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Warehouse/distribution center (DC) automation technology for the retail industry promises to reduce operational costs, improve flexibility and response time for customers, and help improve network productivity, thus making it very relevant for omni/multichannel (OC/MC) settings. However, the investment required to acquire the DC automation technology is high, and hence, the investment decision must be operationally and financially comprehensive. In fact, an automated DC has a network-wide impact: it can benefit players in the network, but in turn is exposed to network risks and the investment must be safeguarded. While the need for a comprehensive decision-making framework and safeguarding strategy is stressed by scholars, such a framework is lacking. Further, corresponding integrated sub-frameworks for key elements in the OC/MC value chain are also missing. In this paper, we address these gaps and contribute by providing a) generalized and integrated three-part framework, b) corresponding sub-frameworks, c) discrete event, economic, and math programming models, d) rapid-sizing/analysis tools based on: i) analysis at the DC-level, ii) network level, iii) economic/business level, and iv) contract level (sustainable supplier/distribution relationship). In this reference, we investigate a new generation 'full-case' technology that has been recognized as a key to warehouse automation. The insights from our research inform several strategic tradeoffs (extent of automation, investment in labor vs. capital, response vs. efficiency, and sustainable supplier management) relevant for decision-making and safeguarding an expensive asset such as an automated DC. Our analysis is based on interviews (retailers, automated and conventional DCs, and DC equipment suppliers), on-site observations, secondary data, and learning from analytical models. We also present an illustrative real-life application/case study of the framework and the modeling details in the E-component.

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The objective of this chapter is to provide an overview of the methods used to investigate the connectivity and structure of the nervous system. These methods allow neuronal cells to be categorized according to their location, shape, and connections to other cells. The Golgi-Cox staining gives a thorough picture of all significant neuronal structures found in the brain that may be distinguished from one another. The most significant characteristic is its three-dimensional integrity since all neuronal structures may be followed continuously from one part to the next. Successions of sections of the brain's neurons are seen with the Golgi stain. The Golgi method is used to serially segment chosen brain parts, and the resulting neurons are produced from those sections.

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Introduction: Patella fracture can occur due to direct injury to the knee or indirect eccentric contraction of the quadriceps tendon. These injuries can present in different configurations which require acceptable reduction and good fixation. Patients are at risk of not only losing their knee extensor mechanism but also having a defective patellofemoral articulation. Hence, the main aim in treating such fractures is to restore the knee extensor mechanism. Surgical options for treating patella fracture include tension band wiring, wiring through cannulated screws, fixation with plate, and suture anchor (SA) fixation. Case Report: We demonstrate a new fixation technique for patella fracture with SAs in two of our patients. They presented with patella fracture following a fall and sustained closed injury with intact distal neurovascular status. The authors describe their technique using double-loaded SAs to obtain anatomical reduction and solid fixation. With three SAs, each inserted in a third portion of a distal fragment. Conclusion: There are several modalities and techniques available for fixation of patella fracture. However, authors recommend that their described novel technique can provide more strength and satisfactory outcome. Furthermore, this technique uses a smaller incision compared to conventional suture tunnel repair as in this technique only the fracture that needs to be exposed distally.

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Disruptions in the supply chains/networks result in both performance failures and a poor return on investment (ROI) of network assets. We propose that addressing this situation requires the governance of exchange relationships through contracts guided by sustainability principles. Specifically, we refer to these contracts in the supply and distribution context as "sustainable network contracts", and the overall framework as the "sustainable contracting framework (SCF)/theory". Despite the critical role of sustainable network contracts for all key stakeholders in the network, we identify a gap in the existing literature regarding the theory of sustainable network contracts. We bridge this gap by extending the extant dimensions of contracts, as described in Transaction Cost Economics and Relational Exchange Theory, to include sustainability dimensions - constituting the 'what' of theory building. To inform sustainable contracts, we propose and employ three factors: costs, benefits, and risks (CBR). We present the 'how' of the theory building, outlined in a five-step approach along with an analytical tool, to demonstrate the practical application of our framework. Additionally, we provide a rationale for adopting sustainable network contracts (the 'why' of the theory building). Our research methodology involves collecting interview-based data from senior executives (CXOs) (secondary and primary), collecting primary and secondary cost data (objective), integrating behavioral elements (subjective), and employing constrained optimization techniques to determine quantity allocation under various contract policies. Further, we map the proposed eight distinct contract types onto the CBR-space, thereby highlight the relevance of the contract types to real-world practices. This mapping considers network externalities, risks, and allows for a coordinated sustainable approach to contracting from the buyer's (retailer's) perspective. For managers, our framework would serve as an important tool that would inform the contract evaluation process, facilitate local versus global decision-making, safeguard network investments, and help align the interests of buyers and suppliers in each contracting cycle.

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Status Epilepticus (SE) is a distributed network disorder, which involves the hippocampus and extra-hippocampal structures. Epileptogenesis in SE is tightly associated with neurogenesis, plastic changes and neural network reorganization facilitating hyper-excitability. On the other hand, dendritic spines are known to be the excitatory synapse in the brain. Therefore, dendritic spine dynamics could play an intricate role in these network alterations. However, the exact reason behind these structural changes in SE are elusive. In the present study, we have investigated the aforementioned hypothesis in the lithium-pilocarpine treated rat model of SE. We have examined cytoarchitectural and morphological changes using hematoxylin-eosin and Golgi-Cox staining in three different brain regions viz. CA1 pyramidal layer of the dorsal hippocampus, layer V pyramidal neurons of anterior temporal lobe (ATL), and frontal neocortex of the same animals. We observed macrostructural and layer-wise alteration of the pyramidal layer mainly in the hippocampus and ATL of SE rats, which is associated with sclerosis in the hippocampus. Sholl analysis exhibited partial dendritic plasticity in apical and basal dendrites of pyramidal cells as compared to the saline-treated weight-/age-matched control group. These findings indicate that region-specific alterations in dendritogenesis may contribute to the development of independent epileptogenic networks in the hippocampus, ATL, and frontal neocortex of SE rats.

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Introduction: The incidence of vascular injuries from arthroscopic surgeries has been reported to be 0.005%. Pseudoaneurysms account for 11% of those injuries. Case Report: In this case report, we discuss a 76-year-old female who presented with a pulsatile swelling in the right shoulder after 10 years following arthroscopic rotator cuff repair. Imaging confirmed the diagnosis of a posterior circumflex artery pseudoaneurysm. The patient was successfully embolised using a transradial approach with thrombosis of the pseudoaneurysm. Conclusion: Vascular injuries following arthroscopic shoulder surgery are rare. However, a pseudoaneurysm should be considered in patients who present with swelling at the surgical site, regardless of the post-operative interval.

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Tumor-induced changes in the peritumoral neocortex play a crucial role in generation of seizures. This study aimed to investigate the molecular mechanisms potentially involved in peritumoral epilepsy in low-grade gliomas (LGGs). Intraoperative peritumoral brain tissues resected from LGG patients with seizures (pGRS) or without seizures (pGNS) were used for RNA sequencing (RNA-seq). Comparative transcriptomics was performed to identify differentially expressed genes (DEGs) in pGRS compared to pGNS using deseq2 and edgeR packages (R). Gene set enrichment analysis (GSEA) using Gene Ontology terms and Kyoto Encyclopedia of Genes & Genomes (KEGG) pathways was performed using the clusterProfiler package (R). The expression of key genes was validated at the transcript and protein levels in the peritumoral region using real-time PCR and immunohistochemistry, respectively. A total of 1073 DEGs were identified in pGRS compared to pGNS, of which 559 genes were upregulated and 514 genes were downregulated (log2 fold-change ≥ 2, padj < 0.001). The DEGs in pGRS were highly enriched in the "Glutamatergic Synapse" and "Spliceosome" pathways, with increased expression of GRIN2A (NR2A), GRIN2B (NR2B), GRIA1 (GLUR1), GRIA3 (GLUR3), GRM5, CACNA1C, CACNA1A, and ITPR2. Moreover, increased immunoreactivity was observed for NR2A, NR2B, and GLUR1 proteins in the peritumoral tissues of GRS. These findings suggest that altered glutamatergic signaling and perturbed Ca2+ homeostasis may be potential causes of peritumoral epilepsy in gliomas. This explorative study identifies important genes/pathways that merit further characterization for their potential involvement in glioma-related seizures.

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Glutamate-receptor-mediated hyperexcitability contributes to seizure generation in temporal lobe epilepsy (TLE). Tryptophan-kynurenine pathway (TKP) metabolites regulate glutamate receptor activity under physiological conditions. This study was designed to investigate alterations in the levels of TKP metabolites and the differential regulation of glutamatergic activity by TKP metabolites in the hippocampus, anterior temporal lobe (ATL), and neocortex samples of a lithium-pilocarpine rat model of TLE. We observed that levels of tryptophan were reduced in the hippocampus and ATL samples but unaltered in the neocortex samples. The levels of kynurenic acid were reduced in the hippocampus samples and unaltered in the ATL and neocortex samples of the TLE rats. The levels of kynurenine were unaltered in all three regions of the TLE rats. The magnitude of reduction in these metabolites in all regions was unaltered in the TLE rats. The frequency and amplitude of spontaneous excitatory postsynaptic currents were enhanced in hippocampus ATL samples but not in the neocortex samples of the TLE rats. The exogenous application of kynurenic acid inhibited glutamatergic activity in the slice preparations of all these regions in both the control and the TLE rats. However, the magnitude of reduction in the frequency of kynurenic acid was higher in the hippocampus (18.44 ± 2.6% in control vs. 30.02 ± 1.5 in TLE rats) and ATL (16.31 ± 0.91% in control vs. 29.82 ± 3.08% in TLE rats) samples of the TLE rats. These findings suggest the differential regulation of glutamatergic activity by TKP metabolites in the hippocampus, ATL, and neocortex of TLE rats.

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Low-grade dysembryoplastic neuroepithelial tumors (DNTs) are a frequent cause of drug-refractory epilepsy. Molecular mechanisms underlying seizure generation in these tumors are poorly understood. This study was conducted to identify altered genes in nonneoplastic epileptogenic cortical tissues (ECTs) resected from DNT patients during electrocorticography (ECoG)-guided surgery. RNA sequencing (RNAseq) was used to determine the differentially expressed genes (DEGs) in these high-spiking ECTs compared to non-epileptic controls. A total of 477 DEGs (180 upregulated; 297 downregulated) were observed in the ECTs compared to non-epileptic controls. Gene ontology analysis revealed enrichment of genes belonging to the following Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways: (i) glutamatergic synapse; (ii) nitrogen metabolism; (iii) transcriptional misregulation in cancer; and (iv) protein digestion and absorption. The glutamatergic synapse pathway was enriched by DEGs such as GRM4, SLC1A6, GRIN2C, GRM2, GRM5, GRIN3A, and GRIN2B. Enhanced glutamatergic activity was observed in the pyramidal neurons of ECTs, which could be attributed to altered synaptic transmission in these tissues compared to non-epileptic controls. Besides glutamatergic synapse, altered expression of other genes such as GABRB1 (synapse formation), SLIT2 (axonal growth), and PROKR2 (neuron migration) could be linked to epileptogenesis in ECTs. Also, upregulation of GABRA6 gene in ECTs could underlie benzodiazepine resistance in these patients. Neural cell-type-specific gene set enrichment analysis (GSEA) revealed transcriptome of ECTs to be predominantly contributed by microglia and neurons. This study provides first comprehensive gene expression profiling of nonneoplastic ECTs of DNT patients and identifies genes/pathways potentially linked to epileptogenesis.

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OBJECTIVES: Temporal lobe epilepsy (TLE) is the most common form of drug-resistant epilepsy. Blood-brain barrier (BBB) leakage occurs during epileptogenesis and several pieces of evidence suggest that this might contribute to the progression of epilepsy. Seizures trigger a pathway involving glutamate signalling through cytosolic phospholipase A2 (cPLA2). This pathway leads to BBB leakage and induces the expression of drug efflux transporters, leading to drug resistance. Therefore, this study aims to determine the mRNA and protein levels of cPLA2, along with its functional activity, in the hippocampus of pilocarpine model of TLE as well as in the surgically resected hippocampal samples of patients with TLE. METHODS: mRNA levels and protein levels of cPLA2 were evaluated by real-time PCR and western blot analysis respectively in animal model of TLE as well as surgically resected hippocampal tissue specimens of TLE. cPLA2 functional activity was measured spectrophotometrically. RESULTS: Significant up-regulation of cPLA2 mRNA was observed in the hippocampal samples obtained from TLE rats (p < 0.05) and-TLE patients (p < 0.01). Increased protein expression of cPLA2 was also demonstrated in the hippocampal samples of TLE rats (p < 0.01) as well as TLE patients (p < 0.01). Similarly, functional activity of cPLA2 was found to be up-regulated in the hippocampus of pilocarpine model of TLE rats (p < 0.01) as well as in the TLE patients (p < 0.01). DISCUSSION: These findings suggest that alterations in cPLA2 expression and activity level in the hippocampus could potentially be a part of dynamic changes associated with TLE.

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Histone deacetylases (HDACs) have been described to have both neurotoxic and neuroprotective roles, and partly, depend on its sub-cellular distribution. HDAC inhibitors have a long history of use in the treatment of various neurological disorders including epilepsy. Key role of HDACs in GABAergic neurotransmission, synaptogenesis, synaptic plasticity and memory formation was demonstrated whereas very less is known about their role in drug-resistant epilepsy pathologies. The present study was aimed to investigate the changes in the expression of HDACs, activity and its sub-cellular distribution in mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) patients. For this study, surgically resected hippocampal tissue specimens of 28 MTLE-HS patients and 20 hippocampus from post-mortem cases were obtained. Real-time PCR was done to analyse the mRNA expression. HDAC activity and the protein levels of HDACs in cytoplasm as well as nucleus were measured spectrophotometrically. Further, sub-cellular localization of HDACs was characterized by immunofluorescence. Significant upregulation of HDAC1, HDAC2, HDAC4, HDAC5, HDAC6, HDAC10 and HDAC11 mRNA were observed in MTLE-HS. Alterations in the mRNA expression of glutamate and gamma-aminobutyric acid (GABA) receptor subunits have been also demonstrated. We observed significant increase of HDAC activity and nuclear level of HDAC1, HDAC2, HDAC5 and HDAC11 in the hippocampal samples obtained from patients with MTLE-HS. Moreover, we found altered cytoplasmic level of HDAC4, HDAC6 and HDAC10 in the hippocampal sample obtained from patients with MTLE-HS. Alterations in the level of HDACs could potentially be part of a dynamic transcription regulation associated with MTLE-HS. Changes in cytoplasmic level of HDAC4, 6 and 10 suggest that cytoplasmic substrates may play a crucial role in the pathophysiology of MTLE-HS. Knowledge regarding expression pattern and sub-cellular distribution of HDACs may help to devise specific HDACi therapy for epilepsy.

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Temporal lobe epilepsy (TLE) is the most common form of intractable epilepsy where hyperactive glutamate receptors may contribute to the complex epileptogenic network hubs distributed among different regions. This study was designed to investigate the region-specific molecular alterations of the glutamate receptors and associated excitatory synaptic transmission in pilocarpine rat model of TLE. We recorded spontaneous excitatory postsynaptic currents (EPSCs) from pyramidal neurons in resected rat brain slices of the hippocampus, anterior temporal lobe (ATL) and neocortex. We also performed mRNA and protein expression of the glutamate receptor subunits (NR1, NR2A, NR2B, and GLUR1-4) by qPCR and immunohistochemistry. We observed significant increase in the frequency and amplitude of spontaneous EPSCs in the hippocampal and ATL samples of TLE rats than in control rats. Additionally, the magnitude of the frequency and amplitude was increased in ATL samples compared to that of the hippocampal samples of TLE rats. The mRNA level of NR1 was upregulated in both the hippocampal as well as ATL samples and that of NR2A, NR2B were upregulated only in the hippocampal samples of TLE rats than in control rats. The mRNA level of GLUR4 was upregulated in both the hippocampal as well as ATL samples of TLE rats than in control rats. Immunohistochemical analysis demonstrated that the number of NR1, NR2A, NR2B, and GLUR4 immuno-positive cells were significantly higher in the hippocampal samples whereas number of NR1 and GLUR4 immuno-positive cells were significantly higher in the ATL samples of the TLE rats than in control rats. This study demonstrated the region-specific alterations of glutamate receptor subunits in pilocarpine model of TLE, suggesting possible cellular mechanisms contributing to generation of independent epileptogenic networks in different temporal lobe structures.

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Focal cortical dysplasia (FCD) is a malformation of the cerebral cortex with poorly-defined epileptogenic zones (EZs), and poor surgical outcome in FCD is associated with inaccurate localization of the EZ. Hence, identifying novel epileptogenic markers to aid in the localization of EZ in patients with FCD is very much needed. High-throughput gene expression studies of FCD samples have the potential to uncover molecular changes underlying the epileptogenic process and identify novel markers for delineating the EZ. For this purpose, we, for the first time performed RNA sequencing of surgically resected paired tissue samples obtained from electrocorticographically graded high (MAX) and low spiking (MIN) regions of FCD type II patients and autopsy controls. We identified significant changes in the MAX samples of the FCD type II patients when compared to non-epileptic controls, but not in the case of MIN samples. We found significant enrichment for myelination, oligodendrocyte development and differentiation, neuronal and axon ensheathment, phospholipid metabolism, cell adhesion and cytoskeleton, semaphorins, and ion channels in the MAX region. Through the integration of both MAX vs non-epileptic control and MAX vs MIN RNA sequencing (RNA Seq) data, PLP1, PLLP, UGT8, KLK6, SOX10, MOG, MAG, MOBP, ANLN, ERMN, SPP1, CLDN11, TNC, GPR37, SLC12A2, ABCA2, ABCA8, ASPA, P2RX7, CERS2, MAP4K4, TF, CTGF, Semaphorins, Opalin, FGFs, CALB2, and TNC were identified as potential key regulators of multiple pathways related to FCD type II pathology. We have identified novel epileptogenic marker elements that may contribute to epileptogenicity in patients with FCD and could be possible markers for the localization of EZ.

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OBJECTIVE: To assess justice system involvement among adolescents in the pediatric emergency department and identify associations with risk and protective factors. STUDY DESIGN: We conducted a cross-sectional, computerized survey of adolescents to assess for personal, justice system involvement, and nonhousehold justice system involvement (ie, important people outside of household). We assessed sexual behaviors, violent behaviors, substance use, school suspension/expulsion, parental supportiveness, and participant mood (score <70 indicates psychological distress). We compared differences between groups using the χ2 tests, Fisher exact tests, t tests, and performed multivariable logistic regression analyses. RESULTS: We enrolled 191 adolescents (mean age 16.1 years, 61% female). Most (68%) reported justice system involvement: personal (13%), household (42%), and nonhousehold (40%). Nearly one-half (47%) were sexually active and 50% reported school suspension/expulsion. The mean score for mood was 70.1 (SD 18); adolescents with justice system involvement had had lower mood scores (68 vs 74, P = .03) compared with those without justice system involvement. In a multivariable model, school expulsion/suspension was significantly associated with reporting any justice system involvement (OR 10.4; 95% CI 4.8-22.4). CONCLUSIONS: We identified the pediatric emergency department as a novel location to reach adolescents at risk for poor health outcomes associated with justice system involvement. Future work should assess which health promotion interventions and supports are desired among these adolescents and families.

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In this study, cluster hypergraphs are introduced to generalize the concept of hypergraphs, where cluster nodes are allowed. Few related terms and properties on cluster hypergraphs are discussed. Some operations, including the Cartesian product, union, intersection, etc., are studied. Different types of matrix representations and isomorphism are also proposed on cluster hypergraphs. The notion of an effective degree for nodes is introduced to capture the group/ cluster effects. At last, the area of applications and future directions with conclusions is deployed.

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Introduction: Lateral end clavicle fractures are rare injuries in pediatric and adolescent population. Most of these injuries can be managed conservatively. However, in patients with acromioclavicular joint (ACJ) "pseudo-dislocations" associated with significant clinical deformity, some patients will benefit from operative intervention. Case Report: Our reported case is a young adolescent with a Type IV Dameron and Rockwood distal clavicle fracture and ACJ pseudo-dislocation, who underwent surgical fixation for this injury. We propose a novel technique of fixation with a suture anchor and endo button with temporary K wire stabilization. These are rare injuries and there are no standardized techniques for reconstruction and fixation. Stabilization with a suture anchor can provide a minimally invasive method of fixation for such injuries without the traditional plating and can lead to excellent final outcomes. Conclusion: ACJ pseudo-dislocations are rare injuries. There is limited evidence in guiding the management of such injuries. Our proposed technique of fixation with suture anchor, endo button and temporary stabilisation with K-wire can provide promising results.

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Introduction: Posterior glenohumeral joint dislocations with associated bony lesions are challenging to treat; namely, reverse Hill-Sachs's lesions increase humeral head excursion predisposing to recurrent dislocations. To add to the complexity of management, posterior shoulder dislocations are often missed on plain radiographs, leading to chronicity in presentation. Case Report: We describe here our technique in our case series of three patients. Case I, 32 years, gentleman, presented 3 days after injury. He had a locked posterior dislocation of shoulder which he sustained while he fell asleep and hit a glass table. Shoulder was not reducible in emergency department. Reverse Hill- Sachs's lesion involved 40% of humeral head. Case II, a 54- years- old gentleman, a keen gym trainer . Following sudden withdrawal of diazepam, he woke up lying on the floor and started experiencing shoulder pain. He presented a week following the injury. The dislocated shoulder could not be reduced in emergency department. Bony defect involved 50% of humeral head. Case III, 45 years gentleman who fell off from bike, presented on the same day to the emergency department. The dislocated shoulder was reduced. Defect size was 40% of humeral head.A thorough physical and radiological examination was performed to evaluate the lesion. Delto-pectoral approach was utilized for surgical exposure. Once fully assessed, the lesion is outlined and an oscillating saw is used to create uniform edges - - a regular "orange slice"- shaped defect. The prepared defect size is measured. Calcium phosphate cement is used to fill the defect and form a mould that represents the dimensions of allograft required to recreate the native sphericity of the humeral head. This mould then acts as a reference when fashioning the osteochondral femoral allograft to make sure this fits the defect anatomically. Once the graft is prepared, it is placed into the defect in the correct orientation and fixed in situ using headless screws. We utilized the same technique in all our patients. Conclusion: Reconstruction with osteochondral allograft is a promising technique to help shoulder surgeons achieve good outcomes for these patients. We propose a novel technique for fashioning allograft to anatomically fill the defects from bone loss, aiming to restores the native sphericity of the humeral head.

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Arthroscopic anterior cruciate ligament (ACL) reconstruction is a common procedure performed for symptomatic ACL tears, especially in athletes. The desired surgical end product with any surgical fixation device remains a taut ACL graft, which is crucial during postoperative rehabilitation to reduce the risk of knee instability and rerupture of the ACL graft. The purpose of this Technical Note and accompanying video is to describe a simple and cost-effective technique to easily retension the ACL graft after tibial fixation in ACL reconstruction using a suture disk device. The technique uses a simple suture disk device to provide strong tibial fixation, along with the unique ability to retension the ACL graft by dialing it in a clockwise direction.