Successful Surgical Management of Giant Mucinous Cystic Neoplasm of Liver (MCN-L) Presenting With Peritoneal Rupture and Biliary Prolapse: Case Report and Review of Literature.

Mucinous cystic neoplasms of liver (MCN-L) are generally considered benign indolent cystic liver lesions, not associated with significant clinical symptoms in majority of patients. However, rarely these benign-appearing lesions may have a complicated clinical course, presenting with jaundice, acute abdomen, or malignant transformation. We report one such rare clinical presentation of MCN-L presenting with obstructive jaundice and abdominal pain due to prolapse of cystic component in biliary system and peritoneal rupture occurring simultaneously. Despite the complex nature of presentation, it was successfully managed surgically with normal follow-up imaging.

Curcumin, inflammation, and neurological disorders: How are they linked?

Background: Despite the extensive research in recent years, the current treatment modalities for neurological disorders are suboptimal. Curcumin, a polyphenol found in Curcuma genus, has been shown to mitigate the pathophysiology and clinical sequalae involved in neuroinflammation and neurodegenerative diseases. Methods: We searched PubMed database for relevant publications on curcumin and its uses in treating neurological diseases. We also reviewed relevant clinical trials which appeared on searching PubMed database using 'Curcumin and clinical trials'. Results: This review details the pleiotropic immunomodulatory functions and neuroprotective properties of curcumin, its derivatives and formulations in various preclinical and clinical investigations. The effects of curcumin on neurodegenerative diseases such as Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), brain tumors, epilepsy, Huntington's disorder (HD), ischemia, Parkinson's disease (PD), multiple sclerosis (MS), and traumatic brain injury (TBI) with a major focus on associated signalling pathways have been thoroughly discussed. Conclusion: This review demonstrates curcumin can suppress spinal neuroinflammation by modulating diverse astroglia mediated cascades, ensuring the treatment of neurological disorders.

Role of Turmeric and Curcumin in Prevention and Treatment of Chronic Diseases: Lessons Learned from Clinical Trials.

Turmeric (Curcuma longa) has been used for thousands of years for the prevention and treatment of various chronic diseases. Curcumin is just one of >200 ingredients in turmeric. Almost 7000 scientific papers on turmeric and almost 20,000 on curcumin have been published in PubMed. Scientific reports based on cell culture or animal studies are often not reproducible in humans. Therefore, human clinical trials are the best indicators for the prevention and treatment of a disease using a given agent/drug. Herein, we conducted an extensive literature survey on PubMed and Scopus following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. The keywords "turmeric and clinical trials" and "curcumin and clinical trials" were considered for data mining. A total of 148 references were found to be relevant for the key term "turmeric and clinical trials", of which 70 were common in both PubMed and Scopus, 44 were unique to PubMed, and 34 were unique to Scopus. Similarly, for the search term "curcumin and clinical trials", 440 references were found to be relevant, of which 70 were unique to PubMed, 110 were unique to Scopus, and 260 were common to both databases. These studies show that the golden spice has enormous health and medicinal benefits for humans. This Review will extract and summarize the lessons learned about turmeric and curcumin in the prevention and treatment of chronic diseases based on clinical trials.

Multifunctionality of Calebin A in inflammation, chronic diseases and cancer.

Chronic diseases including cancer have high case numbers as well as mortality rates. The efficient treatment of chronic diseases is a major ongoing medical challenge worldwide, because of their complexity and many inflammatory pathways such as JNK, p38/MAPK, MEK/ERK, JAK/STAT3, PI3K and NF-κB among others being implicated in their pathogenesis. Together with the versatility of chronic disease classical mono-target therapies are often insufficient. Therefore, the anti-inflammatory as well as anti-cancer capacities of polyphenols are currently investigated to complement and improve the effect of classical anti-inflammatory drugs, chemotherapeutic agents or to overcome drug resistance of cancer cells. Currently, research on Calebin A, a polyphenolic component of turmeric (Curcuma longa), is becoming of growing interest with regard to novel treatment strategies and has already been shown health-promoting as well as anti-tumor properties, including anti-oxidative and anti-inflammatory effects, in diverse cancer cells. Within this review, we describe already known anti-inflammatory activities of Calebin A via modulation of NF-κB and its associated signaling pathways, linked with TNF-α, TNF-ß and COX-2 and further summarize Calebin A's tumor-inhibiting properties that are known up to date such as reduction of cancer cell viability, proliferation as well as metastasis. We also shed light on possible future prospects of Calebin A as an anti-cancer agent.

Is Fatty Liver Associated with Increased Mortality and Morbidity in Coronavirus Disease 2019 (COVID-19) Pneumonia?

Background: Fatty liver has been shown to be associated with severe COVID-19 disease without any impact on mortality. This is based on heterogenous criteria for defining both fatty liver as well as the severity parameters. This study aimed to study the impact of fatty liver on the mortality and severity of disease in patients with COVID-19 pneumonia. Methods: In a case control study design, patients with COVID-19 pneumonia (COVID-19 computed tomography severity index [CTSI] on high-resolution computed tomography chest of ≥1) with fatty liver (defined as liver to spleen attenuation index ≤5 on noncontrast computed tomography cuts of upper abdomen) were compared with those without fatty liver. The primary outcome measure was in-hospital mortality, and the secondary outcome measures were CTSI score, need for intensive care unit (ICU) care, need for ventilatory support, duration of ICU stay, and duration of hospital stay. Results: Of 446 patients with COVID-19 pneumonia, 289 (64.7%)admitted to Max Hospital, Saket, India, between January 1, 2021, and October 30, 2021, had fatty liver. Fifty-nine of 446 patients died during the index admission. In-hospital mortality was not different between patients with fatty liver (38 [13.24%]) or without fatty liver (21 [13.81%]). COVID-19 CTSI score was found to be significantly higher among patients who had fatty liver (13.40 [5.16] vs 11.81 [5.50]; P = 0.003). There was no difference in the requirement of ICU (94 [32%] vs 62 [39.49%]; P = 0.752), requirement of ventilatory support (27 [9.34%] vs 14 [8.91%]; P = 0.385), duration of ICU stay (8.29 [6.87] vs 7.07 [5.71] days; P = 0.208), and duration of hospital stay (10.10 [7.14] vs 10.69 [8.13] days; P = 0.430) between the groups with fatty liver or no fatty liver. Similarly, no difference was found in primary or secondary outcomes measure between the group with severe fatty liver vs mild/moderate or no fatty liver. High total leucocyte count and Fibrosis-4 (FIB-4) index were independently associated with mortality. Conclusions: Fatty liver may not be associated with increased mortality or clinical morbidity in patients who have COVID-19 pneumonia.

A prospective evaluation of breast thermography enhanced by a novel machine learning technique for screening breast abnormalities in a general population of women presenting to a secondary care hospital.

Objective: Artificial intelligence-enhanced breast thermography is being evaluated as an ancillary modality in the evaluation of breast disease. The objective of this study was to evaluate the clinical performance of Thermalytix, a CE-marked, AI-based thermal imaging test, with respect to conventional mammography. Methods: A prospective, comparative study performed between 15 December 2018 and 06 January 2020 evaluated the performance of Thermalytix in 459 women with both dense and nondense breast tissue. Both symptomatic and asymptomatic women, aged 30-80 years, presenting to the hospital underwent Thermalytix followed by 2-D mammography and appropriate confirmatory investigations to confirm malignancy. The radiologist interpreting the mammograms and the technician using the Thermalytix tool were blinded to the others' findings. The statistical analysis was performed by a third party. Results: A total of 687 women were recruited, of whom 459 fulfilled the inclusion criteria. Twenty-one malignancies were detected (21/459, 4.6%). The overall sensitivity of Thermalytix was 95.24% (95% CI, 76.18-99.88), and the specificity was 88.58% (95% CI, 85.23-91.41). In women with dense breasts (n = 168, 36.6%), the sensitivity was 100% (95% CI, 69.15-100), and the specificity was 81.65% (95% CI, 74.72-87.35). Among these 168 women, 37 women (22%) were reported as BI-RADS 0 on mammography; in this subset, the sensitivity of Thermalytix was 100% (95% CI, 69.15-100), and the specificity was 77.22% (95% CI, 69.88-83.50). Conclusion: Thermalytix showed acceptable sensitivity and specificity with respect to mammography in the overall patient population. Thermalytix outperformed mammography in women with dense breasts and those reported as BI-RADS 0.

Multitargeting Effects of Calebin A on Malignancy of CRC Cells in Multicellular Tumor Microenvironment.

BACKGROUND: Tumor microenvironment (TME) provides the essential prerequisite niche for promoting cancer progression and metastasis. Calebin A, a component of Curcuma longa, has long been investigated as a safe multitargeted agent with antitumor and anti-inflammatory properties. However, the multicellular-TME-induced malignancy and the antitumorigenic potential of Calebin A on colorectal cancer (CRC) cells in 3D-alginate cultures are not yet understood, and more in-depth research is needed. METHODS: 3D-alginate tumor cultures (HCT116 cells) in the multicellular proinflammatory TME (fibroblast cells/T lymphocytes), tumor necrosis factor beta (TNF-ß)-TME (fibroblast cells/TNF-ß) were treated with/without Calebin A to address the pleiotropic actions of Calebin A in the CRC. RESULTS: We found that Calebin A downmodulated proliferation, vitality, and migration of HCT116 cells in 3D-alginate cultures in multicellular proinflammatory TME or TNF-ß-TME. In addition, Calebin A suppressed TNF-ß-, similar to multicellular-TME-induced phosphorylation of nuclear factor kappa B (NF-κB) in a concentration-dependent manner. NF-κB-promoting proinflammatory mediators, associated with tumor growth and antiapoptotic molecules (i.e.,MMP-9, CXCR4, Ki-67, ß1-integrin, and Caspase-3) and its translocation to the nucleus in HCT116 cells, were increased in both TME cultures. The multicellular-TME cultures further induced the survival of cancer stem cells (CSCs) (upregulation of CD133, CD44, and ALDH1). Last but not the least, Calebin A suppressed multicellular-, similar to TNF-ß-TME-induced rigorous upregulation of NF-κB phosphorylation, various NF-κB-regulated gene products, CSCs activation, and survival in 3D-alginate tumor cultures. CONCLUSIONS: The downmodulation of multicellular proinflammatory-, similar to TNF-ß-TME-induced CRC proliferation, survival, and migration by the multitargeting agent Calebin A could be a new therapeutic strategy to suppress inflammation and CRC tumorigenesis.

Mcl-1 Inhibition: Managing Malignancy in Multiple Myeloma.

Multiple myeloma (MM) is a plasma cells neoplasm. The overexpression of Bcl-2 family proteins, particularly myeloid cell leukemia 1 (Mcl-1), plays a critical role in the pathogenesis of MM. The overexpression of Mcl-1 is associated with drug resistance and overall poor prognosis of MM. Thus, inhibition of the Mcl-1 protein considered as a therapeutic strategy to kill the myeloma cells. Over the last decade, the development of selective Mcl-1 inhibitors has seen remarkable advancement. This review presents the critical role of Mcl-1 in the progression of MM, the most prominent BH3 mimetic and semi-BH3 mimetic that selectively inhibit Mcl-1, and could be used as single agent or combined with existing therapies.

Evidence That Tumor Microenvironment Initiates Epithelial-To-Mesenchymal Transition and Calebin A can Suppress it in Colorectal Cancer Cells.

Background: Tumor microenvironment (TME) has a pivotal impact on tumor progression, and epithelial-mesenchymal transition (EMT) is an extremely crucial initial event in the metastatic process in colorectal cancer (CRC) that is not yet fully understood. Calebin A (an ingredient in Curcuma longa) has been shown to repress CRC tumor growth. However, whether Calebin A is able to abrogate TME-induced EMT in CRC was investigated based on the underlying pathways. Methods: CRC cell lines (HCT116, RKO) were exposed with Calebin A and/or a FAK inhibitor, cytochalasin D (CD) to investigate the action of Calebin A in TME-induced EMT-related tumor progression. Results: TME induced viability, proliferation, and increased invasiveness in 3D-alginate CRC cultures. In addition, TME stimulated stabilization of the master EMT-related transcription factor (Slug), which was accompanied by changes in the expression patterns of EMT-associated biomarkers. Moreover, TME resulted in stimulation of NF-κB, TGF-ß1, and FAK signaling pathways. However, these effects were dramatically reduced by Calebin A, comparable to FAK inhibitor or CD. Finally, TME induced a functional association between NF-κB and Slug, suggesting that a synergistic interaction between the two transcription factors is required for initiation of EMT and tumor cell invasion, whereas Calebin A strongly inhibited this binding and subsequent CRC cell migration. Conclusion: We propose for the first time that Calebin A modulates TME-induced EMT in CRC cells, at least partially through the NF-κB/Slug axis, TGF-ß1, and FAK signaling. Thus, Calebin A appears to be a potential agent for the prevention and management of CRC.

Radiographic features of COVID-19 infection at presentation and significance of chest X-ray: Early experience from a super-specialty hospital in India.

BACKGROUND: Due to the relative early lockdown in India, relative greater availability of reverse transcription polymerase chain reaction (RT-PCR) testing, and mandate to admit all positive corona virus disease 2019 (COVID-19) patients, the protocol in our hospital is to perform a baseline chest X-ray (CXR) at the time of admission and for follow up. There are currently limited publications demonstrating the radiographic findings and the role of CXR of COVID-19 patients at presentation. AIMS: Evaluatethe radiographic findings on CXR in COVID-19 patients at presentation. Recommend a guideline for its judicious use. SETTINGS AND DESIGN: Retroprospective study performed on RT-PCR confirmed COVID-19 patients admitted in our hospital between March 31,2020 to May 25, 2020. The study included symptomatic and asymptomatic patients. CXR was performed for218 patients. MATERIALS AND METHODS: Portable bedside CXR was performed. The CXRs were evaluated by three radiologists to record the findings and grade the disease. All variables were expressed as mean, ranges, counts, and percentages. RESULTS: 157 patients (72%) were symptomatic and 61 (28%) were asymptomatic. 104 CXRs (48%) were abnormal (97 in symptomatic (62%) and fourin asymptomatic (6%)). 74 patients (47%) in the symptomatic group had known comorbidities and of these, 62 (84%) had abnormal CXR. 97 CXRs (93%) had bilateral findings and 87 CXRs (84%) had peripherally predominant abnormalities. The lower zone was the most common area of involvement (73%). Ground glass opacity (GGO) was the most common finding (94%-98 CXRs). Mild disease was seen in 56 (54%). CONCLUSION: CXR can be used to assess symptomatic COVID-19 patients at presentation and to grade the severity of disease. It may be avoided in asymptomatic patients.

COVID-19, cytokines, inflammation, and spices: How are they related?

BACKGROUND: Cytokine storm is the exaggerated immune response often observed in viral infections. It is also intimately linked with the progression of COVID-19 disease as well as associated complications and mortality. Therefore, targeting the cytokine storm might help in reducing COVID-19-associated health complications. The number of COVID-19 associated deaths (as of January 15, 2021; https://www.worldometers.info/coronavirus/) in the USA is high (1199/million) as compared to countries like India (110/million). Although the reason behind this is not clear, spices may have some role in explaining this difference. Spices and herbs are used in different traditional medicines, especially in countries such as India to treat various chronic diseases due to their potent antioxidant and anti-inflammatory properties. AIM: To evaluate the literature available on the anti-inflammatory properties of spices which might prove beneficial in the prevention and treatment of COVID-19 associated cytokine storm. METHOD: A detailed literature search has been conducted on PubMed for collecting information pertaining to the COVID-19; the history, origin, key structural features, and mechanism of infection of SARS-CoV-2; the repurposed drugs in use for the management of COVID-19, and the anti-inflammatory role of spices to combat COVID-19 associated cytokine storm. KEY FINDINGS: The literature search resulted in numerous in vitro, in vivo and clinical trials that have reported the potency of spices to exert anti-inflammatory effects by regulating crucial molecular targets for inflammation. SIGNIFICANCE: As spices are derived from Mother Nature and are inexpensive, they are relatively safer to consume. Therefore, their anti-inflammatory property can be exploited to combat the cytokine storm in COVID-19 patients. This review thus focuses on the current knowledge on the role of spices for the treatment of COVID-19 through suppression of inflammation-linked cytokine storm.

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.

Inflammation, NF-κB, and Chronic Diseases: How are They Linked?

Most chronic diseases, caused by lifestyle factors, appear to be linked to inflammation. Inflammation is activated mechanistically, and nuclear factor-κB (NF-κB) is a significant mediator. NF-κB, one of the most studied transcription factors, was first identified in the nucleus of B lymphocytes almost three decades ago. This protein has a key function in regulating the human immune system, and its dysregulation has been linked to many chronic diseases including asthma, cancer, diabetes, rheumatoid arthritis, inflammation, and neurological disorders. Physiologically, many cytokines have been discovered that activate NF-κB. Pathologically, environmental carcinogens such as cigarette smoke, radiation, bacteria, and viruses can also activate this transcription factor. NF-κB activation controls expression of more than 500 genes, and most are deleterious to the human body when dysregulated. More than 70,000 articles have been published regarding NF-κB. This review emphasizes the upside and downside of NF-κB in normal and disease conditions and the ways in which we can control this critical transcription factor in patients.

Calebin A Potentiates the Effect of 5-FU and TNF-ß (Lymphotoxin α) against Human Colorectal Cancer Cells: Potential Role of NF-κB.

OBJECTIVE: The majority of chemotherapeutic agents stimulate NF-κB signaling that mediates cell survival, proliferation and metastasis. The natural turmeric non-curcuminoid derivate Calebin A has been shown to suppress cell growth, invasion and colony formation in colorectal cancer cells (CRC) by suppression of NF-κB signaling. Therefore, we hypothesized here that Calebin A might chemosensitize the TNF-ß-treated tumor cells and potentiates the effect of 5-Fluorouracil (5-FU) in advanced CRC. MATERIALS AND METHODS: CRC cells (HCT116) and their clonogenic 5-FU chemoresistant counterparts (HCT116R) were cultured in monolayer or alginate-based 3D tumor environment culture and were treated with/without Calebin A, TNF-ß, 5-FU, BMS-345541 and DTT (dithiothreitol). RESULTS: The results showed that TNF-ß increased proliferation, invasion and resistance to apoptosis in chemoresistant CRC cells. Pretreatment with Calebin A significantly chemosensitized HCT116R to 5-FU and inhibited the TNF-ß-induced enhanced efforts for survival, invasion and anti-apoptotic effects. We found further that Calebin A significantly suppressed TNF-ß-induced phosphorylation and nuclear translocation of p65-NF-κB, similar to BMS-345541 (specific IKK inhibitor) and NF-κB-induced tumor-promoting biomarkers (NF-κB, ß1-Integrin, MMP-9, CXCR4, Ki67). This was associated with increased apoptosis in HCT116 and HCT116R cells. Furthermore, blocking of p65-NF-κB stimulation by Calebin A was imparted through the downmodulation of p65-NF-κB binding to the DNA and this suppression was turned by DTT. CONCLUSION: Our findings indicate, for the first time, that Calebin A chemosensitizes human CRC cells to chemotherapy by targeting of the p65-NF-κB signaling pathway.

Evidence that TNF-ß suppresses osteoblast differentiation of mesenchymal stem cells and resveratrol reverses it through modulation of NF-κB, Sirt1 and Runx2.

It has been established that inflammation plays an important role in bone formation and bone loss. Although a lot is known about the role of TNF-α in bone health, very little is understood about TNF-ß, also called lymphotoxin. In this report, we examine the effect of TNF-ß on osteogenic differentiation of mesenchymal stem cells (MSCs) and its modulation by resveratrol. Monolayer and high-density cultures of MSCs were treated with osteogenic induction medium with/without TNF-ß, Sirt1 inhibitor nicotinamide (NAM), antisense oligonucleotides against Sirt1 (ASO) and/or Sirt1 stimulator resveratrol. We found that TNF-ß inhibits, in a similar way to NAM or Sirt1-ASO, the early stage of osteogenic differentiation of MSCs and this was accompanied with downregulation of bone-specific matrix, ß1-integrin, Runx2 and with upregulation of NF-κB phosphorylation and NF-κB-regulated gene products involved in the inflammatory, degradative processes and apoptosis. However, resveratrol reversed TNF-ß- and NAM-suppressed MSCs osteogenesis by activation of Sirt1 and Runx2 that led to osteoblast differentiation. Furthermore, downregulation of Sirt1 by mRNA inhibited the effect of resveratrol, highlighting the important impact of this enzyme in the TNF-ß signaling pathway. Finally, resveratrol was able to manifest its effect both by suppression of TNF-ß-induced NF-κB and through direct activation of the Sirt1 and Runx2 pathway. Thus, through these studies, we present a mechanism by which a T cell-derived cytokine, TNF-ß can affect bone formation through modulation of MSCs differentiation that involves NF-κB, Sirt1, Runx2 and resveratrol reversed TNF-ß-promoted impairments in MSCs osteogenesis.

Evidence That Calebin A, a Component of Curcuma Longa Suppresses NF-B Mediated Proliferation, Invasion and Metastasis of Human Colorectal Cancer Induced by TNF-ß (Lymphotoxin).

OBJECTIVE: Natural polyphenol Calebin A has been recently discovered as a novel derivate from turmeric with anti-cancer potential. Pro-inflammatory cytokine TNF-ß (lymphotoxin α) is a stimulant for cancer cell malignity via activation of NF-B pathway, also in colorectal cancer (CRC). Here, we investigated the potential of Calebin A to suppress TNF-ß-induced NF-B signalling in CRC. MATERIALS AND METHODS: Three distinct CRC cell lines (HCT116, RKO, SW480) were treated in monolayer or 3-dimensional alginate culture with TNF-ß, Calebin A, curcumin, BMS-345541, dithiothreitol (DTT) or antisense oligonucleotides-(ASO) against NF-B. RESULTS: Calebin A suppressed dose-dependent TNF-ß-induced CRC cell vitality and proliferation in monolayer culture. Further, in alginate culture, Calebin A significantly suppressed TNF-ß-enhanced colonosphere development, as well as invasion and colony formation of all three CRC cell lines investigated. Calebin A specifically blocked TNF-ß-induced activation and nuclear translocation of p65-NF-B, similar to curcumin (natural NF-B inhibitor), BMS-345541 (specific IKK inhibitor) and ASO-NF-B. Moreover, Immunofluorescence and Immunoblotting showed that Calebin A, similar to curcumin or BMS-345541 suppressed TNF-ß-induced activation and nuclear translocation of p65-NF-B and the transcription of NF-B-promoted biomarkers associated with proliferation, migration and apoptosis, in a dose- and time-dependent manner. Those findings were potentiated by the specific treatment of extracted nuclei with DTT, which abrogated Calebin A-mediated nuclear p65-NF-B-inhibition and restored p65-NF-B-activity in the nucleus. CONCLUSION: Overall, these results demonstrate, for the first time, that multitargeted Calebin A has an anti-cancer capability on TNF-ß-induced malignities through inhibitory targeting of NF-B activation in the cytoplasm, as well as by suppressing the binding of p65-NF-B to DNA.

Ultrasound-guided injections in musculo-skeletal system - An overview.

Ultrasound guided musculoskeletal injection has a wide range of indication in joint, muscle, tendon, nerve, ganglion and bursa pathologies. These are less invasive procedures and provide desirable results in short duration. Local anesthetics and corticosteroids are the most commonly injected pharmaceuticals. Platelet rich plasma and autologus blood injections have gained popularity in recent past and provide acceptable results. In this article we aim to review the general consideration, indications, technique and pharmaceuticals used in common therapeutic musculoskeletal injections.

Is curcumin bioavailability a problem in humans: lessons from clinical trials.

Introduction: Since ancient times, turmeric has been used in several folklore remedies against various ailments. The principal component of turmeric is curcumin and its efficacy has been advocated in various in vitro, in vivo and clinical studies for different chronic diseases. However, some studies suggest that curcumin bioavailability is a major problem. Areas covered: This article discusses over 200 clinical studies with curcumin that have demonstrated the pronounced protective role of this compound against cardiovascular diseases, inflammatory diseases, metabolic diseases, neurological diseases, skin diseases, liver diseases, various types of cancer, etc. The review also describes the combination of curcumin with many natural and synthetic compounds as well as various formulations of curcumin that have shown efficacy in multiple clinical studies. Expert opinion: The therapeutic potential of curcumin, as demonstrated by clinical trials has overpowered the myth that poor bioavailability of curcumin poses a problem. Low curcumin bioavailability in certain studies has been addressed by using higher concentrations of curcumin within nontoxic limits. Moreover, curcumin, in combination with other compounds or as formulations, has shown enhanced bioavailability. Hence, bioavailability is not a problem in the curcumin-mediated treatment of chronic diseases. Therefore, this golden nutraceutical presents a safe, low-cost and effective treatment modality for different chronic diseases.