Potential role of immune cell therapy in gynecological cancer and future promises: a comprehensive review.

Gynecological malignancies are most leading causes of death among women worldwide. The high prevalence of gynecologic malignancies remains significant, necessitating to turn the novel treatment approach like immunotherapy, wherein cancer cells are killed by the invasion of immune system. In recent year, immunotherapy has mostly an advanced treatment approach to repressing the tumor cells survival, proliferation, and invasion via the activation of immune systems. Moreover, various types of immune cells including T-cells, B-cells, and dendritic cells are associated with the immunotherapeutic strategy in cancer treatment. Although the significant role of T-cells against cancer is well established, while B-cells and dendritic cells also play an important role against different gynecological cancer by regulating the immune system. This review focuses on that arena and highlight the role of immune cells in the treatment of gynaecological cancer. Various immune cell-based anticancer therapies such as T-cell therapies, Adoptive Cellular transfer, B-cell therapies as well as approaches to Dendritic Cell therapies have been discussed in detail. Furthermore, the clinical settings and future avenues regarding immunotherapy on gynecological cancer have also been reviewed and illuminated in the recent study.

Plant polymerase IV sensitizes chromatin through histone modifications to preclude spread of silencing into protein-coding domains.

Across eukaryotes, gene regulation is manifested via chromatin states roughly distinguished as heterochromatin and euchromatin. The establishment, maintenance, and modulation of the chromatin states is mediated using several factors including chromatin modifiers. However, factors that avoid the intrusion of silencing signals into protein-coding genes are poorly understood. Here we show that a plant specific paralog of RNA polymerase (Pol) II, named Pol IV, is involved in avoidance of facultative heterochromatic marks in protein-coding genes, in addition to its well-established functions in silencing repeats and transposons. In its absence, H3K27 trimethylation (me3) mark intruded the protein-coding genes, more profoundly in genes embedded with repeats. In a subset of genes, spurious transcriptional activity resulted in small(s) RNA production, leading to post-transcriptional gene silencing. We show that such effects are significantly pronounced in rice, a plant with a larger genome with distributed heterochromatin compared with Arabidopsis Our results indicate the division of labor among plant-specific polymerases, not just in establishing effective silencing via sRNAs and DNA methylation but also in influencing chromatin boundaries.

Expansion and contraction of small RNA and methylation machinery throughout plant evolution.

The revolution in sequencing has created a wealth of plant genomes that can be mined to understand the evolution of biological complexity. Complexity is often driven by gene duplication, which allows paralogs to specialize in an activity of the ancestral gene or acquire novel functions. Angiosperms encode a variety of gene silencing pathways that share related machinery for small RNA biosynthesis and function. Recent phylogenetic analysis of these gene families plots the expansion, specialization, and occasional contraction of this core machinery. This analysis reveals the ancient origin of RNA-directed DNA Methylation in early land plants, or possibly their algal ancestors, as well as ongoing duplications that evolve novel small RNA pathways.

A null allele of the pol IV second subunit impacts stature and reproductive development in Oryza sativa.

All eukaryotes possess three DNA-dependent RNA polymerases, Pols I-III, while land plants possess two additional polymerases, Pol IV and Pol V. Derived through duplication of Pol II subunits, Pol IV produces 24-nt short interfering RNAs that interact with Pol V transcripts to target de novo DNA methylation and silence transcription of transposons. Members of the grass family encode additional duplicated subunits of Pol IV and V, raising questions regarding the function of each paralog. In this study, we identify a null allele of the putative Pol IV second subunit, NRPD2, and demonstrate that NRPD2 is the sole subunit functioning with NRPD1 in small RNA production and CHH methylation in leaves. Homozygous nrpd2 mutants have neither gametophytic defects nor embryo lethality, although adult plants are dwarf and sterile.

Apple polyphenol phloretin complexed with ruthenium is capable of reprogramming the breast cancer microenvironment through modulation of PI3K/Akt/mTOR/VEGF pathways.

Our recent investigation directed to synthesize a novel ruthenium-phloretin complex accompanied by the study of antioxidant in addition to DNA binding capabilities, to determine the chemotherapeutic activity against breast carcinoma in vitro and in vivo. Ruthenium-phloretin complex was synthesized and characterized by different spectroscopic methods. The complex was further investigated to determine its efficacy in both MCF-7 and MDA-MB-231 human carcinoma cell lines and finally in an in vivo model of mammary carcinogenesis induced by DMBA in rats. Our studies confirm that the chelation of the metal and ligand was materialize by the 3-OH and 9-OH functional groups of the ligand and the complex is found crystalline and was capable of intercalating with CT-DNA. The complex was capable of reducing cellular propagation and initiate apoptotic events in MCF-7 and MDA-MB-231 breast carcinoma cell lines. Ruthenium-phloretin complex could modulate p53 intervene apoptosis in the breast carcinoma, initiated by the trail of intrinsic apoptosis facilitated through Bcl2 and Bax and at the same time down regulating the PI3K/Akt/mTOR pathway coupled with MMP9 regulated tumor invasive pathways. Ruthenium-phloretin chemotherapy could interrupt, revoke or suspend the succession of breast carcinoma by altering intrinsic apoptosis along with the anti-angiogenic pathway.

Pharmacological basis and new insights of taxifolin: A comprehensive review.

The pharmacological characteristics of phytochemicals have prompted a lot of interest in their application in disease management. Due to the high incidence of cancer related mortality and morbidity throughout the world; experiments have concentrated on identifying the anticancer potential of natural substances. Many phytochemicals such as flavonoids and their derivatives produced from food offer a variety of new anti-cancer agents which prevent the cancer progression. Taxifolin, a unique bioactive flavonoid, is a dietary component that has grabbed the interest of dietitians and medicinal chemists due to its wide range of health benefits. It is a powerful antioxidant with a well-documented effect in the prevention of several malignancies in humans. Taxifolin has shown promising inhibitory activity against inflammation, malignancies, microbial infection, oxidative stress, cardiovascular disease, and liver disease. Anti-cancer activity has been shown to be relatively significant than other activities investigated in vitro and in vivo with a little or no side effects to the normal healthy cells. In summary this review offers the synopsis of recent breakthroughs in the use of taxifolin as a cancer treatment, as well as mechanisms of action. However, to develop a medicine for human usage, more study on pharmacokinetic profile, profound molecular mechanisms, and drug safety criteria should be conducted utilizing well-designed randomized clinical trials.

Embryo CHH hypermethylation is mediated by RdDM and is autonomously directed in Brassica rapa.

BACKGROUND: RNA-directed DNA methylation (RdDM) initiates cytosine methylation in all contexts and maintains asymmetric CHH methylation. Mature plant embryos show one of the highest levels of CHH methylation, and it has been suggested that RdDM is responsible for this hypermethylation. Because loss of RdDM in Brassica rapa causes seed abortion, embryo methylation might play a role in seed development. RdDM is required in the maternal sporophyte, suggesting that small RNAs from the maternal sporophyte might translocate to the developing embryo, triggering DNA methylation that prevents seed abortion. This raises the question of whether embryo hypermethylation is autonomously regulated by the embryo itself or influenced by the maternal sporophyte. RESULTS: Here, we demonstrate that B. rapa embryos are hypermethylated in both euchromatin and heterochromatin and that this process requires RdDM. Contrary to the current models, B. rapa embryo hypermethylation is not correlated with demethylation of the endosperm. We also show that maternal somatic RdDM is not sufficient for global embryo hypermethylation, and we find no compelling evidence for maternal somatic influence over embryo methylation at any locus. Decoupling of maternal and zygotic RdDM leads to successful seed development despite the loss of embryo CHH hypermethylation. CONCLUSIONS: We conclude that embryo CHH hypermethylation is conserved, autonomously controlled, and not required for embryo development. Furthermore, maternal somatic RdDM, while required for seed development, does not directly influence embryo methylation patterns.

Bavachinin mitigates DMH induced colon cancer in rats by altering p53/Bcl2/BAX signaling associated with apoptosis.

Bavachinin is a flavanone obtained from the Chinese herb, Fructus Psoraleae. Flavonoids and flavanones are recognized as cancer preventive agents. We investigated the anticancer properties of bavachinin using a model of dimethylhydrazine (DMH and dextran sodium sulfate (DSS) induced rat colon cancer. We investigated aberrant crypt foci (ACF), hyperplastic lesions, catalase (CAT), superoxide dismutase (SOD) and glutathione (GST) levels in Wistar rats. Expression of cancer biomarkers including IL-6, p53, Bcl2 and BAX was investigated. We found that bavachinin administered to rats re-established the colonic crypts that were damaged by DMH and prevented progression of the cancer.

Decrypting the Molecular Mechanistic Pathways Delineating the Chemotherapeutic Potential of Ruthenium-Phloretin Complex in Colon Carcinoma Correlated with the Oxidative Status and Increased Apoptotic Events.

To explore fresh strategies in colorectal cancer (CRC) chemotherapy, we evaluated the capability of the ruthenium-phloretin complex in exterminating colon cancer by effectively addressing multiple apoptotic mechanisms on HT-29 cancer cells together with an animal model of colorectal cancer activated by 1,2-dimethylhydrazine and dextran sulfate sodium. Our current approach offers tangible evidence of the application of the ruthenium-phloretin complex in future chemotherapy. The complex triggers intrinsic apoptosis triggered by p53 and modulates the Akt/mTOR pathway along with other inflammatory biomarkers. The ruthenium-phloretin complex has been synthesized and successfully characterized by numerous spectroscopic methodologies accompanied by DPPH, FRAP, and ABTS assays assessing its antioxidant potential. Studies conducted in human cell lines revealed that the complex improved levels of p53 and caspase-3 while diminishing the activities of VEGF and mTOR, triggers apoptosis, and induces fragmentation of DNA in the HT-29 cells. Toxicity studies were conducted to identify the therapeutic doses of the novel complex in animal models. The outcomes of the in vivo report suggest that the complex was beneficial in repressing multiplicity of aberrant crypt foci as well as hyperplastic lesions and also promoted increased levels of CAT, SOD, and glutathione. In addition, the ruthenium-phloretin complex was able to control cell proliferation and boosted apoptotic outbursts in cancer cells associated with the increase in cellular response towards Bax while diminishing responses towards Bcl-2, NF-κB, and MMP-9. Our observations from the experiments deliver testament that the ruthenium-phloretin complex has the potential to act as a promising chemotherapeutic agent in colorectal cancer because it can affect the growth of ACF and hyperplastic abrasions in the colon tissues by evoking cell death.

RNA-directed DNA Methylation and sexual reproduction: expanding beyond the seed.

Two trends are changing our understanding of RNA-directed DNA methylation. In model systems like Arabidopsis, tissue-specific analysis of DNA methylation is uncovering dynamic changes in methylation during sexual reproduction and unraveling the contribution of maternal and paternal epigenomes to the developing embryo. These studies indicate that RNA-directed DNA Methylation might be important for mediating balance between maternal and paternal contributions to the endosperm. At the same time, researchers are moving beyond Arabidopsis to illuminate the ancestral role of RdDM in non-flowering plants that lack an endosperm, suggesting that RdDM might play a broader role in sexual reproduction.

Construing the Biochemical and Molecular Mechanism Underlying the In Vivo and In Vitro Chemotherapeutic Efficacy of Ruthenium-Baicalein Complex in Colon Cancer.

In pursuit of a novel approach in colon cancer therapy, we explored the ability of ruthenium baicalein complex to eradicate colon cancer by efficiently targeting various apoptotic pathways on human colon cancer cell line and on a DMH and DSS induced murine model of colorectal cancer. In this study, we provide direct proof of the chemotherapeutic potential of the ruthenium baicalein complex by activating p-53 dependent intrinsic apoptosis and modulating the AKT/mTOR and WNT/ß- catenin pathways. The ruthenium baicalein complex was synthesized and its characterizations were accomplished through various spectroscopic techniques followed by assessment of antioxidant potential by DPPH, FRAP, and ABTS methods. In vitro study established that the complex increased p53 and caspase-3 expressions while down regulating VEGF and mTOR expression, induced apoptosis, and DNA fragmentation in the HT-29 cells. Acute and sub-acute toxicity study was also considered and results from in vivo study revealed that complex was effective in suppressing ACF multiplicity and hyperplastic lesions and also raised the CAT, SOD, and glutathione levels. Furthermore, the complex decreased cell proliferation and increased apoptotic events in tumor cells correlated with the upregulation of Bax and downregulation of Bcl2, WNT and ß- catenin expressions. Our findings from the in vitro and in vivo study provide robust confirmation that ruthenium baicalein complex possesses a potential chemotherapeutic activity against colon cancer and is competent in reducing ACF multiplicity, hyperplastic lesions in the colon tissues of rats by inducing apoptosis.

Potentiating apoptosis and modulation of p53, Bcl2, and Bax by a novel chrysin ruthenium complex for effective chemotherapeutic efficacy against breast cancer.

Breast cancer is the most frequent cause of cancer in women. In the current study, transition metal ruthenium was complexed with flavonoid chrysin to evaluate the chemotherapeutic potential of this compound in Michigan Cancer Foundation-7 (MCF-7) human mammary cancer cell line and 7,12-dimethylbenz(α)anthracene-induced mammary cancer in female Sprague-Dawley rats. The characterizations of the complex were accomplished through UV-visible, NMR, IR, Mass spectra, and XRD techniques and antioxidant activity was assessed by DPPH, FRAP, and ABTS methods. In vitro studies included cell viability, cell cycle analysis, DNA fragmentation, and marker analysis by western blot analysis and found that complex treatment suppressed cell growth-induced cell cycle arrest and enhanced the induction of apoptosis in cancer cells. Moreover, complex treatment modulated signaling pathways including mTOR, VEGF, and p53 in the MCF-7 cells. Acute and subacute toxicity was performed in rats to determine the therapeutic doses. Breast cancer in rats was initiated by the administration of 7,12-dimethylbenz(α)anthracene (0.5 mg/100 g body weight) via single tail vein injection. The histopathological analysis after 24 weeks of carcinogenesis study depicted substantial repair of hyperplastic lesions. Immunohistochemical analysis revealed upregulation of Bax and p53 and downregulation of Bcl2 proteins and TUNEL assay showed an increase in apoptotic index in ruthenium-chrysin-treated groups as compared to the carcinogen control. Our findings from the in vitro and in vivo study support the continued investigation of ruthenium-chrysin complex possesses a potential chemotherapeutic activity against breast cancer and was efficient in reducing hyperplastic lesions in the mammary tissues of rats by inducing apoptosis.

Vanadium quercetin complex attenuates mammary cancer by regulating the P53, Akt/mTOR pathway and downregulates cellular proliferation correlated with increased apoptotic events.

Flavonoid metal ion complexes have been deliberated in recent years and are considered as a new class of medicinal agents with enhanced therapeutic activity and low toxicity. Our study deals with chemotherapeutic effects of vanadium, when coordinated with the flavonoid quercetin on a defined model of chemically induced rat mammary carcinogenesis in vivo and on human breast cancer cell line MCF-7 in vitro. The characterization of the complex was achieved through UV-Visible, IR, and Mass spectra and antioxidant activity was assessed by DPPH, FRAP and ABTS methods. In vitro studies established that the complex upregulated the expressions of p53, Caspase 3 and 9, whereas down regulating Akt, mTOR and VEGF expressions and also induced apoptosis and DNA fragmentation in a dose dependent manner. Acute and Sub-acute toxicity was performed to determine safe doses. 7,12-Dimethylbenz(α)anthracene (0.5 mg/100 g body weight) was used for induction of breast cancer in female Sprague-Dawley rats via single tail vein injection. The histopathological analysis after 24 weeks of carcinogenesis study depicted substantial repair of hyperplastic lesions. TUNEL assay showed an increase in apoptotic index (0.14 ± 0.03; 0.15 ± 0.01) in vanadium-quercetin treated groups as compared to the carcinogen control (0.02 ± 0.01) along with upregulation of Bcl-2 and downregulation of Bax and p53. Immunohistochemical analysis also exhibited decrease in cell proliferation in the vanadium-quercetin treated groups (11.3 ± 0.12; 11.8 ± 0.10). Thus, results from both in vivo and in vitro studies revealed that vanadium-quercetin complex could be a potential candidate for development of approved drug for breast cancer in the near future.

Deciphering the molecular mechanism and apoptosis underlying the in-vitro and in-vivo chemotherapeutic efficacy of vanadium luteolin complex in colon cancer.

The present study is carried out to reveal the chemotherapeutic effects of vanadium luteolin complex against HT-29 human colon carcinoma cell line and chemically induced rat colon carcinoma. Our investigation revealed that the vanadium luteolin complex induces apoptosis in HT-29 cells in a dose-dependent manner. Furthermore, the study also confirmed that the vanadium luteolin complex increased caspase-3 and p53 expression whereas reduced the VEGF, mTOR, Akt expression, and induced DNA fragmentation in HT-29 cells. The oral acute and sub-acute toxicity and the DNA binding efficacy of the complex with CT-DNA were investigated. The vanadium luteolin complex showed mortality at a dose of 120 mg/kg dose. The sub-acute toxicity of the complex at the dose of 90 mg/kg presented an increased level of WBC count, total bilirubin, ALT, AST, ALP, creatinine, blood urea nitrogen, and decreased level of total protein compared with the control group. Histopathological alterations in kidney, liver, stomach, and lungs was observed at a dose of 90 mg/kg of the complex. The dose of 45 mg/kg of the complex was found to have better chemotherapeutic activity by significantly reducing the incidences of aberrant crypt foci formation, upregulation in the expression of p53 and Bax, and downregulation of the expression of Bcl2, and cell proliferation was found in the complex at a dose of 45 mg/kg. Our findings from the study support that the complex possesses a potential chemotherapeutic activity against colon cancer and was efficient in reducing aberrant crypt foci formation multiplicity, hyperplastic lesions in the colon tissues of rats by inducing apoptosis. SIGNIFICANCE: The present study demonstrates that the effect of vanadium-luteolin complex in HT-29 cells and dimethylhydrazine challenged rats, curtail cell proliferation through induction of apoptosis mediated via activation of the key proteins involved in the intrinsic pathway like p53, Bax, caspase-3 and downregulating Bcl2, mTOR/Akt, angiogenic factor VEGF along with aberrant crypt foci formation multiplicity, and PCNA in the colon mucosa. Our combinatorial approach shows higher efficacy at considerably lower doses minimizing side effects. Insights into in-vitro and in-vivo results provide strong proof that low dose chemotherapeutic regimens can suppress, reverse, or delay the progression of colon cancer by modulating intrinsic apoptotic as well as antiangiogenic pathways.

Deciphering the biochemical and molecular mechanism underlying the in vitro and in vivo chemotherapeutic efficacy of ruthenium quercetin complex in colon cancer.

Flavonoids are the most investigated phytochemicals due to their pharmacological and therapeutic activities. Their ability to chelate with metal ions has resulted in the emergence of a new category of molecules with a broader spectrum of pharmacological activities. In this study, the ruthenium quercetin complex has been synthesized and anticancer activity has been evaluated on a well-defined model of DMH followed by DSS induced rat colon cancer and on human colon cancer cell line HT-29. The characterizations accomplished through UV-visible, NMR, IR, Mass spectra and XRD techniques, and antioxidant activity was assessed by DPPH, FRAP, and ABTS methods. In vitro study confirmed that the complex increased p53 expression, reduced VEGF and mTOR expression, apoptosis induction, and DNA fragmentation in the HT-29 cells. Acute and subacute toxicity study was also assessed and results from in vivo study revealed that complex was efficient to suppress ACF multiplicity and hyperplastic lesions and elevated the CAT, SOD, and glutathione levels. Furthermore, the complex was found to decrease cell proliferation and increased apoptotic events in tumor cells correlates upregulation of p53 and Bax and downregulation of Bcl2 expression. Our findings from the in vitro and in vivo study support the continued investigation of ruthenium quercetin complex possesses a potential chemotherapeutic activity against colon cancer and was efficient in reducing ACF multiplicity, hyperplastic lesions in the colon tissues of rats by inducing apoptosis.

Synthesis, characterization and study of antioxidant activity of quercetin-magnesium complex.

Quercetin (3,3',4',5,7-pentahydroxyflavone) one of the most abundant dietary flavonoids, has been investigated in the presence of magnesium (II) in methanol. The complex formation between quercetin and magnesium (II) was examined under UV-visible, Infra-red and (1)H NMR spectroscopic techniques. The spectroscopic data denoted that quercetin can reacts with magnesium cation (Mg(+2)) through the chelation site in the quercetin molecule. The free radical antioxidant activity of the complex with respect to the parent molecule was evaluated using 1,1-diphenyl-2-picrylhydrazyl (DPPH) method. It was observed that the free radical scavenging activity of quercetin was increased after complexation of magnesium (Mg(+2)) cation.

Synthesis, Characterization, Antioxidant Status, and Toxicity Study of Vanadium-Rutin Complex in Balb/c Mice.

A new trend was developed for the formation of a complex between vanadium and flavonoid derivatives in order to increase the intestinal absorption and to reduce the toxicity of vanadium compounds. The vanadium-rutin complex was characterized by several spectroscopic techniques like ultraviolet (UV)-visible, Fourier transform infrared (FTIR), NMR, mass spectrometry, and microscopic evaluation by scanning electron microscopy. The mononuclear complex was formed by the interaction between vanadium and rutin with 1:2 metal to ligand stoichiometry. Antioxidant activity of the complex was evaluated by 1,1-diphenyl-2 picrylhydrazyl, ferric-reducing power, and 2,2'-azin-obis 3-ethylbenzothiazoline-6-sulphonic acid methods. It was shown that radical scavenging activity and ferric-reducing potential of free rutin was lower as compared with vanadium-rutin complex. The study was also investigated for oral acute toxicity and 28 days repeated oral subacute toxicity study of vanadium-rutin complex in balb/c mice. The vanadium-rutin complex showed mortality at a dose of 120 mg/kg in the balb/c mice. In 28 days repeated oral toxicity study, vanadium-rutin complex was administered to both sex of balb/c mice at dose levels of 90, 45, and 20 ppm, respectively. In addition, subacute toxicity study of vanadium-rutin complex (at 90 ppm dose level) showed increase levels of white blood cell (WBC), total bilirubin, alanine aminotransferase (ALT), alkaline phosphatase (ALP), aspartate aminotransferase (AST), creatinine, and blood urea nitrogen and decrease level of total protein (TP) as compared with control group. Histopathological study of vanadium-rutin showed structural alteration in the liver, kidney, and stomach at 90 ppm dose level. No observed toxic level of vanadium-rutin complex at 20 ppm dose level could be good for further study.

Synthesis, characterisation and antioxidant activity of luteolin-vanadium(II) complex.

The complex formation between luteolin (L) and vanadium(IV) oxide sulphate monohydrate (VOSO4·H2O) was examined under UV-visible, infra-red spectroscopy, mass spectroscopy and NMR techniques. The spectroscopic data indicated that luteolin reacts with vanadium oxide cation (VO(+2)) through 4-carbonyl-5-hydroxy chelation site in the two luteolin molecule. The free radical antioxidant activity of the complex with respect to the parent molecule was evaluated using 1,1-diphenyl-2-picrylhydrazyl (DPPH), ferric reducing antioxidant power (FRAP) and 2,2'-azinobis 3-ethylbenzothiazoline-6-sulphonic acid diammonium salt (ABTS) methods. It was observed that the free radical scavenging activity and ferric ion reducing potential of luteolin was increased after the formation of complex with vanadium oxide (VO(+2)) cation.

Reliability and validity analysis of modified Nursing Stress Scale for Indian population.

The original Nursing Stress Scale (NSS) was structurally modified according to results of factorial analysis and a new scale was named as modified nursing stress scale (MNSS). This is the first study to modify and validate NSS for Indian nursing population. Factorial analysis showed different factor loading for two subscales and items were shifted according to their loading to provide a more meaningful structure. After relocation of Items 13, 14, and 15 into first factor, this factor was renamed as "emotional and painful conditions of patients" to provide a more appropriate name to the first factor. Items 24, 25, 26, 27, 28, and 29 were found to be distributed under two different factors; one of these two was renamed as "unpredictable changes" and another retained its original name (i.e., workload). This distribution was also supported by rational analysis. All other items were distributed under factors as in the original scale. Rest of the validity assessment was done with the modified scale. Thus, with minor changes in structure, the scale was found to have better content validity.

Prevalence of musculoskeletal disorders, levels of physical activity and perceived quality of life amongst construction site managers in Mumbai: a case study.

OBJECTIVE: The study aimed to explicate the levels of physical activity, the prevalence of musculoskeletal disorders (MSDs) and the perceived quality of life in construction site managers. PARTICIPANTS: Twenty two site managers working at a site in National Institute of Industrial Engineering (NITIE), Mumbai were selected for the study. METHODS: The participants responded to Nordic Musculoskeletal Questionnaire (NMQ) and the World Health Organization's (WHO), Quality of Life (QOL), and General Physical Activity (GPAQ) Questionnaires. RESULTS: In Quality of Life (QOL), 55% of the participants fell under 'good' psychological domain, while 55% categorized their work environment as 'poor'. Among musculoskeletal problems, low back pain and upper back pain was predominantly reported by the managers. Total physical activity was observed to be 836 Metabolic Equivalent of Task-minutes/week (MET-minutes/week). CONCLUSION: Although the Construction managers were not involved in any kind of rigorous work at the workplace, they were observed to be suffering from musculoskeletal problems of the back. 'Poor' category of environmental domain suggested that the working conditions needed to be improved and could be a reason for their ailment.