Psoriasis is a chronic inflammatory skin disease with a complex mechanism, which is believed to be mainly based on immune disorders and activation of inflammatory pathways. However, we have combed through the literature and found that the pathogenesis of psoriasis might involve a “mobius loop” of “immunity-inflammation-oxidative stress-proliferation” process. The disordered immune environment of the skin might act as the basis, the outbreak of inflammatory factors as the mediator, and the imbalance of oxidative stress homeostasis as the activator. These factors work together, leading to abnormal proliferation of keratinocytes and further immune abnormalities, finally aggravating psoriasis. Therefore, here we review the latest evidence and advance in the pathogenesis of psoriasis, trying to contribute to further understanding and treatment of psoriasis.

Pseudofungus structures in lymph node tissues have been reported on multiple occasions. Despite a variety of investigative tests including histochemical special stains and energy dispersive spectral analysis, the underlying nature and origin of these pseudofungus structures has never been clearly defined. The most common hypothesis suggests that they represent collagen fibers that become coated with iron and calcium. Herein, evidence is given that the pseudofungus structures identified in the lymph node tissues represent fragments of polyurethane catheters. The evidence includes both a comparison of these pseudofungus structures to fragments of polyurethane well documented in the literature and a comparison of polyurethane catheter scrapings to the pseudofungus structures identified in the literature. In both of these comparisons, the morphology of the polyurethane fragments are identical to the pseudofungus structures. This is the first definitive report identifying polyurethane catheter fragments as representing the true nature and etiology of pseudofungus structures in lymph node tissues.

A 69-year-old man presented with a one-month history of a painful mass in the right breast. Pathologic evaluation of the excision of the mass revealed a proliferation of both glandular and stromal elements consistent with gynecomastia. In addition, histologic examination revealed peripheral nerves in the deep portion of the specimen were entrapped in the proliferative changes associated with gynecomastia. It is proposed that the expansile proliferation led to compressive pressure on the nerves and caused the pain associated with gynecomastia.

A case of post-operative agranulocytosis which occurred in a 66-year-old woman following surgery for endometrial carcinoma is reported. The agranulocytosis had a rapid onset, being detected on the first post-operative day. The causative agent, cefazolin was given to the patient intraoperatively. The agranulocytosis persisted until the 22nd postoperative day. A bone marrow biopsy performed on post-operative day four showed a left-shifted myeloid maturation pattern but not a maturation arrest. The pathogenesis of drug-induced neutropenia/agranulocytosis is discussed. It is postulated that reversible binding of cefazolin to albumin accounts for the prolonged duration of agranulocytosis.

In pregnancy, the incidence of pulmonary embolism (PE) is increased fivefold when compared to nonpregnant women of the same age, and PE is one of the leading causes of death during pregnancy.However, the diagnosis of PE among pregnant women is complicated by concerns regarding radiation exposure. Systemic lupus erythematosus (SLE) is an autoimmune disorder with a wide array of presentations and a predilection to affect women of certain ethnic backgrounds. The hallmark of the disease is multisystem involvement, dispersed in time and severity. Usual pulmonary involvement includes pleuritis, pleural effusions, pneumonitis, shrinking lung syndrome, pulmonary hypertension, and alveolar hemorrhage. Pulmonary embolism (PE) is a relatively unusual presentation of SLE. We report the case of a 20-year-old primi at 21 weeks gestation with an acute PE with central chest pain and shortness of breath. The absence of overt signs and symptoms and traditional risk factors prompted a fragmentary workup. This led to the detection of antibodies sensitive for SLE, in the absence of overt signs and symptoms. We revive the concept of latent lupus, a condition construed as early lupus. We firmly suspect direct causation between SLE and PE. Further studies are needed to establish pathogenesis to facilitate early diagnosis and prevent morbidity and mortality from PE. Due to persistent hypotension, thrombolytic therapy with streptokinase was administered and the clinical and hemodynamic response was excellent, with no maternal or fetal hemorrhagic complications. The clinical presentation of pulmonary embolism is sometimes camouflaged by the physiological changes that occur in pregnancy and diagnosis is often delayed by a reluctance to expose the fetus to ionizing radiation. 

Introduction: The world is currently facing the SARS-CoV-2 pandemic with evolving 2nd wave. The COVID-19 patients present most commonly with Severe Acute Respiratory Illness (SARI) in an emergency room with acute onset fever, cough, and breathlessness. However, not all SARI cases as per definition are due to COVID-19 infection, which is well proven in this case series of 113 cases of SARI. This is just the opposite of the other SARI series done in the pre-COVID-19 era. Also, no previous SARI case series data has shown significant association with Diabetes Mellitus, including new-onset diabetes thus figuring out the major Pathophysiological association of COVID-19 with glucose metabolism and has a bearing on the pathogenesis, treatment, and outcome of COVID-19 infection and perpetuity of pandemic of this magnitude. Here we raise concern for the first time about the growing association of an infectious pandemic with the lifestyle disorders which are non-communicable diseases but carry with them the potential of fertile soil for rapidly spreading epidemics.Aim and objective: To find out the etiology, clinical profile, treatment outcome, and mortality rate in different sub-groups of SARI cases in a tertiary care hospital and the incidence of new-onset Diabetes Mellitus in them and to investigate theoretically the hypothesis that maintaining normal glucose metabolism could prevent progression of a mild Flu-like illness (FLI) to a severe form of Severe Acute Respiratory Illness (SARI) and consequent complications such as Cytokine Storm Syndrome and Multi-Organ failure.Design: Retrospective, single-center case series of 113 SARI patients at a tertiary care hospital in Agra India between 1 March- 30 October 2020.Main outcome: The demographics, clinical, pathological, imaging, and treatment outcome data were collected. The SARI cases analyzed were defined as “Severe acute respiratory infections (SARIs) an acute respiratory illness of recent onset (within seven days) manifested by fever (≥38°C), cough and shortness of breath or difficulty in breathing requiring hospitalization and were sub-classified according to the primary etiology producing SARI in them. The findings were compiled and compared. Conclusion: Of the 113 patients of SARI – 32.7 %were associated with Diabetes, with 9.74% new-onset Diabetes and 26 % previously known Diabetes. This was mainly due to SARS-CoV-2 (24 Diabetics out of 52 COVID-19 cases- 46.1 %).The Average hospitalization stay of SARI cases was 10 days with a maximum in SARS-CoV-2 and a minimum stay of 5.22 days in Bacterial Pneumonia and 5.66 days in Koch’s Lungs.The death rate was maximum (4 out of 26) 15.3%. Hospitalized TB/Koch’s Lung patients who presented as SARI and 3.8% in Bacterial Pneumonia, 2.43% in SARS-CoV-2, and <1% in Sepsis.Those SARI cases who were euglycemic at the time of initial presentation recovered early and carried a good prognosis with less mortality as compared to those who were hyperglycemic on presentation. Also, those FLI cases who maintained euglycemia or did not have any other risk factor which predisposes them to stress (Diabetes, Prolonged fasting, Obesity, major organ disorder, Psychological disorder, and Cancer) did not progress to SARI as the endogenous steroid secretion and sympathetic activation did not occur, the intracellular pH levels remained in the alkaline range.10.18% of cases developed new-onset diabetes (a total of 11 cases) out of which 10 were in COVID-19. Thus 19.2% incidence of new-onset diabetes in SARS-CoV-2 and a prevalence of 26.9% in SARS-CoV-2, making total diabetes 46.1% in SARS-CoV-2, and out of all SARI cases, 26 % of patients developed pulmonary fibrosis with consequent long-term complications. In COVID-19 patients, it was seen only in diabetics SARS CoV-2 male patients, thus no death in non-diabetic females in COVID-19 in this case series.

The flat foot can be defined as a syndrome with multiple etiopathogenesis, characterized by an altered structure of the longitudinal arch of the plantar vault with its reduction in height. The plantar arch collapse can be counteracted by strengthening the muscles involved; for many years, specific physical exercises have been proposed for this purpose in physical and rehabilitation medicine. Our work aimed to improve the plantar arch muscles’ tone using high focal vibration therapy (300 Hz). Methods: 49 children with a 3rd degree flat foot (age: 8,7,6) underwent 10 sessions, 2 days/wk, of 30 min of focused high vibratory therapy at a frequency of 300 Hz (Vissman, Italy). Before and after treatment stabilometry (StT), static and dynamic baropodometry tests were performed. Results: Evaluation of StT showed an improvement in stability and a decrease in the sway area and ellipse area. Baropodometry tests showed a decrease in foot surface. Also, dynamic tests showed a decrease in both foot surfaces. Discussion: The results lead us to consider this method as a method of the first choice for a conservative approach in the rehabilitation of flat foot syndrome and also for 3rd grade children [1,2].

The COVID-19 pandemic appeared in late 2019 and became a major health concern with rapid transmission and very high mortality rates across the globe. Although precautionary, preventive, protective and therapeutic measures have been adopted against COVID-19, still the disease has drastically affected people. In order to overcome the challenges of the pandemic, the understanding of the route of transmission, its fusion with receptors and invasion into the human body and hacking the immune system, the viral genome was sequenced. The viral genome keeps on mutating and altering its original form into its subtypes. Moreover, age and comorbid conditions had their impact on developing the disease differing from individual to individual due to interaction varying between the host genome and virus. Considering the pathogenesis of the virus, neutralizing antibodies reduced the viral impact and severity. This review is focused on highlighting the COVID-19 genome, host genetic factors, the pathogenesis of the disease and available therapeutic measures to overcome the pandemic.

The pathogenesis of an ovarian disease is connected with PTN and its receptor protein tyrosine phosphatase receptor Z1 (PTPRZ1). Paclitaxel is the first-line drug for the therapy of ovarian cancer. With the increment of paclitaxel chemotherapy, paclitaxel obstruction happens in the late phase of therapy frequently. By treating A2780 and SKOV-3 cells with PTN, we found the development of the two cell lines was enhanced. Different concentrations of PTN were added to A2780 and SKOV-3 cells treated with paclitaxel and the results of MTT showed that the inhibitory effect of paclitaxel on these two cell lines was weakened. The results of apoptosis assays showed that PTN could slow down the rate of apoptosis and its concentration dependence in both cell lines. To further investigate the impact of PTN on the paclitaxel responsiveness of ovarian malignant growth cells, A2780 and SKOV-3 cells were transfected with sh-PTN-1, sh-PTN-2 and sh-NC plasmids. The results of PCR and Western Blot showed that both RNA-interfering plasmids could inhibit PTN in A2780 and SKOV-3 cells. The results of MTT showed that the inhibitory effect of paclitaxel on cells transfected with sh-PTN-1 expanded compared with the benchmark group. Apoptosis assays showed that the complete apoptosis pace of A2780 and SKOV-3 cells with sh-PTN-1 plasmid induced by paclitaxel was accelerated obviously compared with the benchmark group. To summarize, the results suggested that PTN could enhance the resistance to paclitaxel in ovarian cancer cells, which provides a groundwork for studying on drug resistance of cancer cells to paclitaxel and a new perspective for ovarian cancer therapy.

Recent clinical, experimental and epidemiological studies report that ALS is thought possibly due to a multi-stage process, arising from a combination of genetic susceptibility and environmental factors, which alone or superimposed, perhaps on genetic polymorphism yet to be identified, may contribute to the incidence rate of sporadic ALS. In particular, a large amount of evidence suggests that mercury is toxic to motor neurons and may be a risk factor for ALS, playing a part in its pathogenesis. In fact, there have been case reports of ALS or ALS-like symptoms associated with mercury exposure, thus raising the possibility that mercury could be one of the non-genetic factors of the multistep process that is thought to underlie ALS. In order to give recent elucidations on the putative relationship between mercury exposure and ALS, we reviewed all the papers reported in the literature and published on Pubmed from 2006 to 2022. Despite a number of pathogenetic mechanisms that have been linked to mercury, evidence linking exposure to mercury to ALS is not consistent and discordant and, based on the evaluation of the articles, which emerged from our analysis that to date no convincing correlation between mercury and ALS has been established and no conclusive evidence has been enlightened suggesting increased mercury exposure is associated with ALS.

Introduction: Minimal change disease (MCD) is a common subtype of primary nephrotic syndrome in adults. The pathogenesis of MCD is still not well understood, but some studies suggest that MCD is a T cell-mediated disease related to podocyte dysfunction. Previous research has also indicated the crucial role of B cells in the pathogenesis of MCD. Rituximab (RTX) is a recombinant chimeric mouse/human antibody targeting CD20 antigen. In recent years, RTX has been increasingly used in adult MCD patients.Methodology: We searched the PubMed database using the keywords “Minimal change disease”, “Nephrotic syndrome”, and “Rituximab” and obtained a total of 140 articles. We will now provide a literature review based on these 140 articles, according to our research topic.Discussion: This article provides an overview of the mechanisms and clinical research progress of RTX in the treatment of adult MCD. We have also discussed the current treatment methods for MCD, exploring the potential of using RTX as a first-line therapy for refractory adult MCD.Conclusion: MCD is a common pathological type of nephrotic syndrome, and the exact mechanisms are still not fully understood. Although RTX as a treatment of adult MCD has shown promising clinical results in patients with refractory adult MCD, the safety and efficacy of RTX still lack high-quality clinical evidence. Further research is needed to explore the pathogenesis of MCD and the RTX treatment for MCD.

Background: Asthma, a chronic inflammatory respiratory ailment, is characterized by variable airflow obstruction and heightened bronchial reactivity. Despite therapeutic advancements, a comprehensive comprehension of its underlying metabolic mechanisms remains elusive. Metabolomics has emerged as a powerful approach to investigating the complex connections between serum metabolites and disease pathogenesis. However, exploring the causal relationship between serum metabolites and asthma susceptibility demands meticulous examination to unveil potential therapeutic targets.Methods: Mendelian randomization (MR) approach was explored to investigate the potential causal associations between serum metabolites and asthma risk. The main analysis employed the inverse variance weighted method, supported by supplementary approaches such as MR-Egger, weighted median, weighted mode, and sample mode. To enhance the strength and credibility of our results, we conducted sensitivity analyses encompassing heterogeneity testing, assessment of horizontal pleiotropy, and leave-one-out analysis. Additionally, pathway enrichment analysis was performed to further elucidate the results.Results: We identified 18 known and 12 unknown metabolites with potential associations with asthma risk. Among known metabolites, seven exhibited protective effects (e.g., 4-acetamidobutanoate, allantoin, kynurenine, oxidized bilirubin*), while eleven were considered risk factors (e.g., ornithine, N-acetylornithine, alanine). Through the integration of four additional MR models and sensitivity analyses, we revealed a connection between 4-acetamidobutanoate and approximately 6% lower asthma risk (OR = 0.94, 95% CI: 0.90–0.98).Conclusions: Our MR analysis uncovered protective and risk-associated metabolites, alongside 12 unknown metabolites linked to asthma. Notably, 4-acetamidobutanoate demonstrated a nominal 6% reduction in asthma risk, highlighting its potential significance.

Endometrial Stromal Sarcoma (ESS) is a rare gynecological malignancy originating from endometrial stromal tissue. Representing only a tenth of uterine malignant tumors, ESS is categorized into Low-Grade (LGESS) and High-Grade (HGESS) based on nuclear division. Interestingly, prognostic studies have found no strong correlation between ESS prognosis and nuclear division activity. Undifferentiated Uterine Sarcoma (UUS) represents a spectrum of tumors with varied morphological, clinical, and prognostic features, and lacks a standardized naming convention. In 2014, the World Health Organization grouped ESS into LGESS, HGESS, and UUS based on clinical and pathological attributes. HGESS, despite its rarity, is notorious for its poor prognosis and low survival rate. Its early detection is complicated due to its asymptomatic presentation and ambiguous pathogenesis, leading to debates over treatment approaches. This article delves into the recent research developments concerning HGESS.

Modern medicine has achieved phenomenal success in many areas, turning into a visual and tangible reality the embodiment of some phenomena that in previous years could only be read in works of science fiction.

With the increase in incidence and prevalence of myeloid neoplasms in India, it has become a necessity to understand its molecular mechanisms, acquisition of genomic alterations, and understand its primary and secondary resistance pathways which ultimately impact the decision of therapeutics. The objective of this review is to investigate the molecular aspects of this disease type and identify the biomarkers that help with diagnosis, risk assessment, prognosis, and selecting the best line of treatment for a specific myeloid neoplasm. Advancements and innovations in molecular technologies from simplest Real-Time PCR to high throughput next-generation sequencing have played a vital role in screening the most common mutations and fusions to the novel and rare. Molecular technologies have helped to enumerate the genomic landscape of myeloid malignancies. The understanding of both- the mechanisms and the technology is a strong combination as it has helped revolutionize precision oncology and helped in giving better therapeutic choices with better clinical outcomes. The importance of cellular morphology, clinical symptoms, and molecular pathology in assessing the risk of myeloid malignancies is emphasized and summarized in the review. The review concludes that understanding molecular pathogenesis can be improved by using clinical-pathological-molecular strategies for diagnosis and therapy decision-making.

The article presents materials that make it possible to understand the reason for the absence of one of the classic signs of inflammatory processes in patients with acute pneumonia. The peculiarities of the functional significance of the lungs for the body are the reason that in the case of inflammation in the tissues of the organ, nature has provided for the presence of a more important adaptive mechanism instead of pain as a signal sign. Understanding the causes of the absence of pain in pneumonia in the initial period, which is most responsible for timely and effective care for these patients, allows us to look at the pathogenesis of the disease from a new point of view, which is of fundamental importance for the correction and selection of pathogenetic means of care.