1from sentence_transformers import SparseEncoder
2
3# Download from the 🤗 Hub
4model = SparseEncoder("tomaarsen/splade-modernbert-base-miriad")
5# Run inference
6queries = [
7 "How have infection control measures been effective in preventing nosocomial transmission of TB?\n",
8]
9documents = [
10 'Henry M. Blumberg, MD In this issue of Infection Control and Hospital Epidemiology, a potpourri of tuberculosis (TB)-related articles are being published. 1-7 Tuberculosisrelated issues have been an important focus for the past decade for those in infection control and hospital epidemiology, especially in urban areas where the large majority of TB cases occur, 8 but also, because of federal regulations, for those in low-endemic areas or areas where no TB cases occur (approximately half of the counties in the United States).\n\n The resurgence of TB beginning in the mid1980s in the United States (in large part, due to failure and underfunding of the public health infrastructure and to the epidemic of human immunodeficiency virus [HIV] infection) and outbreaks of TB have highlighted the risk of nosocomial transmission of TB. 9,10 These outbreaks affected both healthcare workers (HCWs) and patients. The fact that outbreaks in New York and Miami, among others, involved multidrug-resistant (MDR) strains that were associated with high morbidity and mortality among HIV-infected individuals punctuated the importance of effective TB infection control measures. Commingling of patients with unsuspected TB and those who were quite immunosuppressed led to amplification of nosocomial transmission. A decade ago, few institutions were prepared for the changing epidemiology of TB.\n\n Several recent studies have demonstrated that infection control measures are effective in preventing nosocomial transmission of TB, 11-13 and two reports in this issue, from institutions in Kentucky 1 and New York, 2 provide additional data on decreases in HCW tuberculin skin-test (TST) conversions following implementation of TB infection control measures. In most studies, multiple interventions (administrative controls, environmental controls, and respiratory protection) were initiated at approximately the same time, making it more difficult to identify the most crucial aspect of the program. The importance of TB infection control measures in contributing to the decline in TB cases in the United States, as well as the reduction in the number of MDR-TB cases in New York City, often has been understated. Increased federal funding for TB control activities and expansion of directly observed therapy clearly are important in efforts to prevent TB, but the initial decline in TB cases and in MDR TB in the United States beginning in 1993 likely was due, in large part, to interruption of TB transmission within healthcare facilities. Unfortunately, increased funding for TB control in the United States in the last 5 years often has not trickled down to inner-city hospitals, which frequently are the first line in the battle against TB.\n\n From our experience and that of others, it appears clear that administrative controls are the most important component of a TB infection control program. At Grady Memorial Hospital in Atlanta, we were able to decrease TB exposure episodes markedly and concomitantly to decrease HCW TST conversions after implementing an expanded respiratory isolation policy. 11 We continue to isolate appropriately approximately 95% of those subsequently diagnosed with TB. We were able to reduce TST conver-sion rates markedly during a period of time in which we had isolation rooms that would be considered suboptimal by Centers for Disease Control and Prevention (CDC) guidelines 14 (rooms that were under negative pressure but had less than six air changes per hour) and were using submicron masks. Implementation of better-engineered isolation rooms (>12 air changes per hour) with the completion of renovations to the hospital may have put us in better compliance with regulatory agencies and made the staff feel more secure, but has had little impact on further reducing low rates of HCW TST conversions. In addition, the termination of outbreaks and reduction of TST conversion rates at several institutions took place before introduction of National Institute for Occupational Safety and Health-approved masks and fit testing. 2,15,16 United States healthcare institutions are required by regulatory mandates to develop a "respiratory protection program" (including fit testing), which can be time-consuming, expensive, and logistically difficult. 17 Data published to date suggest that the impact of formal fit testing on proper mask use is small. 18 These federal mandates also have turned some well-meaning (trying to comply fully with the Occupational Safety and Health Administration [OSHA] regulations) but misguided infection control practitioners into "facial hair police." These types of processes divert time, effort, and resources away from what truly is effective in preventing nosocomial transmission of TB, as well as from other important infection control activities such as preventing nosocomial bloodstream infections or transmission of highly resistant pathogens such as vancomycin-resistant Enterococcus or preparing for the onslaught of vancomycin-resistant Staphylococcus aureus. At a time when US healthcare institutions are under enormous pressure due to healthcare reform, market forces, and managed care, it is essential that federal regulatory agencies look carefully at scientific data when issuing regulations.',
11 'Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) syndrome is a severe and potentially life-threatening hypersensitivity reaction caused by exposure to certain medications (Phillips et al., 2011; Bocquet et al., 1996) . It is extremely heterogeneous in its manifestation but has characteristic delayed-onset cutaneous and multisystem features with a protracted natural history. The reaction typically starts with a fever, followed by widespread skin eruption of variable nature. This progresses to inflammation of internal organs such as hepatitis, pneumonitis, myocarditis and nephritis, and haematological abnormalities including eosinophilia and atypical lymphocytosis (Kardaun et al., 2013; Cho et al., 2017) .\n\n DRESS syndrome is most commonly classified according to the international scoring system developed by the RegiSCAR group (Kardaun et al., 2013) . RegiSCAR accurately defines the syndrome by considering the major manifestations, with each feature scored between −1 and 2, and 9 being the maximum total number of points. According to this classification, a score of < 2 means no case, 2-3 means possible case, 4-5 means probable case, and 6 or above means definite DRESS syndrome. Table 1 gives an overview of the RegiSCAR scoring system. DRESS syndrome usually develops 2 to 6 weeks after exposure to the causative drug, with resolution of symptoms after drug withdrawal in the majority of cases (Husain et al., 2013a) . Some patients require supportive treatment with corticosteroids, although there is a lack of evidence surrounding the most effective dose, route and duration of the therapy (Adwan, 2017) . Although extremely rare, with an estimated population risk of between 1 and 10 in 10,000 drug exposures, it is significant due to its high mortality rate, at around 10% (Tas and The pathogenesis of DRESS syndrome remains largely unknown. Current evidence suggests that patients may be genetically predisposed to this form of hypersensitivity, with a superimposed risk resulting from Human Herpes Virus (HHV) exposure and subsequent immune reactivation (Cho et al., 2017; Husain et al., 2013a) . In fact, the serological detection of HHV-6 has even been proposed as an additional diagnostic marker for DRESS syndrome (Shiohara et al., 2007) . Other potential risk factors identified are family history (Sullivan and Shear, 2001; Pereira De Silva et al., 2011) and concomitant drug use, particularly antibiotics . DRESS syndrome appears to occur in patients of any age, with patient demographics from several reviews finding age ranges between 6 and 89 years (Picard et al., 2010; Kano et al., 2015; Cacoub et al., 2013) . DRESS syndrome was first described as an adverse reaction to antiepileptic therapy, but has since been recognised as a complication of an extremely wide range of medications (Adwan, 2017) . In rheumatology, it has been classically associated with allopurinol and sulfasalazine, but has also been documented in association with many other drugs including leflunomide, hydroxychloroquine, febuxostat and NSAIDs (Adwan, 2017) . Recent evidence has also identified a significant risk of DRESS syndrome with strontium ranelate use (Cacoub et al., 2013) . Thus far, that is the only anti-osteoporotic drug associated with DRESS syndrome, although there are various cases of other adverse cutaneous reactions linked to anti-osteoporotic medications, ranging from benign maculopapular eruption to Stevens-Johnson syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) . Denosumab, an antiresorptive RANK ligand (RANKL) inhibitor licensed for osteoporosis, is currently known to be associated with some dermatological manifestations including dermatitis, eczema, pruritus and, less commonly, cellulitis (Prolia, n.d.).\n\n We hereby describe the first documented case of DRESS syndrome associated with denosumab treatment.\n\n The patient is a 76-year old female with osteoporosis and a background of alcoholic fatty liver disease and lower limb venous insufficiency. Osteoporosis was first diagnosed in 2003 and treated with risedronate, calcium and vitamin D, until 2006. While on this treatment, the patient sustained T12 and L3 fractures, the latter treated with kyphoplasty, and was therefore deemed a non-responder to risedronate.',
12 "The regulation of these events is known to go awry in certain pathologies especially in diseases associated with neurodegeneration. Mitochondrial fission helps to enhance the number of mitochondria, which can be efficiently distributed to each corner of neuronal cells and thus helps them to maintain their energy demands. Mitochondrial fission is highly essential during the periods of energy starvation to produce new, efficient mitochondrial energy generating systems. However, enhanced fission associated with bioenergetic crisis causes BAX foci formation on mitochondrial membrane and thus causes mitochondrial outer membrane permeabilization (MOMP), releasing cytochrome c and other pro apoptotic mediators into cytosol, results in apoptosis [93] . Impairment in the mitochondrial dynamics has also been observed in case of inflammatory neuropathies and oxaliplatin induced neuropathy [94] . Excessive nitric oxide is known to cause s-nitrosylation of dynamin related protein-1 (Drp-1), and increases the mitochondrial fission [95, 96] . Tumor necrosis factor-α (TNF-α) reported to inhibit the kinensin 1 protein, and thus impairs trafficking by halting mitochondrial movement along axons [97] . In addition to impaired dynamics, aggregates of abnormal shaped, damaged mitochondria are responsible for aberrant mitochondrial trafficking, which contributes to axonal degeneration observed in various peripheral neuropathies [81] .\n\n Autophagy is the discerning cellular catabolic process responsible for recycling the damaged proteins/ organelles in the cells [98] . Mitophagy is a selective autophagic process involved in recycling of damaged mitochondria and helps in supplying the constituents for mitochondrial biogenesis [99] . Excessive accumulation and impaired clearance of dysfunctional mitochondria are known to be observed in various disorders associated with oxidative stress [100] . Oxidative damage to Atg 4, a key component involved in mitophagy causes impaired autophagosome formation and clearance of damaged mitochondria [101] . Loss in the function of molecular chaperons and associated accumulation of damaged proteins are known to be involved in various peripheral neuropathies including trauma induced neuropathy [102, 103] . A model of demyelinating neuropathy corresponds to the accumulation of improperly folded myelin protein PMP-22 is also being observed recently [104, 105] .\n\n Mitochondrial dysfunction and associated disturbances are well connected to neuroinflammatory changes that occur in various neurodegenerative diseases [106] . Dysfunctional mitochondria are also implicated in several pathologies such as cardiovascular and neurodegenerative diseases. Several mitochondrial toxins have been found to inhibit the respiration in microglial cells and also inhibit IL-4 induced alternative anti inflammatory response and thus potentiates neuroinflammation [107] . Mitochondrial ROS are well identified to be involved in several inflammatory pathways such as NF-κB, MAPK activation [108] . Similarly, the pro inflammatory mediators released as a result of an inflammatory episode found to be interfere with the functioning of the mitochondrial electron transport chain and thus compromise ATP production [109] . TNF-α is known to inhibit the complex I, IV of ETC and decreases energy production. Nitric oxide (NO) is a potent inhibitor of cytochrome c oxidase (complex IV) and similarly IL-6 is also known to enhance mitochondrial generation of superoxide [110] . Mitochondrial dysfunction initiates inflammation by increased formation of complexes of damaged mitochondrial parts and cytoplasmic pattern recognition receptors (PRR's). The resulting inflammasome directed activation of interleukin-1β production, which starts an immune response and leads to Fig. (4) . Mitotoxicity in peripheral neuropathies: Various pathophysiological insults like hyperglycemic, chemotherapeutic and traumatic injury to the peripheral nerves results in mitochondrial dysfunction through enhanced generation of ROS induced biomolecular damage and bioenergetic crisis. Following the nerve injury accumulation of mitochondria occurs resulting in the release of mtDNA & formyl peptides into circulation which acts as Death associated molecular patterns (DAMP's). These are recognized by immune cells as foreign bodies and can elicit a local immune/inflammatory response. Interaction between inflammatory mediators and structural proteins involved in mitochondrial trafficking will cause impairment in mitochondrial motility. Oxidative stress induced damage to the mt proteins like Atg4, Parkin etc cause insufficient mitophagy. Excess nitrosative stress also results in excessive mt fission associated with apoptosis. In addition, mtDNA damage impairs its transcription and reduces mitochondrial biogenesis. Ca 2+ dyshomeostasis, loss in mitochondrial potential and bioenergetic crisis cause neuronal death via apoptosis/necrosis. All these modifications cause defects in ultra structure, physiology and trafficking of mitochondria resulting in loss of neuronal function producing peripheral neuropathy.",
13]
14query_embeddings = model.encode_query(queries)
15document_embeddings = model.encode_document(documents)
16print(query_embeddings.shape, document_embeddings.shape)
17# [1, 50368] [3, 50368]
18
19# Get the similarity scores for the embeddings
20similarities = model.similarity(query_embeddings, document_embeddings)
21print(similarities)
22# tensor([[25.4833, 0.1418, 0.0000]])
