Sun Raha Hai Na Tu Male 1080p
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I am from maldives I dont know much hindi but I guess the saying 'sun raha hai na tu' can be also reffered for you are not listening. Am I right guys? Correct me If I am wrong Thanks appreciate the hard work of bollymeaning.com~shahin
amezing song dude ...love it heartly...thankx to whos lyrics dis song...Sun rahaa hai naa tuRo rahaa hoon mainSun raha hai naa tuKyun ro raha hoon main......song's awsome ...jitni v tarif kro kam hai.
I really love this...heart touching.. female version of this songe (by shreya goshal) also awesome...am listening to this song at least twice a day...This is gonna be my favorite after "Abhi mujhme kahin" by sonu nigam... awesome song.. love this!
You asked me on phone from India whether I repent what happened. Here is my answer: YES. I got myself into trouble, but nearly got your married life into trouble too. K was planning on coming to DTB to tell him about you and what we were up to. Just then you decided to speak to K. So I tried to warn you against it by sending a message to Cinderella that you shouldn't play with fire or else you'll get burnt. You see what's at stake now don't you? The love of my life, my marriage, my kids AND your married life too! All this mess I did because of 26th JUNE confession! Sun raha hai na? Kyun roh raha hun main?
I have new names for you. Sun raha hai na?Sapna-Because you are now a dream for me.Largesse-means same as Danveera. Because you gave sacrifices such as the sports chat, sports, moms group, your time and most important of all, you value me when no one else does.4:26-Because the sight of this number and you give me peace no matter what my day is like. And my days have mostly been gloomy the last 5 months. Only exception is when K is with me. When he's with me, I dread the sight of 426 and you.Lastly, you are Taboo-because I can't say your name. I am not allowed to. Neither anything associated with you. friends, your family, songs we shared, pictures, emails, things etc. he's managed to restrict me with all physical aspects. Now he's trying to remove you from my memories, from my heart.
Sun Raha Hai LyricsApne karam ki kar adaayein..Yaara Yaara Yaara.. Yaara..Mujhko hi raah dedeKasme de wade deMeri duaaon keIsharon ko sahare deDil ko thikaanein deNaye bahaanein deKhawabon ki barishon koMausam ke paimane deApne karam ki kar adaayeinKar de idher bhi tu nigaaheinSun raha hai na tuRo raha hu main (Repeat 3 times)Manzile.. ruswaa hain..Khoya hai raasta..Aaye le jaayeItni si iltaja..Yeh meri zamanat hai..Tu meri amaanat hai..Haan..Apne karam ki kar adaayein..Kar de idher bhi tu nigahein..Sunn raha hai na tuRo raha hu mainSunn raha hai na tuRo raha hu mainWaqt bhi thahra haiKaise kyun ye huaKaash tu.. aise aayeJaise koi dua..Tu junoon ki rahat hai..Tu meri ibaadat hai..Apne karam ki kar adaayein..Kar de idher bhi tu nigaaheinSun raha hai na tuRo raha hu main (Repeat 3 times)
Tiwari stated that he wants to explore different genres given the right opportunity, though it shouldn't be vulgar and should hold meaning. Satyajit from Glamsham called his second composed song "Saheb Bada Hatila" from Saheb, Biwi Aur Gangster a "rock-musical" arrangement. In his next composition "Sunn Raha Hai", the male version features electronic distortion guitar, zitar and drums while the female version is supported by instruments like ghatam, flute, santoor and acoustic guitar. The variance in composition was particularly applauded by critics.
The Developmental Origins of Health and Disease (DOHaD) Theory proposes that the environment encountered during fetal life and infancy permanently shapes tissue physiology and homeostasis such that damage resulting from maternal stress, poor nutrition or exposure to environmental agents may be at the heart of adult onset disease. Interference with endogenous developmental functions of the aryl hydrocarbon receptor (AHR), either by gene ablation or by exposure in utero to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a potent AHR ligand, causes structural, molecular and functional cardiac abnormalities and altered heart physiology in mouse embryos. To test if embryonic effects progress into an adult phenotype, we investigated whether Ahr ablation or TCDD exposure in utero resulted in cardiac abnormalities in adult mice long after removal of the agent. Ten-months old adult Ahr -/- and in utero TCDD-exposed Ahr +/+ mice showed sexually dimorphic abnormal cardiovascular phenotypes characterized by echocardiographic findings of hypertrophy, ventricular dilation and increased heart weight, resting heart rate and systolic and mean blood pressure, and decreased exercise tolerance. Underlying these effects, genes in signaling networks related to cardiac hypertrophy and mitochondrial function were differentially expressed. Cardiac dysfunction in mouse embryos resulting from AHR signaling disruption seems to progress into abnormal cardiac structure and function that predispose adults to cardiac disease, but while embryonic dysfunction is equally robust in males and females, the adult abnormalities are more prevalent in females, with the highest severity in Ahr -/- females. The findings reported here underscore the conclusion that AHR signaling in the developing heart is one potential target of environmental factors associated with cardiovascular disease. PMID:26555816
Data on cardiac abnormalities in females with untreated hypopituitarism are limited. We investigated echocardiographic abnormalities in females with untreated hypopituitarism and their response to treatment. Twenty-three females with treatment-naïve hypopituitarism and 30 matched healthy controls were evaluated for cardiac structure and function. Echocardiographic evaluation was done at presentation and after achieving a euthyroid and eucortisol state. Fourteen (61%) patients had mitral regurgitation, and 11 (48%) had pericardial effusion as against none among controls. Indices of left ventricular (LV) size like LV end diastolic dimension (LVEDD; 44.5 ± 3.5 mm in cases vs. 47.6 ± 3.8 mm in controls, P = .004), and LV diastolic volume (LVEDV; 91.8 ± 18.0 mL versus 106.5 ± 20.4 mL, P = .009) were significantly lower in the SS group compared with controls. LV mass (LVM) was 70.8 ± 19.2 g in cases and 108.0 ± 33.2 g in controls (P = .02). Similarly, indices of LV systolic function like stroke volume (SV; 59.1 ± 12.0 mL in cases and 74.4 ± 15.8 mL in controls; P = .000), ejection fraction (EF; 64.3 ± 6.2 % in cases against 69.9 ± 9.2 % in controls; P = .03), and fractional shortening (FS; 34.9 ± 4.7% versus 40.1 ± 4.4%, P = .000) were significantly decreased in patients compared with controls. Cardiac abnormalities normalized with restoration of a euthyroid and eucortisol state. Pericardial effusion, mitral regurgitation, and diminished LVM are common in females with untreated hypopituitarism. ACTH = adrenocorticotrophic hormone BMI = body mass index DT = deceleration time EDV = end-diastolic volume EF = ejection fraction FS = fractional shortening GH = growth hormone IGF-1 = insulin growth factor-1 ITT = insulin tolerance test IVSd = interventricular septal diameter LH = luteinizing hormone LV = left ventricular LVEDD = LV end diastolic dimension LVEDV = LV end diastolic volume LVM = LV mass MRI = magnetic resonance imaging MVP = mitral value prolapse PPH
Suwa, Kenichiro; Satoh, Hiroshi; Sano, Makoto; Nobuhara, Mamoru; Saitoh, Takeji; Saotome, Masao; Urushida, Tsuyoshi; Katoh, Hideki; Tawarahara, Kei; Ohtani, Hayato; Wakabayashi, Yasushi; Takase, Hiroyuki; Terada, Hajime; Takehara, Yasuo; Sakahara, Harumi; Hayashi, Hideharu
Methamphetamine use is escalating in Australia and New Zealand, with increasing emergency department attendance and mortality. Cardiac complications play a large role in methamphetamine-related mortality, and it would be informative to assess the frequency of abnormal electrocardiograms (ECGs) amongst methamphetamine users. To determine the frequency and severity of ECG abnormalities amongst methamphetamine users compared to a control group. We conducted a retrospective cohort analysis on 212 patients admitted to a tertiary hospital (106 patients with methamphetamine use, 106 age and gender-matched control patients). Electrocardiograms were analysed according to American College of Cardiology guidelines. Mean age was 33.4 years, with 73.6% male gender, with no significant differences between groups in smoking status, ECG indication, or coronary angiography rates. Methamphetamine users were more likely to have psychiatric admissions (22.6% vs 1.9%, p
It is well established that subclinical hypothyroidism (SCH) is associated with mild cardiac dysfunction, but it is unknown whether there is an underlying impairment of cardiac bioenergetic function. The objective of the study was to quantify the cardiac phosphocreatine to adenosine triphosphate ratio (PCr to ATP) in SCH, compared with healthy controls, and to measure the effect of 6 months of levothyroxine treatment. This was a 6-month, prospective, case-controlled interventional study. The PCr to ATP ratio was measured using phosphorus-31 magnetic resonance spectroscopy in subjects with SCH at baseline and after levothyroxine therapy (1.6 μg/kg · d) and compared with age- and gender-matched euthyroid controls. All subjects were free of overt heart disease. Twenty-one subjects with SCH (normal free T4 and serum TSH between 4.1 and 10 mIU/L) and 17 controls were matched for age (mean age 40.5 vs 43.3 y) and sex (females 81% vs 82%) but differed in mean TSH (6.5 vs 2.1 mIU/L, P < .001). At baseline the mean (± SD) PCr to ATP ratio in SCH was lower than in controls (1.80 ± 0.26 vs 2.07 ± 0.20, P = .001). In the 16 subjects studied after levothyroxine treatment, the PCr to ATP ratio improved (from 1.74 ± 0.24 to 1.91 ± 0.26, P = .004) and approached controls (borderline loss of significance, P = .051). On multivariate analysis, SCH was independently associated with a reduced PCr to ATP ratio, even after adjusting for confounding variables (body mass index and fasting glucose) (P = .001). Our results demonstrate early cardiac bioenergetic impairment in SCH, which is reversible with levothyroxine therapy. This mechanistic insight provides justification for longitudinal trials to determine whether improvement in bioenergetic function improves cardiovascular outcome. 2b1af7f3a8