Common Form Research Articles

The clinical benefits of sodium-glucose cotransporter type 2 inhibitors in people with gout.

Gout is the most common form of inflammatory arthritis worldwide and is characterized by painful recurrent flares of inflammatory arthritis that are associated with a transiently increased risk of adverse cardiovascular events. Furthermore, gout is associated with multiple cardiometabolic-renal comorbidities such as type 2 diabetes, chronic kidney disease and cardiovascular disease. These comorbidities, potentially combined with gout flare-related inflammation, contribute to persistent premature mortality in gout, independently of serum urate concentrations and traditional cardiovascular risk factors. Although better implementation of standard gout care could improve gout outcomes, deliberate efforts to address the cardiovascular risk in patients with gout are likely to berequired to reduce mortality. Sodium-glucose cotransporter type 2 (SGLT2) inhibitors are approved for multiple indications owing to their ability to lower the risk of all-cause and cardiovascular death, hospitalizations for heart failure and chronic kidney disease progression, making them an attractive treatment option for gout. These medications have also been shown to lower serum urate concentrations, the causal culprit in gout risk, and are associated with a reduced risk of incident and recurrent gout, potentially owing to their purported anti-inflammatory effects. Thus, SGLT2 inhibition could simultaneously address both the symptoms of gout and its comorbidities.

Preventive repression: Protest policing in New Delhi

ABSTRACT States view protests as disruptive and police them. Scholarship points to selective policing of protests that endanger law and order as well as those organized by minority groups. A common form of protest policing in cities is requiring protestors to obtain permits in advance. We use interviews with protestors and the police in New Delhi to examine their perception of protest policing. We test these perceptions empirically using an original dataset of 4,921 protest applications submitted to the Delhi police between 2016 and 2019. We find that the rejection of protest applications is driven by the disruptive threat that they pose rather than the identity of the protesting group. However, the police disproportionately flag protest applications by religious minorities for threat assessment. A postcolonial police force, which privileges preservation of order over its other functions, regularly curtails the democratic freedom to protest.

Acquired Forms of Fibroblast Growth Factor 23-Related Hypophosphatemic Osteomalacia.

Fibroblast growth factor 23 (FGF23) is a pivotal humoral factor for the regulation of serum phosphate levels and was first identified in patients with autosomal dominant hypophosphatemic rickets and tumor-induced osteomalacia (TIO), the most common form of acquired FGF23-related hypophosphatemic rickets/osteomalacia (FGF23rHR). After the identification of FGF23, many other inherited and acquired forms of FGF23rHR were reported. In this review article, the detailed features of each acquired FGF23rHR are discussed, including TIO, ectopic FGF23 syndrome with malignancy, fibrous dysplasia/McCune-Albright syndrome, Schimmelpenning-Feuerstein-Mims syndrome/cutaneous skeletal hypophosphatemia syndrome, intravenous iron preparation-induced FGF23rHR, alcohol consumption-induced FGF23rHR, and post-kidney transplantation hypophosphatemia. Then, an approach for the differential diagnosis and therapeutic options for each disorder are concisely introduced. Currently, the majority of endocrinologists might only consider TIO when encountering patients with acquired FGF23rHR; an adequate differential diagnosis can reduce medical costs and invasive procedures such as positron emission tomography/computed tomography and venous sampling to identify FGF23-producing tumors. Furthermore, some acquired FGF23rHRs, such as intravenous iron preparation/alcohol consumption-induced FGF23rHR, require only cessation of drugs or alcohol to achieve full recovery from osteomalacia.

Zinner syndrome: A rarer variant of a rare syndrome

Zinner syndrome, characterized by the combination of absent unilateral kidney, obstructed ejaculatory duct on the same side, and cysts in the seminal vesicle, represents a rare congenital malformation of the mesonephric duct. Its symptoms are often vague, ranging from urinary discomfort to painful ejaculation and infertility, making it difficult to diagnose without imaging. In this report, we discuss a less common form of Zinner syndrome identified through diagnostic imaging.

Cerebral visual impairment: genetic diagnoses and phenotypic associations

BackgroundCerebral visual impairment (CVI) is the most common form of paediatric visual impairment in developed countries. CVI can arise from a host of genetic or acquired causes, but there has...

Prevalence and antimicrobial-resistant patterns of Pseudomonas aeruginosa among burn patients attending Yekatit 12 Hospital Medical College in Addis Ababa, Ethiopia.

Burns are one of the most common forms of trauma globally. P. aeruginosa plays a prominent role as an etiological agent among burn patients. There is a paucity of information about the prevalence and antimicrobial resistance patterns of P. aeruginosa among burn patients in Ethiopia. Hence, this study was designed to assess the prevalence and antimicrobial-resistant patterns of P. aeruginosa among burn patients attending Yekatit 12 Hospital Medical College in Addis Ababa, Ethiopia. Hospital-based cross-sectional study was conducted at Yekatit 12 Hospital Medical College among burn patients from November 2020 to April 2021. Identification of P. aeruginosa was performed using Culture, Biochemical tests, and, Gram staining. Antimicrobial resistance testing was done using the Kirby-Bauer disc diffusion method. Logistic regression was computed to determine associated factors. From 210 burn wound cultures, 27 (12.86%) were found positive for P. aeruginosa. All the isolates showed greater than 70% susceptibility to the tested antibiotics except Gentamycin, Ceftazidime, and, Ciprofloxacin. In addition, 33.33% of P. aeruginosa isolates were multidrug-resistant. Admission type, Hospital stay time and Total body surface area (TBSA) had a statistically significant association (all with P-value <0.05) with the acquisition of P. aeruginosa infection. Overall, the prevalence of P. aeruginosa isolates among burn patients is almost 13%. Most P. aeruginosa isolates were sensitive to Imipenem, while they were most resistant to Gentamycin. One-third of P. aeruginosa were multidrug-resistant. This suggests the need to monitor the treatment of infection with the pathogen to limit the possibility of the emergence of multidrug-resistant isolates in burn centers.

Neuropathological stage-dependent proteome mapping of the olfactory tract in Alzheimer's disease: From early olfactory-related omics signatures to computational repurposing of drug candidates.

Alzheimer's disease (AD) is the most common form of dementia, characterized by an early olfactory dysfunction, progressive memory loss, and behavioral deterioration. Albeit substantial progress has been made in characterizing AD-associated molecular and cellular events, there is an unmet clinical need for new therapies. In this study, olfactory tract proteotyping performed in controls and AD subjects (n = 17/group) showed a Braak stage-dependent proteostatic impairment accompanied by the progressive modulation of amyloid precursor protein and tau functional interactomes. To implement a computational repurposing of drug candidates with the capacity to reverse early AD-related olfactory omics signatures (OMSs), we generated a consensual OMSs database compiling differential omics datasets obtained by mass-spectrometry or RNA-sequencing derived from initial AD across the olfactory axis. Using the Connectivity Map-based drug repurposing approach, PKC, EGFR, Aurora kinase, Glycogen synthase kinase, and CDK inhibitors were the top pharmacologic classes capable to restore multiple OMSs, whereas compounds with targeted activity to inhibit PI3K, Insulin-like growth factor 1 (IGF-1), microtubules, and Polo-like kinase (PLK) represented a family of drugs with detrimental potential to induce olfactory AD-associated gene expression changes. To validate the potential therapeutic effects of the proposed drugs, in vitro assays were performed. These validation experiments revealed that pretreatment of human neuron-like SH-SY5Y cells with the EGFR inhibitor AG-1478 showed a neuroprotective effect against hydrogen peroxide-induced damage while the pretreatment with the Aurora kinase inhibitor Reversine reduced amyloid-beta (Aβ)-induced neurotoxicity. Taken together, our data pointed out that OMSs may be useful as substrates for drug repurposing to propose novel neuroprotective treatments against AD.

Role of RUNX2 in Oral Squamous Cell Carcinoma (OSCC): A Systematic Scoping Review

RUNX2, known as the core-binding factor subunit alpha-1 (Cbfa1), is a protein-coding gene recognized and responsible for its involvement in bone development and osteoblast differentiation. However, its dysregulation and aberrant expression have been linked to the pathogenesis of many diseases, such as oral squamous cell carcinoma (OSCC). This review highlights the significance of the RUNX2 gene in oral squamous cell carcinoma. Objectives. To review the contribution of the RUNX2 gene in oral squamous cell carcinoma and its implication on clinical diagnosis and treatments. Materials and Methods. A systematic scoping review was conducted to elucidate the role of RUNX2 in OSCC. A framework of five stages for scoping reviews outlined by Arksey and O’Malley (2005) was adopted for the current study. Results. The review showed that RUNX2 plays a role in the development and progression of OSCC, a common form of head and neck cancer. Conclusion. RUNX2 is an essential player in the molecular mechanisms underlying the development and progression of oral squamous cell carcinoma, and its dysregulation promotes tumor initiation, progression, and metastasis, making it a potential target therapy for future research aimed at developing novel therapies for oral squamous cell carcinoma. Clinical Relevance. Understanding the precise mechanisms by which RUNX2 contributes to OSCC pathogenesis can lead to target treatment for this challenging form of cancer.

Synaptopathy: presynaptic convergence in frontotemporal dementia and amyotrophic lateral sclerosis.

Frontotemporal dementia and amyotrophic lateral sclerosis are common forms of neurodegenerative disease that share overlapping genetics and pathologies. Crucially, no significantly disease-modifying treatments are available for either disease. Identifying the earliest changes that initiate neuronal dysfunction is important for designing effective intervention therapeutics. The genes mutated in genetic forms of frontotemporal dementia and amyotrophic lateral sclerosis have diverse cellular functions, and multiple disease mechanisms have been proposed for both. Identification of a convergent disease mechanism in frontotemporal dementia and amyotrophic lateral sclerosis would focus research for a targetable pathway, which could potentially effectively treat all forms of frontotemporal dementia and amyotrophic lateral sclerosis (both familial and sporadic). Synaptopathies are diseases resulting from physiological dysfunction of synapses, and define the earliest stages in multiple neuronal diseases, with synapse loss a key feature in dementia. At the presynapse, the process of synaptic vesicle recruitment, fusion and recycling is necessary for activity-dependent neurotransmitter release. The unique distal location of the presynaptic terminal means the tight spatio-temporal control of presynaptic homeostasis is dependent on efficient local protein translation and degradation. Recently, numerous publications have shown that mutations associated with frontotemporal dementia and amyotrophic lateral sclerosis present with synaptopathy characterized by presynaptic dysfunction. This review will describe the complex local signalling and membrane trafficking events that occur at the presynapse to facilitate neurotransmission and will summarize recent publications linking frontotemporal dementia/amyotrophic lateral sclerosis genetic mutations to presynaptic function. This evidence indicates that presynaptic synaptopathy is an early and convergent event in frontotemporal dementia and amyotrophic lateral sclerosis and illustrates the need for further research in this area, to identify potential therapeutic targets with the ability to impact this convergent pathomechanism.

Molecular Mechanisms Linking Osteoarthritis and Alzheimer's Disease: Shared Pathways, Mechanisms and Breakthrough Prospects.

Alzheimer's disease (AD) is a progressive neurodegenerative disease mostly affecting the elderly population. It is characterized by cognitive decline that occurs due to impaired neurotransmission and neuronal death. Even though deposition of amyloid beta (Aβ) peptides and aggregation of hyperphosphorylated TAU have been established as major pathological hallmarks of the disease, other factors such as the interaction of genetic and environmental factors are believed to contribute to the development and progression of AD. In general, patients initially present mild forgetfulness and difficulty in forming new memories. As it progresses, there are significant impairments in problem solving, social interaction, speech and overall cognitive function of the affected individual. Osteoarthritis (OA) is the most recurrent form of arthritis and widely acknowledged as a whole-joint disease, distinguished by progressive degeneration and erosion of joint cartilage accompanying synovitis and subchondral bone changes that can prompt peripheral inflammatory responses. Also predominantly affecting the elderly, OA frequently embroils weight-bearing joints such as the knees, spine and hips leading to pains, stiffness and diminished joint mobility, which in turn significantly impacts the patient's standard of life. Both infirmities can co-occur in older adults as a result of independent factors, as multiple health conditions are common in old age. Additionally, risk factors such as genetics, lifestyle changes, age and chronic inflammation may contribute to both conditions in some individuals. Besides localized peripheral low-grade inflammation, it is notable that low-grade systemic inflammation prompted by OA can play a role in AD pathogenesis. Studies have explored relationships between systemic inflammatory-associated diseases like obesity, hypertension, dyslipidemia, diabetes mellitus and AD. Given that AD is the most common form of dementia and shares similar risk factors with OA-both being age-related and low-grade inflammatory-associated diseases, OA may indeed serve as a risk factor for AD. This work aims to review literature on molecular mechanisms linking OA and AD pathologies, and explore potential connections between these conditions alongside future prospects and innovative treatments.

Impact of Physiotherapy in the Treatment of Pain in Cervical Dystonia.

Cervical dystonia (CD) is the most common form of focal dystonia in adults. Studies show that physiotherapy (PT) in combination with BoNT has an effect on pain in cervical dystonia. We intended to test this hypothesis in a real-world setting to answer the question of whether pain is a good target symptom for prescribing PT. We also aimed to assess which form of PT is most appropriate for the treatment of pain. Study design: cross-sectional survey-based study of 91 patients with a confirmed diagnosis of cervical dystonia. The survey consisted of a questionnaire on type, frequency and content of physiotherapy, an assessment of quality of life with the Craniocervical Dystonia Questionnaire 24 (CDQ 24) and subjective pain scores. 53.8% of patients received physiotherapy, mostly a mixture of exercises to either correct the abnormal posture or to reduce the muscle tone. Additional therapies included stress-reducing exercises (14.3%), psychotherapy (9.9%) and EMG biofeedback (2.2%). Patients who received PT showed a non-significant tendency towards higher pain scores. The severity of dystonia-associated pain was significantly associated with the patients' quality of life (F (1,54) = 22.9, adjusted R2 = 0.286, p < 0.001). Pain is a frequent problem in patients with CD and severely affects quality of life. Physiotherapy could therefore be a valuable treatment option for patients with CD and pain. Our uncontrolled study illustrates the high frequency of physiotherapy in addition to BoNT treatment in a real-life cohort of patients with cervical dystonia. We were able to show that PT reduces patients' perceived pain in a patient reported outcome measure. This highlights the importance of PT in reducing CD-related pain, which considerably impairs quality of life.

Characterization of Novel PHEX Variants in X-linked Hypophosphatemic Rickets and Genotype-PHEX Activity Correlation.

X-linked hypophosphatemia (XLHR) is the most common genetic form of hypophosphatemic rickets (HR), which is caused by phosphate regulating endopeptidase homolog X-linked (PHEX) gene mutation. At present, the genotype-phenotype relationship of XLHR and the pathogenic role of PHEX are not fully understood. In this study, we summarized clinical features in a new cohort of 49 HR patients and detected 16 novel PHEX and 5 novel non-PHEX variants. Subsequently, we studied the pathogenesis of new variants by protein expression, glycosylation analysis, subcellular localization, and endopeptidase activity. The results showed that missense variants (Q189H and X750R) slightly reduced protein expression without obviously altering protein length and localization, whereas truncating variants significantly impaired the synthesis of PHEX and produced a shorter immature protein in cells. Interestingly, no evident correlation was observed between mutation types and clinical phenotypes. However, when we analyzed the relationship between PHEX activity and serum phosphorus level, we found that patients with low PHEX activity tended to have severe hypophosphatemia and high rickets severity score. Following this observation, we established 2 new knock-in XLHR mouse models with 2 novel Phex variants (c.T1349C and c.C426G, respectively) using CRISPR/Cas9 technology. Both mouse models demonstrated clinical manifestations of XLHR seen in patients, and PhexC426G mice showed more severe phenotype than PhexT1349C mice, which further confirmed the rationality of genotype-PHEX enzymatic activity correlation analysis. Therefore, our findings demonstrated that novel PHEX variants could disrupt protein function via affecting protein synthesis, post-translational modification, cellular trafficking, and catalytic activity. Our study facilitates a better understanding of XLHR pathogenic mechanism and PHEX activity-phenotype correlation, which is of crucial importance for future diagnosis and treatment of XLHR.

Cyberbullying and cyber-victimisation among higher secondary school adolescents in an urban city of Nepal: a cross-sectional study

ObjectiveTo assess the prevalence and factors associated with cyberbullying and cyber-victimisation among high school adolescents of Pokhara Metropolitan City, Nepal.DesignA cross-sectional study.SettingPokhara Metropolitan City, Nepal.ParticipantsWe used convenient sampling to enrol...

MISSENSE MUTATIONS IN THE IRAK1 GENE ARE ASSOCIATED WITH AN INCREASED RISK OF SYSTEMIC LUPUS ERYTHEMATOSUS

Single nucleotide polymorphisms (SNPs) are the most common form of genetic variation in humans. Missense SNPs can change protein structure and function. This study aimed to determine missense SNPs of the IRAK1 gene that can affect the amino acid sequence and lead to changes in protein structure and function, as well as their relationship as a risk factor for SLE. In this in silico method, several bioinformatics tools have been used to identify missense SNPs, including their properties and impacts, as well as their interaction networks with proteins. The tools used were PolyPhenv2, SIFT, PhD-SNP, PROVEAN, SNAP, Panthers, I-Mutant 3.0, and GeneMania. Four missense SNPs, rs11465830, rs1059702, rs1059703, and 10127175, were obtained from the NCBI SNP database. The SIFT test results showed that all the SNPs were tolerant. In the test results obtained using PolyPhen, the four SNPs were benign. The results of the probe test indicated that the four SNPs were neutral. When tested with SNAP, one SNP was neutral, and three others had an impact. In the PhD-SNP test, all SNPs were neutral. In the panther test, all SNPs were benign. The I-mutant assay showed that the four SNPs could decrease protein stability. Tests with GeneMania have reported that most interactions between genes were between IRAK1 and MYD88, and physical interactions were the most dominant form of interaction. Conclusion. rs10127175, rs11465830, rs1059702, and rs1059703 are missense SNPs in IRAK1, which can disrupt protein stability and be a risk factor for SLE. Keywords: IRAK1, SNP, Missense, Systemic Lupus Erythematosus

Germline knockout of Nr2e3 protects photoreceptors in three distinct mouse models of retinal degeneration

Retinitis pigmentosa (RP) is a common form of retinal dystrophy that can be caused by mutations in any one of dozens of rod photoreceptor genes. The genetic heterogeneity of RP represents a significant challenge for the development of effective therapies. Here, we present evidence for a potential gene-independent therapeutic strategy based on targeting Nr2e3, a transcription factor required for the normal differentiation of rod photoreceptors. Nr2e3 knockout results in hybrid rod photoreceptors that express the full complement of rod genes, but also a subset of cone genes. We show that germline deletion of Nr2e3 potently protects rods in three mechanistically diverse mouse models of retinal degeneration caused by bright-light exposure (light damage), structural deficiency (rhodopsin-deficient Rho-/- mice), or abnormal phototransduction (phosphodiesterase-deficient rd10 mice). Nr2e3 knockout confers strong neuroprotective effects on rods without adverse effects on their gene expression, structure, or function. Furthermore, in all three degeneration models, prolongation of rod survival by Nr2e3 knockout leads to lasting preservation of cone morphology and function. These findings raise the possibility that upregulation of one or more cone genes in Nr2e3-deficient rods may be responsible for the neuroprotective effects we observe.

Trichosanthis Semen Exerts Neuroprotective Effects in Alzheimer's Disease Models by Inhibiting Amyloid-β Accumulation and Regulating the Akt and ERK Signaling Pathways.

Alzheimer's disease (AD), the most common form of dementia, is characterized by memory loss and the abnormal accumulation of senile plaques composed of amyloid-β (Aβ) protein. Trichosanthis Semen (TS) is a traditional herbal medicine used to treat phlegm-related conditions. While TS is recognized for various bioactivities, including anti-neuroinflammatory effects, its ability to attenuate AD remains unknown. To evaluate the effects of TS extract (TSE) on neuronal damage, Aβ accumulation, and neuroinflammation in AD models. Thioflavin T and western blot assays were used to assess effects on Aβ aggregation in vitro. TS was treated to PC12 cells with Aβ to assess the neuroprotective effects. Memory functions and histological brain features were investigated in TSE-treated 5×FAD transgenic mice and mice with intracerebroventricularly injected Aβ. TSE disrupted Aβ aggregation and increased the viability of cells and phosphorylation of both protein kinase B (Akt) and extracellular signal-regulated kinase (ERK) in vitro. TSE treatment also suppressed the accumulation of Aβ plaques in the brain of 5×FAD mice, protected neuronal cells in both the subiculum and medial septum, and upregulated Akt/ERK phosphorylation in the hippocampus. Moreover, TSE ameliorated the memory decline and glial overactivation observed in 5×FAD mice. As assessing whether TS affect Aβ-induced neurotoxicity in the Aβ-injected mice, the effects of TS on memory improvement and neuroinflammatory inhibition were confirmed. TSE disrupted Aβ aggregation, protected neurons against Aβ-induced toxicity, and suppressed neuroinflammation, suggesting that it can suppress the development of AD.

Abstract B019: Investigating Cannabis sativa bioactive compounds as an anti-cancer treatment in high-grade serous ovarian cancer

Abstract B019: Investigating <i>Cannabis sativa</i> bioactive compounds as an anti-cancer treatment in high-grade serous ovarian cancer

Abstract B085: Carcinoma-associated mesenchymal stem cells promote high-grade serous ovarian cancer metastasis and drive tumor heterogeneity at the metastatic site through direct mitochondrial transfer

Abstract High-grade serous ovarian cancer (HGSC) is the most common and lethal form of ovarian cancer, accounting for over 70% of ovarian cancer cases. HGSC mortality is largely driven by early and diffuse transcoelomic spread from the primary site throughout the peritoneal cavity, resulting in roughly three-quarters of cases presenting with advanced stage disease at time of diagnosis. Following detachment from the primary tumor, disseminated ovarian cancer cells are spread by the peritoneal fluid and ascites where they must adapt to their new microenvironment to survive and successfully form metastases. Crucial to this spread is the formation of multicellular aggregates containing both cancer and non-malignant stromal cells, which enhance cancer cell survival and are associated with poor clinical outcome. While most studies on HGSC multicellular aggregates have focused on ovarian cancer cells alone, the interactions between ovarian cancer cells and other non-malignant cells have yet to be fully elucidated. Prior work by our group have shown that stromal-progenitor cells, termed carcinoma-associated mesenchymal stem/stromal cells (CA-MSCs), enhance HGSC metastasis through direct cellular interaction and formation of heterocellular CA-MSC:cancer cell complexes. Here we demonstrate CA-MSCs enhance metastasis by preferentially donating their mitochondria to cancer cells with the least amount of endogenous mitochondria content (‘mito poor’ cancer cells), increasing their ability to survive and driving tumor heterogeneity at the metastatic site in vivo. Mito poor cancer cells were shown to have decreased proliferative capacity, increased sensitivity to platinum-based chemotherapy and display decreased oxidative phosphorylation (OXPHOS) compared to ‘mito rich’ cancer cells. Primary patient-derived CA-MSCs rescue this vulnerable phenotype by increasing proliferation, chemoresistance and OXPHOS in mito poor cancer cells. These findings were validated in a fully autologous system using CA-MSCs and cancer cells derived from the same patient to prevent confounding effects of cellular response to foreign organelle/DNA. Through lentiviral knockdown of the mitochondrial motor protein MIRO1 we further demonstrate mitochondrial transfer is necessary for CA-MSC-mediated rescue of mito poor cancer cells. Further, we developed a haplotype-specific quantification of mitochondrial DNA to differentiate CA-MSC from endogenous cancer cell mitochondria which was used to quantify the amount of CA-MSC mitochondrial donation and demonstrate donated mitochondria persist in cancer cells up to 14 days. Importantly, CA-MSC mitochondrial donation occurred in vivo and was associated with decreased survival in an orthotopic ovarian cancer murine model. Genomic barcoding was used to quantify tumor cell clonal heterogeneity; using this system we demonstrate CA-MSC mitochondrial donation significantly enhance tumor cell heterogeneity at the metastatic site in vivo. Collectively, we report CA-MSC mitochondrial transfer as a driver of HGSC progression, heterogeneity and metastasis. Citation Format: Leonard G. Frisbie, Catherine A. Pressimone, Roja Baruwal, Geyon L. Garcia, Zanib Javed, Claudette St. Croix, Simon Watkins, Michael Calderone, Huda I. Atiya, Nadine Hempel, Alexander Pearson, Lan G. Coffman. Carcinoma-associated mesenchymal stem cells promote high-grade serous ovarian cancer metastasis and drive tumor heterogeneity at the metastatic site through direct mitochondrial transfer [abstract]. In: Proceedings of the AACR Special Conference on Ovarian Cancer; 2023 Oct 5-7; Boston, Massachusetts. Philadelphia (PA): AACR; Cancer Res 2024;84(5 Suppl_2):Abstract nr B085.

Study on the indoor thermal comfort of cave dwellings in cold areas of China

Cave dwelling, as a common traditional housing form in rural areas, has long been regarded as a low-cost, green, and environmentally friendly living choice. The purpose of this study was to explore and improve the thermal comfort of cave dwellings, and to systematically evaluate and analyse the thermal comfort of cave dwellings through a combination of visit surveys and indoor environmental parameter monitoring. After statistical analysis and comparison of the collected data, the following conclusions were drawn: (1) The thermal neutrality temperature of 25.15 °C determined by Predicted Mean Vote (PMV) in this study was greater than the thermal neutrality temperature of 19.49 °C determined by Thermal Sensation Vote (TSV) model, indicating that cave dwellers prefer a cooler thermal environments under actual conditions. (2) In cold weather, the maximum value of 80% acceptability is 18.12 °C and the minimum value is 12.00 °C. In hot weather, the maximum value of 80% acceptability is 27.17 °C and the minimum value is 23.66 °C. (3) In winter, the average indoor temperature of 9.71 °C is higher than the average outdoor temperature of 7.85 °C; In summer, the average temperature in the naturally ventilated room of 27.44 °C is much lower than the average outdoor temperature of 35.25 °C. The results showed that the building materials and structure of cave houses can provide a certain degree of thermal insulation, which can provide a basis for the design and improvement of low-cost, energy-saving and environmentally friendly houses in rural areas.

Abstract A101: A novel ovarian cancer organotypic tumor slice culture model

Abstract A101: A novel ovarian cancer organotypic tumor slice culture model