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Treatment of mild to moderate carpal tunnel syndrome in patients with diabetic neuropathy using low level laser therapy versus ultrasound controlled comparative study.

BBA clinical

Ahmed OF, Elkharbotly AM, Taha N, Bekheet AB.
PMID: 28856107
BBA Clin. 2017 Jul 20;8:43-47. doi: 10.1016/j.bbacli.2017.07.001. eCollection 2017 Dec.

AIM: The aim of the present study was to investigate and compare between Low Level Laser Therapy (LLLT) and Ultrasound (US) in treatment of Carpal Tunnel Syndrome (CTS) using the advantage of application of treatment directly over the transverse...

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Ahmed OF, Elkharbotly AM, Taha N, et al. Treatment of mild to moderate carpal tunnel syndrome in patients with diabetic neuropathy using low level laser therapy versus ultrasound controlled comparative study. BBA Clin. 2017;8:43-47doi: 10.1016/j.bbacli.2017.07.001.
Ahmed, O. F., Elkharbotly, A. M., Taha, N., & Bekheet, A. B. (2017). Treatment of mild to moderate carpal tunnel syndrome in patients with diabetic neuropathy using low level laser therapy versus ultrasound controlled comparative study. BBA clinical, 843-47. https://doi.org/10.1016/j.bbacli.2017.07.001
Ahmed, Osama F, et al. "Treatment of mild to moderate carpal tunnel syndrome in patients with diabetic neuropathy using low level laser therapy versus ultrasound controlled comparative study." BBA clinical vol. 8 (2017): 43-47. doi: https://doi.org/10.1016/j.bbacli.2017.07.001
Ahmed OF, Elkharbotly AM, Taha N, Bekheet AB. Treatment of mild to moderate carpal tunnel syndrome in patients with diabetic neuropathy using low level laser therapy versus ultrasound controlled comparative study. BBA Clin. 2017 Jul 20;8:43-47. doi: 10.1016/j.bbacli.2017.07.001. eCollection 2017 Dec. PMID: 28856107; PMCID: PMC5567639.
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TCF7L2 polymorphism is associated with low nitric oxide release, endothelial dysfunction and enhanced inflammatory response after myocardial infarction.

BBA clinical

Cintra R, Moura FA, Carvalho LS, Daher M, Santos SN, Costa AP, Figueiredo VN, Andrade JM, Neves FA, Silva JC, Sposito AC.
PMID: 27213136
BBA Clin. 2016 Apr 02;5:159-65. doi: 10.1016/j.bbacli.2016.03.010. eCollection 2016 Jun.

BACKGOUND: The favorable effects of insulin during myocardial infarction (MI) remain unclear due to the divergence between mechanistic studies and clinical trials of exogenous insulin administration. The rs7903146 polymorphism of the transcription factor 7-like 2 (TCF7L2) gene is associated...

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Cintra R, Moura FA, Carvalho LS, et al. TCF7L2 polymorphism is associated with low nitric oxide release, endothelial dysfunction and enhanced inflammatory response after myocardial infarction. BBA Clin. 2016;5:159-65doi: 10.1016/j.bbacli.2016.03.010.
Cintra, R., Moura, F. A., Carvalho, L. S., Daher, M., Santos, S. N., Costa, A. P., Figueiredo, V. N., Andrade, J. M., Neves, F. A., Silva, J. C., Sposito, A. C. (2016). TCF7L2 polymorphism is associated with low nitric oxide release, endothelial dysfunction and enhanced inflammatory response after myocardial infarction. BBA clinical, 5159-65. https://doi.org/10.1016/j.bbacli.2016.03.010
Cintra, Riobaldo, et al. "TCF7L2 polymorphism is associated with low nitric oxide release, endothelial dysfunction and enhanced inflammatory response after myocardial infarction." BBA clinical vol. 5 (2016): 159-65. doi: https://doi.org/10.1016/j.bbacli.2016.03.010
Cintra R, Moura FA, Carvalho LS, Daher M, Santos SN, Costa AP, Figueiredo VN, Andrade JM, Neves FA, Silva JC, Sposito AC. TCF7L2 polymorphism is associated with low nitric oxide release, endothelial dysfunction and enhanced inflammatory response after myocardial infarction. BBA Clin. 2016 Apr 02;5:159-65. doi: 10.1016/j.bbacli.2016.03.010. eCollection 2016 Jun. PMID: 27213136; PMCID: PMC4865630.
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Secretion of salivary statherin is compromised in uncontrolled diabetic patients.

BBA clinical

Izumi M, Zhang BX, Dean DD, Lin AL, Saunders MJ, Hazuda HP, Yeh CK.
PMID: 25793156
BBA Clin. 2015 Jun 01;3:135-140. doi: 10.1016/j.bbacli.2015.01.002.

BACKGROUND: Statherin is an important salivary protein for maintaining oral health. The purpose of the current study was to determine if differences in statherin levels exist between diabetic and healthy subjects.METHODS: A total of 48 diabetic and healthy controls...

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Izumi M, Zhang BX, Dean DD, et al. Secretion of salivary statherin is compromised in uncontrolled diabetic patients. BBA Clin. 2015;3:135-140doi: 10.1016/j.bbacli.2015.01.002.
Izumi, M., Zhang, B. X., Dean, D. D., Lin, A. L., Saunders, M. J., Hazuda, H. P., & Yeh, C. K. (2015). Secretion of salivary statherin is compromised in uncontrolled diabetic patients. BBA clinical, 3135-140. https://doi.org/10.1016/j.bbacli.2015.01.002
Izumi, Masahiro, et al. "Secretion of salivary statherin is compromised in uncontrolled diabetic patients." BBA clinical vol. 3 (2015): 135-140. doi: https://doi.org/10.1016/j.bbacli.2015.01.002
Izumi M, Zhang BX, Dean DD, Lin AL, Saunders MJ, Hazuda HP, Yeh CK. Secretion of salivary statherin is compromised in uncontrolled diabetic patients. BBA Clin. 2015 Jun 01;3:135-140. doi: 10.1016/j.bbacli.2015.01.002. PMID: 25793156; PMCID: PMC4360915.
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Epigenetics in heart failure phenotypes.

BBA clinical

Berezin A.
PMID: 27335803
BBA Clin. 2016 May 30;6:31-7. doi: 10.1016/j.bbacli.2016.05.005. eCollection 2016 Dec.

Chronic heart failure (HF) is a leading clinical and public problem posing a higher risk of morbidity and mortality in different populations. HF appears to be in both phenotypic forms: HF with reduced left ventricular ejection fraction (HFrEF) and...

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Berezin A. Epigenetics in heart failure phenotypes. BBA Clin. 2016;6:31-7doi: 10.1016/j.bbacli.2016.05.005.
Berezin, A. (2016). Epigenetics in heart failure phenotypes. BBA clinical, 631-7. https://doi.org/10.1016/j.bbacli.2016.05.005
Berezin, Alexander. "Epigenetics in heart failure phenotypes." BBA clinical vol. 6 (2016): 31-7. doi: https://doi.org/10.1016/j.bbacli.2016.05.005
Berezin A. Epigenetics in heart failure phenotypes. BBA Clin. 2016 May 30;6:31-7. doi: 10.1016/j.bbacli.2016.05.005. eCollection 2016 Dec. PMID: 27335803; PMCID: PMC4909708.
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Signaling mechanisms implicated in cranial sutures pathophysiology: Craniosynostosis.

BBA clinical

Katsianou MA, Adamopoulos C, Vastardis H, Basdra EK.
PMID: 27957430
BBA Clin. 2016 Apr 29;6:165-176. doi: 10.1016/j.bbacli.2016.04.006. eCollection 2016 Dec.

Normal extension and skull expansion is a synchronized process that prevails along the osteogenic intersections of the cranial sutures. Cranial sutures operate as bone growth sites allowing swift bone generation at the edges of the bone fronts while they...

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Katsianou MA, Adamopoulos C, Vastardis H, et al. Signaling mechanisms implicated in cranial sutures pathophysiology: Craniosynostosis. BBA Clin. 2016;6:165-176doi: 10.1016/j.bbacli.2016.04.006.
Katsianou, M. A., Adamopoulos, C., Vastardis, H., & Basdra, E. K. (2016). Signaling mechanisms implicated in cranial sutures pathophysiology: Craniosynostosis. BBA clinical, 6165-176. https://doi.org/10.1016/j.bbacli.2016.04.006
Katsianou, Maria A, et al. "Signaling mechanisms implicated in cranial sutures pathophysiology: Craniosynostosis." BBA clinical vol. 6 (2016): 165-176. doi: https://doi.org/10.1016/j.bbacli.2016.04.006
Katsianou MA, Adamopoulos C, Vastardis H, Basdra EK. Signaling mechanisms implicated in cranial sutures pathophysiology: Craniosynostosis. BBA Clin. 2016 Apr 29;6:165-176. doi: 10.1016/j.bbacli.2016.04.006. eCollection 2016 Dec. PMID: 27957430; PMCID: PMC5144105.
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Analysis of single nucleotide polymorphisms implicate mTOR signalling in the development of new-onset diabetes after transplantation.

BBA clinical

Chand S, McKnight AJ, Shabir S, Chan W, McCaughan JA, Maxwell AP, Harper L, Borrows R.
PMID: 27051588
BBA Clin. 2016 Jan 08;5:41-5. doi: 10.1016/j.bbacli.2015.12.004. eCollection 2016 Jun.

INTRODUCTION: Despite excellent first year outcomes in kidney transplantation, there remain significant long-term complications related to new-onset diabetes after transplantation (NODAT). The purpose of this study was to validate the findings of previous investigations of candidate gene variants in...

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Chand S, McKnight AJ, Shabir S, et al. Analysis of single nucleotide polymorphisms implicate mTOR signalling in the development of new-onset diabetes after transplantation. BBA Clin. 2016;5:41-5doi: 10.1016/j.bbacli.2015.12.004.
Chand, S., McKnight, A. J., Shabir, S., Chan, W., McCaughan, J. A., Maxwell, A. P., Harper, L., & Borrows, R. (2016). Analysis of single nucleotide polymorphisms implicate mTOR signalling in the development of new-onset diabetes after transplantation. BBA clinical, 541-5. https://doi.org/10.1016/j.bbacli.2015.12.004
Chand, S, et al. "Analysis of single nucleotide polymorphisms implicate mTOR signalling in the development of new-onset diabetes after transplantation." BBA clinical vol. 5 (2016): 41-5. doi: https://doi.org/10.1016/j.bbacli.2015.12.004
Chand S, McKnight AJ, Shabir S, Chan W, McCaughan JA, Maxwell AP, Harper L, Borrows R. Analysis of single nucleotide polymorphisms implicate mTOR signalling in the development of new-onset diabetes after transplantation. BBA Clin. 2016 Jan 08;5:41-5. doi: 10.1016/j.bbacli.2015.12.004. eCollection 2016 Jun. PMID: 27051588; PMCID: PMC4802392.
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Diabetic and dyslipidaemic morbidly obese exhibit more liver alterations compared with healthy morbidly obese.

BBA clinical

Pardina E, Ferrer R, Rossell J, Baena-Fustegueras JA, Lecube A, Fort JM, Caubet E, González Ó, Vilallonga R, Vargas V, Balibrea JM, Peinado-Onsurbe J.
PMID: 27051590
BBA Clin. 2016 Jan 08;5:54-65. doi: 10.1016/j.bbacli.2015.12.002. eCollection 2016 Jun.

BACKGROUND & AIMS: To study the origin of fat excess in the livers of morbidly obese (MO) individuals, we analysed lipids and lipases in both plasma and liver and genes involved in lipid transport, or related with, in that...

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Pardina E, Ferrer R, Rossell J, et al. Diabetic and dyslipidaemic morbidly obese exhibit more liver alterations compared with healthy morbidly obese. BBA Clin. 2016;5:54-65doi: 10.1016/j.bbacli.2015.12.002.
Pardina, E., Ferrer, R., Rossell, J., Baena-Fustegueras, J. A., Lecube, A., Fort, J. M., Caubet, E., González, �. �., Vilallonga, R., Vargas, V., Balibrea, J. M., & Peinado-Onsurbe, J. (2016). Diabetic and dyslipidaemic morbidly obese exhibit more liver alterations compared with healthy morbidly obese. BBA clinical, 554-65. https://doi.org/10.1016/j.bbacli.2015.12.002
Pardina, Eva, et al. "Diabetic and dyslipidaemic morbidly obese exhibit more liver alterations compared with healthy morbidly obese." BBA clinical vol. 5 (2016): 54-65. doi: https://doi.org/10.1016/j.bbacli.2015.12.002
Pardina E, Ferrer R, Rossell J, Baena-Fustegueras JA, Lecube A, Fort JM, Caubet E, González Ó, Vilallonga R, Vargas V, Balibrea JM, Peinado-Onsurbe J. Diabetic and dyslipidaemic morbidly obese exhibit more liver alterations compared with healthy morbidly obese. BBA Clin. 2016 Jan 08;5:54-65. doi: 10.1016/j.bbacli.2015.12.002. eCollection 2016 Jun. PMID: 27051590; PMCID: PMC4802404.
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Reduced inflammatory and muscle damage biomarkers following oral supplementation with bioavailable curcumin.

BBA clinical

McFarlin BK, Venable AS, Henning AL, Sampson JN, Pennel K, Vingren JL, Hill DW.
PMID: 27051592
BBA Clin. 2016 Feb 18;5:72-8. doi: 10.1016/j.bbacli.2016.02.003. eCollection 2016 Jun.

BACKGROUND: Exercise-Induced Muscle Damage (EIMD) and delayed onset muscle soreness (DOMS) impact subsequent training sessions and activities of daily living (ADL) even in active individuals. In sedentary or diseased individuals, EIMD and DOMS may be even more pronounced and...

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McFarlin BK, Venable AS, Henning AL, et al. Reduced inflammatory and muscle damage biomarkers following oral supplementation with bioavailable curcumin. BBA Clin. 2016;5:72-8doi: 10.1016/j.bbacli.2016.02.003.
McFarlin, B. K., Venable, A. S., Henning, A. L., Sampson, J. N., Pennel, K., Vingren, J. L., & Hill, D. W. (2016). Reduced inflammatory and muscle damage biomarkers following oral supplementation with bioavailable curcumin. BBA clinical, 572-8. https://doi.org/10.1016/j.bbacli.2016.02.003
McFarlin, Brian K, et al. "Reduced inflammatory and muscle damage biomarkers following oral supplementation with bioavailable curcumin." BBA clinical vol. 5 (2016): 72-8. doi: https://doi.org/10.1016/j.bbacli.2016.02.003
McFarlin BK, Venable AS, Henning AL, Sampson JN, Pennel K, Vingren JL, Hill DW. Reduced inflammatory and muscle damage biomarkers following oral supplementation with bioavailable curcumin. BBA Clin. 2016 Feb 18;5:72-8. doi: 10.1016/j.bbacli.2016.02.003. eCollection 2016 Jun. PMID: 27051592; PMCID: PMC4802396.
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Urinary myeloid IgA Fc alpha receptor (CD89) and transglutaminase-2 as new biomarkers for active IgA nephropathy and henoch-Schönlein purpura nephritis.

BBA clinical

Moresco RN, Speeckaert MM, Zmonarski SC, Krajewska M, Komuda-Leszek E, Perkowska-Ptasinska A, Gesualdo L, Rocchetti MT, Delanghe SE, Vanholder R, Van Biesen W, Delanghe JR.
PMID: 27051593
BBA Clin. 2016 Feb 17;5:79-84. doi: 10.1016/j.bbacli.2016.02.002. eCollection 2016 Jun.

BACKGROUND: IgA nephropathy (IgAN) and Henoch-Schönlein purpura nephritis (HSPN) are glomerular diseases that share a common and central pathogenic mechanism. The formation of immune complexes containing IgA1, myeloid IgA Fc alpha receptor (FcαRI/CD89) and transglutaminase-2 (TG2) is observed in...

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Moresco RN, Speeckaert MM, Zmonarski SC, et al. Urinary myeloid IgA Fc alpha receptor (CD89) and transglutaminase-2 as new biomarkers for active IgA nephropathy and henoch-Schönlein purpura nephritis. BBA Clin. 2016;5:79-84doi: 10.1016/j.bbacli.2016.02.002.
Moresco, R. N., Speeckaert, M. M., Zmonarski, S. C., Krajewska, M., Komuda-Leszek, E., Perkowska-Ptasinska, A., Gesualdo, L., Rocchetti, M. T., Delanghe, S. E., Vanholder, R., Van Biesen, W., & Delanghe, J. R. (2016). Urinary myeloid IgA Fc alpha receptor (CD89) and transglutaminase-2 as new biomarkers for active IgA nephropathy and henoch-Schönlein purpura nephritis. BBA clinical, 579-84. https://doi.org/10.1016/j.bbacli.2016.02.002
Moresco, Rafael N, et al. "Urinary myeloid IgA Fc alpha receptor (CD89) and transglutaminase-2 as new biomarkers for active IgA nephropathy and henoch-Schönlein purpura nephritis." BBA clinical vol. 5 (2016): 79-84. doi: https://doi.org/10.1016/j.bbacli.2016.02.002
Moresco RN, Speeckaert MM, Zmonarski SC, Krajewska M, Komuda-Leszek E, Perkowska-Ptasinska A, Gesualdo L, Rocchetti MT, Delanghe SE, Vanholder R, Van Biesen W, Delanghe JR. Urinary myeloid IgA Fc alpha receptor (CD89) and transglutaminase-2 as new biomarkers for active IgA nephropathy and henoch-Schönlein purpura nephritis. BBA Clin. 2016 Feb 17;5:79-84. doi: 10.1016/j.bbacli.2016.02.002. eCollection 2016 Jun. PMID: 27051593; PMCID: PMC4802400.
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Low magnesium is not a significant predictor of hard events in acute myocardial infarction.

BBA clinical

Vassalle C, Battaglia D, Vannucci A, Chatzianagnostou K, Landi P, Arvia C, Carpeggiani C.
PMID: 27051600
BBA Clin. 2016 Mar 09;5:130-3. doi: 10.1016/j.bbacli.2016.03.003. eCollection 2016 Jun.

BACKGROUND: Although magnesium (Mg) has recognized cardioprotective properties and hypomagnesemia is common in patients with acute myocardial infarction (AMI), data regarding the role of Mg as prognostic factor for adverse events are scarce, as well as there are conflicting...

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Vassalle C, Battaglia D, Vannucci A, et al. Low magnesium is not a significant predictor of hard events in acute myocardial infarction. BBA Clin. 2016;5:130-3doi: 10.1016/j.bbacli.2016.03.003.
Vassalle, C., Battaglia, D., Vannucci, A., Chatzianagnostou, K., Landi, P., Arvia, C., & Carpeggiani, C. (2016). Low magnesium is not a significant predictor of hard events in acute myocardial infarction. BBA clinical, 5130-3. https://doi.org/10.1016/j.bbacli.2016.03.003
Vassalle, Cristina, et al. "Low magnesium is not a significant predictor of hard events in acute myocardial infarction." BBA clinical vol. 5 (2016): 130-3. doi: https://doi.org/10.1016/j.bbacli.2016.03.003
Vassalle C, Battaglia D, Vannucci A, Chatzianagnostou K, Landi P, Arvia C, Carpeggiani C. Low magnesium is not a significant predictor of hard events in acute myocardial infarction. BBA Clin. 2016 Mar 09;5:130-3. doi: 10.1016/j.bbacli.2016.03.003. eCollection 2016 Jun. PMID: 27051600; PMCID: PMC4818340.
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Inflammatory bowel disease, colorectal cancer and type 2 diabetes mellitus: The links.

BBA clinical

Jurjus A, Eid A, Al Kattar S, Zeenny MN, Gerges-Geagea A, Haydar H, Hilal A, Oueidat D, Matar M, Tawilah J, Hussein IH, Schembri-Wismayer P, Cappello F, Tomasello G, Leone A, Jurjus RA.
PMID: 27051585
BBA Clin. 2015 Nov 05;5:16-24. doi: 10.1016/j.bbacli.2015.11.002. eCollection 2016 Jun.

The co-occurrence of the three disease entities, inflammatory bowel disease (IBD), colorectal cancer (CRC), type 2diabetes mellitus (T2DM) along with inflammation and dismicrobism has been frequently reported. Some authors have even suggested that dysbiosis could be the link through...

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Jurjus A, Eid A, Al Kattar S, et al. Inflammatory bowel disease, colorectal cancer and type 2 diabetes mellitus: The links. BBA Clin. 2015;5:16-24doi: 10.1016/j.bbacli.2015.11.002.
Jurjus, A., Eid, A., Al Kattar, S., Zeenny, M. N., Gerges-Geagea, A., Haydar, H., Hilal, A., Oueidat, D., Matar, M., Tawilah, J., Hussein, I. H., Schembri-Wismayer, P., Cappello, F., Tomasello, G., Leone, A., & Jurjus, R. A. (2016). Inflammatory bowel disease, colorectal cancer and type 2 diabetes mellitus: The links. BBA clinical, 516-24. https://doi.org/10.1016/j.bbacli.2015.11.002
Jurjus, Abdo, et al. "Inflammatory bowel disease, colorectal cancer and type 2 diabetes mellitus: The links." BBA clinical vol. 5 (2016): 16-24. doi: https://doi.org/10.1016/j.bbacli.2015.11.002
Jurjus A, Eid A, Al Kattar S, Zeenny MN, Gerges-Geagea A, Haydar H, Hilal A, Oueidat D, Matar M, Tawilah J, Hussein IH, Schembri-Wismayer P, Cappello F, Tomasello G, Leone A, Jurjus RA. Inflammatory bowel disease, colorectal cancer and type 2 diabetes mellitus: The links. BBA Clin. 2015 Nov 05;5:16-24. doi: 10.1016/j.bbacli.2015.11.002. eCollection 2016 Jun. PMID: 27051585; PMCID: PMC4802401.
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Up-regulation of the human-specific CHRFAM7A gene in inflammatory bowel disease.

BBA clinical

Baird A, Coimbra R, Dang X, Eliceiri BP, Costantini TW.
PMID: 27051591
BBA Clin. 2016 Jan 08;5:66-71. doi: 10.1016/j.bbacli.2015.12.003. eCollection 2016 Jun.

BACKGROUND: The α7-subunit of the α7-nicotinic acetylcholine receptor (α7-nAChR) is an obligatory intermediate for the anti-inflammatory effects of the vagus nerve. But in humans, there exists a second gene called CHRFAM7A that encodes a dominant negative α7-nAChR inhibitor. Here,...

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Baird A, Coimbra R, Dang X, et al. Up-regulation of the human-specific CHRFAM7A gene in inflammatory bowel disease. BBA Clin. 2016;5:66-71doi: 10.1016/j.bbacli.2015.12.003.
Baird, A., Coimbra, R., Dang, X., Eliceiri, B. P., & Costantini, T. W. (2016). Up-regulation of the human-specific CHRFAM7A gene in inflammatory bowel disease. BBA clinical, 566-71. https://doi.org/10.1016/j.bbacli.2015.12.003
Baird, Andrew, et al. "Up-regulation of the human-specific CHRFAM7A gene in inflammatory bowel disease." BBA clinical vol. 5 (2016): 66-71. doi: https://doi.org/10.1016/j.bbacli.2015.12.003
Baird A, Coimbra R, Dang X, Eliceiri BP, Costantini TW. Up-regulation of the human-specific CHRFAM7A gene in inflammatory bowel disease. BBA Clin. 2016 Jan 08;5:66-71. doi: 10.1016/j.bbacli.2015.12.003. eCollection 2016 Jun. PMID: 27051591; PMCID: PMC4802402.
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