Generalized global solar radiation forecasting model via cyber-secure deep federated learning.

Recently, the increasing prevalence of solar energy in power and energy systems around the world has dramatically increased the importance of accurately predicting solar irradiance. However, the lack of access to data in many regions and the privacy concerns that can arise when collecting and transmitting data from distributed points to a central server pose challenges to current predictive techniques. This study proposes a global solar radiation forecasting approach based on federated learning (FL) and convolutional neural network (CNN). In addition to maintaining input data privacy, the proposed procedure can also be used as a global supermodel. In this paper, data related to eight regions of Iran with different climatic features are considered as CNN input for network training in each client. To test the effectiveness of the global supermodel, data related to three new regions of Iran named Abadeh, Jarqavieh, and Arak are used. It can be seen that the global forecasting supermodel was able to forecast solar radiation for Abadeh, Jarqavieh, and Arak regions with 95%, 92%, and 90% accuracy coefficients, respectively. Finally, in a comparative scenario, various conventional machine learning and deep learning models are employed to forecast solar radiation in each of the study regions. The results of the above approaches are compared and evaluated with the results of the proposed FL-based method. The results show that, since no training data were available from regions of Abadeh, Jarqavieh, and Arak, the conventional methods were not able to forecast solar radiation in these regions. This evaluation confirms the high ability of the presented FL approach to make acceptable predictions while preserving privacy and eliminating model reliance on training data.

Anatomical evidence of microbial biofilms in an alloplastic nasal implant.

UNLABELLED: Recently, bacterial biofilms have been proposed as a potential cause of the extreme resistance to antibiotics and impaired host responses in potentially infected facial implants. As opposed to the bacteria in a free-floating or planktonic state, biofilms exist in a sessile form, adherent to a solid or liquid interface and become embedded in a complex matrix that is oftentimes impenetrable to modern day antibiotics. This can lead to chronic infection of implants which ultimately necessitates their removal in a majority of cases. In this novel case report, we show the histomorphological appearance of biofilm formation in a patient with an alloplastic nasal implant that was persistently infected and had to be removed. LEVEL OF EVIDENCE IV: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

Ropivacaine-induced peripheral nerve injection injury in the rodent model.

BACKGROUND: Intraneural administration of local anesthetics has been associated with nerve damage. We undertook the present study to investigate histological changes induced by ropivacaine injection into rat sciatic nerve. METHODS: Fifty-four adult male Lewis rats were randomly distributed into 9 groups, 6 animals per group. Fifty microliters of normal saline, 10% phenol, or 0.75% ropivacaine were administered by intrafascicular injection, extrafascicular injection, or extraneural (topical) placement. At 2 weeks, animals were killed and the sciatic nerve at the injection site was evaluated with light microscopy, quantitative histomorphometry, and electron microscopy. RESULTS: On cross-sectional evaluation, extrafascicular ropivacaine injection and extraneural placement of ropivacaine were both associated with damage to the perineurium, with focal demyelination surrounded by edematous endoneurium. Intrafascicular injection of ropivacaine resulted in a wedge-shaped region of demyelination and focal axonal loss with some regeneration, bordered by a region of normally myelinated axons in a background of edematous endoneurium. Extrafascicular injection resulted in more significant damage than extraneural placement of ropivacaine, but less than intrafascicular injection as shown with quantitative histomorphometry. Quantitatively, ropivacaine-injured specimens had significantly lower nerve density than saline-injured specimens. Wallerian degeneration and perineural edema were also demonstrated qualitatively with electron microscopy. CONCLUSIONS: This study demonstrates that, in the rat model, ropivacaine is associated with marked histological abnormality, including edema of the perineurium and axonal destruction with wallerian degeneration, when injected into or extraneurally placed onto a nerve. Extrafascicular injection and extraneural placement were associated with similar, although milder, histological damage than intrafascicular injection. Further work is needed to investigate the functional implications, if any, of the histological abnormalities observed in this study.

Bipolar electrocautery: A rodent model of Sunderland third-degree nerve injury.

OBJECTIVE: To determine the Sunderland classification of a bipolar electrocautery injury. METHODS: Twenty-two rats received crush (a reproducible Sunderland second-degree injury) or bipolar electrocautery injury and were evaluated for functional, histomorphometric, and immunohistochemical recovery at 21 or 42 days. Animal experiments were performed between July 3 and December 12, 2007. Axonal regeneration and end plate reinnervation were evaluated in double transgenic cyan fluorescent protein-conjugated Thy1 and green fluorescent protein-conjugated S100 mice. RESULTS: Compared with crush injury, bipolar electrocautery injury caused greater disruption of myelin and neurofilament architecture at the injury site and decreased nerve fiber counts and percentage of neural tissue distal to the injury (P =.007). Complete functional recovery was seen after crush but not bipolar electrocautery injury. Serial live imaging demonstrated axonal regeneration at week 1 after crush and at week 3 after bipolar electrocautery injury. Qualitative assessment of motor end plate reinnervation at 42 days demonstrated complete neuromuscular end plate reinnervation in the crush group and only limited reinnervation in the bipolar electrocautery group. CONCLUSION: Bipolar electrocautery injury in a rodent model resulted in a Sunderland third-degree injury, characterized by gradual, incomplete recovery without intervention.

Transcardial perfusion versus immersion fixation for assessment of peripheral nerve regeneration.

Accurate assessment of peripheral nerve regeneration requires fixation techniques that preserve tissue in a natural state with minimal artifact. While transcardial perfusion fixation is accepted as the gold standard for tissue fixation, the less cumbersome approach of immersion fixation has been criticized for introducing artifacts in brain tissue. We investigated whether immersion fixation increased artifact compared to perfusion fixation in the rat sciatic nerve. Eighteen Lewis rats were randomized into three groups: glutaraldehyde immersion fixation; glutaraldehyde transcardial perfusion; and paraformaldehyde transcardial perfusion. All animals underwent sciatic nerve transection and repair followed by tissue harvest and fixation at three weeks. Qualitative assessment of neural architecture and histological features was followed by quantitative analysis of nerve regeneration parameters. Outcome measures included quantitative histomorphometry, analysis of axon/myelin ratios, assessment of fiber distributions, and ultrastructural analysis. No qualitative or quantitative differences were observed with immersion fixation when compared to the transcardial perfusion fixation methods. Immersion fixation is a valid method for assessment of peripheral nerve regeneration in a rat model.

Treatment modality affects allograft-derived Schwann cell phenotype and myelinating capacity.

We used peripheral nerve allografts, already employed clinically to reconstruct devastating peripheral nerve injuries, to study Schwann cell (SC) plasticity in adult mice. By modulating the allograft treatment modality we were able to study migratory, denervated, rejecting, and reinnervated phenotypes in transgenic mice whose SCs expressed GFP under regulatory elements of either the S100b (S100-GFP) or nestin (Nestin-GFP) promoters. Well-differentiated SCs strongly expressed S100-GFP, while Nestin-GFP expression was stimulated by denervation, and in some cases, axons were constitutively labeled with CFP to enable in vivo imaging. Serial imaging of these mice demonstrated that untreated allografts were rejected within 20 days. Cold preserved (CP) allografts required an initial phase of SC migration that preceded axonal regeneration thus delaying myelination and maturation of the SC phenotype. Mice immunosuppressed with FK506 demonstrated mild subacute rejection, but the most robust regeneration of myelinated and unmyelinated axons and motor endplate reinnervation. While characterized by fewer regenerating axons, mice treated with the co-stimulatory blockade (CSB) agents anti-CD40L mAb and CTLAIg-4 demonstrated virtually no graft rejection during the 28 day experiment, and had significant increases in myelination, connexin-32 expression, and Akt phosphorylation compared with any other group. These results indicate that even with SC rejection, nerve regeneration can occur to some degree, particularly with FK506 treatment. However, we found that co-stimulatory blockade facilitate optimal myelin formation and maturation of SCs as indicated by protein expression of myelin basic protein (MBP), connexin-32 and phospho-Akt.

The impact of motor and sensory nerve architecture on nerve regeneration.

Sensory nerve autografting is the standard of care for injuries resulting in a nerve gap. Recent work demonstrates superior regeneration with motor nerve grafts. Improved regeneration with motor grafting may be a result of the nerve's Schwann cell basal lamina tube size. Motor nerves have larger SC basal lamina tubes, which may allow more nerve fibers to cross a nerve graft repair. Architecture may partially explain the suboptimal clinical results seen with sensory nerve grafting techniques. To define the role of nerve architecture, we evaluated regeneration through acellular motor and sensory nerve grafts. Thirty-six Lewis rats underwent tibial nerve repairs with 5 mm double-cable motor or triple-cable sensory nerve isografts. Grafts were harvested and acellularized in University of Wisconsin solution. Control animals received fresh motor or sensory cable isografts. Nerves were harvested after 4 weeks and histomorphometry was performed. In 6 animals per group from the fresh motor and sensory cable graft groups, weekly walking tracks and wet muscle mass ratios were performed at 7 weeks. Histomorphometry revealed more robust nerve regeneration in both acellular and cellular motor grafts. Sensory groups showed poor regeneration with significantly decreased percent nerve, fiber count, and density (p<0.05). Walking tracks revealed a trend toward improved functional recovery in the motor group. Gastrocnemius wet muscle mass ratios show a significantly greater muscle mass recovery in the motor group (p<0.05). Nerve architecture (size of SC basal lamina tubes) plays an important role in nerve regeneration in a mixed nerve gap model.

Role of timing in assessment of nerve regeneration.

Small animal models are indispensable for research on nerve injury and reconstruction, but their superlative regenerative potential may confound experimental interpretation. This study investigated time-dependent neuroregenerative phenomena in rodents. Forty-six Lewis rats were randomized to three nerve allograft groups treated with 2 mg/(kg day) tacrolimus; 5 mg/(kg day) Cyclosporine A; or placebo injection. Nerves were subjected to histomorphometric and walking track analysis at serial time points. Tacrolimus increased fiber density, percent neural tissue, and nerve fiber count and accelerated functional recovery at 40 days, but these differences were undetectable by 70 days. Serial walking track analysis showed a similar pattern of recovery. A "blow-through" effect is observed in rodents whereby an advancing nerve front overcomes an experimental defect given sufficient time, rendering experimental groups indistinguishable at late time points. Selection of validated time points and corroboration in higher animal models are essential prerequisites for the clinical application of basic research on nerve regeneration.

Axotomy or compression is required for axonal sprouting following end-to-side neurorrhaphy.

End-to-side (ETS) nerve repair remains an area of intense scrutiny for peripheral nerve surgeon-scientists. In this technique, the transected end of an injured nerve, representing the "recipient" is sutured to the side of an uninjured "donor" nerve. Some works suggest that the recipient limb is repopulated with regenerating collateral axonal sprouts from the donor nerve that go on to form functional synapses. Significant, unresolved questions include whether the donor nerve needs to be injured to facilitate regeneration, and whether a single donor neuron is capable of projecting additional axons capable of differentially innervating disparate targets. We serially imaged living transgenic mice (n=66) expressing spectral variants of GFP in various neuronal subsets after undergoing previously described atraumatic, compressive, or epineurotomy forms of ETS repair (n=22 per group). To evaluate the source, and target innervation of these regenerating axons, nerve morphometry and retrograde labeling were further supplemented by confocal microscopy as well as Western blot analysis. Either compression or epineurotomy with inevitable axotomy were required to facilitate axonal regeneration into the recipient limb. Progressively more injurious models were associated with improved recipient nerve reinnervation (epineurotomy: 184+/-57.6 myelinated axons; compression: 78.9+/-13.8; atraumatic: 0), increased Schwann cell proliferation (epineurotomy: 72.2% increase; compression: 39% increase) and cAMP response-element binding protein expression at the expense of a net deficit in donor axon counts distal to the repair. These differences were manifest by 150 days, at which point quantitative evidence for pruning was obtained. We conclude that ETS repair relies upon injury to the donor nerve.

Retrograde labeling in peripheral nerve research: it is not all black and white.

Retrograde labeling has become an important method of evaluation for peripheral nerve regeneration after injury. We review the features of the commonly used retrograde tracers Fast Blue, Fluoro-Gold, and Fluoro Ruby in addition to the various application methods (conduit reservoir, intramuscular injection, and crystal powder application) and the techniques used to count stained neurons. Upon application of the staining techniques and dyes in a rat and mouse nerve injury model, Fluoro-Gold was found to stain the greatest number of neurons with all application methods. However, due to variability of staining intensity, neuron size, and background staining, it is difficult to count the stained neurons accurately. Fast Blue stains consistently using intramuscular injection in the mouse but fails to provide adequate staining using the muscle injection method in the rat model and shows high failure rates using the conduit reservoir technique. However, crystal dye application with Fast Blue to the cut nerve end provides excellent results. We believe that it is imperative to use the various tracers and application methods prior to their experimental use to develop a consistent standardized approach to retrograde labeling.

Pregabalin does not impact peripheral nerve regeneration after crush injury.

Timely repair and robust regeneration after traumatic peripheral nerve injury are essential to ensure optimal recovery. Pregabalin (Lyrica; Pfizer Inc., Morris Plains, NJ), frequently prescribed to attenuate neuropathic pain in patients with traumatic nerve injury, was evaluated for its potential to alter nerve regeneration in the rat sciatic crush model. Rats were randomly assigned to one of three groups of 12 animals each: (1) sham surgery and pregabalin injections; (2) crush injury and pregabalin injections; and (3) crush injury and saline vehicle injections. Nerve regeneration was evaluated with weekly walking tracks and histomorphometry. There were no significant differences in sciatic function index or histomorphometric parameters at the 21-day endpoint between the pregabalin-treated rats undergoing crush injury and the saline-treated controls. Although we have observed a subjectively improved clinical course in human patients treated with pregabalin after traumatic nerve injury, the effect does not appear to be due to accelerated nerve regeneration.

Induction of regional collateral sprouting following muscle denervation.

OBJECTIVES/HYPOTHESIS: Anecdotal clinical findings suggest that denervated muscle may regain modest functional recovery via spontaneous collateral sprouts from intact adjacent nerve fibers. The current study evaluates the conditions needed for the denervated masseter muscle to induce axonal sprouting from the facial nerve. We hypothesize that epineurial injury is required to induce collateral sprouting toward a neighboring denervated muscle. STUDY DESIGN: Twelve thy1-yellow fluorescent protein-16 (thy1-YFP-16) transgenic mice whose axons express yellow fluorescent protein were allocated into six groups, with four degrees of facial nerve injury (intact, crush, transection, removed segment) with or without masseter denervation. METHODS: Animals underwent serial in vivo imaging analyses under the fluorescent microscope weekly for 5 or 7 weeks and were subsequently perfused for analysis. Masseter muscle acetylcholine receptors (AChRs) were stained with Alexa Fluor 594 conjugated alpha-bungarotoxin, and whole mounts were imaged with confocal microscopy. RESULTS: In groups with intact or crushed facial nerves, no evidence of collateral sprouting was demonstrated. Mice with transected facial nerve branches or removed segments demonstrated sprouting from the proximal stump into the denervated masseter. Staining of the AChRs confirmed that new neuromuscular junctions were established between the facial nerve and the denervated masseter. CONCLUSIONS: This study suggests that epineurial injury is required to stimulate axonal sprouting into adjacent denervated muscle. Nerves with compromised epineurium may be useful in promoting neo-neurotization after muscle denervation.

Binary imaging analysis for comprehensive quantitative histomorphometry of peripheral nerve.

Quantitative histomorphometry is the current gold standard for objective measurement of nerve architecture and its components. Many methods still in use rely heavily upon manual techniques that are prohibitively time consuming, predisposing to operator fatigue, sampling error, and overall limited reproducibility. More recently, investigators have attempted to combine the speed of automated morphometry with the accuracy of manual and semi-automated methods. Systematic refinements in binary imaging analysis techniques combined with an algorithmic approach allow for more exhaustive characterization of nerve parameters in the surgically relevant injury paradigms of regeneration following crush, transection, and nerve gap injuries. The binary imaging method introduced here uses multiple bitplanes to achieve reproducible, high throughput quantitative assessment of peripheral nerve. Number of myelinated axons, myelinated fiber diameter, myelin thickness, fiber distributions, myelinated fiber density, and neural debris can be quantitatively evaluated with stratification of raw data by nerve component. Results of this semi-automated method are validated by comparing values against those obtained with manual techniques. The use of this approach results in more rapid, accurate, and complete assessment of myelinated axons than manual techniques.

The use of vacuum-assisted closure therapy for the treatment of a large infected facial wound.

Chronic wounds in difficult locations pose constant challenges to health care providers. Negative-pressure wound therapy is a relatively new treatment to promote wound healing. Laboratory and clinical studies have shown that the vacuum-assisted closure (VAC) therapy increases wound blood flow, granulation tissue formation, and decreases accumulation of fluid and bacteria. VAC therapy has been shown to hasten wound closure and formation of granulation tissue in a variety of settings. Accepted indications for VAC therapy include the infected sternum, open abdomen, chronic, nonhealing extremity wounds and decubitus ulcers. We report the first case of VAC therapy successfully used on a large infected wound to the face to promote healing.