Tuina Intervention in Sodium Monoiodoacetate Injection-Induced Rat Model of Knee Osteoarthritis.

Knee osteoarthritis (KOA), a common degenerative joint disorder, is characterized by chronic pain and disability, which can progress to irreparable structural damage of the joint. Investigations into the link between articular cartilage, muscles, synovium, and other tissues surrounding the knee joint in KOA are of great importance. Currently, managing KOA includes lifestyle modifications, exercise, medication, and surgical interventions; however, the elucidation of the intricate mechanisms underlying KOA-related pain is still lacking. Consequently, KOA pain remains a key clinical challenge and a therapeutic priority. Tuina has been found to have a regulatory effect on the motor, immune, and endocrine systems, prompting the exploration of whether Tuina could alleviate KOA symptoms, caused by the upregulation of inflammatory factors, and further, if the inflammatory factors in skeletal muscle can augment the progression of KOA. We randomized 32 male Sprague Dawley (SD) rats (180-220 g) into four groups of eight animals each: antiPD-L1+Tuina (group A), model (group B), Tuina (group C), and sham surgery (group D). For groups A, B, and C, we injected 25 µL of sodium monoiodoacetate (MIA) solution (4 mg MIA diluted in 25 µL of sterile saline solution) into the right knee joint cavity, and for group D, the same amount of sterile physiological saline was injected. All the groups were evaluated using the least to most stressful tests (paw mechanical withdrawal threshold, paw withdrawal thermal latency, swelling of the right knee joint, Lequesne MG score, skin temperature) before injection and 2, 9, and 16 days after injection.

Euglycemic Ketoacidosis in Two Patients Without Diabetes After Introduction of Sodium-Glucose Cotransporter 2 Inhibitor for Heart Failure With Reduced Ejection Fraction.

OBJECTIVE: Ketoacidosis induced by sodium-glucose cotransporter 2 inhibitor (SGLT2i) treatment has been consistently observed in clinical practice in patients with type 2 diabetes despite minimal indication from the landmark cardiovascular outcome trials. It has been postulated that individuals without diabetes will not develop this complication due to an adequate insulin secretory capacity, which will protect against significant ketone formation. Cardiovascular outcome trials examining SGLT2i use in individuals with heart failure but not diabetes have not reported ketoacidosis. RESEARCH DESIGN AND METHODS: We describe the first two case reports of severe nondiabetic ketoacidosis after initiation of an SGLT2i for the treatment of heart failure with reduced ejection fraction, and we describe the management strategies employed and implication for the pathophysiology of SGLT2i-associated ketoacidosis. RESULTS: Each individual presented with ketoacidosis triggered by reduced oral nutrition intake. For both individuals, ketoacidosis resolved with intravenous glucose administration, encouragement of consumption of oral glucose-containing fluid, and minimal insulin administration. CONCLUSIONS: These two cases demonstrate that SGLT2i-associated ketoacidosis is possible in individuals without diabetes.

Anti-Inflammatory Effect and Signaling Mechanism of Glycine max Hydrolyzed with Enzymes from Bacillus velezensis KMU01 in a Dextran-Sulfate-Sodium-Induced Colitis Mouse Model.

The purpose of this study was to investigate the effect that Glycine max hydrolyzed with enzymes from Bacillus velezensis KMU01 has on dextran-sulfate-sodium (DSS)-induced colitis in mice. Hydrolysis improves functional health through the bioconversion of raw materials and increase in intestinal absorption rate and antioxidants. Therefore, G. max was hydrolyzed in this study using a food-derived microorganism, and its anti-inflammatory effect was observed. Enzymatically hydrolyzed G. max (EHG) was orally administered once daily for four weeks before DSS treatment. Colitis was induced in mice through the consumption of 5% (w/v) DSS in drinking water for eight days. The results showed that EHG treatment significantly alleviated DSS-induced body weight loss and decreased the disease activity index and colon length. In addition, EHG markedly reduced tumor necrosis factor-α, interleukin (IL)-1ß, and IL-6 production, and increased that of IL-10. EHG improved DSS-induced histological changes and intestinal epithelial barrier integrity in mice. Moreover, we found that the abundance of 15 microorganisms changed significantly; that of Proteobacteria and Escherichia coli, which are upregulated in patients with Crohn's disease and ulcerative colitis, decreased after EHG treatment. These results suggest that EHG has a protective effect against DSS-induced colitis and is a potential candidate for colitis treatment.

SSRI/SNRI -induced Hyponatremia: A Case Series of 26 Patients in a Single Institution from 2018 to 2020.

Antidepressant medications are widely used by patients with depression or a depressive disorder. In spite of a generally favorable safety profile of selective serotonin reuptake inhibitors or serotonin - norepinephrine reuptake inhibitors (SSRI/SNRI), several cases of a possible connection between SSRI/SNRI and hyponatremia have been reported. To describe the clinical characteristics of patients with hyponatremia after SSRI/SNRI exposure, and to examine the association between SSRI/SNRI exposure and the presence of hyponatremia in a Chinese population. A retrospective single-center case series study. We performed a retrospective evaluation of inpatients with SSRI/SNRI-induced hyponatremia from a single institution in China between 2018 and 2020. Clinical data were obtained through review of medical records. Patients who met the initial inclusion criteria but did not develop hyponatremia acted as controls. The study was approved by the Clinical Research Ethics Board of Beijing Hospital (Beijing, P.R. China). We identified 26 patients with SSRI/SNRI-induced hyponatremia. The incidence rate of hyponatremia was 1.34% (26/1937) in the study population. The mean age at diagnosis was 72.58 (±12.84) years, with a male: female ratio of 1:1.42. The duration between SSRI/SNRI exposure and the onset of hyponatremia was 7.65 (±4.88) days. The minimum serum sodium level was 2328.23 (±107.25) mg/dL in the study group. Seventeen patients (65.38%) received sodium supplements. Four patients (15.38%) switched to another antidepressant. Fifteen patients (57.69%) recovered by the time of discharge. There were significant differences in serum potassium, serum magnesium and serum creatinine level between the two groups (p < 0.05). The rate of use of sertraline was significantly higher in the study group compared with the control group (p < 0.05). This pattern was not found in other SSRI/SNRI (p > 0.05). The results of our study show that SSRI/SNRI exposure, in addition to hyponatremia, may also affect the level of serum potassium, serum magnesium and serum creatinine. A history of hyponatremia and exposure to SSRI/SNRI may be potential risk factors for the development of hyponatremia. Future prospective studies are needed to validate these findings.

Morroniside ameliorates glucocorticoid-induced osteoporosis and promotes osteoblastogenesis by interacting with sodium-glucose cotransporter 2.

CONTEXT: Morroniside (MOR) possesses antiosteoporosis (OP) effects, but its molecular target and relevant mechanisms remain unknown. OBJECTIVE: We investigated the effects of MOR on glucocorticoid-induced OP and osteoblastogenesis and its underlying mechanisms. MATERIALS AND METHODS: The effects of MOR (10-100 µM) on the proliferation and differentiation of MC3T3-E1 cells were studied in vitro. The glucocorticoid-induced zebrafish OP model was treated with 10, 20 and 40 µM MOR for five days to evaluate its effects on vertebral bone density and related osteogenic markers. In addition, molecular targets prediction and molecular docking analysis were carried out to explore the binding interactions of MOR with the target proteins. RESULTS: In cultured MC3T3-E1 cells, 20 µM MOR significantly increased cell viability (1.64 ± 0.12 vs. 0.95 ± 0.16; p < 0.01) and cell differentiation (1.57 ± 0.01 vs. 1.00 ± 0.04; p < 0.01) compared to the control group. MOR treatment significantly ameliorated vertebral bone loss in the glucocorticoid-induced OP zebrafish model (0.86 ± 0.02 vs. 0.40 ± 0.03; p < 0.01) and restored the expression of osteoblast-specific markers, including ALP, Runx2 and Col-І. Ligand-based target prediction and molecular docking revealed the binding interaction between MOR and the glucose pockets in sodium-glucose cotransporter 2 (SGLT2). DISCUSSION AND CONCLUSIONS: These findings demonstrated that MOR treatment promoted osteoblastogenesis and ameliorated glucocorticoid-induced OP by targeting SGLT2, which may provide therapeutic potential in managing glucocorticoid-induced OP.

Dietary sodium restriction prevents vascular endothelial growth factor inhibitor-induced hypertension.

BACKGROUND: Vascular endothelial growth factor inhibitors (VEGFIs) are effective anticancer agents which often induce hypertension. VEGFI-induced hypertension is sodium-sensitive in animal studies. Therefore, the efficacy of dietary sodium restriction (DSR) to prevent VEGFI-induced hypertension in cancer patients was studied. METHODS: Cancer patients with VEGFI-induced hypertension (day mean >135/85 mmHg or a rise in systolic and/or diastolic BP ≥ 20 mmHg) were treated with DSR (aiming at <4 g salt/day). The primary endpoint was the difference in daytime mean arterial blood pressure (MAP) increase between the treatment cycle with and without DSR. RESULTS: During the first VEGFI treatment cycle without DSR, mean daytime MAP increased from 95 to 110 mmHg. During the subsequent treatment cycle with DSR, mean daytime MAP increased from 94 to 102 mmHg. Therefore, DSR attenuated the increase in mean daytime MAP by 7 mmHg (95% CI 1.3-12.0, P = 0.009). DSR prevented the rise in the endothelin-1/renin ratio that normally accompanies VEGFI-induced hypertension (P = 0.020) and prevented the onset of proteinuria: 0.15 (0.10-0.25) g/24 h with DSR versus 0.19 (0.11-0.32) g/24 h without DSR; P = 0.005. DISCUSSION: DSR significantly attenuated VEGFI induced BP rise and proteinuria and thus is an effective non-pharmacological intervention.

EXPERIMENTAL RESEARCH OF THE EFFECT OF COXIBS ON THE CERULOPLASMIN LEVEL IN RAT SERUM ON THE FORMALIN-INDUCED EDEMA MODEL.

OBJECTIVE: The aim: To estimate anti-inflammatory action of coxibs (3-(4-methylsulfonylphenyl)-4-phenyl-2H-furan-5-one, 2,3,5,6-tetradeuterio-4-[5-(4-methylphenyl)-3-(trifluoromethyl) pyrazol-1-yl]benzenesulfonamide) compared to reference drug - 2-[(2,6-Dichlorophenyl)amino]benzeneacetic acid sodium salt. PATIENTS AND METHODS: Materials and methods: The anti-inflammatory effect of studied substances was investigated using the ceruloplasmin test as serum ceruloplasmin is a routinely investigated biochemical index. Formalin-induced hind paw edema was used as the most commonly used animal model to simulate acute inflammation. 3-(4-methylsulfonylphenyl)-4-phe¬nyl-2H-furan-5-one (1.5 mg/kg) and celecoxib (5 mg/kg) were administrated intragastrically in 4 hours after induction of inflammation with formalin. The ceruloplasmin level in the serum was investigated using the Ravin's method. RESULTS: Results: The levels of serum ceruloplasmin under conditions of formalin edema was 3.11 ± 0.02 µmol/L, that is 2.5 times greater than in intact animals. It was shown that at the injection of 3-(4-methylsulfonylphenyl)-4-phenyl-2H-furan-5-one serum сeruloplasmin level demonstrated a statistically significant reduction in comparison with formalin edema. There is no statistically significant difference between groups. 3-(4-methylsulfonylphenyl)-4-phenyl-2H-furan-5-one affected the serum ceruloplasmin levels in rats under the conditions of formalin edema effectively. 2,3,5,6-tetradeuterio-4-[5-(4-methylphenyl)-3-(trifluoromethyl)pyrazol-1-yl]benzenesulfonamide had only tendency to decrease the inflammatory marker ceruloplasmin in serum of rats in reference to formalin edema. CONCLUSION: Conclusions: Results of biochemical research of the effect of coxibs on the serum ceruloplasmin level in rats show that 3-(4-methylsulfonylphenyl)-4-phenyl-2H-furan-5-one has marked anti-inflammatory activity while 2,3,5,6-tetradeuterio-4-[5-(4-methylphenyl)-3-(trifluoromethyl)pyrazol-1-yl]benzenesulfonamide has only tendency to decrease the inflammatory marker ceruloplasmin in serum of rats.

A Rare Case of Acne Medication-Induced Drug Reaction With Eosinophilia and Systemic Symptoms.

INTRODUCTION: Acne vulgaris is the most common skin condition in late adolescence and frequently requires systemic treatment with antibiotics or androgen receptor blockers in moderateto- severe cases. CASE PRESENTATION: We report the case of a 17-year-old adolescent female with new onset fever, headache, and pruritic rash 1 month after she started doxycycline and spironolactone for the treatment of acne vulgaris. Later, she developed eosinophilia and transaminitis. Infectious workup was negative. DISCUSSION: This presentation was consistent with a definite case of drug reaction with eosinophilia and systemic symptoms (DRESS). DRESS is a severe, systemic hypersensitivity drug reaction that typically occurs 2 to 8 weeks following exposure to the offending medication. CONCLUSIONS: Although doxycycline and spironolactone are uncommon triggers of DRESS, they are common medications used to treat acne, and clinicians should be aware of this potential complication when counseling patients, especially adolescents.

Hyponatremia Associated With Standard-Dose Trimethoprim-Sulfamethoxazole Use in an Immunocompetent Patient.

INTRODUCTION: Trimethoprim-sulfamethoxazole (TMP-SMX) use in immunocompromised patients can cause dose-dependent electrolyte irregularities including hyponatremia, hyperkalemia, and metabolic acidosis. We report a case of isolated hyponatremia caused by low-dose TMP-SMX use in an immunocompetent patient that mimicked the syndrome of inappropriate antidiuretic hormone secretion (SIADH). CASE PRESENTATION: A 72-year-old woman was admitted to the hospital for acute onset of weakness and ambulatory dysfunction after starting TMP-SMX (160 mg/800 mg). She was found hyponatremic (sodium level, 125 mmol/L, down from 141 mmol/L prior to medication initiation). After ruling out diuretics use, and adrenal and thyroid dysfunction, we started her on intravenous saline infusion to manage her TMP-SMX-induced hyponatremia, and her symptoms resolved. DISCUSSION: Electrolyte problems in immunocompromised patients treated for opportunistic infections with high-dose TMP-SMX (≥ 8 mg/kg/d TMP) are well-documented. However, the effects in immunocompetent patients are uncommon when standard dose (< 8 mg/kg/d TMP) is used. CONCLUSIONS: TMP-SMX blocks the aldosterone-mediated sodium reabsorption in the collecting ducts, and the trimethoprim component itself is structurally similar to potassium-sparing diuretics, which block sodium uptake at the distal nephron-both of which can cause hyponatremia.

The protective effect of pomegranate peel aqueous extract on selenite-induced cataract in rats.

The present study was performed to evaluate the preventive effect of pomegranate peel extract on sodium-induced cataract in rats. Sprague-Dawley suckling male rats were divided into four groups: group C: rats received no treatment, group P: rats received pomegranate peel aqueous extract (PPE) orally, group Se: rats received an injection of sodium selenite, group Se + P: rats received PPE and sodium selenite concomitantly. After 4 weeks, rats were sacrificed, and their lenses were homogenized and evaluated for biochemical parameters and sodium dodecyl sulfate-polyacrylamide gel electrophoresis. In the Se group, developed cataract with significant lens opacity was observed. Other changes in enzymatic and non-enzymatic antioxidants, oxidative parameters, solubility of proteins, in NO and Ca levels and the electrophoresis pattern of proteins were observed in lenses of the Se group compared to control groups. After the preventive administration of PPE, most of these parameters were normalized due to antioxidant and anti-inflammatory activities of the extract. PRACTICAL APPLICATIONS: Cataract is one of the leading causes of vision impairment among the elderly, and surgery is the major therapeutic step taken to cure it. However, surgery has its limitations and complications. Therefore, prevention of cataract development, especially in high-risk individuals, can be better than cure. Pomegranate peel extract has a high potential to prevent cataract in these people.

[The effect of natural mineral bicarbonate sodium-calcium water «Tib-1¼ on the antioxidant status of rats with adjuvant rheumatoid arthritis]. / Vliyanie prirodnoi mineral'noi gidrokarbonatnoi natrievo-kal'tsievoi vody «Tib-1¼ na antioksidantnyi status krys s ad"yuvantnym revmatoidnym artritom.

The combination of traditional basic pharmacotherapy for rheumatoid arthritis (RA) and physiotherapeutic methods can reduce the activity of the disease and accelerate the onset of remission, and therefore the development of new non-drug methods for the treatment of RA is relevant. PURPOSE OF THE STUDY: Study of the effect of natural mineral water « Tib-1¼ on the lipid peroxidation system in an experiment with a model adjuvant-induced RA in rats. MATERIAL AND METHODS: The object of the study were Wistar rats, divided into three groups: negative control (solvents), positive control (model of adjuvant-induced RA by subcutaneous injection of complete Freund's adjuvant) and experimental (correction of RA with mineral water « Tib-1¼, diluted in a ratio of 1:3 during the first 2 weeks from the moment the model was formed in the ad libitum mode). On the 3rd and 7th weeks in the blood of the animals were determined: the total number of leukocytes, the content of hydroperoxides according to Gavrilov, the level of malondialdehyde (MDA), catalase activity. Pathological changes in the hip and knee joints were recorded using radiography. RESULTS: The inflammatory process in the positive control group by the 3rd week was characterized by an increase in the number of leukocytes by 66% (p<0.01) and was accompanied by an increase in MDA by 60% (p<0.001). By the 7th week, despite a relative increase in catalase activity (16%), the MDA level continued to be elevated compared to the negative control by 67% (p<0.001). Against the background of exposure to mineral water, inflammation decreased (the number of leukocytes in the "model/experiment" groups turned out to be reduced by 41%; p<0.01) and an increase in compensatory-adaptive reactions in the form of catalase activation was noted (by 8%; p<0.01), which was accompanied by a persistent (weeks 3 and 7) decrease in MDA output (by 20%; p<0.01). Using the method of radiation diagnostics, positive changes in the articular apparatus of experimental animals were revealed, consisting in the relief of signs of subchondral sclerosis of the bone heads, which were noted for animals of the model group. CONCLUSION: The use of natural mineral water «Tib-1¼ helps to reduce the acute inflammatory response during the formation of adjuvant-induced RA in Wistar rats, initiates the normalization of the balance of pro- and antioxidant processes in the body, and minimizes the intensity of degenerative-inflammatory joint lesions.

Sodium-Glucose Cotransporter-2 Inhibitors and Urinary Tract Infections: A Propensity Score-matched Population-based Cohort Study.

OBJECTIVES: Sodium-glucose cotransporter-2 (SGLT2) inhibitor-induced glycosuria is hypothesized to increase the risk of urinary tract infections (UTIs). We assessed the risk of UTIs associated with SGLT2 inhibitor initiation in type 2 diabetes. METHODS: We conducted a population-based cohort study using primary care data from the United Kingdom's Clinical Practice Research Datalink (CPRD) and administrative health-care data from Alberta, Canada. From a base cohort of new metformin users, we constructed 5 comparative cohorts, wherein the exposure contrast was defined as new use of SGLT2 inhibitors or 1 of 5 active comparators: dipeptidylpeptidase-4 (DPP-4) inhibitors, sulfonylureas (SU), glucagon-like peptide-1 receptor agonists (GLP-1 RA), thiazolidinediones (TZD) and insulin. We defined a composite UTI outcome based on hospitalizations or physician visit records. For each comparative cohort, we used high-dimensional propensity score matching to adjust for confounding and Cox proportional hazards regression to estimate the hazard ratios (HRs) in each database. We meta-analyzed estimates using a random-effects model. RESULTS: SGLT2 inhibitor use was not associated with a higher risk of UTI compared with DPP-4 inhibitors (pooled HR, 1.08; 95% confidence interval [CI], 0.89 to 1.30), SU (pooled HR, 1.08; 95% CI, 0.90 to 1.30), GLP-1 RA (pooled HR, 0.81; 95% CI, 0.61 to 1.09) or TZD (pooled HR, 0.81; 95% CI, 0.55 to 1.19). The risk of UTI was lower compared with insulin (pooled HR, 0.74; 95% CI, 0.63 to 0.87). The risk of UTI did not differ based on the SGLT2 inhibitor agent or dose. Last, SGLT2 inhibitor initiation was not associated with an increased risk of UTI recurrence. CONCLUSION: SGLT2 inhibitor use is not associated with an increased risk of UTIs, compared with other antidiabetic agents.

A case of anti-HMGCR myopathy triggered by sodium/glucose co-transporter 2 (SGLT2) inhibitors.

Inflammatory myopathies, including immune-mediated necrotizing myopathy (IMNM), are a rare and heterogeneous group of autoimmune diseases which can even involve extramuscular districts and seriously impact patients' quality of life. We report the case of a 76-year-old woman who developed muscle weakness, fatigue, and increased CK, following treatment with dapagliflozin, a sodium/glucose co-transporter 2 (SGLT2) inhibitor, and metformin. Neurophysiology, muscle biopsy, and antibody dosage confirmed the diagnosis of IMNM. The temporal correlation between the onset of clinical manifestations and the increase in the dosage of antidiabetic drugs, the improvement of symptoms with the dechallenge of dapagliflozin, and the exclusion of other possible causes triggering myopathy suggests that this may be the first case of dapagliflozin-induced myopathy, different from the former one associated with the use of SGLT2 inhibitors.

Venous thromboembolism and severe hypernatremia in a patient with lithium-induced nephrogenic diabetes insipidus and acute kidney injury: a case report.

We report a case of thromboembolism in a patient with hypernatremia resulting from lithium-induced nephrogenic diabetes insipidus (NDI). A 49-year-old female patient on chronic lithium therapy due to bipolar disorder was transferred to the emergency department with signs of dehydration, altered mental status, and increased oxygen demand. She was admitted to a local psychiatric clinic first because of an exacerbation of a manic episode. When she was transferred to our clinic, her blood pressure was 130/80 mmHg, she was tachycardic (110 beats/min), had tachypnea (24 breaths/min), normal body temperature (36.5 ℃), and an oxygen saturation of 94% via a face mask (10 L/min). Laboratory results showed hypertonic hypernatremia (osmolality, 363 mOsm/kg; sodium, 171 mEq/L), low urine osmolality (osmolality, 231 mOsm/kg), and normal urine sodium (Na, 63 mEq/L). Her serum lithium concentration was above the therapeutic range (1.52 mmol/L). An increase in cardiac markers and changes in electrocardiogram were detected; therefore, echocardiography was performed, which showed right ventricular dysfunction and small left ventricular chamber size. Computed tomography of the chest and lower extremities showed pulmonary thromboembolism (PTE) and deep venous thrombosis (DVT). She was treated with hypotonic fluid to correct hypernatremia and intravenous heparin for thromboembolism. The size of the thromboembolism decreased, and hypernatremia was corrected. She was discharged with a direct oral anticoagulant (DOAC). Here, we report a case of severe hypernatremia and venous thromboembolism in lithium-induced NDI.

High-Salt Diet Impairs the Neurons Plasticity and the Neurotransmitters-Related Biological Processes.

Salt, commonly known as sodium chloride, is an important ingredient that the body requires in relatively minute quantities. However, consuming too much salt can lead to high blood pressure, heart disease and even disruption of circadian rhythms. The biological process of the circadian rhythm was first studied in Drosophila melanogaster and is well understood. Their locomotor activity gradually increases before the light is switched on and off, a phenomenon called anticipation. In a previous study, we showed that a high-salt diet (HSD) impairs morning anticipation behavior in Drosophila. Here, we found that HSD did not significantly disrupt clock gene oscillation in the heads of flies, nor did it disrupt PERIOD protein oscillation in clock neurons or peripheral tissues. Remarkably, we found that HSD impairs neuronal plasticity in the axonal projections of circadian pacemaker neurons. Interestingly, we showed that increased excitability in PDF neurons mimics HSD, which causes morning anticipation impairment. Moreover, we found that HSD significantly disrupts neurotransmitter-related biological processes in the brain. Taken together, our data show that an HSD affects the multiple functions of neurons and impairs physiological behaviors.

Association of Estimated Salt and Miso Intake with the Prevalence of Obesity in People with Type 2 Diabetes: A Cross-Sectional Study.

Salt intake is often estimated by the amount of sodium excreted in urine, and miso has been reported to increase it. This cross-sectional study investigated the relationship between obesity and high estimated salt intake with and without habitual miso consumption. Estimates of salt intake (g/day) were calculated using urinary sodium excretion, and a high estimated intake was defined as greater than the median amount of 9.5 g/day. Participants were divided into four groups based on estimated salt intake and miso consumption. Among 300 people, the proportions of obesity were 77.8% (n = 14/18), 40.2% (n = 53/132), 26.0% (n = 33/127), and 34.8% (n = 8/23) in the (+/-), (+/+), (-/+), and (-/-) groups of high estimated salt intake/habitual miso consumption, respectively. Compared with the (+/-) group, the adjusted odds ratios for obesity were 0.07 (95% confidence interval (CI): 0.02-0.26, p < 0.001), 0.16 (95% CI: 0.03-0.76, p = 0.022), and 0.14 (95% CI: 0.04-0.51, p = 0.003) in the (-/+), (-/-), and (+/+) groups, respectively. The presence of obesity was not much higher in people with high estimated salt intake with habitual miso consumption than that in people without. Clinicians should be aware that miso consumption promotes salt excretion, which may lead to an apparently higher estimated salt intake than actual.

Pharmacological investigations on efficacy of Phlorizin a sodium-glucose co-transporter (SGLT) inhibitor in mouse model of intracerebroventricular streptozotocin induced dementia of AD type.

OBJECTIVES: The study has been commenced to discover the potential of Phlorizin (dual SGLT inhibitor) in streptozotocin induced dementia of Alzheimer's disease (AD) type. MATERIAL AND METHODS: Injection of Streptozotocin (STZ) was given via i.c.v. route (3 mg/kg) to induce dementia of Alzheimer's type. In these animals learning and memory was evaluated using Morris water maze (MWM) test. Glutathione (GSH) and thiobarbituric acid reactive species (TBARS) level was quantified to evaluate the oxidative stress; cholinergic activity of brain was estimated in term of acetylcholinesterase (AChE) activity; and the levels of myeloperoxidase (MPO) were measured as inflammation marker. RESULTS: The mice model had decreased performance in MWM, representing impairment of cognitive functions. Biochemical evaluation showed rise in TBARS level, MPO and AChE activity, and fall in GSH level. The histopathological study revealed severe infiltration of neutrophils. In the study, Phlorizin/Donepezil (serving as positive control) treatment mitigate streptozotocin induced cognitive decline, histopathological changes and biochemical alterations. CONCLUSIONS: The results suggest that Phlorizin decreased cognitive function via its anticholinesterase, antioxidative, antiinflammatory effects and probably through SGLT inhibitory action. It can be conferred that SGLTs can be an encouraging target for the treatment of dementia of AD.