Antimicrobial Resistance Patterns of Pathogens Isolated from Patients with Wound Infection at a Teaching Hospital in Vietnam.

Purpose: At a teaching Hospital in Vietnam, the persistently high incidence of diagnosed wound infection poses ongoing challenges to treatment. This study seeks to explore the causative agents of wound infection and their antimicrobial and multidrug resistance patterns. Methods: A cross-sectional study was conducted at the Department of Microbiology, Military Hospital 103, Vietnam. Data on microorganisms that caused wound infection and their antimicrobial resistance patterns was recorded from hospitalized patients from 2014 to 2021. Using the chi-square test, we analyzed the initial isolation from wound infection specimens collected from individual patients. Results: Over a third (34.9%) of wound infection samples yielded bacterial cultures. Staphylococcus aureus was the most prevalent bacteria, followed by Pseudomonas aeruginosa. Worryingly high resistance rates were observed for several antibiotics, particularly among Gram-negative bacteria. Ampicillin displayed the highest resistance (91.9%), while colistin and ertapenem remained the most effective. In Gram-positive bacteria, glycopeptides like teicoplanin and vancomycin (0% and 3.3% resistance, respectively) were most effective, but their use was limited. Clindamycin and tetracycline showed decreasing effectiveness. Resistance rates differed between surgical and non-surgical wards, highlighting the complex dynamics of antimicrobial resistance within hospitals. Multidrug resistance (MDR) was substantial, with Gram-negative bacteria exhibiting a 63.6% MDR rate. Acinetobacter baumannii showed the highest MDR rate (88.0%). Conclusion: This study investigated wound infection characteristics, antibiotic resistance patterns of common bacteria, and variations by hospital ward. S. aureus was the most prevalent bacteria, and concerning resistance rates were observed, particularly among Gram-negative bacteria. These findings highlight the prevalence of multidrug resistance in wound infections, emphasizing the importance of infection control measures and judicious antibiotic use.

Antimicrobial Resistance Patterns of Staphylococcus Aureus Isolated at a General Hospital in Vietnam Between 2014 and 2021.

Purpose: Staphylococcus aureus is a commensal bacteria species that can cause various illnesses, from mild skin infections to severe diseases, such as bacteremia. The distribution and antimicrobial resistance (AMR) pattern of S. aureus varies by population, time, geographic location, and hospital wards. In this study, we elucidated the epidemiology and AMR patterns of S. aureus isolated from a general hospital in Vietnam. Methods: This was a cross-sectional study. Data on all S. aureus infections from 2014 to 2021 were collected from the Microbiology department of Military Hospital 103, Vietnam. Only the first isolation from each kind of specimen from a particular patient was analyzed using the Cochran-Armitage and chi-square tests. Results: A total of 1130 individuals were diagnosed as S. aureus infection. Among them, 1087 strains were tested for AMR features. Most patients with S. aureus infection were in the age group of 41-65 years (39.82%). S. aureus isolates were predominant in the surgery wards, and pus specimens were the most common source of isolates (50.62%). S. aureus was most resistant to azithromycin (82.28%), erythromycin (82.82%), and clindamycin (82.32%) and least resistant to teicoplanin (0.0%), tigecycline (0.16%), quinupristin-dalfopristin (0.43%), linezolid (0.62%), and vancomycin (2.92%). Methicillin-resistant S. aureus (MRSA) and multidrug-resistant (MDR) S. aureus were prevalent, accounting for 73.02% and 60.90% of the total strains respectively, and the strains isolated from the intensive care unit (ICU) had the highest percentage of multidrug resistance (77.78%) among the wards. Conclusion: These findings highlight the urgent need for continuous AMR surveillance and updated treatment guidelines, particularly considering high resistance in MRSA, MDR strains, and ICU isolates. Future research focusing on specific resistant populations and potential intervention strategies is crucial to combat this rising threat.

Structure, anticoagulant and cytotoxic activity of a sulfated polysaccharide from green seaweed Chaetomorpha linum.

In this article, chemical structure and conformation in an aqueous solution of a new sulfated polysaccharide, PCL, extracted from green seaweed Chaetomorpha linum were elucidated by SEC-MALL, IR, NMR and SAXS. The results indicated that the obtained polysaccharide is a sulfated arabinogalactan with a molecular weight of 223 kDa, and is mainly composed of →3,6)-α-D-Galp4S→ and →2)-α-L-Araf→ connecting together through 1→3 glycoside linkages. It has a broken rod-like conformation in solution with Rgc estimated as 0.43 nm from SAXS measurements. The polysaccharide exhibited a notable anticoagulant activity measured by the assays of activated partial thromboplastintime, thrombintime and prothrombine time as well as a significant cytotoxic activity against hepatocellular, human breast cancer, and cervical cancer cell lines.

Modular desalination concept with low-pressure reverse osmosis and capacitive deionization: Performance study of a pilot plant in Vietnam in comparison to seawater reverse osmosis.

Membrane capacitive deionization (MCDI) has shown many advances, however, its performance in combination with other treatment technologies has not been widely reported. In this study, a pilot-scale low-pressure reverse osmosis (LPRO) (FilmTec™ XLE-2540) with MCDI (CapDI© C17, Voltea) was developed and tested as a promising modular desalination system. The systems were evaluated individually at different salinities and tested together as a modular system. The study focused in the comparison to conventional seawater reverse osmosis (SWRO) (FilmTec™ SW30-2540) at pilot-scale and in theory using the software Water Application Value Engine (WAVE, DuPont™), including a cost evaluation of the systems. Pilot tests were carried out in Can Gio, a riverine estuary region in South Vietnam, which is affected by progressive salinization (TDS ≈ 1-25 g/L). Drinking water quality (TDS < 600 mg/L) was achieved with a specific energy consumption (SEC) of 5.2 kWh/m³. Additionally, fouling mitigation was investigated for the ultrafiltration (UF) pre-treatment by periodic hydraulic and chemical enhanced backwashing. While the SWRO had a slightly lower SEC of 5.0 kWh/m³, WAVE calculations showed that lowering the SEC to 3.6 kWh/m³ is possible by improving the LPRO pump design and an optimization of the MCDI operation.

Bosentan versus nifedipine in the treatment of vasculopathy in systemic sclerosis patients: A randomized control trial.

BACKGROUND: Bosentan is effective agent in scleroderma vasculopathy. However, there are no studies evaluating effectiveness of bosentan in Vietnamese patients, where nifedipine is still the common treatment. OBJECTIVE: To compare the efficacy of bosentan versus nifedipine in scleroderma vasculopathy in Vietnamese patients. METHODS: We randomly assigned 70 patients in a 2:1 ratio to receive oral bosentan or oral nifedipine for 16 weeks, respectively. The primary outcomes were the change in Raynaud's Condition Score (RCS), appearance of new digital ulcers (DUs) and change in World Health Organization (WHO) functional class. Secondary outcomes were the change in the nailfold capillaries disease stage and systolic pulmonary arterial pressure (sPAP) value. RESULTS: At week 16, patients in bosentan group had no RCS imprvement, the mean difference was 0.8 ± 0.2 (95% CI, 0.4 to 1.1, p < 0.001) and improved WHO functional class, a mean treatment effect of 35.6% in favor of bosentan (95% CI, 13.4 to 57.7%, p < 0.05). Bosentan treatment was associated with a 58% reduction in the number of new DUs compared with nifedipine (mean ± standard error: 0.22 ± 0.42 vs 0.52 ± 0.59 new DUs, p < 0.05). sPAP was decreased by 4.1 ± 3.8 mmHg (95% CI, 3.0 to 5.3, p < 0.001) in bosentan group, versus 1.0 ± 2.9 mmHg (95% CI, -0.2 to 2.1, p > 0.05) in nifedipine group. Headache was the most common adverse event in both groups. CONCLUSIONS: Bosentan significantly limited the occurrence of new DUs, reduced symptoms of pulmonary arterial hypertension and sPAP value and all were better than nifedipine.

The compound LG283 inhibits bleomycin-induced skin fibrosis via antagonizing TGF-ß signaling.

BACKGROUND: Systemic sclerosis (SSc) is a collagen disease that exhibits intractable fibrosis and vascular injury of the skin and internal organs. Transforming growth factor-ß (TGF-ß)/Smad signaling plays a central role in extracellular matrix (ECM) production by α-SMA-positive myofibroblasts. Myofibroblasts may be partially derived from various precursor cells in addition to resident fibroblasts. Recently, our high-throughput in vitro screening discovered a small compound, LG283, that may disrupt the differentiation of epithelial cells into myofibroblasts. This compound was originally generated as a curcumin derivative. METHODS: In this study, we investigated the effect of LG283 on inhibiting fibrosis and its mechanism. The action of LG283 on TGF-ß-dependent fibrogenic activity and epithelial-mesenchymal transition (EMT) was analyzed in vitro. The effects of LG283 were also examined in a bleomycin-induced skin fibrosis mouse model. RESULTS: LG283 suppressed TGF-ß-induced expression of ECM, α-SMA, and transcription factors Snail 1 and 2, and Smad3 phosphorylation in cultured human dermal fibroblasts. LG283 was also found to block EMT induction in cultured human epithelial cells. During these processes, Smad3 phosphorylation and/or expression of Snail 1 and 2 were inhibited by LG283 treatment. In the bleomycin-induced skin fibrosis model, oral administration of LG283 efficiently protected against the development of fibrosis and decrease of capillary vessels without significantly affecting cell infiltration or cytokine concentrations in the skin. No apparent adverse effects of LG283 were found. LG283 treatment remarkably inhibited the enhanced expression of α-SMA and phosphorylated Smad3, as well as those of Snail 1 and 2, in the bleomycin-injected skin. CONCLUSIONS: The LG283 compound exhibits antagonistic activity on fibrosis and vascular injury through inhibition of TGF-ß/Smad/Snail mesenchymal transition pathways and thus, may be a candidate therapeutic for the treatment of SSc. Although the involvement of EMT in the pathogenesis of SSc remains unclear, the screening of EMT regulatory compounds may be an attractive approach for SSc therapy.

Iron-based subsurface arsenic removal (SAR): Results of a long-term pilot-scale test in Vietnam.

The principle of subsurface arsenic removal (SAR) from groundwater is based on oxidation and adsorption reactions by infiltrating oxygen into the anoxic aquifer and the immobilization of arsenic (As) onto freshly formed iron (Fe)-(hydr)oxides. In this study, a pilot-scale plant for SAR has been subject to long term testing in the Mekong Delta, Vietnam. Initial concentrations of Fe (8.4 ± 1.3 mg L-1) and As (81 ± 8 µg L-1) in the exploited groundwater were successfully lowered to below the WHO guideline value limits for drinking water of 0.3 mg L-1 and 10 µg L-1, respectively. Adsorption and co-precipitation of As with Fe-(hydr)oxides could be identified as the principal mechanism responsible for the As removal from groundwater, demonstrating the feasibility of SAR as a low-cost and zero-waste solution over a period of two years. However, naturally occurring geochemical reducing conditions and high ammonium levels in the groundwater delayed the removal of manganese (Mn). An additional post-treatment filtration for Mn-removal was temporarily used to comply with the Vietnamese drinking water standard until a Mn-mitigation was achieved by the SAR process. In contrast to most As-remediation technologies, SAR appears to be a long-term, sustainable treatment option with the salient advantage of negligible production of toxic waste, which with ex-situ processes require additionally management costs.

Homeostatic Function of Dermokine in the Skin Barrier and Inflammation.

Dermokine is a chiefly skin-specific secreted glycoprotein localized in the upper epidermis, and its family consists of three splice variants in mice and five in humans. To investigate the pathophysiological impact of dermokine, we generated mice deficient for two (ßγ) or all dermokine isoforms (αßγ). Both variants, especially dermokine αßγ-deficient mice exhibited scale and wrinkle formation resembling ichthyosis accompanied by transepidermal water imbalance at the neonatal stage. Several dermokine αßγ-deficient mice died by postnatal day 21 when reared under low humidity. Moreover, the cornified envelope was vulnerable, and skin barrier lipid ceramides were reduced in the epidermis of dermokine αßγ-deficient mice. cDNA microarray and quantitative reverse transcriptase-PCR assays of the epidermis revealed the upregulation of small proline-rich protein and late cornified envelope family members, as well as antimicrobial peptides in the dermokine αßγ-deficient mice. These barrier gene signatures were similar to that seen in psoriasis, whereas recent studies demonstrated that congenital ichthyosis has gene profiles resembling psoriasis. In line with these findings, adult dermokine αßγ-deficient mice exhibited aggravated phenotypes in psoriasis-like dermatitis models but not in allergic dermatitis models. Dermokine may play a regulatory role in inflammatory dyskeratotic diseases, such as congenital ichthyosis and psoriasis, in the crosstalk between barrier dysfunction and inflammation.

Inhibition of the Progression of Skin Inflammation, Fibrosis, and Vascular Injury by Blockade of the CX3 CL1/CX3 CR1 Pathway in Experimental Mouse Models of Systemic Sclerosis.

OBJECTIVE: To assess the preclinical efficacy and mechanism of action of an anti-CX3 CL1 monoclonal antibody (mAb) in systemic sclerosis (SSc). METHODS: Cultured human dermal fibroblasts were used to evaluate the direct effect of anti-CX3 CL1 mAb on fibroblasts. In addition, bleomycin-induced and growth factor-induced models of SSc were used to investigate the effect of anti-CX3 CL1 mAb on leukocyte infiltration, collagen deposition, and vascular damage in the skin. RESULTS: Anti-CX3 CL1 mAb treatment significantly inhibited Smad3 phosphorylation (P < 0.05) and expression of type I collagen and fibronectin 1 (P < 0.01) in dermal fibroblasts stimulated with transforming growth factor ß1 (TGFß1). In the bleomycin model, daily subcutaneous bleomycin injection increased serum CX3 CL1 levels (P < 0.05) and augmented lesional CX3 CL1 expression. Simultaneous administration of anti-CX3 CL1 mAb or CX3 CR1 deficiency significantly suppressed the dermal thickness, collagen content, and capillary loss caused by bleomycin (P < 0.05). Injection of bleomycin induced expression of pSmad3 and TGFß1 in the skin, which was inhibited by anti-CX3 CL1 mAb. Further, the dermal infiltration of CX3 CR1+ cells, macrophages (inflammatory and alternatively activated [M2-like] subsets), and CD3+ cells significantly decreased following anti-CX3 CL1 mAb therapy (P < 0.05), as did the enhanced skin expression of fibrogenic molecules, such as thymic stromal lymphopoietin and secreted phosphoprotein 1 (P < 0.05). However, the treatment did not significantly reduce established skin fibrosis. In the second model, simultaneous anti-mCX3 CL1 mAb therapy significantly diminished the skin fibrosis induced by serial subcutaneous injection of TGFß and connective tissue growth factor (P < 0.01). CONCLUSION: Anti-CX3 CL1 mAb therapy may be a novel approach for treating early skin fibrosis in inflammation-driven fibrotic skin disorders such as SSc.

Blockade of TGF-ß/Smad signaling by the small compound HPH-15 ameliorates experimental skin fibrosis.

BACKGROUND: Transforming growth factor-ß (TGF-ß)/Smad signaling is well known to play a critical role in the pathogenesis of systemic sclerosis (SSc). We previously developed an artificial molecule, the histidine-pyridine-histidine ligand derivative HPH-15, which may have an antifibrotic effect. The purpose of the present study was to clarify the effects of this drug in human skin fibroblasts and in a preclinical model of SSc. METHODS: The effects of HPH-15 on expression of extracellular matrix components and TGF-ß signaling in human dermal fibroblasts were analyzed. The antifibrotic properties of HPH-15 and its mechanisms were also examined in a bleomycin-induced skin fibrosis mouse model. RESULTS: HPH-15 suppressed the TGF-ß-induced phosphorylation of Smad3 and inhibited the expression of collagen I, fibronectin 1, connective tissue growth factor, and α-smooth muscle actin induced by TGF-ß in cultured human skin fibroblasts. In the bleomycin-induced skin fibrosis model, oral administration of HPH-15 protected against the development of skin fibrosis and ameliorated established skin fibrosis. Additionally, HPH-15 suppressed the phosphorylation of Smad3 in various cells, including macrophages in the bleomycin-injected skin. Further, in the treated mice, dermal infiltration of proinflammatory macrophages (CD11b+Ly6Chi) and M2 profibrotic macrophages (CD11b+CD204+ or CD11b+CD206+) was significantly decreased during the early and late stages, respectively. HPH-15 treatment resulted in decreased messenger RNA (mRNA) expression of the M2 macrophage markers arginase 1 and Ym-1 in the skin, whereas it inversely augmented expression of Friend leukemia integration 1 and Krüppel-like factor 5 mRNAs, the transcription factors that repress collagen synthesis. No apparent adverse effects of HPH-15 were found during the treatment. CONCLUSIONS: HPH-15 may inhibit skin fibrosis by inhibiting the phosphorylation of Smad3 in dermal fibroblasts and possibly in macrophages. Our results demonstrate several positive qualities of HPH-15, including oral bioavailability, a good safety profile, and therapeutic effectiveness. Thus, this TGF-ß/Smad inhibitor is a potential candidate therapeutic for SSc clinical trials.

Iron-based subsurface arsenic removal technologies by aeration: A review of the current state and future prospects.

Arsenic contamination in groundwater is a critical issue and one that raises great concern around the world as the cause of many negative health impacts on the human body, including internal and external cancers. There are many ways to remove or immobilize arsenic, including membrane technologies, adsorption, sand filtration, ion exchange, and capacitive deionization. These exhibit many different advantages and disadvantages. Among these methods, in-situ subsurface arsenic immobilization by aeration and the subsequent removal of arsenic from the aqueous phase has shown to be very a promising, convenient technology with high treatment efficiency. In contrast to most of other As remediation technologies, in-situ subsurface immobilization offers the advantage of negligible waste production and hence has the potential of being a sustainable treatment option. This paper reviews the application of subsurface arsenic removal (SAR) technologies as well as current modeling approaches. Unlike subsurface iron removal (SIR), which has proven to be technically feasible in a variety of hydrogeochemical settings for many years, SAR is not yet an established solution since it shows vulnerability to diverse geochemical conditions such as pH, Fe:As ratio, and the presence of co-ions. In some situations, this makes it difficult to comply with the stringent guideline value for drinking water recommended by the WHO (10 µg L-1). In order to overcome its limitations, more theoretical and experimental studies are needed to show long-term application achievements and help the development of SAR processes into state-of-the-art technology.

The determinants of trichiasis recurrence differ at one and two years following lid surgery in Vietnam: A community-based intervention study.

AIM: To compare determinants for recurrence of trichiasis at one and two years following lid surgery in Vietnam. STUDY DESIGN: Community-based intervention study. METHODS: This study was carried out between 2000 and 2003 in four trachoma-endemic districts of Vietnam. Trained trichiasis surgeons performed modified Cuenod Nataf lid surgery on 648 eyes of 472 patients with Trachomatous trichiasis (TT). Trained investigators collected information on ocular and lid status before surgery and at one and two years following surgery. Trichiasis recurrence was calculated after adjusting for one or both eyes of each operated individual. RESULTS: Fifty-six eyes developed recurrence at one year with adjusted prevalence of 8.8% (95% CI 6.60-11.01). One hundred and one eyes [15.9% (95% CI 13.04-18.72)] had recurrence two years following surgery. Female gender, older age group, study area, severe grade of trachomatous scarring (TS), past history of lid surgery, postoperative suture adjustment and surgeon were risk factors for recurrence at the end of one year. Study area and previous lid surgery were risk factors for recurrence in the second year. Recurrence at one year could be predicted if study area and severity of Trachomatous Scarring (TS) are known. CONCLUSIONS: One and two year recurrence rates with modified Cuenod Nataf lid surgeries for TT in Vietnam were acceptably low. Early recurrence could be reduced by proper case selection. However, late recurrence seems to be dependent on interaction of risk factors. Only age of the patient was the reliable predictor of recurrence.

Impact of annual targeted treatment on infectious trachoma and susceptibility to reinfection.

CONTEXT: The World Health Organization developed the SAFE strategy (Surgery for trichiasis; Antibiotics for Chlamydia trachomatis infection; Facial cleanliness; and Environmental improvement) to eliminate blinding trachoma globally by the year 2020. Despite a number of studies using various intervals of treatment for different prevalence rates, there has been a lack of sufficient follow-up beyond the final treatment point to determine rates of recurrence of disease and infection and the risk factors that may contribute to each. OBJECTIVE: To evaluate the impact of 2 annual targeted azithromycin treatments on active trachoma and C trachomatis infection rates over 3 years in Vietnam. DESIGN, SETTING, AND PARTICIPANTS: Three communes were randomly selected for a longitudinal study in Vietnam from November 2000 through November 2003. Individuals (n = 3186) were graded for trachoma followed by conjunctival sampling to detect chlamydiae by commercial polymerase chain reaction. Grading and chlamydial detection were repeated every 6 months for 3 years. INTERVENTION: Azithromycin was given to children aged 5 through 15 years with active trachoma and their household members in SAFE and SA communes at baseline and 12 months; these communes were compared with the S-only control commune that did not receive azithromycin targeted treatment. MAIN OUTCOME MEASURES: Prevalence and incidence of active trachoma and C trachomatis infection in all communes at baseline, 6, 12, 18, 24, and 36 months. Subgroup analysis evaluated new infection, continuing infection, and reinfection at 6, 12, 18, 24, and 36 months and risk factors for each. RESULTS: Reinfection rates increased significantly between 12 and 36 months for SAFE (from 1.6 to 29.3 per 1000; P<.001) and SA (5.1 to 25.3 per 1000; P = .002) communes but not for the S-only commune (13.4 to 6.7 per 1000; P = .55) after 24 months. Compared with the S-only commune, mixed-effects and generalized estimating equations (GEE) logistic models showed that reinfection risk was significantly higher for SAFE (odds ratio [OR], 4.1; 95% confidence interval [CI], 1.5-9.8; P = .005) and SA (OR, 4.2; 95% CI, 1.1-17.3; P = .04) communes at 36 months. CONCLUSIONS: Increasing reinfection rates suggest that treatment may interrupt the duration of infection required for developing immunity, increasing the number of individuals susceptible to reinfection and adversely affecting disease prevalence over time. Additional research is needed to determine optimal trachoma control strategies, including evaluation of the "F" and "E" components. TRIAL REGISTRATION: www.actr.org.au Identifier: 12606000360516.

Association between the G protein beta3 subunit 825t allele and radial artery hypertrophy.

The GNB3 C825T gene polymorphism has recently been identified and associated with hypertension, obesity and left ventricular hypertrophy. The aim of the study was to determine the relationship between the C825T polymorphism of the gene encoding for the G protein beta3 subunit (GNB3 C825T) and vascular hypertrophy. We studied a cohort of 306 subjects (age 49 +/- 12 years) without evidence of cardiovascular disease and never treated with cardiovascular drugs. Vascular phenotypes were evaluated for the common carotid and radial arteries using high-resolution echo-tracking devices. Genotype frequencies were in agreement with the Hardy-Weinberg equilibrium. For the radial artery, mean wall thickness was significantly higher in subjects carrying the 825T allele than in CC genotype subjects (240 +/- 54 microm for CT genotype and 241 +/- 53 microm for TT genotype vs. 222 +/- 52 microm for CC genotype, p = 0.01). The frequency of the 825T allele was significantly different in subjects with (52%) and without (35%) radial artery hypertrophy (chi(2) = 10.88, p < 0.001). The relative risk of radial artery hypertrophy in subjects carrying the 825T allele compared with those with the CC genotype was 3.02 (95% CI 1.53- 5.95). A logistic regression analysis indicated that the positive and significant association between the 825T allele and radial artery hypertrophy was independent of age, blood pressure, gender and BMI. In contrast, no association between genotypes and carotid artery wall thickening was observed. These results suggest that some genetic characteristics determine in part the patterns of radial artery geometrical changes. As the 825T allele is associated with vascular hypertrophy of a muscular artery but not with structural changes of an elastic artery, we hypothesize that the 825T allele may be a genetic marker of arteriolosclerosis.