My students Babisweta Swain, Abhishek Raj and Piyush Barwal had presented this topic in our 22nd Student Scientific Society Conference in the department of Propaedeutic of Internal Diseases No.2
Diabetic drugs is a very important topic for pg entrance.....so all about it has been discussed in detail as required for pg entrance....do make use of it...
Shedding the lights on SUs Translating evidence into patients’ benefits mhrsrs2011
Sulfonylureas were discovered by the french chemist Marcel Janbon and co-workers during World War II
, who were studying sulfonamide antibiotics and discovered that the compound sulfonylurea induced hypoglycemia in animals.
Controlling blood sugar (glucose) levels is the major goal of diabetes treatment, in order to prevent complications of the disease.
Type 1 diabetes is managed with insulin as well as dietary changes and exercise.
Type 2 diabetes may be managed with non-insulin medications, insulin, weight reduction, or dietary changes.
Medications for type 2 diabetes are designed to
increase insulin output by the pancreas,
decrease the amount of glucose released from the liver,
increase the sensitivity (response) of cells to insulin,
decrease the absorption of carbohydrates from the intestine, and
slow emptying of the stomach, thereby delaying nutrient digestion and absorption in the small intestine.
O futuro na terapia baseada em incretins.Ruy Pantoja
Neste belo artigo realcei em amarelo as partes que mais me instigaram. Depois traço um paralelismo com a bela conferência do Prof. Buse, realizada em San Diego há um mês.
Diabetic drugs is a very important topic for pg entrance.....so all about it has been discussed in detail as required for pg entrance....do make use of it...
Shedding the lights on SUs Translating evidence into patients’ benefits mhrsrs2011
Sulfonylureas were discovered by the french chemist Marcel Janbon and co-workers during World War II
, who were studying sulfonamide antibiotics and discovered that the compound sulfonylurea induced hypoglycemia in animals.
Controlling blood sugar (glucose) levels is the major goal of diabetes treatment, in order to prevent complications of the disease.
Type 1 diabetes is managed with insulin as well as dietary changes and exercise.
Type 2 diabetes may be managed with non-insulin medications, insulin, weight reduction, or dietary changes.
Medications for type 2 diabetes are designed to
increase insulin output by the pancreas,
decrease the amount of glucose released from the liver,
increase the sensitivity (response) of cells to insulin,
decrease the absorption of carbohydrates from the intestine, and
slow emptying of the stomach, thereby delaying nutrient digestion and absorption in the small intestine.
O futuro na terapia baseada em incretins.Ruy Pantoja
Neste belo artigo realcei em amarelo as partes que mais me instigaram. Depois traço um paralelismo com a bela conferência do Prof. Buse, realizada em San Diego há um mês.
List of GLP-1 Receptor Agonists for Diabetes & Weight Loss.pdfDoriaFang
The development of GLP-1 long-acting receptor agonists has become a research hotspot worldwide. There are 9 GLP-1RA hypoglycemic drugs have been approved for diabetes & weight loss.
Impact of sodium glucose cotransporter 2 (SGLT2) inhibitors on atherosclerosi...OlgaGoryacheva4
My student Joisy Aloor had presented this topic in our 22nd Student Scientific Society Conference in the department of Propaedeutic of Internal Diseases No.2
International Journal of Pharmaceutical Science Invention (IJPSI)inventionjournals
International Journal of Pharmaceutical Science Invention (IJPSI) is an international journal intended for professionals and researchers in all fields of Pahrmaceutical Science. IJPSI publishes research articles and reviews within the whole field Pharmacy and Pharmaceutical Science, new teaching methods, assessment, validation and the impact of new technologies and it will continue to provide information on the latest trends and developments in this ever-expanding subject. The publications of papers are selected through double peer reviewed to ensure originality, relevance, and readability. The articles published in our journal can be accessed online.
Herbal therapies for type 2 diabetes mellitusDwie Craph
dm type 2
Similar to GLP-1 receptor agonists (GLP-1RAs): cardiovascular actions and therapeutic potential by Babisweta Swain, Abhishek Raj and Piyush Barwal (20)
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
2. So what’s GLP-1?
Glucagon-like peptide-1 (GLP-1) is a 30 or 31 amino acid long peptide hormone
deriving from the tissue-specific posttranslational processing of the proglucagon
peptide. It is produced and secreted by intestinal enteroendocrine L-cells and
certain neurons within the nucleus of the solitary tract in the brainstem upon food
consumption. The initial product GLP-1 (1–37) is susceptible to amidation and
proteolytic cleavage which gives rise to the two truncated and equipotent
biologically active forms, GLP-1 (7–36) amide and GLP-1 (7–37). Active GLP-1
composes two α-helices from amino acid position 13–20 and 24–35 separated by
a linker region.
3. Alongside glucose-dependent insulinotropic peptide (GIP), GLP-1 is an incretin;
thus, it has the ability to decrease blood sugar levels in a glucose-dependent
manner by enhancing the secretion of insulin. Beside the insulinotropic effects,
GLP-1 has been associated with numerous regulatory and protective effects.
Unlike GIP, the action of GLP-1 is preserved in patients with type 2 diabetes and
substantial pharmaceutical research has therefore been directed towards the
development of GLP-1-based treatment.
4. Endogenous GLP-1 is rapidly degraded primarily by dipeptidyl peptidase-4 (DPP-
4), as well as neutral endopeptidase 24.11 (NEP 24.11) and renal clearance,
resulting in a half-life of approximately 2 minutes. Consequently, only 10–15 % of
GLP-1 reaches circulation intact, leading to fasting plasma levels of only 0–15
pmol/L. To overcome this, GLP-1 receptor agonists and DPP-4 inhibitors have
been developed to increase GLP-1 activity. As opposed to common treatment
agents such as insulin and sulphonylurea, GLP-1-based treatment has been
associated with weight loss and a lower risk of hypoglycemia, two important
considerations for patients with type 2 diabetes.
5. What’s GLP-1 RA?
Glucagon-like peptide-1 receptor agonists, also known as GLP-1 receptor agonists or incretin
mimetics, are agonists of the GLP-1 receptor. This class of medications is used for the treatment
of type 2 diabetes.[1][2] One of their advantages over older insulin secretagogues, such as
sulfonylureas or meglitinides, is that they have a lower risk of causing hypoglycemia.[3] GLP-1 has
a short duration of action, so to overcome this limitation several modifications either in the drug or
the formulations are being developed. [4]
There is some dispute over the safety profile of these drugs due to proliferative effects in the
pancreas.[citation needed] Diabetes is associated with both acute pancreatitis and pancreatic
cancer. While some recent studies have not found that these drugs can cause either pancreatitis
or cancer,[5] a 2017 study found that recent prescription of incretins was associated with an
increased detection of occult pancreatic cancer over non-insulin anti diabetic drugs (NIADs)
6. Effects of GLP-1 RA Cardiovascular outcome trials of
GLP-1RAs
In the past decade, CVOTs with GLP-1RAs have
been conducted with at least seven agents including
liraglutide, lixisenatide, exenatide, semaglutide,
dulaglutide, albiglutide and oral semaglutide (Table
2). In CVOTs, liraglutide, semaglutide a
dulaglutide demonstrated appreciable cardiovascular
and renal protective effects, among which liraglutide
had an appreciable effect on mitigating the risk of
cardiovascular death [4], while semaglutide and
dulaglutide conferred a risk reduction on non-fatal
stroke [22, 23]. Moreover, liraglutide also had effects
on reducing the incidence of MI in high-risk patients
7. Cardiovascular actions of GLP-1RAs in
pre-clinical studiesEffects of GLP-1RAs on atherosclerosis and
atherosclerosis in the setting of diabetes, Atherosclerosis with multiple and diverse
drivers is a dominant complicating process in T2DM
[53]. Exposure to western diets pathologically alters the expression of many genes leading to
atherosclerosis [16]. According to a recent study, GLP-1R is mainly expressed in the macrophage
enrichment region of atherosclerotic plaques, which
provide us a new perspective on pharmacological modification of GLP-1R upon signal in
atherosclerosis
8. Preclinical studies have shown that large doses
of GLP-1RAs can reduce lipid deposition
and plaque volume on the aortic surface of hyperglycemic mice via an AMPK-independent
action in streptozotocin
(STZ)-induced hyperglycemic and hyperlipidemic mice or type 1 diabetic rats [55]. GLP-
1RAs have
direct anti-atherosclerotic effects in euglycemic mice, ApoE-/- mice or Watanabe heritable
hyperlipidemic (WHHL) rabbits in a GLP-1R-dependent manner
[56-58]. Therefore, these studies demonstrated that
GLP-1RAs have an impact on preventing and
stabilizing atherosclerotic vascular disease, which
may translate into its protective effects against MACE
in human subjects
9. Effects of GLP-1RAs on hypertension
,Hypertension and accompanying cardiovascular
remodeling are amongst the leading drivers of
atherosclerosis and causes of CVD. Endogenous , GLP-1R signaling exerts a physiologically
relevant effect on BP control, which may be attributable, in
part, to its tonic actions on proximal tubule Na/H
mediated sodium reabsorption, and the intrarenal renin-angiotensin II system [67]. In
spontaneously hypertensive rats, GLP-1 treatment mediates renal vasodilation and
attenuates renal autoregulatory responses [68]. In addition, acute renal infusion with GLP-1
can augment renal blood flow and promote natriuresis and dieresis [69]. In summary, GLP-1
or GLP-1RA treatment can make a positive impact on
reducing the impact of hypertension in affected
patients .
10. Effects of GLP-1RAs on myocardial
infarction(MI)
MI and its consequent tissue damage leading to heart failure are mainly responsible for the fatality in
patients with T2DM. Evidence indicates that GLP-1RAs can reduce the occurrence of MI [70]. Among
patients with acute MI undergoing percutaneous interventions, GLP-1 treatment can reduce infarctsize,
together with improving left ventricular ejection fraction (LVEF)
. GLP-1RA (such as exendin-4) treatment can reduce the size of MI impacted cardiac volume in rats,
inhibit ventricular dilation, myocardial fibrosis and hypertrophy in vivo [72].
Mechanically, GLP-1RAs regulate insulin-like growth
factor-1/2 and upregulate α-estrogen receptors to exert cardioprotective actions in isoprenaline-
induced MI []. In addition, another report demonstrated the reparative role of GLP-1RAs in MI via
modulating sirtulin (SIRT)1/Parkin/mitophagy [74].
Interestingly, even in obese swine, GLP-1R activation can improve cardiac function and augment
cardiac output after MI [75]. Accordingly, it is suggested that GLP-1RAs have properties of alleviating
MI and repairing damaged cardiac tissue to improve cardiac function.
11. Effects of GLP-1RAs on heart failure
Myocardial remodeling has a critical role in heart
failure following MI. Disturbances in cardiac calcium
metabolism are a hallmark of heart failure. GLP-1RAs prevent post-MI remodeling by having
an impact on the extracellular matrix changes rather than dependency on its glycemic
control [76]. There is another mechanism showing that GLP-1RA treatment
regulates Ca2+ levels due to reductions in the ryanodine receptor (RyR)2 phosphorylation
and suppression of the activation of calmodulin-
dependent protein kinase (CaMK)-II [77]. Moreover, a favorable impact of GLP-1RAs on
cardiac remodeling can occur through activation of the eNOS/cyclic guanosine
monophosphate (cGMP)/protein kinase G (PKG) nexus Cardiac hypertrophy leads to heart
failure at the later decompensated stage of the disease process, which is a primary cause of
morbidity and mortality.Evidence has recently revealed that GLP-1RAs inhibit cardiac
hypertrophy by upregulating GLP-1R expression and activating the AMPK/mechanistic
target of the rapamycin (mTOR) signaling pathway.
12. Mitochondrial dysfunction, apoptosis and oxidative stress are in part due to methylglyoxal
accumulation. Therefore, the attenuation ofmethylglyoxal-induced mitochondrial abnormalities
may suppress the progression of heart failure. In cultured H9c2 cells, GLP-1RAs attenuate the
production of mitochondrial and intracellular reactive oxygen species (ROS) induced by
methylglyoxal. As a result, GLP-1RAs display suppressive effects on mitochondrial functions
and oxidative stress on heart failure [79].
Although GLP-1RAs can play a favorable role in improving heart failure based on pre-clinical
studies, whereas some clinical evidence relevantly have reported that GLP-1RAs treatment could
be associated with adverse heart failure events, eg.
increasing heart rate, reducing LVEF . Therefore, overall, the benefit of GLP-1RAs for heart
failure has been difficult to confirm.
13. The potential cardiovascular benefits of
GLP-1RA
. GLP-1RAs have effects on limiting atherosclerosis, controlling hypertension, and delaying the
progression
of heart failure, myocardial infarction, and cardiomyopathy. For a brief description, GLP-1RAs
attenuate and stabilize the development of atherosclerotic plaques through
anti-inflammatory mechanisms and preventing vascular remodeling, and inhibit activation and
recruitment of macrophages in atherosclerosis. For hypertension, GLP-1RAs
augment renal blood flow and promote natriuresis and diuresis. For myocardial infarction, GLP-1RAs
alleviate and repair MI via SIRT1/Parkin/mitophagy, insulin-like growth
factor-1/2 and upregulating α-estrogen receptor. For heart failure, GLP-1RAs remodel calcium
circulation disorders, inhibit cardiac hypertrophy by activating the AMPK/ mTOR
signaling pathway and attenuate methylglyoxal-induced mitochondrial abnormalities. For
cardiomyopathy, GLP-1RAs improve mitochondrial function via regulating autophagy and
inflammatory signaling, as well as not only mediate the inhibition of myocardial apoptosis, but also
improve cardiac energy metabolism.
14. Effects of GLP-1RAs on cardiomyopathy
Diabetic cardiomyopathy is an important cardiac
complication which is accompanied by cardiac hypertrophy []. Chronic inflammation results
in the loss of cardiomyocytes in diabetic hearts. GLP-1RAs have the potential to inhibit
cardiac inflammation via retarding the production of pyroptotic cytokines, caspase-1 and the
AMPK-thioredoxin interacting protein (TXNIP) pathway in high-fat diet-fed rats .
15. Specifically, GLP-1RAs exert protective effects on
exercise-induced cardiomyopathy via increasing
autophagy, reducing inflammation-related proteins
and ROS generation via restoring the expression of catalase and manganese superoxide
dismutase (MnSOD) [81].GLP-1RAs attenuate apoptosis in cardiomyocytes induced by
hyperglycemia via inhibiting receptor of advanced glycation end
products (RAGE) receptor [82]. In H9c2 cardiomyoblasts, GLP-1RAs protect against cell
apoptosis and inhibit the expression of tumor protein
P53 (p53). GLP-1RAs not only mediate the inhibition
of myocardial apoptosis, but also improve cardiac energy metabolism. These studies illustrate
that GLP-1RAs may confer protective effects on the progression of cardiomyopathy.
16. GLP-1RA treatment also mitigates experimental
diabetic cardiomyopathy by the indirect mechanisms
of augmenting glucose oxidation in cardiomyocytes ]. In terms of mechanisms, GLP-
1RAs can block
C/EBP homologous protein (CHOP)-mediated endoplasmic reticulum (ER) stress via
attenuating the irreversible electroporation (IRE)-α unfolded protein response (UPR) [85].
There is a further action that the reduction of HOX transcript antisense RNA (HOTAIR)
expression gives rise to cardiomyopathy.
As a result, GLP-1RAs demonstrate a new therapeutic action in cirrhotic rats with
cardiomyopathy through the protective role of HOTAIR via SIRT1 activationfer
17. Improving cardiomyocyte/cardiac fibroblast
dysfunction by GLP-1RAs
Cardiomyocyte/cardiac fibroblast dysfunction is
related to abnormal proliferation,apoptosis,
hypertrophy, as well as inflammation and fibrosis,
which may be caused by mitochondrial dysfunction
and metabolic disorders. Persistent hyperglycemia
can mediate hypoxic or ischemic injury, as well as
elicit cardiomyocyte contractile dysfunction and the
NF-κB signaling pathway activation, thus inducing
ER stress [152]. GLP-1RA can help maintain a balance
of energy metabolism in cardiomyocytes through
activating PI3K/Akt as well as p38 MAPK pathways
as well as activating Nrf-2/heme oxygenase-1 (HO-1),
contributing to augmented adenosine triphosphate
formation and glucose ingestion by cardiomyocytes
18. Based on these pathways, GLP-1RAs
improve metabolic disorders to alleviate
cardiomyocyte dysfunction.
Apoptosis of cardiomyocytes is usually
irreversible, leading to myocardial damage.
GLP-1RAs make an impact on anti-apoptosis through
multiple pathways. Firstly, the impact is partly due to
ameliorating caspase-3 and Bax activity and
upregulating Bcl-2 [156]. Secondly, GLP-1RAs
attenuate apoptosis induced by TNF-α by
ameliorating mitochondrial dysfunction related to