Loss Of Fibers Research Articles

Transmission of signal and idler using optical parametric amplifier based on PPLN waveguide

In this study, we attempted the repeated transmission of S-band signals by compensating for the loss of the transmission fiber using an optical parametric amplifier (OPA) based on a periodically poled LiNbO3 waveguide. We examined and compared the two configurations. The first method involved wavelength conversion of the signal to an idler, while the second method amplified the signal itself. In the latter case, we demonstrated repeated transmissions using external dispersion compensation. In the former case, we demonstrated that it was possible not only to compensate for fiber loss but also to reduce the accumulation of dispersion in transmission fibers by utilizing spectral inversion.

Scleromyxedema

Scleromyxedema or generalized diffuse lichen myxoedematosus is arare mucinosis that is associated with monoclonal gammopathy and which frequently affects multiple extracutaneous organ systems. The pathogenesis of scleromyxedema has not been fully elucidated, but includes stimulation of glycosaminoglycan synthesis. The clinical course of scleromyxedema is chronic and often progressive, leading to severe morbidity and even death. The characteristic skin findings encompass multiple waxy papules often on indurated plaques, while thickening of skin leads to conspicuous folds on glabella and dorsal aspects of finger joints. Microscopical manifestations are dermal deposits of glycosaminoglycans between collagen bundles in reticular dermis, increased numbers of fibroblasts and fibrosis as well as loss of elastic fibers. Progressive skin involvement results in decreased mobility of the mouth and joints and even contractures. Extracutaneous manifestations occur in the musculoskeletal or cardiovascular system, in the gastrointestinal or respiratory tract, in the kidneys or in the central and peripheral nervous system. There are no in-label or evidence-based treatments available for scleromyxedema, but by expert consensus high-dose immunoglobulins are considered as treatment of choice, followed in case of insufficient efficacy by systemic glucocorticosteroids and then lenalidomide or thalidomide. In severe and refractory cases, autologous hematopoietic stem cell transplantation has been performed. Long-term maintenance treatment is usually required to prevent recurrences. Close interdisciplinary follow-up is recommended.

Characterization of graded 6-Hydroxydopamine unilateral lesion in medial forebrain bundle of mice

Parkinson’s disease (PD) is the second most common age-related neurodegenerative disease, with a progressive loss of dopaminergic cells and fibers. The purpose of this study was to use different doses of 6-hydroxydopamine (6-OHDA) injection into the medial forebrain bundle (MFB) of mice to mimic the different stages of the disease and to characterize in detail their motor and non-motor behavior, as well as neuropathological features in the nigrostriatal pathway. MFB were injected with 0.5 μg, 1 μg, 2 μg of 6-OHDA using a brain stereotaxic technique. 6-OHDA induced mitochondrial damage dose-dependently, as well as substantia nigra pars compacta (SNpc) tyrosine hydroxylase-positive (TH+) cell loss and striatal TH fiber loss. Activation of astrocytes and microglia in the SNpc and striatum were consistently observed at 7 weeks, suggesting a long-term glial response in the nigrostriatal system. Even with a partial or complete denervation of the nigrostriatal pathway, 6-OHDA did not cause anxiety, although depression-like behavior appeared. Certain gait disturbances were observed in 0.5 μg 6-OHDA lesioned mice, and more extensive in 1 μg group. Despite the loss of more neurons from 2 μg 6-OHDA, there was no further impairment in behaviors compared to 1 μg 6-OHDA. Our data have implications that 1 μg 6-OHDA was necessary and sufficient to induce motor and non-motor symptoms in mice, thus a valuable mouse tool to explore disease progression and new treatment in PD.

Microstructural integrity of the locus coeruleus and its tracts reflect noradrenergic degeneration in Alzheimer’s disease and Parkinson’s disease

BackgroundDegeneration of the locus coeruleus (LC) noradrenergic system contributes to clinical symptoms in Alzheimer’s disease (AD) and Parkinson’s disease (PD). Diffusion magnetic resonance imaging (MRI) has the potential to evaluate the integrity of the LC noradrenergic system. The aim of the current study was to determine whether the diffusion MRI-measured integrity of the LC and its tracts are sensitive to noradrenergic degeneration in AD and PD.MethodsPost-mortem in situ T1-weighted and multi-shell diffusion MRI was performed for 9 AD, 14 PD, and 8 control brain donors. Fractional anisotropy (FA) and mean diffusivity were derived from the LC, and from tracts between the LC and the anterior cingulate cortex, the dorsolateral prefrontal cortex (DLPFC), the primary motor cortex (M1) or the hippocampus. Brain tissue sections of the LC and cortical regions were obtained and immunostained for dopamine-beta hydroxylase (DBH) to quantify noradrenergic cell density and fiber load. Group comparisons and correlations between outcome measures were performed using linear regression and partial correlations.ResultsThe AD and PD cases showed loss of LC noradrenergic cells and fibers. In the cortex, the AD cases showed increased DBH + immunoreactivity in the DLPFC compared to PD cases and controls, while PD cases showed reduced DBH + immunoreactivity in the M1 compared to controls. Higher FA within the LC was found for AD, which was correlated with loss of noradrenergic cells and fibers in the LC. Increased FA of the LC-DLPFC tract was correlated with LC noradrenergic fiber loss in the combined AD and control group, whereas the increased FA of the LC-M1 tract was correlated with LC noradrenergic neuronal loss in the combined PD and control group. The tract alterations were not correlated with cortical DBH + immunoreactivity.ConclusionsIn AD and PD, the diffusion MRI-detected alterations within the LC and its tracts to the DLPFC and the M1 were associated with local noradrenergic neuronal loss within the LC, rather than noradrenergic changes in the cortex.

Aortic elastic fiber degeneration during acute type a aortic dissection and reverse aortic remodeling

BackgroundProgression of proximal or distal aortic dilatation is defined as reverse aortic remodeling after surgery for acute type A aortic dissection (ATAAD) that may be dependent on aortic wall degeneration.MethodsWe investigated whether aortic wall degeneration is associated with reverse aortic remodeling leading to aortic reoperation after surgery for ATAAD. Altogether, 141 consecutive patients undergoing surgery for ATAAD at Tampere were evaluated. The resected ascending aortic wall at surgery was processed for 42 degenerative, atherosclerotic and inflammatory histological variables. Patients undergoing aortic reoperations (Redos) were compared with those without aortic reoperations (Controls) during a mean 4.9-year follow-up.ResultsRedos were younger than Controls (56 and 66 years, respectively, P < 0.001), and had less frequently previous cardiac surgery prior to ATAAD. Initial surgery encompassed replacement of the ascending aorta in the majority. There were 21 Redos in which one patient died during follow-up as compared with 51 deaths in Controls (log Rank P = 0.002). Histology of the aortic wall revealed increased elastic fiber fragmentation, loss, and disorganization in Redos as compared with Controls (2.1 ± 0.5 vs. 1.9 ± 0.5, Point score unit (PSU), P = 0.043 and 1.7 ± 0.8 vs. 1.2 ± 0.8, PSU, P = 0.016, respectively). Moderate atherosclerosis occurred less often in Redos vs. Controls (9.5% vs. 33%, PSU, P = 0.037, respectively).ConclusionsAccording to this exploratory study, histopathology reveals distinctive aortic wall degeneration during ATAAD. Reverse aortic remodeling after ATAAD is associated with the presence of ascending aortic wall elastic fiber fragmentation, loss and disorganization during ATAAD.

Imaging mass cytometry analysis of Becker muscular dystrophy muscle samples reveals different stages of muscle degeneration

Becker muscular dystrophy (BMD) is characterised by fiber loss and expansion of fibrotic and adipose tissue. Several cells interact locally in what is known as the degenerative niche. We analysed muscle biopsies of controls and BMD patients at early, moderate and advanced stages of progression using Hyperion imaging mass cytometry (IMC) by labelling single sections with 17 markers identifying different components of the muscle. We developed a software for analysing IMC images and studied changes in the muscle composition and spatial correlations between markers across disease progression. We found a strong correlation between collagen-I and the area of stroma, collagen-VI, adipose tissue, and M2-macrophages number. There was a negative correlation between the area of collagen-I and the number of satellite cells (SCs), fibres and blood vessels. The comparison between fibrotic and non-fibrotic areas allowed to study the disease process in detail. We found structural differences among non-fibrotic areas from control and patients, being these latter characterized by increase in CTGF and in M2-macrophages and decrease in fibers and blood vessels. IMC enables to study of changes in tissue structure along disease progression, spatio-temporal correlations and opening the door to better understand new potential pathogenic pathways in human samples.

Continuous-wave operation of 1550 nm low-threshold triple-lattice photonic-crystal surface-emitting lasers

Benefitting from narrow beam divergence, photonic crystal surface-emitting lasers are expected to play an essential role in the ever-growing fields of optical communication and light detection and ranging. Lasers operating with 1.55 μm wavelengths have attracted particular attention due to their minimum fiber loss and high eye-safe threshold. However, high interband absorption significantly decreases their performance at this 1.55 μm wavelength. Therefore, stronger optical feedback is needed to reduce their threshold and thus improve the output power. Toward this goal, photonic-crystal resonators with deep holes and high dielectric contrast are often used. Nevertheless, the relevant techniques for high-contrast photonic crystals inevitably complicate fabrication and reduce the final yield. In this paper, we demonstrate the first continuous-wave operation of 1.55 μm photonic-crystal surface-emitting lasers by using a ‘triple-lattice photonic-crystal resonator’, which superimposes three lattice point groups to increase the strength of in-plane optical feedback. Using this geometry, the in-plane 180° coupling can be enhanced threefold compared to the normal single-lattice structure. Detailed theoretical and experimental investigations demonstrate the much lower threshold current density of this structure compared to ‘single-lattice’ and ‘double-lattice’ photonic-crystal resonators, verifying our design principles. Our findings provide a new strategy for photonic crystal laser miniaturization, which is crucial for realizing their use in future high-speed applications.

Fresh Fruit Bunch (FFB) Processing Modification to Increase Crude Palm Oil (CPO) Rendement

Oil palm has grown from an area of 300 thousand ha in 1980 to now 16.1 million ha (according to GAPKI) with CPO production of 40 million tons. People’s plantations continue to increase and currently account for 52 percent of the total area of oil palm plantations. In this research, pressing pressure experiments were carried out at 60 bar, 70 bar, and 80 bar, respectively, oil losses in fiber were obtained at 13.22%,9.34%, and 7.63%. Through regression analysis, it was found that oil loss in the mesocarp was 1.1% at a pess pressure of 106 Bar. So from this experiment it can be concluded that separating the mesocarp and kernel before pressing provides an increase in oil yield, minimizing oil loss in fiber. The standard oil loss in fiber is 5% in the current palm oil processing process. After modifying the process, very small oil loss in the fiber can be achieved.

Netazepide, an Antagonist of Cholecystokinin Type 2 Receptor, Prevents Vincristine-Induced Sensory Neuropathy in Mice.

Among the vinca-alkaloid class, vincristine is a potent chemotherapeutic agent with significant neurotoxic effects and is employed to address a wide spectrum of cancer types. Recently, the therapeutic potential of the cholecystokinin type 2 receptor (CCK2R) as a target for vincristine-induced peripheral neuropathy (VIPN) was demonstrated. In this study, the impact of preventive CCK2R blockade using netazepide (Trio Medicines Ltd., London, UK) was investigated in a mouse model of vincristine-induced peripheral neuropathy. Netazepide is a highly selective CCK2R antagonist under development for the treatment of patients with gastric neuroendocrine tumors caused by hypergastrinemia secondary to chronic autoimmune atrophic gastritis. Vincristine-induced peripheral neuropathy was induced by intraperitoneal injections of vincristine at 100 µg/kg/d for 7 days (D0 to D7). Netazepide (2 mg/kg/d or 5 mg/kg/d, per os) was administered one day before vincristine treatment until D7. Vincristine induced a high tactile allodynia from D1 to D7. VIPN was characterized by dorsal root ganglion neuron (DRG) and intraepidermal nerve fiber (IENF) loss, and enlargement and loss of myelinated axons in the sciatic nerve. Netazepide completely prevented the painful symptoms and nerve injuries induced by vincristine. In conclusion, the fact that netazepide protected against vincristine-induced peripheral neuropathy in a mouse model strongly supports the assessment of its therapeutic potential in patients receiving such chemotherapy.

Design of A Chaos-based Digital Radio over Fiber Transmission Link using ASK Modulation for Wireless Communication Systems

Secured broadband radio communications are becoming increasingly pivotal for high-speed connectivity in radio access networks, playing a crucial role in both mobile information systems and wireless IoT connections. This paper introduces a chaos-based two-channel digital radio communication system utilizing fiber optic radio transmission technology. The system comprises two radio channels operating at up to 1 Gbps using amplitude shift keying (ASK) modulation, followed by modulation with a chaotic sequence before conversion to the optical domain using the MZM modulator. To compensate for fiber loss, the system utilizes an Erbium Doped Fiber Amplifier (EDFA) and employs the optical links through standard ITU-G.655 optical fibers. Numerical simulation of the designed system is performed using the commercialized simulation software Optisystem V.15 to assess and characterize transmission performance. The results demonstrate the system’s effective operation on two channels with a fiber transmission distance of up to 110 km, maintaining a bit error ratio of less than 10−9. This feature ensures reliable performance for high-speed radio connections, particularly in applications such as fronthaul networks in cloud radio access and wireless sensor network connections.

ΔFosB is part of a homeostatic mechanism that protects the epileptic brain from further deterioration.

Activity induced transcription factor ΔFosB plays a key role in different CNS disorders including epilepsy, Alzheimer's disease, and addiction. Recent findings suggest that ΔFosB drives cognitive deficits in epilepsy and together with the emergence of small molecule inhibitors of ΔFosB activity makes it an interesting therapeutic target. However, whether ΔFosB contributes to pathophysiology or provides protection in drug-resistant epilepsy is still unclear. In this study, ΔFosB was specifically downregulated by delivering AAV-shRNA into the hippocampus of chronically epileptic mice using the drug-resistant pilocarpine model of mesial temporal epilepsy (mTLE). Immunohistochemistry analyses showed that prolonged downregulation of ΔFosB led to exacerbation of neuroinflammatory markers of astrogliosis and microgliosis, loss of mossy fibers, and hippocampal granule cell dispersion. Furthermore, prolonged inhibition of ΔFosB using a ΔJunD construct to block ΔFosB signaling in a mouse model of Alzheimer's disease, that exhibits spontaneous recurrent seizures, led to similar findings, with increased neuroinflammation and decreased NPY expression in mossy fibers. Together, these data suggest that seizure-induced ΔFosB, regardless of seizure-etiology, is part of a homeostatic mechanism that protects the epileptic brain from further deterioration.

J24335 exerts neuroprotective effects against 6-hydroxydopamine-induced lesions in PC12 cells and mice

Parkinson's disease is the second most prevalent age-related neurodegenerative disease and disrupts the lives of people aged >60 years. Meanwhile, single-target drugs becoming inapplicable as PD pathogenesis diversifies. Mitochondrial dysfunction and neurotoxicity have been shown to be relevant to the pathogenesis of PD. The novel synthetic compound J24335 (11-Hydroxy-1-(8-methoxy-5-(trifluoromethyl)quinolin-2-yl)undecan-1-one oxime), which has been researched similarly to J2326, has the potential to be a multi-targeted drug and alleviate these lesions. Therefore, we investigated the mechanism of action and potential neuroprotective function of J24335 against 6-OHDA-induced neurotoxicity in mice, and in PC12 cell models. The key target of action of J24335 was also screened. MTT assay, LDH assay, flow cytometry, RT-PCR, LC–MS, OCR and ECAR detection, and Western Blot analysis were performed to characterize the neuroprotective effects of J24335 on PC12 cells and its potential mechanism. Behavioral tests and immunohistochemistry were used to evaluate behavioral changes and brain lesions in mice. Moreover, bioinformatics was employed to assess the drug-likeness of J24335 and screen its potential targets. J24335 attenuated the degradation of mitochondrial membrane potential and enhanced glucose metabolism and mitochondrial biosynthesis to ameliorate 6-OHDA-induced mitochondrial dysfunction. Animal behavioral tests demonstrated that J24335 markedly improved motor function and loss of TH-positive neurons and dopaminergic nerve fibers, and contributed to an increase in the levels of dopamine and its metabolites in brain tissue. The activation of both the CREB/PGC-1α/NRF-1/TFAM and PKA/Akt/GSK-3β pathways was a major contributor to the neuroprotective effects of J24335. Furthermore, bioinformatics predictions revealed that J24335 is a low toxicity and highly BBB permeable compound targeting 8 key genes (SRC, EGFR, ERBB2, SYK, MAPK14, LYN, NTRK1 and PTPN1). Molecular docking suggested a strong and stable binding between J24335 and the 8 core targets. Taken together, our results indicated that J24335, as a multi-targeted neuroprotective agent with promising therapeutic potential for PD, could protect against 6-OHDA-induced neurotoxicity via two potential pathways in mice and PC12 cells.

Pedestal-cladding-pumped holmium fiber laser optimization using an analytical model

An analytical model of holmium-doped fiber laser is used to calculate optimal fiber length, pump wavelength and signal wavelength under in-band pumping conditions while considering fiber losses. The calculations show the advantages of a new type of pedestal-cladding-pumped fiber.

Episodic Neurological Dysfunction in X-Linked Charcot-Marie-Tooth Disease: Expansion of the Phenotypic and Genetic Spectrum.

X-linked Charcot-Marie-Tooth disease type 1 (CMTX1) is characterized by peripheral neuropathy with or without episodic neurological dysfunction. We performed clinical, neuropathological, and genetic investigations of a series of patients with mutations of the gap-junction beta-1 gene (GJB1) to extend the phenotypic and genetic description of CMTX1. Detailed clinical evaluations, sural nerve biopsy, and genetic analysis were applied to patients with CMTX1. We collected 27 patients with CMTX1 with GJB1 mutations from 14 unrelated families. The age at onset (AAO) was 20.9±12.2 years (mean±standard deviation; range, 2-45 years). Walking difficulties, weakness in the legs, and pes cavus were common initial symptoms. Compared with female patients, males tended to have a younger AAO (males vs. females=15.4±9.6 vs. 32.0±8.8 years, p=0.002), a longer disease course (16.8±16.1 vs. 5.5±3.8 years, p=0.034), and more-severe electrophysiological results. Besides peripheral neuropathy, six of the patients had special episodic central nervous system (CNS) evidence from symptoms, signs, and/or reversible white-matter lesions. Neuropathology revealed the loss of large myelinated fibers, increased number of regenerated axon clusters with abnormally thin myelin sheaths, and excessively folded myelin. Genetic analysis identified 14 GJB1 variants, 6 of which were novel. These findings expand the phenotypic and genetic spectrum of CMTX1. Although CMTX1 was found to have high phenotypic and CNS involvement variabilities, detailed neurological examinations and nerve conduction studies will provide critical clues for accurate diagnoses. Further exploration of the underlying mechanisms of connexin 32 involvement in neuropathy or CNS dysfunction is warranted to develop promising therapies.

Sarcopenia as a non-motor symptom of Parkinson's disease

Sarcopenia is a progressive generalized skeletal muscle disease that is accompanied by an accelerated loss of muscle mass and function, affecting the quality of life and the ability to perform self-care. The prevalence of sarcopenia in the world today ranges from 10 to 25%, which represents a certain danger as it is a prognostic factor for possible injury and increased disability in the elderly population. Sarcopenia often accompanies a large number of different diseases, including neurodegenerative ones, so it is actively studied in this category of patients, for example, as one of the early symptoms of Parkinson's disease (PD). PD and sarcopenia have overlapping pathophysiological mechanisms of muscle fiber loss: inflammation, muscle autophagy, oxidative stress and apoptosis. Loss of muscle mass due to malnutrition is common in PD. According to some studies, the prevalence of sarcopenia in PD varies from 6 to 55.8%; weakness and sarcopenia are more common in patients with PD than in society as a whole, which is associated with an unfavorable course of the disease. The presence of both diseases simultaneously in one patient can impose certain restrictions on the treatment of the patient, worsen his physical and mental condition, which determines the need for early detection of sarcopenia in patients with PD.

Melatonin supplementation counteracts fiber loss in knee ligaments of diabetes-induced rats.

Diabetes mellitus (DM) is a prevalent metabolic disease. The clinical impact of sustained hyperglycemia on ligament healing has not been well characterized. Diabetes is a known cause of macro-, microvascular, and diabetic ulcer healing difficulties among tissues. Therefore, we aimed to investigate the healing potential occurring in injured and healthy ligaments among diabetic and healthy individuals using a rat model. We hypothesize that DM may contribute to altering the knee medial collateral ligament (MCL), thus its morphology, biochemical fitness, and functionality. The study cohort consisted of 40 rats. The animals were randomized into four equal groups. Groups I and II (20 rats) received saline subcutaneously and served as controls. Groups III and IV (20 rats) were injected with a single dose of streptozotocin (STZ). All animals underwent surgery to cut the left tibial collateral ligament in the hind limb and suture it. The access site was sutured to create inflammation and study the regenerative capacities of animals with normal carbohydrate metabolism and pharmacologically induced diabetes. Each animal then underwent sham surgery to access and suture the right tibial collateral ligament in the hind limb without ligament intervention. After the animals had undergone surgeries, groups II and IV were given melatonin supplementation for 4weeks. Rats with DM presented with more fibrosis and calcification of the MCL and decreased healing potential. Treatment with melatonin in diabetic rats mitigated alterations and improved the antioxidant status of ligaments from the diabetic group.

Endothelial Glycocalyx in the Peripheral Capillaries is Injured Under Oxaliplatin-Induced Neuropathy

Oxaliplatin, a platinum-based anticancer drug, is associated with peripheral neuropathy (oxaliplatin-induced peripheral neuropathy, OIPN), which can lead to worsening of quality of life and treatment interruption. The endothelial glycocalyx, a fragile carbohydrate-rich layer covering the luminal surface of endothelial cells, acts as an endothelial gatekeeper and has been suggested to protect nerves, astrocytes, and other cells from toxins and substances released from the capillary vessels. Mechanisms underlying OIPN and the role of the glycocalyx remain unclear. This study aimed to define changes in the three-dimensional ultrastructure of capillary endothelial glycocalyx near nerve fibers in the hind paws of mice with OIPN. The mouse model of OPIN revealed disruption of the endothelial glycocalyx in the peripheral nerve compartment, accompanied by vascular permeability, edema, and damage to the peripheral nerves. To investigate the potential treatment interventions, nafamostat mesilate, a glycocalyx protective agent was used in tumor-bearing male mice. Nafamostat mesilate suppressed mechanical allodynia associated with neuropathy. It also prevented intra-epidermal nerve fiber loss and improved vascular permeability in the peripheral paws. The disruption of endothelial glycocalyx in the capillaries that lie within peripheral nerve bundles is a novel finding in OPIN. Furthermore, these findings point toward the potential of a new treatment strategy targeting endothelial glycocalyx to prevent vascular injury as an effective treatment of neuropathy as well as of many other diseases. PerspectiveOIPN damages the endothelial glycocalyx in the peripheral capillaries, increasing vascular permeability. In order to prevent OIPN, this work offers a novel therapy approach that targets endothelial glycocalyx.

Clinical applications of confocal microscopy to corneal innervation

In vivo corneal confocal microscopy (IVCM) is a non‐invasive ophthalmic imaging technique that provides images of the cornea at the cellular level. Despite the uses in ocular surface pathologies, in the last decades IVCM has been used to provide more knowledge in refractive surgery wound healing (LASIK and PRK), dry eye disease, and in some corneal infections (amoebas and filamentous fungi). The observation of the corneal cells, both normal and inflammatory, and the possibility of quantification of the corneal nerve density and quality with manual or automated tools, makes IVCM have a significant potential to improve the diagnosis and prognosis in several systemic and corneal conditions. Neuropathic pain has multiple aetiologies, but a major feature is small fibre dysfunction or damage. IVCM has been utilized to show small nerve fibre loss in patients with diabetic and other neuropathies. IVCM has comparable diagnostic utility to intraepidermal nerve fibre density for diabetic neuropathy, fibromyalgia and amyloid neuropathy and predicts the development of diabetic neuropathy. Moreover, in clinical intervention trials of patients with diabetic and sarcoid neuropathy, corneal nerve regeneration occurs early and precedes an improvement in symptoms and neurophysiology. Corneal nerve fibre loss also occurs and is associated with disease progression in multiple sclerosis, Parkinson's disease, and dementia. Patients with small fibre neuropathy have IVCM nerve changes. In conclusion, IVCM has good diagnostic and prognostic capability and fulfils the criteria as an end point for clinical trials in corneal, and peripheral and central neurodegenerative diseases.

중요 시설물 감시용 광센서 시스템 구성 및 감시기법 연구

A buried optical fiber sensor that can be detected over a large area per unit length was designed and manufactured, and study was conducted on the signal characteristics according to the load of an external intrusion object. The optical fiber used was designed and manufactured for external intrusion detection that generated bending loss of the optical fiber using a single mode optical fiber for general optical communication with a length of 4 km. This study investigated the change in the output of the optical fiber sensor and the change in the sensor output signal and detection signal owing to the invasion of external intruders according to the width of the pulse pumping light. Therefore, when changing the width of the pulse pumping light, the minimum detectable conditions according to the detection of external intruders were investigated. Finally, a monitoring technique was presented by developing a signal processing algorithm for an optical fiber sensor.

Extraction and characterization of cattail fibre and lignin recovery from retting bath

Cattail is an aquatic perennial with upright, flat, rhizomatous leaves that can grow to heights of 2.5 to 5 m and looks capable of filling this need. The main objective of this research was to separate and individualize the fibres by partial delignification of cattail fibre and recovery of lignin from the used retting bath of cattail fibre. The alkaline formulations were opted to the separation and removing gummy lignin materials for effective retting of cattail fibre. The retting parameters were studied to obtain the least strength loss and optimum lignin removal in the cattail fibres. The lignin recovery yielded 6.75 gram per litre (gpl) by keeping acidic medium for 1 h at room temperature. Recovered lignin was characterized through Fourier infrared spectroscopy and particle size analysis. The retted Cattail single fibre average diameter and fineness was 109 μm and tex, respectively. Tensile strength retained up to 60 % after retting.