Urea 10% / Lactic acid 5% cream

Keratosis pilaris (KP) is a highly prevalent, benign disorder of follicular keratinization characterized by rough keratotic papules and variable perifollicular erythema, most commonly affecting the extensor upper arms, thighs, and buttocks. Although medically harmless, KP is frequently associated with cosmetic distress, reduced self-confidence, and persistent dissatisfaction with skin texture and appearance. The fundamental pathological process involves follicular hyperkeratosis with retention keratosis and abnormal desquamation, often occurring in the context of xerosis and epidermal barrier dysfunction, including associations with atopic dermatitis, ichthyosis vulgaris, and filaggrin-related barrier impairment. These mechanisms provide a strong rationale for topical keratolytic therapy, which aims to reduce corneocyte cohesion, facilitate desquamation, soften keratin plugs, and improve hydration of the stratum corneum. Topical keratolytics remain reasonable first-line, symptom-directed options for KP, with AHAs, BHAs, and urea all demonstrating potential benefit. However, the overall evidence base is constrained by small sample sizes, heterogeneous outcome measures, limited blinding, and short follow-up, with sparse long-term maintenance data and limited differentiation between texture-dominant and erythematous KP phenotypes.

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Objectives: This study aimed to clarify the effect of lactic acid bacteria-fermented corn protein hydrolysate (FCH) on fatigue in mice and explore the connection between fatigue-related indicators and intestinal microbial flora. Methods: The fatigue model of mice was constructed by exercise endurance experiment. The anti-fatigue level of FCH was evaluated by measuring physiological and biochemical indexes in mouse serum, liver and skeletal muscle. The relationship between FCH, intestinal flora and fatigue was explored through the analysis of intestinal microbial diversity in mice, and the anti-fatigue mechanism of FCH was further analyzed. Results: The results showed that the weight-bearing swimming time of mice was prolonged by 1.96 times, and the running time of mice was prolonged by 2.63 times in the high-dose FCH (FCH-H) group. Moreover, the lactic acid contents in the blood were reduced by 16.00%, and lactate dehydrogenase activity and urea nitrogen contents basically returned to the normal level. Meanwhile, the malondialdehyde contents were reduced by 31.24%, and superoxide dismutase activity and glutathione contents were increased by 1.84 times and 1.72 times, respectively. In addition, the glycogen contents of the body were restored, and the muscle glycogen and liver glycogen were increased by 1.81 and 5.81 times, respectively. Analysis of intestinal microbial flora diversity in mice showed that the highest relative abundance was Lactobacillus, and the FCH group could recover and even increase its relative abundance. Lactobacillus was significantly positively correlated with muscle glycogen and SOD. Conclusions: FCH can alleviate fatigue by regulating fatigue-related indicators and improving the intestinal microbial flora of the organism.

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Abstract This study aims to investigate the performance of deep eutectic solvents (DESs) as plasticizers in low‐density polyethylene (LDPE) films and to compare them with di(2‐ethylhexyl) phthalate (DEHP). DESs were produced by mixing choline chloride with lactic acid and urea in 1:1 and 1:2 molar ratios. The prepared DESs were added to LDPE at two different ratios (10% and 30%), and films with 10 different compositions were produced by the extrusion method. The densities, viscosities, pH, volatility, and thermal values of the produced DESs were determined between 1.14 and 1.18 g/cm 3 , 22 and 99 mPa.s, 0.05 and 9.02, 0.7% and 18.9%, and <−70 and 63°C, respectively. When the DESs were examined in terms of their bond structure, it was observed that they could be produced successfully. The LDPE films with DES were characterized by thickness, mechanical, barrier, optical, DSC, FTIR, SEM, water behavior properties, heat sealability, and overall migration (OM) properties. According to the results of some basic analyses performed on the films, the first three films with the best properties (CL1:30, CL2:30, and DEHP:30) were determined using TOPSIS from the multi‐criteria decision hierarchy techniques. It was determined that the DES films with the most suitable properties had better properties than the control and DEHP films in terms of tensile strength (10–12 MPa), elongation at break (500%–545%), water vapor permeance (0.03–0.04 g/m 2 /h/kPa), and oxygen transmission rate (13–14 cm 3 /m 2 /day), water contact angle (>99°), and UV light barrier analyses. DES did not cause any change in the DSC and OM values of LDPE films. In general, important results were obtained regarding the use of DES as effective plasticizers in LDPE films. Highlights DES is a sustainable alternative to DEHP for LDPE plasticization. DES‐plasticized films showed 400% better elongation performance. DES‐plasticized films showed 25% better water vapor and 80% better oxygen barriers. DES‐plasticized films have superior UV light barrier and hydrophobic properties. DES‐plasticized films did not affect thermal stability or OM.

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The aim of this study was to investigate the effect of Lactiplantibacillus paraplantarum ST1 and Limosilactobacillus fermentum G3 and their combination with urea on the aerobic stability of sugarcane tops silages. The fermentation profile was not affected by the interaction between urea and lactic acid bacteria (LAB), except for the lactic acid content (P = 0.012). Lactic acid content was higher in LAB silage (P = 0.008). The use of urea resulted in higher levels of pH value, butyric acid, and ammonia-nitrogen compared to LAB. The addition of urea increased the crude protein, and fiber content in silage and decreased the in vitro dry matter digestibility of silage by 7.1% (P < 0.001). In the urea-treated silages, the pH values remained stable, and the yeast counts remained low during five days of air exposure. In contrast, yeast counts increased in the silages without urea treatment, irrespective of the use of LAB. Clostridium sensu stricto 12 was found exclusively in urea-treated silages. The use of LAB additives without urea appears to be advantageous for the fermentation process of sugarcane tops silage. Despite improving the aerobic stability, the addition of urea is not warranted because it results in a poor-quality silage.

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Many physiological processes rely on a constant pH of about 7.4. Several buffers maintain intravascular pH, most importantly the bicarbonate system, in which a weak acid dissociates: [1]CO2 +H2O⇌H2CO3⇌H+ + HCO3− Adding acid increases the concentration of H+ (denoted as [H+]). As there is now excess H+ on the right side of the equation, the equilibrium shifts to the left to reduce it, consuming H+ and HCO3− to form H2O and CO2. Conversely, adding base decreases [H+], so the equilibrium shifts to the right to replace it, generating H+ and HCO3−. Across a range of CO2 and HCO3− concentrations, the pH is maintained, governed by the HCO3−/CO2 ratio (Henderson–Hasselbalch equation): [2]pH=pKa+log[HCO3−]α⋅pCO2=6.1+log[HCO3−]0.03⋅pCO2 where pKa = dissociation constant = 6.1, α = solubility constant for CO2 = 0.03, pCO2 is the partial pressure of CO2 in mmHg and [HCO3−] is the concentration of HCO3− in mmol/L Adding H+ ions, such as lactic acid or ketoacid, not only consumes HCO3− but also generates an anion, which is unmeasured in the renal (metabolic) panel—giving a high anion gap (AG) metabolic acidosis (HAGMA). Alternatively, direct HCO3− loss (in diarrhoea or renal tubular acidosis) causes acidaemia without generating unmeasured anions, producing a normal AG metabolic acidosis (NAGMA). The two may be distinguished by the AG, which is the difference between unmeasured anions and unmeasured cations: Based on charge balance: Sum of cations = Sum of anions Only measuring Na+, Cl− and HCO3−: [Na+] + [Unmeasured cation] = [Cl−] + [HCO3−] + [Unmeasured anion] AG = Unmeasured anion – Unmeasured cation = [Na+] – [Cl−] – [HCO3−] [3] There are normally more unmeasured anions than unmeasured cations, so AG is positive. As albumin is the predominant unmeasured anion, AG is corrected for hypoalbuminaemia: Corrected AG = Calculated AG + 0.25 (40 – albumin [in g/L]) [4] The AG is a well-accepted, readily available and simple-to-calculate fundamental tool in the diagnostic approach to metabolic acidosis.[1] However, it depends on the measurement methodology and traceability (calibration) of Na+, Cl− and HCO3−. Since its initial clinical use in the 1970s, significant advances have been made in the measurement of Na+, Cl− and HCO3−. This has led to wide reference intervals in literature and uncertainty about the AG cut-off that best distinguishes HAGMA from NAGMA. In this issue, Chionh et al.[2] addressed this matter in a large, single-centre cohort of patients who had lactate, ketone or salicylate levels measured with urea, electrolytes and creatinine. Of the 16,475 patients, 2366 had lactic acidosis, 217 had ketosis, 36 had both lactic acidosis and ketosis, and 2 had elevated salicylate. The AG was a good indicator of lactic acidosis and ketoacidosis with a C-statistic of 0.873. Although an AG cut-off of >19 mEq/L best predicted lactic acidosis or ketoacidosis (sensitivity 81% and specificity 77%), the authors propose a lower cut-off of ≥15 mEq/L, prioritising clinical sensitivity (98%) at the cost of reduced specificity (34%). This is reasonable when using AG as an initial screening test for metabolic acidosis, which prompts further investigation if elevated. This important study affirms that the AG, first described in 1936 by James Gamble, remains a valid and clinically sensitive test for HAGMA with modern high-throughput analysers and that the performance is consistent across patient subgroups. A noteworthy advantage of the study is the validation of an AG cut-off against clinically significant conditions, instead of theoretical or laboratory considerations alone. Interestingly, a quarter of patients in this cohort with raised lactate or ketone had a HCO3− >20 mmol/L, which may not be regarded as clinically significant metabolic acidosis. This highlights the importance of always calculating AG in every renal panel, as concomitant metabolic alkalosis can mask a HAGMA, giving spuriously ‘normal’ HCO3− [Box 1].Box 1: Stepwise acid–base analysis and the importance of calculating anion gap (AG).A limitation of this study is that it considered only a subset of HAGMA causes, omitting renal insufficiency, toxic alcohol and 5-oxoproline (seen in chronic paracetamol use in the elderly). Among patients without elevated lactate, ketone or salicylate levels, the 25th percentile HCO3− was 20 mmol/L and the 75th percentile corrected AG was 19 mEq/L, suggesting that a quarter of patients had HAGMA unexplained by raised lactate, ketone or salicylate levels. The positive predictive value of AG ≥15 mEq/L for elevated lactate, ketones or salicylate levels was only 22%. Physiologically, these patients likely have unmeasured anion leading to elevated AG, which was not captured in the study. Renal insufficiency is a common and particularly important cause of HAGMA. The specificity of AG ≥15 mEq/L decreases with declining glomerular filtration rate (GFR) (44%, 26% and 10% for GFR ≥60, 30–59 and <30 mL/min/1.73 m², respectively) and with rising urea levels (44% for urea ≤7.7 mmol/L; 18% for urea >7.7 mmol/L). Hence, patients with poorer renal function appear more likely to have raised AG with normal lactate, ketone or salicylate levels. Further analysis of the association between AG and GFR or urea in this cohort may be meaningful, and conclusions about the applicability of the proposed AG cut-off to uraemia cannot be made. Another limitation is that the AG cut-off remains institution-specific, as methodology and traceability (calibration) of its measured components differ. Although Na+ and Cl− measurements have seen great advancements with the use of ion-selective electrode potentiometry and are numerically comparable across laboratory platforms, harmonisation of HCO3− measurement remains challenging. Regulated test accuracy (as per the US Clinical Laboratory Improvement Amendments proficiency testing criteria[4]) for Na+ is ±4% and Cl− ±5%, whereas HCO3− values may vary by ±20%, affecting AG interpretation. Furthermore, test sensitivity and specificity are dependent on population prevalence, which varies with context (e.g. a laboratory mainly serving primary care vs. tertiary referral centre). Hence, the proposed AG cut-off may not be directly applicable without validation and verification. It would be ideal for every laboratory to conduct a similar analysis of its AG reference range and cut-off, and the authors have provided a replicable methodology to do so. There are some nuances when applying AG to clinical practice. Firstly, it is only an initial step in approaching metabolic acidosis. To dissect complex acid–base disorders, detailed stepwise analysis is necessary [Box 1], with additional steps such as calculating osmolar gap (for toxic alcohols) or urine AG (which distinguishes NAGMA due to gastrointestinal or urinary HCO3− loss). Secondly, some causes of acidosis do not fall neatly into the HAGMA/NAGMA dichotomy. For instance, the acidosis of chronic kidney disease is typically NAGMA in earlier stages (due to reduced capacity for ammonium excretion), with superimposed HAGMA later (due to accumulation of sulfates and phosphates, which are unmeasured anions).[5] Similarly, although diabetic ketoacidosis is classically HAGMA, NAGMA is seen during the recovery phase due to large-volume normal saline infusion and rapid excretion of the ketoacid anion (an indirect loss of base).[6] Thirdly, the interpretation of AG must consider the causes of spurious changes and the effect of unmeasured cations (e.g. reduced AG in immunoglobulin G myeloma) [Box 2]. Finally, the bicarbonate-centred HAGMA/NAGMA approach has intrinsic limitations. It does not adequately explain why 0.9% NaCl infusion causes acidosis, which is better rationalised using the strong ion difference.[8] Although the HAGMA/NAGMA framework is one of several approaches to acid–base physiology, it remains the simplest and most clinically useful framework for everyday practice.Box 2: Causes of metabolic acidosis and changes in AG.In conclusion, the AG is basic chemistry with powerful clinical applications. It should be calculated when interpreting every renal panel, and further evaluation of HAGMA should be considered if AG ≥15 mEq/L, even if bicarbonate is normal. Renal panels contain a huge amount of information, for those who know where to look. Acknowledgement This article is co-authored by Fong JMN and his mentor (See KC) as part of the SMJ Editorial Fellowship programme 2026. Financial support and sponsorship Nil. Conflicts of interest See KC is a member of the SMJ Editorial Board and was thus not involved in the peer review and publication decisions of this article.

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and C=O groups on organic molecules significantly degrades the anode because the generated polymers block the catalytically active sites. This knowledge will contribute to the effective design of catalysts/electrodes and benefit the communities in electrolytic synthesis and fuel cells.

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Background: Simiao Pill (SP) is a traditional Chinese medicine used to treat hyperuricemia (HUA). Microbial fermentation can enhance the effectiveness of herbal medicines. Objectives: This study aimed to evaluate the effects of composite lactic acid bacteria fermentation on the chemical components of SP and its anti-HUA effect. Methods: This study revealed the contents of fermented Simiao Pill (FSP), and optimized the optimal fermentation conditions. The anti-HUA effects were evaluated by testing the biochemical indicators of liver and kidney function, and the histology of liver and kidney. Immunohistochemistry, Western blot and RT-qPCR analysis were applied to investigate key proteins and mRNAs. Results: After fermentation with composite lactic acid bacteria, the contents of ferulic acid and berberine in fermented Simiao Pill (FSP) were increased by 40.0% and 20.7%, respectively, compared with those in SP. The optimal fermentation conditions were: time of 24 h, temperature of 35 °C, and inoculation of 1%. FSP significantly reduced the serum levels of uric acid, blood urea nitrogen, creatinine. FSP ameliorated the damage of the kidney and the degree of renal interstitial fibrosis. FSP downregulated the protein expressions of URAT1, upregulated that of OAT1, and inhibited the expression of XOD activity and protein, with its efficacy being superior to that of SP. Conclusion: Fermentation with composite lactic acid bacteria increased the contents of ferulic acid and berberine in SP. FSP lowered uric acid by increasing OAT1 to promote uric acid excretion, decreasing URAT1 to reduce uric acid reabsorption, and inhibiting XOD to reduce uric acid production.

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