Strength and Functional Recovery Following Repair of Flexor Digitorum Superficialis in Zone 2

1993 ◽  
Vol 18 (1) ◽  
pp. 22-25 ◽  
Author(s):  
H. J. BOULAS ◽  
J. W. STRICKLAND

A two-pronged study was designed to evaluate the strength in vitro and functional recovery in vivo of FDS repairs in zone 2. In part I, horizontal mattress or Tajima grasping repairs were performed on fresh-frozen cadaveric digits, using 3/0 or 4/0 braided nylon suture material. The Tajima repair was significantly stronger than the mattress suture, using either 3/0 ( P = 0.0001) or 4/0 ( P = 0.0027) suture material. The 3/0 Tajima repair appeared strong enough to permit gentle early active motion. Furthermore, the clinical portion of the study (part II) demonstrated restoration of FDS function following repair in relatively isolated injuries in 13 out of 15 digits (86.7%), with PIP flexion averaging 80° and grip strength 89% of that in the uninjured hand.

2020 ◽  
pp. 1-14
Author(s):  
Shelby Shrigley ◽  
Fredrik Nilsson ◽  
Bengt Mattsson ◽  
Alessandro Fiorenzano ◽  
Janitha Mudannayake ◽  
...  

Background: Human induced pluripotent stem cells (hiPSCs) have been proposed as an alternative source for cell replacement therapy for Parkinson’s disease (PD) and they provide the option of using the patient’s own cells. A few studies have investigated transplantation of patient-derived dopaminergic (DA) neurons in preclinical models; however, little is known about the long-term integrity and function of grafts derived from patients with PD. Objective: To assess the viability and function of DA neuron grafts derived from a patient hiPSC line with an α-synuclein gene triplication (AST18), using a clinical grade human embryonic stem cell (hESC) line (RC17) as a reference control. Methods: Cells were differentiated into ventral mesencephalic (VM)-patterned DA progenitors using an established GMP protocol. The progenitors were then either terminally differentiated to mature DA neurons in vitro or transplanted into 6-hydroxydopamine (6-OHDA) lesioned rats and their survival, maturation, function, and propensity to develop α-synuclein related pathology, were assessed in vivo. Results: Both cell lines generated functional neurons with DA properties in vitro. AST18-derived VM progenitor cells survived transplantation and matured into neuron-rich grafts similar to the RC17 cells. After 24 weeks, both cell lines produced DA-rich grafts that mediated full functional recovery; however, pathological changes were only observed in grafts derived from the α-synuclein triplication patient line. Conclusion: This data shows proof-of-principle for survival and functional recovery with familial PD patient-derived cells in the 6-OHDA model of PD. However, signs of slowly developing pathology warrants further investigation before use of autologous grafts in patients.


2018 ◽  
Vol 44 (4) ◽  
pp. 354-360 ◽  
Author(s):  
Koji Moriya ◽  
Takea Yoshizu ◽  
Naoto Tsubokawa ◽  
Hiroko Narisawa ◽  
Yutaka Maki

We report seven patients requiring tenolysis after primary or delayed primary flexor tendon repair and early active mobilization out of 148 fingers of 132 consecutive patients with Zone 1 or 2 injuries from 1993 to 2017. Three fingers had Zone 2A, two Zone 2B, and two Zone 2C injuries. Two fingers underwent tenolysis at Week 4 or 6 after repair because of suspected repair rupture. The other five fingers had tenolysis 12 weeks after repair. Adhesions were moderately dense between the flexor digitorum superficialis and profundus tendons or with the pulleys. According to the Strickland and Tang criteria, the outcomes were excellent in one finger, good in four, fair in one, and poor in one. Fingers requiring tenolysis after early active motion were 5% of the 148 fingers so treated. Indications for tenolysis were to achieve a full range of active motion in the patients rated good or improvement of range of active motion of the patients rated poor or fair. Not all of our patients with poor or fair outcomes wanted to have tenolysis. Level of evidence: IV


2020 ◽  
Author(s):  
Steven F. Grieco ◽  
Xin Qiao ◽  
Xiaoting Zheng ◽  
Yongjun Liu ◽  
Lujia Chen ◽  
...  

SummarySubanesthetic ketamine evokes rapid and long-lasting antidepressant effects in human patients. The mechanism for ketamine’s effects remains elusive, but ketamine may broadly modulate brain plasticity processes. We show that single-dose ketamine reactivates adult mouse visual cortical plasticity and promotes functional recovery of visual acuity defects from amblyopia. Ketamine specifically induces down-regulation of neuregulin-1 (NRG1) expression in parvalbumin-expressing (PV) inhibitory neurons in mouse visual cortex. NRG1 downregulation in PV neurons co-tracks both the fast onset and sustained decreases in synaptic inhibition to excitatory neurons, along with reduced synaptic excitation to PV neurons in vitro and in vivo following a single ketamine treatment. These effects are blocked by exogenous NRG1 as well as PV targeted receptor knockout. Thus ketamine reactivation of adult visual cortical plasticity is mediated through rapid and sustained cortical disinhibition via downregulation of PV-specific NRG1 signaling. Our findings reveal the neural plasticity-based mechanism for ketamine-mediated functional recovery from adult amblyopia.Highlights○ Disinhibition of excitatory cells by ketamine occurs in a fast and sustained manner○ Ketamine evokes NRG1 downregulation and excitatory input loss to PV cells○ Ketamine induced plasticity is blocked by exogenous NRG1 or its receptor knockout○ PV inhibitory cells are the initial functional locus underlying ketamine’s effects


Hand Surgery ◽  
2013 ◽  
Vol 18 (03) ◽  
pp. 375-379 ◽  
Author(s):  
Muntasir Mannan Choudhury ◽  
Shian Chao Tay

Surgical treatment for trigger finger involves division of the A1 pulley. Some surgeons perform an additional step of traction tenolysis by sequentially bringing the flexor digitorum superficialis and flexor digitorum profundus tendons out of the wound gently with a Ragnell retractor. There is currently no study which states whether flexor tendon traction tenolysis should be routinely performed or not. The objective of this study is to compare the outcome in patients who have traction tenolysis performed (A group) versus those who did not have traction tenolysis (B group) performed. It was noted that even though the mean total active motion (TAM) for the B group in our study was lower preoperatively, it was consistently higher than the A group in all the 3 post-operative visits demonstrating a better outcome in the B group. Even though it was not statistically significant, our data also showed that patients with traction tenolysis appeared to have more postoperative pain compared to those without.


2021 ◽  
pp. 175319342110612
Author(s):  
Angelina Garkisch ◽  
Stefanie Schmitt ◽  
Nicole Kim ◽  
Dagmar-C. Fischer ◽  
Karl-Josef Prommersberger ◽  
...  

The flexor digitorum superficialis tendon of the ring finger can be transferred to the thumb flexor. We followed ten patients after such a transfer for 5–128 months and measured grip strength and force transmission of the fingers and individual phalanges while the patients gripped 10-cm or 20-cm diameter cylinders. The grip strength of the middle, ring and little fingers was reduced when gripping the 10-cm cylinder, with a significantly larger decrease in the ring finger. With the 20-cm cylinder, grip forces of all fingers were almost identical, with slightly lower force of the ring finger and slightly higher forces in the index and small fingers. We conclude that after transfer of flexor digitorum superficialis tendon from a ring finger, grip strength of the ring finger is reduced. Finger forces are more hampered while gripping objects with smaller circumferences than large ones.


Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Huiling Zhang ◽  
Zhong-Sheng Li ◽  
Yong Ni ◽  
Xian-Yong Zhou ◽  
Shi-Gang Qiao

During the recovery phase of ischemic stroke, one of the major barriers for the spontaneous neuronal axon regeneration is the formation of astrogliosis and glial scar, and targeting astrogliosis becomes a therapeutic strategy for ischemic stroke. However, the mechanism regulating the process of scar components after ischemia still remains poorly understood. The aim of this study was to observe the role of RIP1 kinase (RIP1K), the key regulator of necroptosis (programmed necrosis) in the brain functional recovery after ischemic stroke and in the ischemic stroke-induced astrogliosis and glial scar formation in both in vitro and in vivo glial scar models. The glial scar formation model in vitro or in vivo was established by using primary cultured astrocyte subjected to 6 hours of oxygen-glucose deprivation (OGD) following 12 hours or 24 hours reperfusion, or by 90 min of transient middle cerebral artery occlusion (tMCAO) and reperfusion in rats. Western blotting analysis and immunohistochemical assay showed that knockdown of RIP1K by lentivirally-delivered shRNAs against RIP1K (shRNA RIP1K) could decrease several protein levels of glial scar markers such as glial fibillary acidic protein (GFAP), neurocan and phosphacan both in in vitro and in vivo glial scar models. Furthermore, western blotting analysis showed that knockdown of RIP1K reduced the protein levels of VEGF-D receptor 3 in in vitro glial scar models. In addition, knockdown of RIP1K also notably reduced the shrinking volume and ameliorated the behavioral symptoms in the recovery phase of rats after tMCAO. And immunocytochemistry assay demonstrated that RIP1K knockdown promoted the neuronal axonal generation in a neuron and astrocyte co-culture system. Our data indicates that RIP1K might play an important role in the formation of glial scar after ischemic stroke via promoting the function of VEGF-D receptor 3 in astrocytes.


Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 2003 ◽  
Author(s):  
Mon-Chien Lee ◽  
Yi-Ju Hsu ◽  
Hsiao-Li Chuang ◽  
Pei-Shan Hsieh ◽  
Hsieh-Hsun Ho ◽  
...  

In recent years, probiotics of human origin have shown superior results and performance compared to probiotics from plant or dairy sources, in both in vitro and animal studies. Towards this end, the current study was conducted to explore the ergogenic properties of Bifidobacterium longum subsp. longum OLP-01 isolated from the intestinal microbiome of the gold medalist from the 2008 Beijing Olympics women’s 48 kg weightlifting competition. Male Institute of Cancer Research (ICR) mice were divided into four groups (n = 10 per group) and orally administered OLP-01 for 4 weeks at 0 (vehicle), 2.05 × 109 (OLP-01-1X), 4.10 × 109 (OLP-01-2X), and 1.03 × 1010 (OLP-01-5X) CFU/kg/day. Physical performance tests including grip strength and endurance time were measured, with OLP-01 supplementation dose-dependently elevating grip strength and endurance. The anti-fatigue activity levels of serum lactate, ammonia, glucose, blood urea nitrogen (BUN), and creatine kinase (CK) were measured after an acute exercise challenge, and OLP-01 was found to significantly decrease lactate, ammonia, and CK levels. OLP-01 treatment was also found to significantly increase the resting levels of both hepatic and muscular glycogen, an indicator of energy storage. Supplementation by OLP-01 showed no subchronic toxic effects while supporting many health-promoting, performance-improving, and fatigue-ameliorating functions.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
D Mori ◽  
S Miyagawa ◽  
T Kawamura ◽  
H Hata ◽  
T Ueno ◽  
...  

Abstract Background Although transplantation of human Adipose-derived Mesenchymal stem cell (hADSC) shows efficacy in the treatment of ischemic cardiomyopathy, its therapeutic mechanisms have not been fully elucidated. It has been already reported that mitochondria transfer to recipient cells have impact on resistance to injury and tissue regeneration, however this phenomenon has not been elucidated in the damaged heart. Therefore, we hypothesized that ADSC transfer own mitochondria to cardiomyocytes in-vivo and in-vitro under ischemic condition, resulting in the functional recovery of cardiomyocyte. Method and result Transplantation of hADSC (group A) to the heart surface or sham operation (group C) was performed in rats that were subjected to LAD ligation 2 weeks prior to the treatment (n=10 each). The number of transplant cell was 1x106/body. Three days after transplantation, transferred hADSCs' mitochondria were observed in recipient cardiomyocytes histologically (Figure). Quantitative PCR analysis revealed that mitochondrial genome of recipient myocytes increased over time. The cardiac function assessed with echocardiography was significantly better in group A. Furthermore, live-imaging of hADSC transplantation revealed the suspected transfer of mitochondria to beating heart. In-vitro, the co-culture of rat cardiomyocytes (rCM) and hADSC was observed with time-lapse photography and demonstrated mitochondrial transfer under the hypoxic condition. The measuring the oxygen consumption rate (OCR) of these cells showed that OCR of rCM was reinforced by co-culture with hADSC conspicuously. Figure 1 Conclusion Mitochondrial transfer from hADSC to rCM was suggested in-vivo and in-vitro ischemic condition and suspected to be related to functional recovery of ischemic cardiomyocyte.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
J Chen ◽  
Y N Song ◽  
Z Y Huang

Abstract Background Poor cell homing limits efficacy of cardiac cellular therapy. The cysteine–arginine–glutamic acid–lysine–alanine (CREKA) homing peptide binds with high specificity to fibrin which is involved in repair of tissue injury. Purpose We assessed if CREKA-modified stem cells had enhanced fibrin-mediated homing ability resulting in better functional recovery and structural preservation in a rat myocardial injury model. Methods CREKA-modified mesenchymal stem cells (CREKA-MSCs) were obtained via membrane fusion with CREKA-modified liposomes. The fibrin targeting ability of CREKA-MSCs was examined both in vitro and in vivo. Results Under both static and flow conditions in vitro, CREKA significantly enhanced MSCs binding ability to fibrin clots. CREKA-MSCs showed much more higher accumulation than unmodified MSCs in injured rat myocardium, colocalizing with fibrin and resulting in better cardiac function. Stem cell-CREKA-fibrin targeting system Conclusions Modification of MSCs with the homing peptide CREKA favored their migration and retention in the infarcted area, resulting in better structural preservation and functional recovery. Fibrin is therefore a novel target for enhancing homing of transplanted cells to injured myocardium and the fibrin-targeting delivery system represents a generalizable platform technology for regenerative medicine.


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