Corrigendum: Serological and molecular prevalence of Brucella spp. among livestock species in Rajasthan, India.

[This corrects the article DOI: 10.3389/fvets.2023.1157211.].

Serological and molecular prevalence of Brucella spp. among livestock species in Rajasthan, India.

A seroprevalence and molecular study was carried out in six districts of the state of Rajasthan, India to detect brucellosis in major livestock species. This study involves the testing of 3,245 livestock samples using the Rose Bengal Plate Test (RBPT), Indirect Enzyme-Linked Immunosorbent Assay (i-ELISA), and genus-specific polymerase chain reaction (PCR) markers for molecular diagnosis of the disease. In the tested samples, seroprevalence was 5.06% (CI: 1.96-8.15) using the RBPT test and 6.88% (CI: 1.98-11.78) using the i-ELISA test, while the cumulative seroprevalence (RBPT and i-ELISA) was 3.63% (CI: 0.44-6.83). The prevalence of the disease was 1.27% (CI: 0.56-3.11) when tested using molecular markers. The highest prevalence of brucellosis was detected in Cattle (7.00, 3.22%), followed by camels (5.50, 2.50%), buffalo (2.66, 0.00%), sheep (2.43, 0.41%), and goats (0.58, 0.23%) when serological (cumulative) and molecular diagnosis were considered preferred methods of detection. Cattle (3.22%) and camels (2.50%) also showed a high prevalence of disease when tested using molecular markers. The results of this study reveal that cattle, camel, and sheep brucellosis is prevalent in the study areas.

Nanotechnology Based Approaches in Phage Therapy: Overcoming the Pharmacological Barriers.

With the emergence and spread of global antibiotic resistance and the need for searching safer alternatives, there has been resurgence in exploring the use of bacteriophages in the treatment of bacterial infections referred as phage therapy. Although modern phage therapy has come a long way as demonstrated by numerous efficacy studies but the fact remains that till date, phage therapy has not received regulatory approval for human use (except for compassionate use).Thus, to hit the clinical market, the roadblocks need to be seriously addressed and gaps mended with modern solution based technologies. Nanotechnology represents one such ideal and powerful tool for overcoming the pharmacological barriers (low stability, poor in-vivo retention, targeted delivery, neutralisation by immune system etc.) of administered phage preparations.In literature, there are many review articles on nanotechnology and bacteriophages but these are primarily focussed on highlighting the use of lytic and temperate phages in different fields of nano-medicine such as nanoprobes, nanosensors, cancer diagnostics, cancer cell targeting, drug delivery through phage receptors, phage display etc. Reviews specifically focused on the use of nanotechnology driven techniques strictly to improve phage therapy are however limited. Moreover, these review if present have primarily focussed on discussing encapsulation as a primary method for improving the stability and retention of phage(s) in the body.With new advances made in the field of nanotechnology, approaches extend from mere encapsulation to recently adopted newer strategies. The present review gives a detailed insight into the more recent strategies which include 1) use of lipid based nano-carriers (liposomes, transfersomes etc.) 2) adopting microfluidic based approach, surface modification methods to further enhance the efficiency and stability of phage loaded liposomes 3) Nano- emulsification approach with integration of microfluidics for producing multiple emulsions (suitable for phage cocktails) with unique control over size, shape and drop morphology 4) Phage loaded nanofibers produced by electro-spinning and advanced core shell nanofibers for immediate, biphasic and delayed release systems and 5) Smart release drug delivery platforms that allow superior control over dosing and phage release as and when required. All these new advances are aimed at creating a suitable housing system for therapeutic bacteriophage preparations while targeting the multiple issues of phage therapy i.e., improving phage stability and titers, improving in-vivo retention times, acting as suitable delivery systems for sustained release at target site of infection, improved penetration into biofilms and protection from immune cell attack. The present review thus aims at giving a complete insight into the recent advances (2010 onwards) related to various nanotechnology based approaches to address the issues pertaining to phage therapy. This is essential for improving the overall therapeutic index and success of phage therapy for future clinical approval.

Antiangiogenic activity of zinc and zinc-sorafenib combination using the chick chorioallantoic membrane assay: A descriptive study.

AIM: Zinc, a trace element, is known for downregulating several proangiogenic growth factors and cytokines. However, its antiangiogenic activity is not adequately studied. The present study was aimed to evaluate the possible antiangiogenic activity of zinc via the chick chorioallantoic membrane (CAM) assay. Furthermore, the antiangiogenic activity of the combination therapy of zinc with various doses of sorafenib, a tyrosine kinase inhibitor, was evaluated. MATERIALS AND METHODS: A pilot study was initially conducted so as to select suitable doses of zinc and sorafenib. The antiangiogenic activity after combining zinc 2.5 µg/embryo with sorafenib 1 and 2 µg/embryo was also evaluated. The antiangiogenic activity was quantified in terms of total length of blood vessels, number of junctions, number of branching points, and mean length of the blood vessels. RESULTS: Zinc 2.5 µg/embryo showed significant (P < 0.05) antiangiogenic activity, as compared to the control group. However, its effect was not comparable to that of sorafenib 2 µg/embryo. The combination of zinc 2.5 µg/embryo with sorafenib 2 µg/embryo did not show an additive/synergistic effect. The combination of zinc 2.5 µg/embryo with sorafenib 1 µg/embryo produced an antiangiogenic activity which was comparable (P > 0.05) to that of sorafenib 2 µg/embryo. CONCLUSION: Zinc caused significant antiangiogenic activity in the CAM assay. The lack of addition/synergism in the zinc-sorafenib combination could have been due to the variability in the dose/ratio selection. Addition of zinc to sorafenib therapy could improve treatment tolerability, reduce cost of therapy, and reduce the emergence of drug resistance. Future mechanistic studies could identify the exact pharmacodynamics of zinc as an angiogenesis inhibitor.

Postprandial Hypertriglyceridemia Predicts Development of Insulin Resistance Glucose Intolerance and Type 2 Diabetes.

Insulin resistance (IR) and type 2 diabetes mellitus (T2DM) have been found to be associated with postprandial hypertriglyceridemia (PPHTg). However, whether PPHTg can cause IR and diabetes is not clear. We therefore investigated the role of PPHTg in development of T2DM in rat model of T2DM. 96 male Wistar rats were randomized into four groups (24 rats each). Control Group A, high sucrose diet (HSD) Group B, HSD+Pioglitazone (10 mg/kg/day) Group C and HSD+Atorvastatin (20 mg/kg/day) Group D. Fat and glucose tolerance tests were done at regular intervals in all groups besides insulin and body weight measurement. At 26 weeks, low dose streptozotocin (15 mg/kg, i.p.) was given to half of the rats. All rats were followed up till 48 weeks. PPHTg developed as early as week 2 in Group B and stabilized by week 14. Group B displayed highest PPHTg compared to other groups. Atorvastatin treatment (Group D) abolished PPHTg which became comparable to controls, pioglitazone treatment partially blunted PPHTg resulting in intermediate PPHTg. Group B with highest PPHTg showed highest subsequent IR, glucose intolerance (GI) and highest incidence of prediabetes at week 26 and diabetes at week 34 and 46 compared to other groups. Group D rats displayed lower IR, GI, low incidence of prediabetes and diabetes at these time points compared to Groups B and C. ROC analysis showed that triglyceride area under the curve of each time point significantly predicts the risk of diabetes. Present study provides the evidence that PPHTg predicts the development of IR, GI and T2DM in rat model of diet induced T2DM.

Cadmium exposure during lactation causes learning and memory-impairment in F1 generation mice: amelioration by quercetin.

Cadmium (Cd) is a known pollutant present in the environment at low levels and is reported to affect reproduction in many ways. The present study was undertaken to explore the effect of Cd in F1 generation mice on cognitive parameters, and to further investigate whether quercetin could modulate these effects. In this study, female lactating mice were exposed to cadmium for seven days just after delivery. The new born pups in their adulthood were tested for learning and memory parameters by passive avoidance task and Morris water maze (MWM) test. It was observed that pups exposed to Cd showed significant impairment of memory in step down latency test, which was reversed by quercetin (100 mg/kg). In MWM test for spatial memory, animals exposed to Cd exhibited increased escape latency, which was reversed by quercetin (50 mg/kg) significantly. Quercetin alone (50 and 100 mg/kg) also demonstrated improved spatial memory, and showed improved retention memory in the passive avoidance paradigm at dose 50 mg/kg. On testing oxidative stress parameters, we observed significantly increased malondialdehyde (MDA) levels in brain tissue of Cd-treated mice. Moreover, co-treatment with quercetin (50 mg/kg) and Cd significantly reduced these MDA levels. The other doses (25 and 100 mg/kg) also showed reduction in MDA levels as compared to the group exposed to Cd alone, though the difference was not statistically significant. Hence, this study highlights the possibility of cognitive impairment in adulthood if there is Cd exposure during lactation and oxidative stress could possibly attribute to this effect.

Atorvastatin prevents type 2 diabetes mellitus--an experimental study.

Recent reports of increased diabetes risk have raised concerns regarding the use of statins. The present study was therefore planned to clarify whether atorvastatin can prevent diabetes development in a rat model of type 2 diabetes mellitus. Eight week old male Wistar rats were randomized into three groups (n = 12 each group). Group A was given standard chow diet, while group B and group C were offered high sucrose diet. In addition to high sucrose diet, group C was given atorvastatin (20mg/kg/day) from beginning of study till 26th week. After 26 weeks, a low dose of streptozotocin (15 mg/kg, i.p.) was given to all 3 groups and further followed for 4 weeks. Oral glucose tolerance tests were done at week 4, 26 and week 30. Development of impaired glucose tolerance at week 26 (16.66% vs 100%, P = <0.001) and diabetes at week 30 (16.66% vs 81.81%, P = 0.002) was significantly lower in rats pretreated with atorvastatin along with high sucrose diet viz group C compared to group B rats who received high sucrose diet only respectively. Also, metabolic indices like body weight, hypertriglyceridemia, glucose area under the curve (Gl-AUC) were significantly lower in group C compared to group B (P = <0.05) while insulin resistance (HOMA-IR) was also lower in group C (P = 0.05). This study clearly demonstrates for the first time in a rat model of type 2 diabetes mellitus that atorvastatin prevents development of type 2 diabetes.