that an increase in job accessibility leads to an increase in housing prices, whereas it is not related to rents.

(H2) Increased ‘external’ competition measured by the price level on the market for single-family owner occupied housing, leads to lower rents.

We also present evidence consistent with our hypothesis that regulation is constraining the supply of housing so that increased demand leads to much higher prices, not many more units, in a number of other high price housing markets across the country.

The study finds that a decreasing internal rate of return on developers' housing investments, caused mainly by high land prices, has led to a reduction in housing supply.

The main findings are that the housing market has been a contributor to past volatility in the UK economy, and that moving to a fixed rate structure would reduce the impact of a change in interest rates on key macroeconomic indicators.

Using a spatial equilibrium model, I show that less elastic housing supplies increase governments' abilities to extract rents.

Empirical results provide strong evidence that an increase in land supply will bring forth a decrease in housing prices.

However, any observed impact on housing prices may be mitigated by density effects and stigma effects that decrease demand for market-rate units.

At the same time, high rental vacancies, lagging rents and high inflation rates per se also are found to raise structure prices relative to market-clearing rents, suggesting significant adjustment lags from the durability of the housing stock, transaction costs, and segmentation between owner and rental submarkets.

This paper argues that income inequality is one important factor driving up both the housing price relative to income and the housing vacancy rate.

A possible conclusion is that policies that make it easier for households to leave the rental market are important for increasing the pressure on the firms in the rental sector and reducing rents.

Thus, this paper demonstrates that the demise of social rent has accelerated under conditions of market-oriented housing restructuring, and increasingly occurs in high demand neighbourhoods where current housing policies push gentrification.

Finally, we show that the response of housing rents accounts for a large proportion of the “price puzzle” found in the literature.

In addition, we find that falling average rents caused entry to the housing market to become more affordable, and that this was linked to significantly higher household formation rates.

We find that a developed rental market attenuates fluctuations in the housing sector, especially for the common currency area sample.

Despite finding attitudes that genetic links to mental illness would increase rather than decrease stigma, we found strong community acceptance of depression risk genotyping, even though a predisposition to depression may only manifest upon exposure to stressful life events.

The study also provides support for the contention that certain forms of mental illness may still exist in the gene pool because particular personality traits associated with milder forms of mental illness (i.e., Neuroticism & schizotypy) are also associated directly with creativity and indirectly with short-term mating success.

The study is among the first to show that a normal genetic variant can increase the risk of mental illness.

Just as critically, by spreading the message that genetic risk for psychiatric disorders is biological and fundamentally no different than for other human conditions, we can dispel the stigma associated with mental illness.

Therefore, inherited genetic risk may partly account for the association of childhood abuse with mental illness.

Genetic risk factors that shape the brain transcriptome may contribute to diagnostic differences between broad classes of mental illness.

Our finding of a substantial decrease in risk of psychotic illness associated with familial liability for psychosis following adjustment for other environmental stressors highlights potentially modifiable risk factors on the trajectory to psychotic illness and suggests that interventions that reduce or manage exposure to these risks may be protective, despite a genetic liability.

Although it cannot be determined from these data whether specific treatments for mental illness contribute to the observed associations, elevated risk across different diagnoses suggests that some aspects of mental illness itself may confer risk.

Genetic explanations may be suggested to reduce the stigma associated with mental illnesses, however, these explanations work in complex ways and may not uniformly reduce illness related stigma.

Our respondents strongly endorsed the importance of physical and mental illness genetic research.

Tests based on the genetic contributors to psychiatric illness offer another troubling example.

The genetic factors that influence self-report psychiatric illness also influence psychiatric illness as described by relatives.

Although the mental illness in this family may not be typical of that in the general population, the findings suggest that the q21-22 region of chromosome 11 may be a promising area to examine for genes predisposing to major mental illness.

Furthermore, the association of childhood abuse with parental mental illness suggests that genetic and environmental factors are difficult to separate as etiological factors in vulnerability.

The results are consistent with a causal relation between adolescent motherhood and offspring mental health problems, and they highlight the usefulness of behavior genetic designs when examining putative environmental risks for the development of psychopathology.

Psychiatric genetics appears to be poised for significant advances in our knowledge and understanding of the molecular genetic basis of mental illness.

Taken together, these data suggested that AST may be used to treat patients with allergic skin diseases through a mechanism, which may be associated with that involved in anti‑inflammatory or anti-allergic activities.

GENERAL SIGNIFICANCE These data suggest that AST may be useful as a preventive/therapeutic agent for cardiac dysfunction and myocardial fibrosis.

Taken together, our results showed the potential of AST as a countermeasure to immune dysfunction and suggest its use as immunosuppressant compound in inflammatory disease.

Our findings suggest that AST has the ability to inhibit T cell proliferation and cytokine secretion both in vitro and in vivo by interfering with MAPK signaling pathway.

It was concluded that AST could be considered as a potential mitochondrial-targeted agent in the therapy of pathological conditions associated with oxidative damage and mitochondrial dysfunction.

AST is overused in hospitalized patients.

These results suggest that Ast might act as an ROS scavenger, providing benefits to SS patients with impaired salivary secretion.

These results prove that ASD may serve as a better source of AST for human nutrition than does free AST.

In conclusion, AST could prevent the development of chronic asthma, thus reducing asthma attacks.

Therefore, AST is a promising therapeutic agent for the prevention and treatment of endometritis.

Our study provides a novel mechanism of the renoprotective effects by AST.

Collectively, our data suggest that the renoprotective effect of AST on DN depends on Nrf2/ARE signaling activation, which could be a potentially therapeutic strategy in the treatment of DN.

One-third of the genetic contribution was unique to perinatal depression and not shared with nonperinatal depression, suggesting only partially overlapping genetic etiologies for perinatal depression and nonperinatal depression.

Together these findings suggest that an inherited predisposition to bipolar depressive illness does not involve inherited variations in levels of type A MAO activity.

Our results suggest that having a marriage-like relationship acts as a protective factor in reducing the impact of inherited liability to symptoms of depression in the general population.

The transmission of depression symptoms is due in part to environmental processes independent of inherited effects and is not accounted for by shared adversity measurements.

Birth-weight for gestation is moderated by genetic and familial risk for depression in influencing early depression symptoms.

The association between paternal depression in the postnatal period and depression in girls at age 18 years is partially explained by maternal depression.

IMPORTANCE Some small studies suggest that maternal postnatal depression is a risk factor for offspring adolescent depression.

BMI does not significantly predict the development of depression in the offspring of parents with recurrent depression.

Maternal depression in pregnancy is a key vulnerability factor for offspring depression in early adulthood.

Our findings supported the hypothesis that depression spectrum disease is a variant of neurotic depression, whereas familial pure depressive disease overlaps with endogenous depression.

ME and depression are both heritable (ME 0.42, depression 0.37) and share common genetic factors, suggesting an overlap in etiology and the relevance of circadian rhythms to depression.

The association between LBW and depression was stronger among children of depressed parents than among children of nondepressed parents, with an interaction term (BW and parental depression status) significant for MDD (P = .05), suggesting that parental depression may augment the impact of LBW on offspring depression:

Prevalence of depression.

Chronic depression is distinguished from episodic depression by a more severe familial liability.

Among patients with PD, depression is associated with polymorphism at rs78162420 and rs1545843, both previously linked with depression.

This finding may represent a risk factor for depression or constitute an effect of developing depression.

Results revealed that maternal depression and paternal depression had an additive effect on youth externalizing disorders.

Resilience and depression had significant associations with self-rated successful aging, with effects comparable in size to that for physical health.

Meaning Results suggest that the prevention of psychopathology and monitoring of individuals with mental disorders for signs of accelerated aging may have the potential to reduce health inequalities and extend healthy lives.

Awareness of the age-related changes in adult mentalizing is important to differentiate normal aging effects from ToM impairments due to neuropsychiatric diseases.

In the U. S., positive mental health was higher among the older adults, but there was no effect of age for negative mental health.

In addition to poor clinical outcomes, such measures have profound negative effects on the mental health of older populations.

These results suggest that older molecular brain aging is a common feature of severe mental illnesses and neurodegeneration.

This indicates that the general perception of aging moderates the toll that feeling old takes on mental health.

The COVID-19 pandemic has had serious deleterious effects on the mental health of older adults worldwide.

Of 601 men followed for 4.8 years, 76.0% enjoyed successful mental health aging.

Considering rapid aging of the Chinese population, anticipated increases in chronic disease burden, and possible attenuation of filial care, this analysis suggests that older adults in China may increasingly face health and social conditions detrimental to their mental health.

DISCUSSION The mental health benefit of working, among persons aged 65 and older, may be due to the healthy worker effect.

Subjective aging has a small significant effect on health, health behaviors, and survival.

This might lead to decreased mental health and long-term effects.

However, these effects seem to be short-lived, and thus we do not expect strong negative consequences for older adults mental health downstream.

Positive aging is more evident in Sardinia, especially in rural areas, where the maintenance of an adequate social status and physical activity help guarantee a positive level of mental health in later life.

The study found that retirement at age 60 had no effects on physical health functioning and, if anything, was associated with an improvement in mental health, particularly among high socioeconomic status groups.

We favor the explanation that leg cramps, particularly developing in night sleep, may be triggered by reduced blood flow due to postural changes.

Prolonged standing at work may be a more important risk factor for varicose veins and nocturnal leg cramps than biological differences between women and men.

Muscle cramps in patients with varicose veins occur more frequently and more often at night and in the calf in comparison with those from the general population.

The results suggest that magnesium may be effective in treatment of nocturnal leg cramps.

We conclude that leg cramps are still a common symptom in pregnancy and may compromize sleep and hence the ability to work.

Our study demonstrated that nocturnal leg cramps were significantly more frequent in LSCS patients than in the control group.

Magnesium was not effective for the treatment of nocturnal leg cramps.

The results indicate that quinine can prevent nocturnal leg cramps in general ambulatory populations.

There was a significant, positive association between rest cramps and symptoms of angina or intermittent claudication although these two factors only accounted for 12% of the variance, suggesting that peripheral vascular disease may play a relevant but limited role in the aetiology of rest cramps.

Thus, it is hypothesizable that either peripheral and central mechanisms may together contribute in producing muscle cramps.

Calf-stretching exercises are not effective in reducing the frequency or severity of night cramps.

It is suggested that the cause of these cramps is plasma-volume contraction.

These findings suggest the relevance of spinal involvement in both the origin and sustenance of muscle cramps.

We identified an association between alcohol consumption and nocturnal leg cramps among patients aged 60 years and older attending general practices.

I would agree with Ayres and Mihan that the medication is almost universally effective on idiopathic nocturnal leg cramps.

They also highlight the need to develop and evaluate physical activity interventions in the treatment of Nocturnal Legs Cramps.