1. Type 1 diabetes (due to b-cell destruction, usually leading to absolute insulin deficiency) 2. Type 2 diabetes (due to a progressive insulin secretory defect on the background of insulin resistance) 3. Gestational diabetes mellitus (GDM) (diabetes diagnosed in the second or third trimester of pregnancy that is not clearly overt diabetes) 4. Specific types of diabetes due to other causes, e.g., monogenic diabetes syndromes (such as neonatal diabetes and maturity-onset diabetes of the young [MODY]), diseases of the exocrine pancreas (such as cystic fibrosis), and drugor chemical-induced diabetes (such as in the treatment of HIV/AIDS or after organ transplantation)

Classification and diagnosis of diabetes

In 1962, Caraway I highlighted the potential for therapeutic drugs and endogenous compounds to modify the concentrations of various analytes in body fluids. A few years later, others, including Elking and Kabat! and Sunderman;' amplified Caraway's earlier report. These early papers prompted many clinical chemists to begin to question their test results, something that clinicians often did when the results did not appear to fit the clinical picture of their patients. At the time these papers were written there was legitimate concern about the analytical specificity of many laboratory methods, and clinicians did not have confidence in the test results. The clinician's view was that any test result that did not conform to his or her clinical impression was erroneous. My personal interest in the effects of drugs on clinical laboratory tests was triggered by physicians criticizing certain test results that my laboratory produced. They felt that the results were not in keeping with their clinical impressions. They concluded the test results were wrong. Yet I knew that quality assurance data were within acceptable limits. Obtaining drug histories often identified likely causes of abnormal results. Sometimes, the clinicians were not aware of all the in vivo effects of the drugs they were using. It was possible to show that the abnormal test result was related to a side-effect. Sometimes we were able to demonstrate an interference of a drug with an analytical method. It seemed worth capturing the effort put into tracking the causes of spurious results so that other laboratory staff might find it easier to explain unanticipated test results. The information I accumulated was first published in a regular issue of Clinical Chemistry.' updated in a special issue of the journal, and then, periodically, in books published by the American Association for Clinical Chemistry (AACC), the most recent in 1995.5 The amount of information related to the effect of drugs on clinical laboratory tests is growing. One continuing concern is the point at which data should be considered obsolete and not reported. Generally, data on analytical interferences of drugs have been deleted from the master file when references are more than 15 years old. However, for procedures that continue to be widely used, e.g. urine dipsticks, the reported effects have been republished. In the early editions of the publication there was considerable emphasis on the effects of drugs on the analytical methods. In the later editions there has been less emphasis on analytical interferences as analytical specificity has improved. In all the editions I have adopted the philosophy that it is as important to document that a drug has been demonstrated not to have an effect on a particular method as it is to describe the effects that it does have. The clinician is often faced with an unexpected abnormal result. He or she needs to know all the possible causes. Invariably, clinicians are unaware of the analytical methods used to measure the analytes that they require to be measured. They are also often unaware of some of the side-effects of drugs that they use relatively infrequently. Thus, to provide all the information that clinicians and laboratory staff need to properly interpret the test results, the database of the effects of drugs must be fully comprehensive. A repeatedly asked question is whether the availability of databases of effects of drugs on clinical laboratory tests can influence medical practice. Most users of the database can provide anecdotal accounts of instances when it was able to provide an explanation for unexpected abnormal results. Shortly after the publication of the second compilation of the database.P we embarked on a study at the University of Wisconsin Hospitals? to determine whether automatic reporting to physicians of potential drug-induced causes of abnormal test results could modify medical practice. More than 13 000 patient-days in patients in general surgical, minimal or moderate medical care, or intensive care units, were followed.

Effects of drugs on clinical laboratory tests

Psychomotor abnormalities have been abundantly observed in psychiatric disorders like major depressive disorder (MDD), bipolar disorder (BD), and schizophrenia (SCH) Although early psychopathological descriptions highlighted the truly psychomotor nature of these abnormalities, more recent investigations conceive them rather in purely motor terms This has led to an emphasis of dopamine-based abnormalities in subcortical–cortical circuits including substantia nigra, basal ganglia, thalamus, and motor cortex Following recent findings in MDD, BD, and SCH, we suggest a concept of psychomotor symptoms in the literal sense of the term by highlighting three specifically psychomotor (rather than motor) mechanisms including their biochemical modulation These include: (i) modulation of dopamine- and substantia nigra-based subcortical–cortical motor circuit by primarily non-motor subcortical raphe nucleus and serotonin via basal ganglia and thalamus (as well as by other neurotransmitters like glutamate and GABA); (ii) modulation of motor cortex and motor network by non-motor cortical networks like default-mode network and sensory networks; (iii) global activity in cortex may also shape regional distribution of neural activity in motor cortex We demonstrate that these three psychomotor mechanisms and their underlying biochemical modulation are operative in both healthy subjects as well as in MDD, BD, and SCH subjects; the only difference consists in the fact that these mechanisms are abnormally balanced and thus manifest in extreme values in psychiatric disorders We conclude that psychomotor mechanisms operate in a dimensional and cross-nosological way as their degrees of expression are related to levels of psychomotor activity (across different disorders) rather than to the diagnostic categories themselves Psychomotor mechanisms and their biochemical modulation can be considered paradigmatic examples of a dimensional approach as suggested in RDoC and the recently introduced spatiotemporal psychopathology

All roads lead to the motor cortex: psychomotor mechanisms and their biochemical modulation in psychiatric disorders

Sedentary lifestyle and consumption of high-calorie foods have caused a relentless increase of overweight and obesity prevalence at all ages. Its presently epidemic proportion is disquieting due to the tight relationship of obesity with metabolic syndrome and several other comorbidities which do call for urgent workarounds. The usual ineffectiveness of present therapies and failure of prevention campaigns triggered overtime a number of research studies which have unveiled some relevant aspects of obesity genetic and epigenetic inheritable profiles. These findings are revealing extremely precious mainly to serve as a likely extra arrow to allow the clinician’s bow to achieve still hitherto unmet preventive goals. Evidence now exists that maternal obesity/overnutrition during pregnancy and lactation convincingly appears associated with several disorders in the offspring independently of the transmission of a purely genetic predisposition. Even the pre-conception direct exposure of either father or mother gametes to environmental factors can reprogram the epigenetic architecture of cells. Such phenomena lie behind the transfer of the obesity susceptibility to future generations through a mechanism of epigenetic inheritance. Moreover, a growing number of studies suggests that several environmental factors such as maternal malnutrition, hypoxia, and exposure to excess hormones and endocrine disruptors during pregnancy and the early postnatal period may play critical roles in programming childhood adipose tissue and obesity. A deeper understanding of how inherited genetics and epigenetics may generate an obesogenic environment at pediatric age might strengthen our knowledge about pathogenetic mechanisms and improve the clinical management of patients. Therefore, in this narrative review, we attempt to provide a general overview of the contribution of heritable genetic and epigenetic patterns to the obesity susceptibility in children, placing a particular emphasis on the mother-child dyad.

/pdf/genetics-epigenetics-and-transgenerational-transmission-of-27zij7e9.pdf

Genetics, epigenetics and transgenerational transmission of obesity in children

Bronchial asthma is a complex heterogeneous airway disease, which has emerged as a global health issue. A comprehensive understanding of the different molecular mechanisms of bronchial asthma may be an efficient means to improve its clinical efficacy in the future. Increasing research evidence indicates that some types of programmed cell death (PCD), including apoptosis, autophagy, pyroptosis, ferroptosis, and necroptosis, contributed to asthma pathogenesis, and may become new targets for future asthma treatment. This review briefly discusses the molecular mechanism and signaling pathway of these forms of PCD focuses on summarizing their roles in the pathogenesis and treatment strategies of asthma and offers some efficient means to improve clinical efficacy of therapeutics for asthma in the near future. 

/pdf/programmed-cell-death-in-asthma-apoptosis-autophagy-n4q4e12f.pdf

Programmed Cell Death in Asthma: Apoptosis, Autophagy, Pyroptosis, Ferroptosis, and Necroptosis

Bronchial asthma is a common chronic respiratory disease in children with complex pathogenesis, characterized by airway hyper‐responsiveness, obstruction, mucus hyperproduction, and airway remodeling. Autophagy is important for cellular physiology, and the ATG5 rs510432 has recently been implicated in several fundamental characteristics of childhood asthma pathogenesis and may play a role in the disease progression. This study aims to assess the expression of ATG5 messenger RNA (mRNA) according to rs510432 polymorphism in asthmatic children and to evaluate their possible relation with the development of the disease.

Autophagy‐related 5 gene mRNA expression and ATG5 rs510432 polymorphism in children with bronchial asthma

Background Recent emerging evidence supports the role of miR-196a2 in various human diseases. However, its role in type 1 diabetes mellitus (T1DM) is still underestimated. We aimed, for the first time, to investigate the expression of miR-196a2 in T1DM and the association of miR-196a2 (rs11614913) polymorphism with susceptibility of T1DM in a sample of patients from Cairo, Egypt. Methods The study included 150 patients and 150 healthy subjects. Evaluation of rs11614913 genotypes and miR-196a2 expression was done using the allelic discrimination and quantitative reverse transcriptase polymerase chain reaction (PCR) method, respectively. Results The Hardy-Weinberg equilibrium of single nucleotide polymorphism(SNP) was detected among controls (p = 0.2). Our results revealed that the TT genotype was more frequent in patients (22.6%) than controls (10%) while the CC genotype was more frequent in controls (47.3%) than patients (39.3%) (p = 0.01). The frequency of the T allele was significantly higher in patients than in controls (41.7 vs. 31.3%), while the C allele was more frequent in controls (p = 0.008). After adjustment for traditional risk factors, the association of the TT genotype with T1DM remained significant (TT vs. CC, odds ration [OR] = 3.2, 95% confidence interval [CI]: 1.4-7.4, p = 0.005). Power analysis of the data yielded a statistical power of 80% for the miR-196a2 rs11614913 with T1DM. Relative expression of miR-196a2 showed significant decrease in patients compared to controls (median = 0.09, 0.5, interquartile range [IQR] = 0.03-1.6, 0.1-2.1). However, miR-196a2 expression showed no significant difference between different rs11614913 genotypes (p = 0.5). Conclusions Our findings demonstrated that miR-196a rs11614913 is associated with T1DM and decreased expression of miR-196a2 may play a role in pathogenesis of T1DM.

Micro-RNA 196a2 expression and miR-196a2 (rs11614913) polymorphism in T1DM: a pilot study.

Screening of the most common MEFV mutations in a large cohort of Egyptian patients with Familial Mediterranean fever

VDR gene expression in asthmatic children patients in relation to vitamin D status and supplementation

Patterns of microRNAs 142-3p, 106a, 17 and 20a expression in patients with systemic lupus erythematosus

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