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Journal of Nutritional Therapeutics

Process Standardization for the Manufacture of Shrikhand Spread - Pages 22-30
 
S. Sarkar, A. Sur, K. Sarkar, R. Majhi, K. Chatterjee, B. Sikder, S. Basu and S. Paul

DOI: https://doi.org/10.6000/1929-5634.2018.07.01.3

Published: 30 April 2018

 

 

Abstract: Purpose: Shrikhand Spread, a unique sweetened fermented Indian milk product is made by separation of whey from dahi, the Indian counterpart of Western yoghurt, followed by addition of sugar. Production of dahi employing traditional method involved undefined mixed starter cultures, uncontrolled fermentation and longer production time resulting in wide variation in its chemical and microbiological qualities. In order to cater to a product with desirable properties like lower post-acidification, higher flavour profile, firm body and lower syneresis coupled with shorter production time, conjugated application of yoghurt cultures and dahi cultures were tried. Since the shelf-life of dahi is limited, conversion into shrikhand spread may be used as a tool to extend the shelf-life and therefore the market reach towards commercialization into the global market as a potential functional food.

Design/Methodology/Approach: Different batches of dahi were made from homogenized (Stage I - 2500 psi, Stage II - 500 psi) and pasteurized (74-78 °C/16-19 Sec) milk, pre-adjusted to 3.15-3.20% fat and 11.40% snf with diverse starter combinations selected upon the extent of post acidification, volatile acid production, syneresis and rheological characteristics. Homogenized, pasteurized and regulated milk was further subjected to a heat-treatment (90°C/10 min) and seeded with selected starter combinations to obtain firm curd intended for shrikhand spread manufacture. Shelf-life of shrikhand spread was evaluated in terms of chemical and microbiological criteria upto 7 days of storage at 8±1°C.

Findings: Starter combination of eXactDahi 2+YoFlex Express 1.0 at an incubation temperature-time combination of 45°C/5h was found most suitable for producing dahi with smooth body, higher volatile acidity and low syneresis. Utilization of dahi obtained employing the above starter combination for the manufacture shrikhand spread was suggested and the product was found to retain its goodness when stored for 7 days at 8±1°C.

Originality/Value: Conjugated use of yoghurt cultures with dahi cultures was suggested to overcome the drawbacks of traditional process of dahi manufacture suitable for conversion into shrikhand spread. This dahi was found capable of enhancing its dietetic value in addition. 

Keywords: Lactic acid bacteria Dahi, Chakka, Shrikhand spread, Shelf-life.

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Journal of Nutritional Therapeutics

Camel Milk and the Prevention of Glucose Cataract, an Organ Culture Study - Pages 31-39
 
Ali H.S. Alghamdi, Hasabelrasoul Mohamed, Jonathan Austin, Collin Henry, Kayla Massey, Shanzeh Sayied, Samiyyah Sledge, Aliza Williams and Douglas Borchman

DOI: https://doi.org/10.6000/1929-5634.2018.07.02.1
Published: 16 August 2018

 

 

Abstract: Purpose: To test if camel milk affects glucose-induced opacity in organ cultured rat and human lenses.

Methods: Whole human and rat lenses were cultured in various media containing either 55 mM glucose, camel milk, or a combination of both glucose and milk. Some lenses were cultured in a media containing neither moiety to establish a control. Absorbance spectra of human and rat lenses were measured daily using a visible/ultraviolet light spectrometer. Lens opacities were graded by a blinded grader from photographs taken daily. Aldose reductase activity, catalase activity, glutathione and receptor for advanced glycation end products levels were assayed.

Results: The optical density and light scattering intensity of human lenses cultured with glucose were higher after two to four days in organ culture compared with lenses cultured without glucose. Camel milk in the culture media attenuated the glucose-induced increase in optical density, light scattering intensity and opacity grade after two to four days for both human and rat lenses. Aldose reductase activity, catalase activity and glutathione levels were restored but the receptor for advanced glycation end products was similar in rat lenses cultured with glucose compared with those cultured with glucose and camel milk. There were no differences between the assayed moieties in human lenses cultured with glucose or glucose plus milk. Since camel milk restored rat lens glutathione levels, it is possible that camel milk may protect the lens from oxidation and significantly reduce the glucose-induced increase in light scattering of human lenses. Structurally and physiologically, rat lenses are distinct from human lenses, therefore, the rat lens data was highly variable when compared with the human lens data, highlighting the importance of using human lenses in future studies.

Conclusions: Camel milk present in the organ culture medium inhibited the glucose-induced opacity in human lenses and restored the amount of glutathione to the same levels of lenses not cultured in glucose. The positive results of the current study leads to future studies to determine the moieties in camel milk that are responsible for cataract inhibition and in vivo studies involving camel milk.

Keywords: Camel milk, Cataract, Glucose, Human, Lens, Organ culture.

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Journal of Nutritional Therapeutics

Safety and Efficacy of Methanol Fraction of Moringa oleifera as Antihypertensive in L-NAME Induced Hypertensive Rabbits: Bedside to Bench, Implications for Bench Back to Bedside - Pages 51-58
 
Josef Hyánek, František Pehal, Ladislava Dubská, Blanka Miková, Věra Martiníková, Jana Privarová, Jana Brtnová and Luděk Táborský

DOI: https://doi.org/10.6000/1929-5634.2018.07.02.3

Published: 16 August 2018

 

 

Abstract: Context: Hypertension, a global menace requires innovative research into the use of Moringa oleifera being promoted and traditionally used as alternative therapy.

Objective: To innovatively evaluate the mechanistic effect, safety and efficacy of the methanol fraction of M. oleifera (MMO) leaves on L-NAME induced hypertensive rabbits.

Methods: Rabbits were divided into six groups: Control, L-NAME alone, L-NAME with 100, 200 or 400 mg/kg of MMO and enalapril. Inclusion and exclusion criteria were similar baseline parameters and Day 3 systolic blood pressure (SBP) less than baseline SBP respectively. The primary outcome was a 10% reduction of SBP on Day 21. Enalapril group was excluded from analysis. Safety was assessed with liver and renal functions, hydrogen peroxide and nitric oxide concentrations to elucidate mechanistic effect.

Results: Moringa 100 mg/kg, 200 mg/kg and 400 mg/kg reduced SBP by 4.75, 18.00 and 15.25 mmHg (F=22.123, p=0.000). SBP control was achieved with MMO 200mg/kg, 14% reduction and 400mg/kg, 12% reduction. Nitric oxide concentration, 0.06, 0.094 and 0.114mmol (F= 30.255, p= 0.000) dose-dependently increased and was most predictive of SBP control (r2=0.802, p=0.000). Nitric oxide production was inversely related to heart/body weight ratio which was dose-dependently reduced. MMO reduced hydrogen peroxide and ALT level but no significant effect on urea, HDL, and TG.

Conclusion: MMO reduced SBP and dose-dependently increased nitric oxide concentration in L-NAME induced hypertensive rabbits. The effect may be mediated via activation of nitric oxide pathway. MMO demonstrated a potent anti-oxidant activity and safety. Effect on ventricular hypertrophy needs further evaluation.

Keywords: Moringa, hypertension, nitric-oxide, anti-oxidant, intention-to-treat, per protocol.

Journal of Nutritional Therapeutics

Lathosterol and other Noncholesterol Sterols in Treatment of Hereditary Hypercholesterolemias: 20-Year Experience among School Children and Adolescents - Pages 40-50
 
Josef Hyánek, František Pehal, Ladislava Dubská, Blanka Miková, Věra Martiníková, Jana Privarová, Jana Brtnová and Luděk Táborský

DOI: https://doi.org/10.6000/1929-5634.2018.07.02.2

Published: 16 August 2018

 

 

Abstract: Aims: This paper presents our 20-year experience with diagnosing heterozygous familial hypercholesterolemia (HFH) and monitoring its diet and drug treatment in 94 children (6-18 years) by means of noncholesterol sterols (NCS), namely lathosterol (Lat) and desmosterol (Des) as cholesterol synthesis precursors, and campesterol (Cam) and sitosterol (Sit) as cholesterol absorption precursors.

Patients and Methods:Four groups were included in the study: (1) 64 children with genetically confirmed HFH; (2) 30 children with clinical and laboratory symptoms of HFH where the relevant genetic mutations have not been found; (3) 77 children with alimentary hyperlipidemia (AH), and (4) 84 healthy children as a control group. The followed-up markers were routine lipid profile comprising total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and triacylglycerides (TAG), complemented by apolipoprotein A1 (ApoA), apolipoprotein B (ApoB), lipoprotein(a) (Lp(a)), low-density lipoprotein receptor (LDL-R), apolipoprotein E (ApoE) polymorphism, and plasma NCS (Lat, Des, Cam and Sit), the latter being established by means of GC/MS. The medical treatment of HFH patients consisted of simvastatin and ezetimibe. Correlations between TC lowering and decrease in Lat and other NCS values during combination treatment were examined in various types of hypercholesterolemia.

Results: HFH patients, whether genetically confirmed or not, exhibit a significant decrease in Lat (and in milder concentrations also Des) which correlates directly to the TC lowering during the combination therapy (r = 0.912 for Lat; r = 0.798 for Des; p<0.001). Cam and Sit do not correlate with the TC lowering at all (r = -0.378 for Cam; r = -0.208 for Sit). By contrast, high TC levels in AH patients are not accompanied by significantly elevated Lat levels, and, therefore, caloric restriction cannot result in significant Lat or Des decrease (p<0.001). Lat and Des levels are also high following drug treatment interruption during long vacations or when the drug treatment is neglected. Compensatory elevation of Cam and Sit occurs in 50% of treated children patients after the desirable TC level below 4.8 mmol/l has been achieved and maintained. In our experience, the combination of statin and ezetimibe is the most efficacious therapy to lower TC together with Lat and Des in children with HFH.

Conclusions: Inclusion precursors for cholesterol synthesis and absorption in laboratory testing improve differential diagnosis of HFH, and makes monitoring and/or treatment of pediatric patients more precise and convenient.

Keywords: Noncholesterol sterols, lathosterol, desmosterol, campesterol, sitosterol, phytosterols, heterozygous familial hypercholesterolemia, alimentary hyperlipidemia, monitoring diet and drug treatment, simvastatins, ezetimibe.

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Journal of Nutritional Therapeutics

Non-Muscle Myosin IIA (Myh9) is in the Nucleus of S-Phase Entering NT2-D1 Cells - Pages 59-66
 
Gabriela Naum-Onganía and Rolando Rivera-Pomar

DOI: https://doi.org/10.6000/1929-5634.2018.07.02.4

Published: 16 August 2018

 

 

Abstract: Non-muscle myosin IIA is a cytoplasmic protein that works in concert with F-actin to produce cell movement. The heavy chain of this protein is codified by the MYH9 gene. The presence of motor proteins as myosin or mono and F-actin and their role in transcription has recently been observed. Prep1–the transcription factor of HOXB genes– constitutes a dimer with Pbx1, which induces HOXB gene expression. Prep1 has been found purifying with β-actin and Myh9. HOXB transcription initiates when cells enter in S-phase, during which DNA duplication and transcription occur at the same time. Here, we have shown that Myh9 co-localizes with Prep1 in the nucleus and in the periphery of the nucleolus in S-phase NT2-D1 cells. Furthermore, we have shown that Myh9 purifies with Pbx1 from nuclear extracts of S-phase entering NT2-D1 cells –and not from cytoplasmic extracts. Taking into account these results, we conclude that Myh9 is in the nucleus of the S-phase entering NT2-D1 cells and might have a role in HOXB transcription.

Keywords: Myosin9, Hox genes, NT2-D1 cells, S-phase.

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