The Association of Olfactory Impairment with Charcot Neuroarthropathy and Possible Links to Causation.

BACKGROUND: Charcot neuroarthropathy (CN) is a devastating complication of some diseases affecting the peripheral nervous system. Initial subjective and objective presentation of the disease can be variable. Common among all presentations seems to be uncontrolled inflammation yielding dislocations and/or fractures. The exact cause remains the subject of much debate. METHODS: Our study retrospectively looks at the function of olfactory function in consecutive patients with CN and compares the findings with a nonaffected population. The University of Pennsylvania Smell Identification Test was used to assess olfaction and document microsomia. RESULTS: Twenty consecutive patients presenting with CN demonstrated significant (P < .0001) microsomia when compared to an unaffected population with diabetes. CONCLUSIONS: Microsomia is strongly associated with CN. This finding may be correlated to voltage-gated sodium 1.7 channel impairment and appears to be a candidate precursor for the development of CN.

Thermostability in endoglucanases is fold-specific.

BACKGROUND: Endoglucanases are usually considered to be synergistically involved in the initial stages of cellulose breakdown-an essential step in the bioprocessing of lignocellulosic plant materials into bioethanol. Despite their economic importance, we currently lack a basic understanding of how some endoglucanases can sustain their ability to function at elevated temperatures required for bioprocessing, while others cannot. In this study, we present a detailed comparative analysis of both thermophilic and mesophilic endoglucanases in order to gain insights into origins of thermostability. We analyzed the sequences and structures for sets of endoglucanase proteins drawn from the Carbohydrate-Active enZymes (CAZy) database. RESULTS: Our results demonstrate that thermophilic endoglucanases and their mesophilic counterparts differ significantly in their amino acid compositions. Strikingly, these compositional differences are specific to protein folds and enzyme families, and lead to differences in intramolecular interactions in a fold-dependent fashion. CONCLUSIONS: Here, we provide fold-specific guidelines to control thermostability in endoglucanases that will aid in making production of biofuels from plant biomass more efficient.

The football: an intuitive dressing for offloading neuropathic plantar forefoot ulcerations.

A reproducible, affordable, efficacious and safe modality for offloading neuropathic plantar foot ulcerations was previously presented in a pilot study. A follow-up retrospective multicentre analysis of the football dressing is now presented. Wound healing rates are compared with published data on the total contact cast (TCC) and instant total contact cast (iTCC). Overall wound healing rates for University of Texas Health Science Center class 1A, 1B, 1C, 1D, 2A, 2B, 2C and 3B plantar forefoot ulcerations is 2.91 weeks with a 95% confidence interval of 2.36-3.47 weeks for complete wound epithelialisation. The cost associated with this dressing technique is a fraction of that associated with the TCC and iTCC. The ease of application coupled with reliable healing rates and affordable materials makes the football dressing a worthy partner against the sequelae of plantar forefoot ulcerations.

Diagnostic Ultrasound of the Soleal Sling.

The soleal sling may be a site of tibial nerve entrapment. Objective diagnosis of this syndrome is difficult with current nerve conduction study techniques, magnetic resonance imaging, and neurosensory testing. Diagnostic ultrasound is ideally suited to visualize the tibial nerve statically and dynamically as it enters the soleal sling, thus making an objective diagnosis of soleal sling impingement much easier.

Surgical decompression in lower-extremity diabetic peripheral neuropathy.

Peripheral neuropathy can be a devastating complication of diabetes mellitus. This article describes surgical decompression as a means of restoring sensation and relieving painful neuropathy symptoms. A prospective study was performed involving patients diagnosed as having type 1 or type 2 diabetes with lower-extremity peripheral neuropathy. The neuropathy diagnosis was confirmed using quantitative sensory testing. Visual analog scales were used for subjective assessment before and after surgery. Treatment consisted of external and as-needed internal neurolysis of the common peroneal, deep peroneal, tibial, medial plantar, lateral plantar, and calcaneal nerves. Subjective pain perception and objective sensibility were significantly improved in most patients who underwent the described decompression. Surgical decompression of multiple peripheral nerves in the lower extremities is a valid and effective method of providing symptomatic relief of neuropathy pain and restoring sensation.

Nerve decompression after diabetic foot ulceration may protect against recurrence: a 3-year controlled, prospective analysis.

BACKGROUND: Nerve entrapment, common in diabetes, is considered an associated phenomenon without large consequence in the development of diabetes complications such as ulceration, infection, amputation, and early mortality. This prospective analysis, with controls, of the ulcer recurrence rate after operative nerve decompression (ND) offers an objective perspective on the possibility of frequent occult nerve entrapment in the diabetic foot complication cascade. METHODS: A multicenter cohort of 42 patients with diabetic sensorimotor polyneuropathy, failed pharmacologic pain control, palpable pulses, and at least one positive Tinel's nerve percussion sign was treated with unilateral multiple lower-leg external neurolyses for the indication of pain. All of the patients had healed at least one previous ipsilateral plantar diabetic foot ulceration (DFU). This group was retrospectively evaluated a minimum of 12 months after operative ND and again 3 years later. The recurrence risk of ipsilateral DFU in that period was prospectively analyzed and compared with new ulcer occurrence in the contralateral intact, nonoperated control legs. RESULTS: Operated legs developed two ulcer recurrences (4.8%), and nine contralateral control legs developed ulcers (21.4%), requiring three amputations. Ulcer risk is 1.6% per patient per year in ND legs and 7% in nonoperated control legs (P = .048). CONCLUSIONS: Adding operative ND at lower-leg fibro-osseous tunnels to standard postulcer treatment resulted in a significantly diminished rate of subsequent DFU in neuropathic high-risk feet. This is prospective, objective evidence that ND can provide valuable ongoing protection from DFU recurrence, even years after primary ulcer healing.

Bioengineered human dermal tissue grafting of necrobiosis lipoidica diabeticorum ulcerations: a case series.

A retrospective case series of sequential patients with recurrent ulcerations associated with necrobiosis lipoidica diabeticorum (NLD) is presented. Standard wound care required 40 ± 7.21 weeks to attain complete epithelialization. Standard wound care plus weekly applications of bioengineered neonatal human dermal tissue shortened healing to 7.14 ± 3.44 weeks. .

Low long-term risk of foot ulcer recurrence after nerve decompression in a diabetes neuropathy cohort.

BACKGROUND: Use of nerve decompression in diabetic sensorimotor polyneuropathy is a controversial treatment characterized as being of unknown scientific effectiveness owing to lack of level I scientific studies. METHODS: Herein, long-term follow-up data have been assembled on 65 diabetic patients with 75 legs having previous neuropathic foot ulcer and subsequent operative decompression of the common peroneal and tibial nerve branches in the anatomical fibro-osseous tunnels. RESULTS: The cohort's previously reported low recurrence risk of less than 5% annually at a mean of 2.49 years of follow-up has persisted for an additional 3 years, and cumulative risk is now 2.6% per patient-year. Nine of 75 operated legs (12%) have developed an ulcer in 4,218 months (351 patient-years) of follow-up. Of the 53 contralateral legs without decompression, 16 (30%) have ulcerated, of which three have undergone an amputation. Fifty-nine percent of patients are known to be alive with intact feet a mean of 60 months after decompression. CONCLUSIONS: The prospective, objective, statistically significant finding of a large, long-term diminution of diabetic foot ulcer recurrence risk after operative nerve decompression compares very favorably with the historical literature and the contralateral legs of this cohort, which had no decompression. This finding invites prospective randomized controlled studies for validation testing and reconsideration of the frequency and contribution of unrecognized nerve entrapments in diabetic sensorimotor polyneuropathy and diabetic foot complications.

Endoglucanases: insights into thermostability for biofuel applications.

Obtaining bioethanol from cellulosic biomass involves numerous steps, among which the enzymatic conversion of the polymer to individual sugar units has been a main focus of the biotechnology industry. Among the cellulases that break down the polymeric cellulose are endoglucanases that act synergistically for subsequent hydrolytic reactions. The endoglucanases that have garnered relatively more attention are those that can withstand high temperatures, i.e., are thermostable. Although our understanding of thermostability in endoglucanases is incomplete, some molecular features that are responsible for increased thermostability have been recently identified. This review focuses on the investigations of endoglucanases and their implications for biofuel applications.

Symmetry of sensory loss in developing diabetic sensory polyneuropathy.

The medical literature presents diabetic sensory polyneuropathy (DSPN) as an axonal length-dependent symmetric pathology producing a stocking-like pattern of anesthesia in the lower extremities. This has been based on anecdotal reports. Objective research has shown that damage may not occur in a purely length-dependent manner. A stocking distribution of sensory loss is atypical, and plantar sensory loss predominates. A single-blinded, age-matched, control/experimental study was performed of the symmetry of nerve damage in developing DSPN. Control (n = 46) and experimental (n = 83) subjects were examined. The patterns of sensory loss and the severity of axonal damage were evaluated. The right/left symmetry of pathology was recorded for each individual. Although there was not a stocking pattern of anesthesia found in developing DSPN, the pattern and severity of anesthesia were found to be generally symmetric. The severity of sensory impairment was symmetric at the dorsal foot (93%), lateral foot (95%), and plantar foot (69%). The most predominant site of sensory impairment was also symmetric (81%). This argues against a purely metabolic etiology for axonal damage. An anatomic component is implied. Further research will need to include examination of the unique physical characteristics of predominantly affected nerves.

Characteristics of lower extremity pressure sensation impairment in developing diabetic sensory polyneuropathy.

The medical literature presents diabetic sensory polyneuropathy as a length-dependent process producing a stocking distribution of sensory loss in the lower extremities. If a purely length-dependent etiology for diabetic sensory polyneuropathy were true, then a validated comparison of sensory loss at any equidistant site about the forefoot will reveal findings consistent with the accepted stocking pattern of anesthesia. A single-blinded, age-matched, control/experimental study is made into the frequency of apparent purely length-dependent A-beta fiber pathology in developing diabetic sensory polyneuropathy. Control (n = 46) and experimental (n = 83) central US subjects are examined with a subjective neuropathy screening questionnaire, vibratory threshold, and single-point pressure threshold testing. There is a plantar predominant pattern (61.5%) of sensory loss in developing diabetic sensory polyneuropathy, even after adjusting for sensitivity differences between different areas of the foot. A typical stocking pattern of sensory loss was not found. Although axonal pathology is length dependent, it is not apparently a purely length-dependent process. Therefore, a purely metabolic explanation for sensory loss is unlikely. In addition, an anatomic component for A-beta fiber pathology is implied by this study.