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Postępująca inwazja bakteryjna w tkankach zęba prowadzi do zapalenia miazgi, powstawania w niej mikroropnii, zniszczenia a w konsekwencji do zapalenia ozębnej. Z tego względu celem leczenia endodontycznego stało się trójwymiarowe oczyszczenie kanału korzeniowego od jego ujścia do przewężenia fizjologicznego. Dlatego celem pracy jest analiza konfiguracji, ilości kanałów korzeniowych, istnienia kanałów bocznych oraz delty korzeniowej w grupie pierwszych zębów trzonowych stałych w uzębieniu ludzkim. Jednocześnie ocenie poddawana jest dodatkowo swoistość badania radiologicznego (zdjęcia zębowe), poprzez porównanie zdjęć rentgenowskich wykonanych przed preparacją zębów z obrazem systemu kanałowego uzyskanego na podstawie mikrotomografii oraz po wykonaniu szlifów poprzecznych i ich obserwacji na mikroskopie świetlnym. Celem tej oceny jest zaprezentowanie rozbieżności pomiędzy oceną radiologiczną systemu kanałowego a kliniczną.

The abnormal accumulation of the tau protein into aggregates is a hallmark in neurodegenerative diseases collectively known as tauopathies. In normal conditions, tau binds off and on microtubules aiding in their assembly and stability dependent on the phosphorylation state of the protein. In disease-affected neurons, hyperphosphorylation leads to the accumulation of the tau protein into aggregates, mainly neurofibrillary tangles (NFT) which have been seen to colocalise with other protein aggregates in neurodegeneration. One such protein is α-synuclein, the main constituent of Lewy bodies (LB), a hallmark of Parkinson's disease (PD). In many neurodegenerative diseases, including PD, the colocalisation of tau and α-synuclein has been observed, suggesting possible interactions between the two proteins. To explore the cytotoxicity and interactions between these two proteins, we expressed full length human tau and α-synuclein in Dictyostelium discoideum alone, and in combination. We show that tau is phosphorylated in D. discoideum and colocalises closely (within 40 nm) with tubulin throughout the cytoplasm of the cell as well as with α-synuclein at the cortex. Expressing wild type α-synuclein alone caused inhibited growth on bacterial lawns, phagocytosis and intracellular Legionella proliferation rates, but activated mitochondrial respiration and non-mitochondrial oxygen consumption. The expression of tau alone impaired multicellular morphogenesis, axenic growth and phototaxis, while enhancing intracellular Legionella proliferation. Direct respirometric assays showed that tau impairs mitochondrial ATP synthesis and increased the "proton leak," while having no impact on respiratory complex I or II function. In most cases depending on the phenotype, the coexpression of tau and α-synuclein exacerbated (phototaxis, fruiting body morphology), or reversed (phagocytosis, growth on plates, mitochondrial respiratory function, Legionella proliferation) the defects caused by either tau or α-synuclein expressed individually. Proteomics data revealed distinct patterns of dysregulation in strains ectopically expressing tau or α-synuclein or both, but down regulation of expression of cytoskeletal proteins was apparent in all three groups and most evident in the strain expressing both proteins. These results indicate that tau and α-synuclein exhibit different but overlapping patterns of intracellular localisation, that they individually exert distinct but overlapping patterns of cytotoxic effects and that they interact, probably physically in the cell cortex as well as directly or indirectly in affecting some phenotypes. The results show the efficacy of using D. discoideum as a model to study the interaction of proteins involved in neurodegeneration., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Mroczek, Fernando, Fisher and Annesley.)

Alpha synuclein has been linked to both sporadic and familial forms of Parkinson's disease (PD) and is the most abundant protein in Lewy bodies a hallmark of Parkinson's disease. The function of this protein and the molecular mechanisms underlying its toxicity are still unclear, but many studies have suggested that the mechanism of α-synuclein toxicity involves alterations to mitochondrial function. Here we expressed human α-synuclein and two PD-causing α-synuclein mutant proteins (with a point mutation, A53T, and a C-terminal 20 amino acid truncation) in the eukaryotic model Dictyostelium discoideum . Mitochondrial disease has been well studied in D. discoideum and, unlike in mammals, mitochondrial dysfunction results in a clear set of defective phenotypes. These defective phenotypes are caused by the chronic hyperactivation of the cellular energy sensor, AMP-activated protein kinase (AMPK). Expression of α-synuclein wild type and mutant forms was toxic to the cells and mitochondrial function was dysregulated. Some but not all of the defective phenotypes could be rescued by down regulation of AMPK revealing both AMPK-dependent and -independent mechanisms. Importantly, we also show that the C-terminus of α-synuclein is required and sufficient for the localisation of the protein to the cell cortex in D. discoideum .

The misfolding and aggregation of the largely disordered protein, α-synuclein, is a central pathogenic event that occurs in the synucleinopathies, a group of neurodegenerative disorders that includes Parkinson's disease. While there is a clear link between protein misfolding and neuronal vulnerability, the precise pathogenic mechanisms employed by disease-associated α-synuclein are unresolved. Here, we studied the pathogenicity of misfolded α-synuclein produced using the protein misfolding cyclic amplification (PMCA) assay. To do this, previous published methods were adapted to allow PMCA-induced protein fibrillization to occur under non-toxic conditions. Insight into potential intracellular targets of misfolded α-synuclein was obtained using an unbiased lipid screen of 15 biologically relevant lipids that identified cardiolipin (CA) as a potential binding partner for PMCA-generated misfolded α-synuclein. To investigate whether such an interaction can impact the properties of α-synuclein misfolding, protein fibrillization was carried out in the presence of the lipid. We show that CA both accelerates the rate of α-synuclein fibrillization and produces species that harbour enhanced resistance to proteolysis. Because CA is virtually exclusively expressed in the inner mitochondrial membrane, we then assessed the ability of these misfolded species to alter mitochondrial respiration in live non-transgenic SH-SY5Y neuroblastoma cells. Extensive analysis revealed that misfolded α-synuclein causes hyperactive mitochondrial respiration without causing any functional deficit. These data give strong support for the mitochondrion as a target for misfolded α-synuclein and reveal persistent, hyperactive respiration as a potential upstream pathogenic event associated with the synucleinopathies.This article has an associated First Person interview with the first author of the paper., Competing Interests: Competing interestsThe authors declare no competing or financial interests., (© 2020. Published by The Company of Biologists Ltd.)

Post-traumatic ankle arthritis can be a very disabling condition especially in young patients. Localization of the pain is important to allow appropriate treatment. Non-surgical treatment options include anti-inflammatory medications and use of bracing. Multiple surgical options range from joint sparing procedures for the younger patient to total ankle replacement for the older, less active patient. Arthrodesis remains the gold standard and is the procedure of choice for younger patients who are heavy laborers and in patients with severe arthritis who are not candidates for a total ankle replacement. Joint sparing operations include allograft resurfacing, arthroscopic debridement and osteophyte resection, joint distraction arthroplasty, and supramalleolar osteotomy. In older low demand patients, the surgeon may consider a total ankle arthroplasty as an alternative to arthrodesis.

Background: The hip joint is a multiaxial articulation and the most mobile joint of the lower extremity. It can be subject to overloading by the repetition of a motor pattern produced by imbalanced muscle groups., Objectives: To determine mean torque values of the external forces acting on the hip joint in various age groups; to compare the relations between the torque values of antagonistic hip muscles; to correlate changes in mean torque values of the hip muscles with age., Material and Methods: The study involved a group of 120 women aged 19-85 years divided into 6 age groups of 20 subjects each. The presence of knee or hip pathology was an exclusion criterion. The tests were carried out in the Zamość Rehabilitation Department of CMPA in an SPB2-FM unit., Results: The highest mean torque values for all muscle groups were seen in women aged 19-25 years. The values gradually decreased with age., Conclusions: 1. The SPB2-FM unit is an objective tool for evaluating torques of the hip muscles and makes it possible to monitor changes occurring in the process of rehabilitation, as well as to diagnose risks resulting from a decrease in hip muscle strength. 2. The present study of healthy subjects provides baseline data for further comparisons with patients suffering from hip pathology and preliminary input for determining reference values of pelvic girdle muscle strength.

Background: Atypical claudication is a relatively uncommon problem within the general population. However, suspicion for the diagnosis is raised when young and athletic patients present with symptoms of claudication during exercise. The most common causes of atypical claudication are anatomical variants, including popliteal artery entrapment syndrome and tarsal tunnel syndrome. These variants result in impaired arterial flow and nerve compression, respectively. In this report, we present a seminal case of dorsalis pedis artery entrapment by the extensor hallucis brevis tendon during active dorsiflexion of the foot., Methods: The patient was a 42-year-old male without significant past medical history, who presented with claudication in both feet upon active dorsiflexion. He underwent dynamic arterial duplex studies that first revealed normal flow in the neutral position and then revealed complete cessation of flow in both duplex and Doppler modes on dorsiflexion of the foot. He also underwent dynamic magnetic resonance angiography of bilateral lower extremities that revealed an incomplete pedal arch with early termination of the posterior tibial artery on static images and termination of the dorsalis pedis artery at notching on the dorsum of the foot during dorsiflexion. The patient was taken to the operating room for bilateral dorsalis pedis artery exploration. During exploration, the patient was found to have entrapment of the dorsalis pedis artery by the extensor hallucis brevis (EHB) tendon. This was documented by both direct visualization and intraoperative cessation of Doppler signal on dorsiflexion. Since the EHB tendon provides only secondary function to the extensor hallucis longus (EHL) tendon, the EHB was transected near its insertion and transposed directly to the EHL tendon. This allowed for normal extensor function of the great toe and restored triphasic Doppler signals during dorsiflexion., Conclusion: Dorsalis pedis arterial entrapment is a novel cause of atypical claudication. It is extremely uncommon as patients must have both abnormal anatomy and an incomplete pedal arch to display symptoms. Similar to other entrapment syndromes, if identified before permanent arterial scarring, the treatment does not require a bypass procedure. Removal of the tendon along with transposition will allow cessation of symptoms without impaired dorsiflexion of the great toe., (Copyright 2010. Published by Elsevier Inc.)

This prospective study was designed to evaluate a nonoperative-based treatment protocol for patients with the clinical diagnosis of a degenerative medial meniscus tear and to determine if a significant percent of patients with degenerative medial meniscus tears improve with nonoperative treatment and do not elect operative treatment. Twenty-six patients were followed for 37 months and evaluated clinically, radiographically, and with standardized, validated Modified Lysholm Knee Scoring System (MLKS) and Standardized Activities of Daily Living Scale of the Knee (SADL) questionnaires. Patients were initially treated with 4 weeks of nonsteroidal anti-inflammatory drugs. After 4 weeks, they were offered arthroscopic partial meniscectomy or continued nonoperative treatment. Forty-six percent of patients (12 of 26) declined operative treatment. The mean length of time between enrollment and surgery was 3 months (range, 1-13 months). Both groups improved significantly over baseline (P<.05). The initial and final SADL and initial MLKS scores of the 2 groups were not significantly different (P>.05). The final MLKS score of the operative treatment group was significantly greater than the nonoperative group (P=.04). Both the nonoperative and operative treatment groups improved significantly at 3-year follow-up. Forty-six percent of the patients received nonoperative treatment and improved to a functional level that allowed them to avoid surgery. Therefore, we recommend an initial course of nonoperative treatment for all patients with a clinical diagnosis of degenerative medial meniscus tears prior to considering surgery.

The current study evaluated a new pressure alarm and compared the ability of subjects to limit weightbearing to 20 lb with and without the alarm. The 28 subjects were divided into four groups (Group 1, n = 7, mean age, 33 years, with normal sensation; Group 2, n = 7, mean age, 59 years, with normal sensation; Group 3, n = 6, mean age, 56 years, without protective lower limb sensation, and Group 4, n = 8, mean age, 39 years, with transtibial amputation). All subjects were instructed in partial weightbearing ambulation and then practiced weight shifting onto a scale set at 20 lb for 2 minutes. Average peak force was measured using the F-scan in-shoe sensor while subjects ambulated in two trials: one with a deactivated pressure alarm and the other with an activated alarm. Data were analyzed using two-tailed t tests. In Groups 1, 2, and 4, significantly lower average peak force with the activated alarm versus deactivated alarm occurred in 43%, 86%, and 100% of subjects, respectively. Weightbearing was limited to less than 20 lb with the activated alarm in 86%, 57%, 33%, and 38% of subjects versus 71%, 14%, 0%, and 0% of subjects with the deactivated alarm, respectively.

A retrospective radiographic and chart review was performed for the initial 50 patients who underwent Agility (DePuy, Warsaw IN) total ankle arthroplasty by the senior author (M.S.M.). The review focused on the perioperative complications of nerve or tendon lacerations, intraoperative fractures, acute deep infections, wound complications and component positioning. Major wound complications were defined as those requiring a soft-tissue coverage procedure. Minor wound complications did not require soft tissue coverage and included wound breakdowns, wound edge necrosis, and superficial infections. The immediate mortise and lateral postoperative radiographs were reviewed to measure component positioning. The patients were divided into two groups to compare the initial 25 patients (Group A) with the subsequent 25 patients (Group B). There were no major wound complications in either group. Minor wound complications decreased from six in Group A to two in Group B. There were four lacerations (flexor hallucis longus, posterior tibial tendon, deep peroneal nerve, and superficial peroneal nerve), all occurring in Group A. Five patients sustained intraoperative fractures in Group A, as compared with two fractures in Group B. The number of components varying greater than 4 degrees from neutral as measured by the lateral talar, lateral tibial and mortise tibial component angles decreased by 9% from Group A to Group B. The only tibial component to be placed in more than 4 degrees of valgus occurred in Group A. It seems that a notable learning curve exists in the performance of total ankle arthroplasty as demonstrated by a comparison of the initial 25 patients with the subsequent 25 patients performed by one orthopaedic surgeon. This improvement most likely resulted from the use of enhanced techniques and further training with the prosthesis. This information can be used as a teaching tool to decrease the incidence of complications for surgeons performing their initial arthroplasties with this potentially technically demanding procedure.

Purpose: The purpose of this study was to determine, first, if there is measurable deficit in proprioception in an anterior cruciate ligament (ACL)-deficient knee, either compared to the contralateral knee or external controls; second, if this deficit, if present, improves after ACL reconstruction; and third, if improvement occurs, what the time course of improvement is., Type of Study: Prospective cohort study., Methods: Patients undergoing ACL reconstruction at the University of Chicago, demonstrating a full and painless range of motion and no other knee ligament injury or history of previous knee surgery, were eligible. Twenty-six patients, with an average age of 25 years (range, 16 to 48) were enrolled. Average time from injury to reconstruction was 8 weeks. The patients' contralateral knee served as an internal control, and 26 age-matched and gender-matched healthy volunteers were enrolled as an external control group. ACL reconstructions were performed using a single-incision technique with either bone-patellar tendon-bone or quadrupled hamstring autograft. They were allowed immediate weightbearing as tolerated and participated in a standardized rehabilitation program, with the goal of returning to sport at approximately 6 months. Proprioception testing was carried out using an electrogoniometer, in a seated position. Joint position sense (JPS) and threshold to detection of passive motion (TDPM) were measured preoperatively and at 3 and 6 weeks and 3 and 6 months postoperatively., Results: Mean KT-2000 values 6 months postoperatively were 1.38 mm (+/-2). Modified Lysholm score improved significantly (P <.01). Calculated r values were 0.65 for JPS and 0.96 for TDPM. No significant differences in postoperative proprioception were found between hamstring and patellar tendon grafts or among patients with meniscus injury, meniscus repair, or chondral injury. Preoperatively, the mean TDPM in both the injured and contralateral knees was significantly higher (worse) than in the external control knees (P =.008; P =.016). Evaluation of changes in proprioception from preoperative to 6 months postoperative showed significant improvement in both injured and contralateral knees (P =.04; P =.01). At 6-month follow-up, there was no significant difference from controls., Conclusions: TDPM was a more reliable method than JPS for testing proprioception before and after ACL reconstruction in this study. Bilateral deficits in knee joint proprioception (TDPM) were documented after unilateral ACL injury. Reconstruction of a mechanical restraint (ACL graft) was believed to have a significantly positive impact on early and progressive improvement in proprioception.

Mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes syndrome (MELAS) is a maternally inherited multisystem disease caused by mutations of the mitochondrial DNA. The characteristic clinical features are: encephalopathy manifesting as dementia and seizures, stroke-like episodes at young age (usually < 40), lactic acidosis and myopathy with ragged-red fibres. Other frequent manifestations include: sensorineural deafness, diabetes, hypoparathyroidism, peripheral neuropathy and cardiomyopathy. We present two patients with MELAS who were diagnosed 4 and 9 years respectively following the onset of the disease despite the characteristic clinical pictures. The differential diagnostics of inborn and acquired disorders causing stroke is included. We regard that mitochondrial diseases are still insufficiently known and are frequently misdiagnosed. The knowledge is indispensable for establishing diagnosis and accurate genetic counselling. Although there is no specific therapy for mitochondrial diseases to date, coenzyme Q and various vitamins as well as moderate degree exercise might be recommended.

Leber hereditary optic neuropathy (LHON), which is a relatively rare disease, is an inherited form of bilateral atrophy of optic nerves. This atrophy is related to degeneration of retinal ganglion cells and optic nerve axons. The aetiology of this disease is complex and involves primary mutations of mitochondrial DNA, as well as secondary genetic and/or epigenetic changes. We compared the clinical course of LHON in the patients with identical mitochondrial mutations. The molecular PCR-diagnosis was performed in 8 patients, representing 2 generations of the tested family. The group included 2 women suspected of being carriers and 6 men, 3 of whom were diagnosed with LHON and 3 suspected of being at risk of LHON. The primary 11,778 mtDNA mutation was diagnosed in all tested patients with one exception of the son of a male with LHON, which is in agreement with inheritance of mtDNA mutations.

In every human cell there are hundreds of mitochondria, which are required for oxidative phosphorylation as well as many other metabolic processes. Each mitochondrion contains approximately 5 mitochondrial DNA molecules. These circular DNAs of 16.5 kb in size contain only 39 genes. Mutations in mitochondrial DNA are responsible for many diseases. Alterations in these molecules may also play a role in ageing and in tumour formation.

MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) is a disease mainly due to a mutation at position 3243 (A --> G) in the leucine tRNA gene in mitochondrial DNA. Symptoms of the disorder are complex and the exact pathogenesis is not understood. A review of the literature on the subject is presented.

Increasing numbers of diseases due to disturbances in mitochondrial DNA (mtDNA) are being discovered. Mutations in mtDNA mainly cause malfunctioning of muscle and nerve cells. The most common diseases and their molecular diagnosis are briefly described.

Study Design: Computed tomography scans of the dens were performed on patients who had no atlantoaxial pathology., Objectives: To determine whether one or two screws is optimal for fracture fixation and whether two screws can always negotiate the intramedullary odontoid cavity., Summary of Background Data: Fixation of Type II dens fractures traditionally has used C1-C2 posterior wiring and fusion. Two screws placed across an odontoid fracture as a method of rigid internal fixation also has been described. However, it is not known whether two screws can always negotiate the odontoid canal., Methods: Ninety-two consecutive computerized tomography scans of the dens were performed on adults who had no atlantoaxial pathology. Measurements were taken from the scan and compared with the cross-sectional diameter of two odontoid screws., Results: The critical diameter for the placement of two 3.5-mm cortical screws with tapping was 9.0 mm. This dimension was present in 95% of the patients studied., Conclusions: Correct orientation of the computerized tomography scanner is critical for accurate measurements. Two 3.5-mm screws can be used in internal fixation of Type II dens fractures in 95% of the patients if the inner cortex is tapped.

The perception of depth in monocularly viewed pictures has been investigated with the use of a binocular rangefinder developed by Gregory. Two experiments are reported which focus upon stimulus conditions that were identified by Haber as conventions for rendering depth in pictures. Several conclusions, which concern assumptions that must be made in interpreting pictures according to such conventions, are supported by the results. There is a default or assumed layout of background space. The interpretation of a point in a depiction depends upon the interpretation of neighboring points, so that interpretations of local features influence the interpretations of nearby 'empty' areas. In photographs, the magnitude of apparent depth depends upon the degree of discrepancy between the position of the illuminating source and the observer's supposed light-source position. Also in photographs, apparent depth increases as the contrast between highlights and attached shadows increases.