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As tour package sales by travel agents increase, tour wholesalers are becoming more important in the travel marketplace. This article reports the results of two mail surveys and a series of follow-up personal interviews. The results indicate that travel agents' purchases are based on the wholesaler's reputation for reliability, quality, and service. Factors which travel agents perceive as influencing clients' purchases are also reported. [ABSTRACT FROM PUBLISHER]

In a University Hospital of Southern India, 255 men and 91 women with diabetes died during a 18-month period. Their age at onset (diagnosis) of diabetes, known duration of diabetes, age at death and major morbidity at death were studied. Life tables (1998-2002) of reference populations (rural and urban, men and women) in Andhra Pradesh state were used to calculate reduction in life expectancy at age at onset (ie. life expectancy at age at diagnosis-known duration of diabetes) in both genders with diabetes. Diabetes was diagnosed at about same age (mean±SD) in men (52.2±12.8 yrs) and women (51.24±13.4 yrs, ns). Known duration of diabetes was 5.6±7.5 yrs in men, while women had diabetes for longer period (6.9±7.7 yrs, ns). Age at death (men 57.8±12.3, women 58.1±13.4 yrs, ns) and reduction in life expectancy (men 18.3±9.4, women 19.0±11.7 yrs, ns) were similar in both genders. In men who died below 30, between 30-44, 45-59 and above 60 years age, reduction in life expectancy was 29.0±25.7, 14.8±14.9, 12.0±11.0 and 9.7±4.3 yrs, respectively. In women, corresponding values were 31.4±26.0, 12.3±14.2, 8.33±12.7 and 8.47±5.0 yrs, respectively. Reduction in life expectancy in diabetes (men vs. women) as associated with following major complications at death was, coronary heart disease (16.2±7.0 vs. 14.5±8.7 yrs, ns), cerebrovascular disease (17.6±10.1 vs. 16.0±8.1 yrs, ns), nephropathy (16.9±7.5 vs. 19.5±12.9 yrs, ns), congestive heart failure (16.1±7.7 vs.18.9±13.2 yrs, ns), hepatic disease (19.8±9.9 vs. 20.1 ± 9.96, ns), metabolic disorder (19.2±11.0 vs. 24.0±14.6, ns), malignancy (17.0±7.8 vs. 17.9±9.5, ns) and others (18.4±9.4 and 18.54±10.8 yrs, ns). Reduction in life expectancy in men and women in above categories of age and its association with major complications at the time of death was not different between men and women. However, women with diabetes and infections died earlier (54.6±10.6 yrs) than men (59.3±11.54 yrs, p<0.05). Reduction in life expectancy in these women was 22.0±9.31 as compared to 17.4±8.4 yrs in men (p<0.01). This study highlighted that both men and women with diabetes died about two decades earlier compared to reference populations. The gender differences reported here warranted early identification of diabetic women at high risk for developing infections and their aggressive management. [ABSTRACT FROM AUTHOR]

During a 18-month period, 255 men and 91 women with diabetes and 601 men and 275 women without diabetes died in a University Hospital of Hyderabad in Southern India. Their age at onset (diagnosis) of diabetes, known duration of diabetes, age at death, data on major vascular and non vascular complications at death (in addition to causes of death), hospital stay and hospitalization costs were studied. Life tables (1998-2002) of reference populations (rural and urban, men and women) in Andhra Pradesh state were used to calculate reduction in life expectancy. Vascular complications (% in diabetics vs. non diabetics) in men (M) and women (F) at death, coronary artery disease (M 13.3 vs. 6.4, F 11.3 vs.5.0) and nephropathy (M 11.9 vs.8.9, F 13.3 vs.8.6) were significantly more (chi-square p<0.001) in diabetics, while cerebrovascular disease events (M 8.5 vs.8.1, F 9.2 vs.8.5) were not different. Among non vascular complications (%), congestive heart failure (M 5.9 vs.4.4, F 5.0 vs.3.8) and metabolic disorder (M 4.4 vs.2.2, F 6.3 vs.2.5) were more common in diabetics, while non diabetics were more susceptible to develop hepatic disease (M 2.1 vs.4.1, F 1.3 vs.2.8), infection (M 13.6 vs. 15.0, F 12.1 vs. l5.3), malignancy (M 3.7 vs.5.9, F 4.2 vs.8.5) or others (M 36.7 vs.45.0, F 37.5 vs.45.0). Within diabetics, mean (±SD) age at diagnosis (M 52.2±1.2.8, F 51.2±13.4 yrs), age at death (M 57.8±12.3, F 58.1±13.4 yrs), reduction in life expectancy (M 18.3±9.4, F 19.0±11.7 yrs), hospital stay (M 7.3±8.1, F 7.4±8.5 days) and hospitalization costs (mean Indian Rs. M 30, 595, F 26,632, I Rs.46∼US$) were not significantly different between genders and in those with different vascular or non vascular complications. These findings were in contrast to an earlier study report from this center in 1994, which recorded higher mortality in women with diabetes due to vascular disease. Present study demonstrated that women had improved access to health care as diabetes was diagnosed at about same age in both genders and received better medical attention as evidenced by similar hospital stay period and hospital costs. This mortality data analysis heightened our attention to early diagnosis and delaying progression of coronary and renal disease in diabetes. [ABSTRACT FROM AUTHOR]

Interest in botanicals, particularly as dietary supplement ingredients, is growing steadily. This growth, and the marketing of new ingredients and combination products as botanical dietary supplements, underscores the public health need for a better understanding of potential toxicities associated with use of these products. This article and accompanying template outline the resources to collect literature and relevant information to support the design of botanical toxicity studies. These resources provide critical information related to botanical identification, characterization, pre-clinical and clinical data, including adverse effects and interactions with pharmaceuticals. Toxicologists using these resources should collaborate with pharmacognosists and/or analytical chemists to enhance knowledge of the botanical material being tested. Overall, this guide and resource list is meant to help locate relevant information that can be leveraged to inform on decisions related to toxicity testing of botanicals, including the design of higher quality toxicological studies., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Polybrominated diphenyl ethers (PBDEs) were used as flame retardants and from their end-use products they can be released to accumulate within indoor environments. This may result in exposures to pregnant women with potential adverse effects on the developing fetus. While studies have shown associations between prenatal PBDE exposure and poor birth outcomes, research has mainly focused on birth weight and gestational age and may miss important indicators of newborn size., Methods: The sample included a cohort of Dominican and African American mother-child pairs from New York City recruited from 1998 to 2006. PBDE congeners (BDE-47, BDE-99, BDE-100, and BDE-153) were measured in cord serum at birth and dichotomized into low (<80th percentile) and high (>80th percentile) categories. Weight, length, head circumference, and gestational age were measured at birth and the ponderal index (birth weight/length x 100), size for gestational age, and population-based z-scores were calculated (n = 305). Separate regression analyses were conducted to estimate associations between PBDEs or PBDE sum (ng/g lipid) and birth outcomes. Quantile g-computation was performed to estimate the effect of total PBDE mixture. We also assessed effect modification by sex and ethnicity., Results: Adjusting for relevant covariates, the high exposure category of BDE-153 was associated with lower birth weight z-score (-0.25, 95% CI: -0.5, 0.0) and longer gestation (0.43 weeks, 95% CI: 0.07, 0.79). The high exposure category of BDE-99 was associated with lower birth length z-score (-0.55, 95% CI: -0.98, -0.12). There was a negative association between the overall PBDE mixture and birth length z-score (-0.10, 95% CI: -0.21, 0.00) per 1 quintile increase in PBDEs. There was no effect modification by sex or ethnicity., Conclusions: These results suggest that prenatal exposures to BDE-153, BDE-99, and total PBDE mixture are associated with birth outcomes in a cohort of Dominican and African American newborns., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Peroxisome proliferator-activated receptor γ (PPARγ) is a ligand-activated transcription factor that regulates lipid/glucose homeostasis and adipocyte differentiation. While the role of PPARγ in adipogenesis and diabetes has been extensively studied, little is known about PPARγ function during early embryonic development. Within zebrafish, maternally-loaded pparγ transcripts are present within the first 6 h post-fertilization (hpf), and de novo transcription of zygotic pparγ commences at ~48 hpf. Since maternal pparγ transcripts are elevated during a critical window of cell fate specification, the objective of this study was to test the hypothesis that PPARγ regulates gastrulation and dorsoventral patterning during zebrafish embryogenesis. To accomplish this objective, we relied on (1) ciglitazone as a potent PPARγ agonist and (2) a splice-blocking, pparγ-specific morpholino to knockdown pparγ. We found that initiation of ciglitazone-a potent human PPARγ agonist-exposure by 4 hpf resulted in concentration-dependent effects on dorsoventral patterning in the absence of epiboly defects during gastrulation, leading to ventralized embryos by 24 hpf. Interestingly, ciglitazone-induced ventralization was reversed by co-exposure with dorsomorphin, a bone morphogenetic protein signaling inhibitor that induces strong dorsalization within zebrafish embryos. Moreover, mRNA-sequencing revealed that lipid- and cholesterol-related processes were affected by exposure to ciglitazone. However, pparγ knockdown did not block ciglitazone-induced ventralization, suggesting that PPARγ is not required for dorsoventral patterning nor involved in ciglitazone-induced toxicity within zebrafish embryos. Our findings point to a novel, PPARγ-independent mechanism of action and phenotype following ciglitazone exposure during early embryonic development., Competing Interests: The authors declare that they have no competing interests., (© 2019 Cheng et al.)

Triphenyl phosphate (TPHP) is a commonly used organophosphate flame retardant and plasticizer in the United States. Using zebrafish as a model, the overall objective of this study was to identify potential organs that might be targeted by TPHP during embryonic development. Based on mRNA-sequencing, TPHP exposure from 24 to 30 h post fertilization (hpf) and 24 to 48 hpf significantly affected the abundance of 305 and 274 transcripts, respectively, relative to vehicle (0.1% DMSO) controls. In addition to minor effects on cardiotoxicity- and nephrotoxicity-related pathways, ingenuity pathway analysis (IPA) of significantly affected transcripts within 30- and 48-hpf embryos revealed that hepatotoxicity-related pathways were strongly affected following exposure to TPHP-alone. Moreover, although pretreatment with fenretinide (a retinoic acid receptor agonist) mitigated TPHP-induced pericardial edema and liver enlargement at 72 and 128 hpf, respectively, IPA revealed that fenretinide was unable to block TPHP-induced effects on cardiotoxicity-, nephrotoxicity-, and hepatotoxicity-related pathways at 48 hpf, suggesting that TPHP-induced effects on the transcriptome were not associated with toxicity later in development. In addition, based on Oil Red O staining, we found that exposure to TPHP nearly abolished neutral lipids from the embryonic head and trunk and, based on metabolomics, significantly decreased the total abundance of metabolites-including betaine, a known osmoprotectant-at 48 and 72 hpf. Overall, our data suggest that, in addition to the heart, TPHP exposure during early development results in adverse effects on the liver, lipid utilization, and osmoregulation within embryonic zebrafish., (© The Author(s) 2019. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Diphenyl phosphate (DPHP) is an aryl phosphate ester (APE) used as an industrial catalyst and chemical additive and is the primary metabolite of flame retardant APEs, including triphenyl phosphate (TPHP). Minimal DPHP-specific toxicity studies have been published despite ubiquitous exposure within human populations following metabolism of TPHP and other APEs. Therefore, the objective of this study was to determine the potential for DPHP-induced toxicity during embryonic development. Using zebrafish as a model, we found that DPHP significantly increased the distance between the sinus venosus and bulbus arteriosis (SV-BA) at 72 h postfertilization (hpf) following initiation of exposure before and after cardiac looping. Interestingly, pretreatment with d-mannitol mitigated DPHP-induced effects on SV-BA length despite the absence of DPHP effects on pericardial area, suggesting that DPHP-induced cardiac defects are independent of pericardial edema formation. Using mRNA-sequencing, we found that DPHP disrupts pathways related to mitochondrial function and heme biosynthesis; indeed, DPHP significantly decreased hemoglobin levels in situ at 72 hpf following exposure from 24 to 72 hpf. Overall, our findings suggest that, similar to TPHP, DPHP impacts cardiac development, albeit the potency of DPHP is significantly less than TPHP within developing zebrafish.