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Other studies (Mendelson et al. ; Hu, B.F.; Camargo, C.A., Jr.; et al. In addition, CRF and ACTH have immuno-potentiating and proinflammatory properties (figure 1) (Besedovsky and del Rey 1996). 2008). Thus, it is not surprising that cognitive processes are exquisitely sensitive to the effects of chemicals such as alcohol. ; et al. Glucocorticoids achieve their effects by binding to widely distributed high-affinity mineralocorticoid receptors and low-affinity glucocorticoid receptors on their target cells. 2000). A role for increased TRH section in blunting the TSH response also is supported by observations that abstinent patients with AUD who had a severely blunted TSH response to TRH showed increased levels of TRH in the cerebrospinal fluid (Adinoff et al. Rachdaoui N, Sarkar DK. The hippocampus is a structure that is vital to learning and the formation of memory. To understand the effects alcohol causes, its important to understand the different parts of the brain and alcohols impact on them. 2001; Tomie Furuya et al. Block, G.D.; Yamamoto, M.E. ; Hiney, J.K.; et al. Alcoholism: Clinical and Experimental Research 24(12):18361849, 2000. Initiation and progression of puberty are controlled by signals from the central nervous system that stimulate the pulsatile diurnal secretion of luteinizing hormone-releasing hormone (LHRH) from the hypothalamus into the hypothalamicpituitary portal system (Sarkar and Fink 1979; Sarkar et al. Metabolism 37(3):229233, 1988. Like the other hormone systems discussed so far, the GH/IGF-1 axis is under the control of the hypothalamus. Moreover, the body doesn't get able to absorb vitamins and nutrients. PMID: 6316391, Sarkar, D. K.; Kuhn, P.; Marano, J.; et al. PMID: 12397512, Pedersen, C.A. ; Verma, P.; and Weinberg, J. Prenatal alcohol exposure: Fetal programming and later life vulnerability to stress, depression and anxiety disorders. PMID: 18191055, Beulens, J.W. Finally, people with a family history of alcohol use disorder (AUD) exhibited hyperresponsiveness of the stress response mediated by the HPA axis (Uhart et al. PMID: 11988580, Sonntag, W.E., and Boyd, R.L. There are many ways alcohol consumption affects the body's glucose levels. 1990), and kisspeptins (Navarro et al. Reproductive Neuroendocrinology of Aging and Drug Abuse. Hormonal responses to psychological stress and family history of alcoholism. The hypothalamus produces and secretes LHRH, also called gonadotropin-releasing hormone, into the hypothalamicpituitary portal network. Autonomic Nervous System: Part of the nervous system that connects the central nervous system to the organs and controls involuntary bodily functions, such as respiration and digestion. As part of the HPA axis, it releases adrenocorticotropic hormone (ACTH) in response to AVP and CRH, triggering the adrenals into completing the stress response. 2009). 2001; Sarkar 2010). Alcohol and Alcoholism 19(3):235242, 1984. ; and Skupny, A. Gamma-aminobutyric acid up- and downregulates insulin secretion from beta cells in concert with changes in glucose concentration. Ethanol inhibits the naloxone-induced release of luteinizing hormone-releasing hormone from the hypothalamus of the male rat. These findings clearly indicate that chronic alcohol exposure induces a -cell dysfunction and not an enteroinsular incretin dysfunction, because the decrease in insulin response compared with the control group also was observed when glucose was administered intravenously. Bo, W.J., Krueger, W.A. Alcoholism: Clinical and Experimental Research 12(6):731734, 1988. Finally, ethanol treatment had differential effects on various G-proteins in cells expressing only D2S or D2L, eliciting a marked increase in Gs expression and a decrease in Gi3 expression in D2S cells but a moderate increase in Gs and marked increase in Gi3 expression in D2L (Sengupta and Sarkar 2012). 2015). 2006). . Get help when you need it. Update on pancreatic cancer and alcohol-associated risk. The short-term effects of consuming excess alcohol can result in: lapse of judgment loss of coordination nausea vomiting blacking out slurred speech impaired memory Prolonged use of alcohol is toxic to neurons and can result in neuron death. ; ODell, L.E. Genetics certainly influence our likelihood of developing AUD, but the story isn't so simple. Conversely, the -cells of the pancreas produce insulin, which lowers blood glucose levels after a meal by stimulating the absorption of glucose by liver, muscle, and adipose tissues and promoting the storage of glucose in the form of glycogen in these tissues. PMID: 3131791, Moller, N., and Jorgensen, J.O. This can cause injuries, poor decision-making, and other detrimental events that can affect the rest of your life. The hypothalamus controls body temperature, thirst, hunger and other bodily functions involved in sleep and emotional activity. Little research has assessed the effects of alcohol use on the hypothalamicpituitarygonadal (HPG) axis during puberty in humans. PMID: 8373011, Vescovi, P.P., and Coiro, V. Effect of diazepam on growth hormone secretion in abstinent alcoholic men. People are curious about how alcohol affects our bodies. Proceedings of the National Academy of Sciences of the United States of America 97(5):23372342, 2000. Proceedings of the National Academy of Sciences of the United States of America 87(24):96989702, 1990. Human studies have documented that moderate alcohol consumption induces disruptions in normal hormone levels during puberty, including a decrease in estrogen levels in adolescent girls that was sustained for long periods of time (Block et al. Dose-response determinations revealed that alcohol produced a biphasic effect on serum testosterone and LH: low doses of alcohol significantly increased testosterone and LH, whereas high doses decreased the levels of both hormones. C-peptide: Part of the precursor molecule of insulin that gets excised during the final processing of the insulin molecule; has no physiologic activity. However, prolactin also has been implicated in a plethora of other biological functions or responses, such as mammary-gland development; reproduction; immune functions; and behavioral functions, including learning, memory, and adaptation. Alcohol consumption and total estradiol in premenopausal women. Alcoholism: Clinical and Experimental Research 22(5 Suppl. The beneficial metabolic effects of moderate alcohol use on insulin sensitivity and glucose homeostasis therefore might explain the significant reduction in the risk of development of type 2 diabetes and of cardiovascular disorders (Avogaro et al. 2, Part of the Thus, fetal ethanol exposure increased methylation of a regulatory element (i.e., the promoter) of the D2R gene, thereby reducing transcription. For example, jokes start to seem funnier, and a user may be less afraid to talk to new people or do something outside of their comfort zone.. PMID: 11505028, Emanuele, N.V.; LaPaglia, N.; Steiner, J.; et al. Hypothalamus. Diabetologia 49(4):697705, 2006. Endocrine 14(2):213219, 2001b. Alcohol use, urinary cortisol, and heart rate variability in apparently healthy men: Evidence for impaired inhibitory control of the HPA axis in heavy drinkers. It's the unsteady, staggering walk of a long-term alcoholic. Endocrinol Metab Clin North Am. This suggests that chronic exposure to ethanol induces dysfunction of the thyroid gland, which then is no longer able to properly respond to TRH stimulation. Alcohol 42(5):349361, 2008. PMID: 18709650, Sierksma, A.; Patel, H.; Ouchi, N.; et al. Role of microglia in ethanols apoptotic action on hypothalamic neuronal cells in primary cultures. Ethanol exposure affects prolactin production not only in adults but also in the developing fetus. PMID: 16447058, Feng, L.; Han, B.; Wang, R.; et al. PMID: 7832470, Hoffman, P.L., and Tabakoff, B. Centrally acting peptides and tolerance to ethanol. Peripubertal paternal EtOH exposure. Annals of the New York Academy of Sciences, Journal of Pharmacology and Experimental Therapeutics, Proceedings of the National Academy of Sciences of the United States of America, Asian Pacific Journal of Cancer Prevention, Current Opinion in Clinical Nutrition and Metabolic Care, American Journal of Physiology: Endocrinology and Metabolism, Journal of Gastroenterology and Hepatolog, This research was supported by National Institutes of Health. 2004), or remained unchanged (Beulens et al. Alcohol and the hormonal control of lactation. PMID: 11394639, Fernandez-Lizarbe, S.; Pascual, M.; and Guerri, C. Critical role of TLR4 response in the activation of microglia induced by ethanol. Though damage may be reversible in some cases, others may not be as lucky. Some of these are neurons whose cell bodies are in the hypothalamus and that extend to limbic and forebrain areas, where they release oxytocin from their terminals. Journal of Clinical Investigation 108(9):13791385, 2001. In these analyses, the HPA response after several weeks of daily 30-minute self-administration of alcohol was highest in the animals with the lowest level of consumption (<0.2 mg/kg/session) and most blunted in animals with the highest level of consumption (~1.0 mg/kg/session). 1995). 1995) and the development of hypogonadism (Castilla-Cortazar et al. Zimmermann, U.; Spring, K.; Kunz-Ebrecht, S.R. The .gov means its official. doi:10.1016/j.ecl.2013.05.008, Steiner JL, Crowell KT, Lang CH. The higher alcohol levels that are achieved in a maturing brain increases the adolescent's risk for neurotoxicity and memory problems. ; and You, M. Adiponectin and alcoholic fatty liver disease. However, the effects differed between different subtypes of thyroid cancer, with a stronger inverse association for papillary thyroid cancer (relative risk = 0.58) compared with follicular thyroid cancer (relative risk = 0.86) (Meinhold et al. PMID: 12824819, Sarkar, D.K. Specifically, ethanol exposure of ovariectomized rats for 2 to 4 weeks decreased the levels of growth-inhibitory molecules (e.g., transforming growth factor beta-1 [TGF-1]) and increased the levels of growth-stimulatory factors, such as TGF-3 and basic fibroblast growth factor, in the pituitary gland; similar results were found in isolated cell cultures enriched for lactotropes and exposed to ethanol for 24 hours (Sarkar and Boyadjieva 2007). She helps individuals recover from drug, alcohol and gambling dependencies through group and individual therapy and regularly speaks at treatment centers. Its ideal to catch the disorder before it gets this far, but, sadly, this is not always a reality.. Alcoholism: Clinical and Experimental Research 31(9):15811588, 2007. The reduced hormone levels affected the monthly pattern of menstruation in the rhesus macaques and induced a lengthening of the intervals between menses in the alcohol-exposed monkeys (Dees et al. The pancreas, which lies behind the stomach, serves two major functions. Ethanol affects prolactin levels not only through its impact on D2R but also through changes in the production and secretion of growth factors in the pituitary that help control lactotropic cell proliferation. That affects how signals flow through your body, making you think, speak, and move more slowly. ; and Teoh, S.K. ; and Ylikahri, R. Effect of ethanol on serum concentrations of somatomedin C and the growth hormone (GH) secretion stimulated by the releasing hormone (GHRH). 2008). Emanuele, M.A. Augment insulin secretion, causing temporary hypoglycemia. 2013). ; Tentler, J.J.; Kirsteins, L.; et al. Nadia Rachdaoui, Ph.D., and Dipak K. Sarkar, Ph.D., D.Phil. 2013; Haas et al. PMID: 9712595, Kim, S.J. Continued meth abuse can severely damage dopamine and serotonin neurons, affecting how a person feels, acts and thinks. It controls just about everything we do: thoughts, motor skills, emotions, etc.. PMID: 19862001, Mendelson, J.H., and Mello, N.K. PMID: 10866524, Chiao, Y.B., and Van Thiel, D.H. Biochemical mechanisms that contribute to alcohol-induced hypogonadism in the male. Other studies have shown that long-term moderate alcohol consumption can decrease the number and quality of a womans oocytes (i.e., ovarian reserve), which was associated with increased FSH levels (Li et al. PMID: 16213844, Muti, P.; Trevisan, M.; Micheli, A.; et al. 1 The D2S isoform results from an exclusion of the sixth exon of the D2R gene in the mature transcript. A blunted TSH response also was observed during early withdrawal and was positively correlated with severity of withdrawal symptoms; in fact, it may be an important predictor of relapse (Pienaar et al. For example, acute ethanol administration increased serum prolactin levels in male (Seilicovich et al. The hypothalamicpituitary axis can be considered the coordinating center of the endocrine system. 2009; Nagy 2004). PMID: 20346754, Iovino, M.; Guastamacchia, E.; Giagulli, V.A. PMID: 18336630, De, A.; Boyadjieva, N.; Oomizu, S.; and Sarkar, D.K. Adiponectin, an adipocyte-derived plasma protein, inhibits endothelial NF-kappaB signaling through a cAMP-dependent pathway. Thus, glucocorticoids bind to mineralocorticoid (type 1) receptors and glucocorticoid (type 2) receptors in the hypothalamus, hippocampus, and pituitary. ; et al. 3. The frequency of daily ethanol consumption influences the effect of ethanol on insulin sensitivity in rats fed a high-fat diet. The effect of binge ethanol exposure on growth hormone and prolactin gene expression and secretion. Fetal alcohol exposure reduces dopamine receptor D2 and increases pituitary weight and prolactin production via epigenetic mechanisms. The neurotoxic effects of alcohol lead to thiamine deficiency and global cell death within, particularly vulnerable areas within the brain. Thus, the amount of GH secreted by the anterior pituitary is tightly regulated by GHRH, IGF-1, and somatostatin. Alcoholism: Clinical and Experimental Research 27(5):849861, 2003. It also appears vulnerable to damage from . Direct actions of ethanol on thyroid hormone metabolism, specifically on the activity of enzymes that catalyze the conversion of T4 to T3 (i.e., 5II deiodinase) or inactivate T3 to 3,3-T2 (i.e., 5-II deiodinase), also have been proposed. The levels of free T4 and T3, however, were lower in people with AUD during withdrawal and early abstinence compared with nonalcoholic healthy control subjects (Hegedus et al. Moreover, chronic alcohol has inhibitory actions on LHRH-producing neurons. Gavaler, J.S. Scientists believe that alcohol-seeking behavior is regulated in part by the hypothalamic pituitary adrenal axis. Journal of Obstetrics and Gynaecology Research, Cancer Epidemiology, Biomarkers & Prevention. ; Yang, S.Q. Life Sciences 93(21):778782, 2013. ; Shaw, G.K.; and Thomson, A.D. Thyroid status in chronic alcoholics. However, there are two main exceptions when long-term damage can be severe and life-altering. One of the tools that can assist with managing your alcohol addiction is Soberlink. Differential effect of desglycinamide9-(Arg8)-vasopressin on cognitive functions of diabetes insipidus and alcoholic patients. This activity prevents the intestines from digesting food. Alter the effectiveness of medications for diabetes. Long-term, alcohol can affect both our brain and other parts of our body and can cause: Ongoing mental health conditions An increased risk of diabetes and weight gain Increased risk of a range of cancers Heart issues, such as high blood pressure, heart damage and heart attacks Liver failure Brain related damage impairment (ARBI) Fertility issues PMID: 2672958, Boyadjieva, N.I., and Sarkar D.K. Research proves alcohol has a clear effect on the brain. Alcohol can stimulate neurons in the paraventricular nucleus (PVN) of the hypothalamus to release corticotropin-releasing factor (CRF) and arginine vasopressin (AVP). In addition to the effects of alcohol on the adolescent brain drinking alcohol at an early age has other risks. 1986). PMID: 11141043, Richardson, H.N. After puberty, the levels again decrease slowly to reach the adult level. Vasopressin secretion control: Central neural pathways, neurotransmitters and effects of drugs. Alcohol Health & Research World 21(1):1320, 1997. How the Body Responds to Alcohol Alcohol acts primarily on the nerve cells within the brain. PMID: 9727642, Maeda, N.; Shimomura, I.; Kishida, H.; et al. This amount is present in 12 ounces of beer; 8 ounces of malt . ; Floreani, N.; et al. The researchers also detected a decrease in the glucose transporter Glut2 in -cells as well as a decrease in insulin synthesis, further exacerbating the effects of chronic alcohol exposure. British Medical Journal 2(5608):804805, 1968. In premenopausal women, chronic heavy drinking contributes to reproductive disorders, including:. PMID: 11198718, Obradovic, T., and Meadows, G.G. Learning and memory are crucial events during adolescence, when the brain is maturing both physically and functionally. It is responsible for making hormones that affect many body functions. ; Song, E.H.; Lee, H.J. 1998) and rodents (Emanuele et al. 1993; Stoop 2014). Sign up for text support. Over the last decade, however, numerous studies have demonstrated that WAT is a dynamically active endocrine organ that can produce and secrete biologically active peptides and proteins called adipokines, which have autocrine, paracrine, and endocrine actions. In addition, exposure of ovariectomized rats to ethanol for 2 to 4 weeks reduced the expression of two other G-proteins, Gi2 and Gi3 (Chaturvedi and Sarkar 2008). Accountability is a vital and required part of sustaining recovery. After 20 minutes, your liver starts processing alcohol. 6. PMID: 22031825, Bantle, A.E. Taken together these studies indicate that ethanol diminishes dopamines ability to inhibit prolactin secretion by altering the processing (i.e., splicing) of D2R mRNA, promoting the increase of the D2L isoform, as well as by differentially altering the expression of various Gi and Gs proteins in lactotropic cells. ; Krampe, H.; et al. Similarly, healthy men who were in the top percentile of self-reported alcohol consumption had higher levels of excreted cortisol in urine (Thayer et al. ; Pritchard, M.T. 2005). ; Castellano, J.M. Hyperprolactinemia following chronic alcohol administration. Neuroendocrinology 48(5):495499, 1988. Various mechanisms have been proposed for the blunted HPA axis responsiveness to chronic alcohol consumption. PMID: 23025690, Pienaar, W.P. In the testes, in contrast, LH stimulates testosterone production and release, whereas FSH controls spermatogenesis. Thank you! 2013). Alcohol may induce inflammation through both direct and indirect mechanisms. Some studies found normal concentrations of total plasma T4 (tT4) during early withdrawal (Majumdar et al. 2012). It is absorbed through the lining of your stomach into your bloodstream. 1982; Dees et al. PMID: 1656797, Aoun, E.G. Its production and actions are regulated by TNF, with the two compounds suppressing each others production and antagonizing each others actions in target tissues (Maeda et al. A review published in 2015 reported that chronic heavy drinking can cause glucose intolerance in healthy people. Insulin Resistance: Impairment of the normal physiological response to insulin that may be the result of a variety of abnormalities; occurs in diabetes mellitus. 2013). 2003). Federal government websites often end in .gov or .mil. High circulating TNF levels, in turn, have been implicated in the development of peripheral insulin resistance (Hotamisligil et al. For more information, see the sidebar Alcohols Effects on the HypothalamicPituitaryGonadal Axis During Puberty.. Alcohol use has been shown to affect many hormone systems, including the hypothalamicpituitaryadrenal (HPA) axis, the hypothalamicpituitarygonadal (HPG) axis, the hypothalamicpituitarythyroid (HPT) axis, the hypothalamicpituitarygrowth hormone/insulin-like growth factor-1 (GH/IGF-1) axis, and the hypothalamicposterior pituitary (HPP) axis. Moreover, intravenous injection of 10 mg diazepam, an allosteric modulator of GABA receptor function, had no effect on GH secretion in men with AUD who had maintained a 5-week abstinence, whereas control subjects without AUD showed a striking increase of GH secretion in response to diazepam (Vescovi and Coiro 1999). Endocrinology 141(4):13251331, 2000. This decrease seems to be related to reduced activity of the gene resulting from epigenetic modifications of the D2R gene. 2006). Sobriety is challenging, but your health is worth it. PMID: 19481567, Rowe, P.H. ; Hendriks, H.F.; et al. 2005). Unlike other cells within the human body, brain cells do not regenerate. Substantial evidence from animal research and a growing number of studies in humans indicate that marijuana exposure during development can cause long-term or possibly permanent adverse changes in the brain. ; Smedley, K.L. 2006; Zimmermann et al. Endocrine Reviews 29(5):535559, 2008. PMID: 23839524, Wang, S.; Luo, Y.; Feng, A.; et al. ; et al. PMID: 3001809, Seki, M.; Yoshida, K.; and Okamura, Y. PMID: 10961870, Zhang, Y.; Proenca, R.; Maffei, M.; et al. Inverse relationship between CSF TRH concentrations and the TSH response to TRH in abstinent alcohol-dependent patients. ; and Nyomba, B.L. Corticotropin-releasing hormone (CRH) is released from the hypothalamus, which stimulates the anterior pituitary to release adrenocorticotropic hormone (ACTH). PMID: 6307074, Cicero, T.J.; Newman, K.S. The researchers noted that testosterone, estrogen, and glucocorticoids interact with each. 2009; Li et al. PMID: 26519603, Majumdar, S.K. Leptin acts centrally to induce the prepubertal secretion of luteinizing hormone in the female rat. This could account at least for part of the alcohol-induced impairment in -cell function, because activation of GABA receptors in pancreatic -cells increases insulin secretion (Bansal et al. Alcohol abuse disrupts all of these systems and causes hormonal disturbances that may result in various disorders, such as stress intolerance, reproductive dysfunction, thyroid problems, immune abnormalities, and psychological and behavioral disorders. A 2014 study looked at how stress and sex hormones affect dopamine neurotransmission during adolescence. 2010). Diet-induced insulin resistance in mice lacking adiponectin/ACRP30. For those who drink mass amounts of alcohol, the following body parts are at risk for damage: One other major risk from overdrinking is a higher chance of cancer. IUBMB Life 60(12):790797, 2008. By Buddy T Studies found that heavy alcohol consumption results in reduced testosterone ; Boldt, B.M. Together, GH and IGF-1 regulate important physiological processes in the body, such as pre- and postnatal growth and development (Giustina et al. Alcoholism: Clinical and Experimental Research 19(6):14671473, 1995. For example, acute exposure to ethanol is associated with suppressed production of certain cytokines (e.g., tumor necrosis factor alpha [TNF] and IL-1) (Pruett et al. Hypothalamic releasing and inhibiting hormones are carried directly to the anterior pituitary gland via hypothalamic-hypophyseal portal veins. Verywell Mind articles are reviewed by board-certified physicians and mental healthcare professionals. 1983). Therefore, some problems like bloating, gassiness, or diarrhea can occur. Hepatology 31(6):1379, 2000. Another proposed mechanism for the alcohol-induced decrease in LH secretion during puberty is that even though the hypothalamus produced more LHRH, the release of the hormone to the pituitary gland was diminished (Dees and Skelley 1990). PMID: 12766631, Ehrenreich, H.; tom Dieck, K.; Gefeller, O.; et al. Hegedus, L.; Rasmussen, N.; Ravn, V.; et al. Insulin lowers glucose levels, while glucagon raises it. PMID: 22302180, Nagy, L.E. Mechanism of alcohol-induced oxidative stress and neuronal injury. PMID: 24259947, Kim, J.Y. Alcohol can permeate virtually every organ and tissue in the body, resulting in tissue injury and organ dysfunction. Acute exposure to alcohol activates the HPA axis, leading to a dose-related increase in circulating ACTH and glucocorticoids and inducing anxiolytic-like responses (Richardson et al. The pituitary gland comprises two sectionsthe adenohypophysis, or anterior lobe, and the neurohypophysis, or posterior lobe. the testes, and the hypothalamus.2 Alcohol affects each of these parts of the male reproductive system, preventing . Alcohol exposure also can interfere with these hormonal systems. PMID: 10189054, De Marinis, L.; Mancini, A.; Fiumara, C.; et al. 1990; Wei et al. Endocrine Reviews 17(1):64102, 1996. There are two isoforms of the D2R, a long (D2L) and a short (D2S) isoform.1 Chronic exposure to ethanol increases the expression of prolactin mRNA and of D2L mRNA but decreases expression of D2S both in the pituitary of Fischer-344 rats and in primary cultures of anterior pituitary cells (Oomizu et al.
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As a part of Jhan Dhan Yojana, Bank of Baroda has decided to open more number of BCs and some Next-Gen-BCs who will rendering some additional Banking services. We as CBC are taking active part in implementation of this initiative of Bank particularly in the states of West Bengal, UP,Rajasthan,Orissa etc.
We got our robust technical support team. Members of this team are well experienced and knowledgeable. In addition we conduct virtual meetings with our BCs to update the development in the banking and the new initiatives taken by Bank and convey desires and expectation of Banks from BCs. In these meetings Officials from the Regional Offices of Bank of Baroda also take part. These are very effective during recent lock down period due to COVID 19.
Information and Communication Technology (ICT) is one of the Models used by Bank of Baroda for implementation of Financial Inclusion. ICT based models are (i) POS, (ii) Kiosk. POS is based on Application Service Provider (ASP) model with smart cards based technology for financial inclusion under the model, BCs are appointed by banks and CBCs These BCs are provided with point-of-service(POS) devices, using which they carry out transaction for the smart card holders at their doorsteps. The customers can operate their account using their smart cards through biometric authentication. In this system all transactions processed by the BC are online real time basis in core banking of bank. PoS devices deployed in the field are capable to process the transaction on the basis of Smart Card, Account number (card less), Aadhar number (AEPS) transactions.